CAD & Atherosclerosis

Mounting evidence supports that chronic environmental exposure to low levels of lead, cadmium, and arsenic contribute significantly to cardiovascular disease (CVD), the American Heart Association says in a new scientific statement.

“In reality, identifying a new type of cardiovascular risk factor leads to more questions than answers,” Gervasio A. Lamas, MD, chair of the statement writing group, said in an interview.

“For the most part, as cardiologists, we are used to risk factors we can manage with antihypertensives, statins, weight loss, exercise, and avoidance of smoking. Unfortunately, the ubiquity of toxic metals and their multiple sources increases the complexity of potential treatment,” said Dr. Lamas, chairman of medicine and chief of the Columbia University division of cardiology at Mount Sinai Medical Center in Miami Beach, Fla.

The statement addressing contaminant metals as CV risk factors was published online in the Journal of the American Heart Association.
 

Involuntary exposure harms the heart

Exposure to contaminant metals most often happens involuntarily through air, water, soil, and food, and extensive industrial and public use, the writing group notes.

These contaminant metals interfere with critical intracellular reactions and functions, leading to oxidative stress and chronic inflammation; this in turn leads to endothelial dysfunction, hypertension, epigenetic dysregulation, dyslipidemia, and changes in myocardial excitation and contractile function, the authors point out.

Lead, cadmium, and arsenic have been linked to subclinical atherosclerosis, coronary artery stenosis and calcification, as well as to an increased risk for ischemic heart disease and stroke, left ventricular hypertrophy, and heart failure and peripheral artery disease.

Epidemiologic studies show that exposure to lead, cadmium, or arsenic is associated with cardiovascular death mostly attributable to ischemic heart disease. In the United States alone, one study suggested that more than 450,000 deaths annually could be attributed to lead exposure.

“This is a global issue in which lower-income communities are disproportionately exposed to toxic metals through contaminated air, water, and soil,” Ana Navas-Acien, MD, PhD, vice chair of the statement writing group, said in a news release.

“Addressing metal exposure in these populations may provide a strategy to reduce cardiovascular disease disparities and advance environmental justice,” adds Dr. Navas-Acien, professor of environmental health sciences at Columbia University, New York.

Dr. Lamas said in an interview that the writing group is “hopeful that there will be a multilevel response” to publication of the scientific statement.

“On the societal level, we believe more effort can be made to measure these pollutants and protect the public. On the physician level, knowledge of metal levels could become part of the routine risk evaluation of the cardiac patient. On the individual level, patients can try to avoid these pollutants, by knowing arsenic levels of well-water, lead and cadmium levels of drinking water, avoiding tobacco and vaping, and using filters when available or necessary,” Dr. Lamas said.

“On the scientific level, identifying ubiquitous pollutants should spur scientists and pharmaceutical companies to develop preventive and therapeutic approaches.”

Finally, clinical trials should be encouraged to assess existing drugs that can remove these atherogenic toxins from the body or treat their ill effects. One such trial is expected to be completed within a year, Dr. Lamas added.

This scientific statement was prepared by the volunteer writing group on behalf of the AHA Council on Epidemiology and Prevention; the Council on Cardiovascular and Stroke Nursing; the Council on Lifestyle and Cardiometabolic Health; the Council on Peripheral Vascular Disease; and the Council on the Kidney in Cardiovascular Disease.
 

A version of this article originally appeared on Medscape.com.

Mounting evidence supports that chronic environmental exposure to low levels of lead, cadmium, and arsenic contribute significantly to cardiovascular disease (CVD), the American Heart Association says in a new scientific statement.

“In reality, identifying a new type of cardiovascular risk factor leads to more questions than answers,” Gervasio A. Lamas, MD, chair of the statement writing group, said in an interview.

“For the most part, as cardiologists, we are used to risk factors we can manage with antihypertensives, statins, weight loss, exercise, and avoidance of smoking. Unfortunately, the ubiquity of toxic metals and their multiple sources increases the complexity of potential treatment,” said Dr. Lamas, chairman of medicine and chief of the Columbia University division of cardiology at Mount Sinai Medical Center in Miami Beach, Fla.

The statement addressing contaminant metals as CV risk factors was published online in the Journal of the American Heart Association.
 

Involuntary exposure harms the heart

Exposure to contaminant metals most often happens involuntarily through air, water, soil, and food, and extensive industrial and public use, the writing group notes.

These contaminant metals interfere with critical intracellular reactions and functions, leading to oxidative stress and chronic inflammation; this in turn leads to endothelial dysfunction, hypertension, epigenetic dysregulation, dyslipidemia, and changes in myocardial excitation and contractile function, the authors point out.

Lead, cadmium, and arsenic have been linked to subclinical atherosclerosis, coronary artery stenosis and calcification, as well as to an increased risk for ischemic heart disease and stroke, left ventricular hypertrophy, and heart failure and peripheral artery disease.

Epidemiologic studies show that exposure to lead, cadmium, or arsenic is associated with cardiovascular death mostly attributable to ischemic heart disease. In the United States alone, one study suggested that more than 450,000 deaths annually could be attributed to lead exposure.

“This is a global issue in which lower-income communities are disproportionately exposed to toxic metals through contaminated air, water, and soil,” Ana Navas-Acien, MD, PhD, vice chair of the statement writing group, said in a news release.

“Addressing metal exposure in these populations may provide a strategy to reduce cardiovascular disease disparities and advance environmental justice,” adds Dr. Navas-Acien, professor of environmental health sciences at Columbia University, New York.

Dr. Lamas said in an interview that the writing group is “hopeful that there will be a multilevel response” to publication of the scientific statement.

“On the societal level, we believe more effort can be made to measure these pollutants and protect the public. On the physician level, knowledge of metal levels could become part of the routine risk evaluation of the cardiac patient. On the individual level, patients can try to avoid these pollutants, by knowing arsenic levels of well-water, lead and cadmium levels of drinking water, avoiding tobacco and vaping, and using filters when available or necessary,” Dr. Lamas said.

“On the scientific level, identifying ubiquitous pollutants should spur scientists and pharmaceutical companies to develop preventive and therapeutic approaches.”

Finally, clinical trials should be encouraged to assess existing drugs that can remove these atherogenic toxins from the body or treat their ill effects. One such trial is expected to be completed within a year, Dr. Lamas added.

This scientific statement was prepared by the volunteer writing group on behalf of the AHA Council on Epidemiology and Prevention; the Council on Cardiovascular and Stroke Nursing; the Council on Lifestyle and Cardiometabolic Health; the Council on Peripheral Vascular Disease; and the Council on the Kidney in Cardiovascular Disease.
 

A version of this article originally appeared on Medscape.com.

Mounting evidence supports that chronic environmental exposure to low levels of lead, cadmium, and arsenic contribute significantly to cardiovascular disease (CVD), the American Heart Association says in a new scientific statement.

“In reality, identifying a new type of cardiovascular risk factor leads to more questions than answers,” Gervasio A. Lamas, MD, chair of the statement writing group, said in an interview.

“For the most part, as cardiologists, we are used to risk factors we can manage with antihypertensives, statins, weight loss, exercise, and avoidance of smoking. Unfortunately, the ubiquity of toxic metals and their multiple sources increases the complexity of potential treatment,” said Dr. Lamas, chairman of medicine and chief of the Columbia University division of cardiology at Mount Sinai Medical Center in Miami Beach, Fla.

The statement addressing contaminant metals as CV risk factors was published online in the Journal of the American Heart Association.
 

Involuntary exposure harms the heart

Exposure to contaminant metals most often happens involuntarily through air, water, soil, and food, and extensive industrial and public use, the writing group notes.

These contaminant metals interfere with critical intracellular reactions and functions, leading to oxidative stress and chronic inflammation; this in turn leads to endothelial dysfunction, hypertension, epigenetic dysregulation, dyslipidemia, and changes in myocardial excitation and contractile function, the authors point out.

Lead, cadmium, and arsenic have been linked to subclinical atherosclerosis, coronary artery stenosis and calcification, as well as to an increased risk for ischemic heart disease and stroke, left ventricular hypertrophy, and heart failure and peripheral artery disease.

Epidemiologic studies show that exposure to lead, cadmium, or arsenic is associated with cardiovascular death mostly attributable to ischemic heart disease. In the United States alone, one study suggested that more than 450,000 deaths annually could be attributed to lead exposure.

“This is a global issue in which lower-income communities are disproportionately exposed to toxic metals through contaminated air, water, and soil,” Ana Navas-Acien, MD, PhD, vice chair of the statement writing group, said in a news release.

“Addressing metal exposure in these populations may provide a strategy to reduce cardiovascular disease disparities and advance environmental justice,” adds Dr. Navas-Acien, professor of environmental health sciences at Columbia University, New York.

Dr. Lamas said in an interview that the writing group is “hopeful that there will be a multilevel response” to publication of the scientific statement.

“On the societal level, we believe more effort can be made to measure these pollutants and protect the public. On the physician level, knowledge of metal levels could become part of the routine risk evaluation of the cardiac patient. On the individual level, patients can try to avoid these pollutants, by knowing arsenic levels of well-water, lead and cadmium levels of drinking water, avoiding tobacco and vaping, and using filters when available or necessary,” Dr. Lamas said.

“On the scientific level, identifying ubiquitous pollutants should spur scientists and pharmaceutical companies to develop preventive and therapeutic approaches.”

Finally, clinical trials should be encouraged to assess existing drugs that can remove these atherogenic toxins from the body or treat their ill effects. One such trial is expected to be completed within a year, Dr. Lamas added.

This scientific statement was prepared by the volunteer writing group on behalf of the AHA Council on Epidemiology and Prevention; the Council on Cardiovascular and Stroke Nursing; the Council on Lifestyle and Cardiometabolic Health; the Council on Peripheral Vascular Disease; and the Council on the Kidney in Cardiovascular Disease.
 

A version of this article originally appeared on Medscape.com.

MANNHEIM, GERMANY – Patients with high lipoprotein(a) (Lp[a]) levels not only have an almost twofold higher coronary plaque burden than those with low levels but also a faster rate of plaque progression, an observational imaging study shows.

This could explain the greater risk for major adverse cardiovascular events seen in patients with high Lp(a) levels, suggests the research, presented during the annual European Atherosclerosis Society Congress.

The team performed follow-up coronary CT angiography (CCTA) on almost 275 patients who had undergone imaging approximately 10 years earlier, finding that almost one-third had high Lp(a) levels.

At baseline, per cent plaque volumes were 1.8 times greater in high Lp(a) patients versus those with low levels of the protein. After 10 years, plaque volumes were 3.3 times larger in patients with high Lp(a) levels.

Over this period, the rate of increase of plaque volume was 1.9 times greater in patients with high Lp(a) levels.

Study presenter Nick S. Nurmohamed, MD, PhD candidate, department of vascular medicine, Amsterdam University Medical Centers, also showed that high Lp(a) levels were associated with a 2.1-fold increase in rates of MACE.

He said in an interview that this finding could be related to Lp(a) increasing inflammatory signaling in the plaque, “making it more prone to rupture, and we saw that on the CCTA scans,” where high Lp(a) levels were associated with the presence of more high-risk plaques.

He added that in the absence of drugs that target Lp(a) levels directly, the results underline the need to focus on other means of lipid-lowering, as well as “creating awareness that Lp(a) is associated with plaque formation.”

Dr. Nurmohamed said that “for the moment, we have to treat patients with high Lp(a) with other risk-lowering therapies, such as low-density lipoprotein [LDL] cholesterol–lowering drugs, and the management of other risk factors.”

However, he noted that “there are a couple of Lp(a)-lowering medications in trials,” with results expected in the next 2-3 years.

“Then we will have the means to treat those patients, and with CCTA we can identify the patients with the biggest risk,” Dr. Nurmohamed added.
 

Plaque burden

Philippe Moulin, MD, PhD, head of endocrinology and professor of human nutrition at Faculté Lyon Est, Claude Bernard Lyon (France) 1 University, said that the association between Lp(a) and plaque burden has been seen previously in the literature in a very similar study but with only 1-year follow-up.

Similarly, registry data have suggested that Lp(a) is associated with worsening plaque progression over time.

“Here, with 10-year follow-up, [the study] is much more interesting,” due to its greater statistical power, he said in an interview. It is also “well-documented” and uses an “appropriate” methodology.

But Dr. Moulin underlined that the number of patients with high Lp(a) levels included in the study is relatively small.

Consequently, the researchers were not able to look at the level and rate of progression of atherosclerosis between different quartiles of Lp(a), “so you have no dose-response analysis.”

It also does not “establish causality,” as it remains an observational study, despite being longitudinal, “well done, and so on.”

Dr. Moulin added that the study nevertheless adds “one more stone” to the construct of the idea of high risk around high Lp(a) levels, and “prepares the ground” for the availability of two drugs to decrease Lp(a) levels, expected in 2026 and 2027.

These are expected to substantially reduce Lp(a) levels and achieve a reduction in cardiovascular risk of around 20%-40%, “which would be interesting,” especially as “we have patients who have Lp(a) levels four times above the upper normal value.”

Crucially, they may already have normal LDL cholesterol levels, meaning that, for some patients, “there is clearly a need for such treatment, as long as it is proven that it will decrease cardiovascular risk.”

For the moment, however, the strategy for managing patients with high Lp(a) remains to increase the dose of statin and to have more stringent targets, although Dr. Moulin pointed out that, “when you give statins, you raise slightly Lp(a) levels.”

Dr. Nurmohamed said in an interview that “we know from largely genetic and observational studies that Lp(a) is causally associated with atherosclerotic cardiovascular disease.”

What is less clear is the exact underlying mechanism, he said, noting that there have been several imaging studies in high and low Lp(a) patients that have yielded conflicting results in terms of the relationship with plaque burden.

To investigate the impact of Lp(a) levels on long-term coronary plaque progression, the team invited patients who had taken part in a previous CCTA study to undergo repeat CCTA, regardless of their underlying symptoms.

In all, 299 patients underwent follow-up imaging a median of 10.2 years after their original scan. Plaque volumes were quantified and adjusted for vessel volumes, and the patients were classified as having high (≥ 70 nmol/L) or low (< 70 nmol/L) Lp(a) levels.

After excluding patients who had undergone coronary artery bypass grafting, the team analyzed 274 patients with a mean age at baseline of 57 years. Of these, 159 (58%) were men. High Lp(a) levels were identified in 87 (32%) patients.

The team found that at baseline, patients with high Lp(a) levels had significantly larger percent atheroma volumes than those with low levels, at 3.92% versus 2.17%, or an absolute difference of 1.75% (P = .013).

The difference between the two groups was even greater at the follow-up, when percent atheroma volumes reached 8.75% in patients with high Lp(a) levels versus 3.90% for those with low levels, or an absolute difference of 4.85% (P = .005).

Similar findings were seen when looking separately at percentage of noncalcified and calcified plaque volumes as well as when analyzing for the presence of low-density plaques.

Multivariate analysis taking into account clinical risk factors, statin use, and CT tube voltage found that high Lp(a) levels were associated with a greater percent atheroma volume at baseline, at an odds ratio versus low Lp(a) of 1.83 (95% confidence interval, 0.12-3.54; P = .037).

High Lp(a) levels were also linked to a larger percent atheroma volume on follow-up imaging, at an odds ratio of 3.25 (95% CI, 0.80-5.71; P = .010), and a significantly greater change in atheroma volume from baseline to follow-up imaging, at an odds ratio of 1.86 (95% CI, 0.59-3.14; P = .005)

Finally, the team showed that, after adjusting for clinical risk factors, high baseline Lp(a) levels were associated with an increased risk of MACE during the follow-up period, at a hazard ratio versus low Lp(a) levels of 2.10 (95% CI, 1.01-4.29, P = .048).

No funding was declared. Dr. Nurmohamed is cofounder of Lipid Tools. Other authors declare relationships with Amgen, Novartis, Esperion, Sanofi-Regeneron, Ackee, Cleerly, GW Heart and Vascular Institute, Siemens Healthineers, and HeartFlow.

A version of this article first appeared on Medscape.com.

MANNHEIM, GERMANY – Patients with high lipoprotein(a) (Lp[a]) levels not only have an almost twofold higher coronary plaque burden than those with low levels but also a faster rate of plaque progression, an observational imaging study shows.

This could explain the greater risk for major adverse cardiovascular events seen in patients with high Lp(a) levels, suggests the research, presented during the annual European Atherosclerosis Society Congress.

The team performed follow-up coronary CT angiography (CCTA) on almost 275 patients who had undergone imaging approximately 10 years earlier, finding that almost one-third had high Lp(a) levels.

At baseline, per cent plaque volumes were 1.8 times greater in high Lp(a) patients versus those with low levels of the protein. After 10 years, plaque volumes were 3.3 times larger in patients with high Lp(a) levels.

Over this period, the rate of increase of plaque volume was 1.9 times greater in patients with high Lp(a) levels.

Study presenter Nick S. Nurmohamed, MD, PhD candidate, department of vascular medicine, Amsterdam University Medical Centers, also showed that high Lp(a) levels were associated with a 2.1-fold increase in rates of MACE.

He said in an interview that this finding could be related to Lp(a) increasing inflammatory signaling in the plaque, “making it more prone to rupture, and we saw that on the CCTA scans,” where high Lp(a) levels were associated with the presence of more high-risk plaques.

He added that in the absence of drugs that target Lp(a) levels directly, the results underline the need to focus on other means of lipid-lowering, as well as “creating awareness that Lp(a) is associated with plaque formation.”

Dr. Nurmohamed said that “for the moment, we have to treat patients with high Lp(a) with other risk-lowering therapies, such as low-density lipoprotein [LDL] cholesterol–lowering drugs, and the management of other risk factors.”

However, he noted that “there are a couple of Lp(a)-lowering medications in trials,” with results expected in the next 2-3 years.

“Then we will have the means to treat those patients, and with CCTA we can identify the patients with the biggest risk,” Dr. Nurmohamed added.
 

Plaque burden

Philippe Moulin, MD, PhD, head of endocrinology and professor of human nutrition at Faculté Lyon Est, Claude Bernard Lyon (France) 1 University, said that the association between Lp(a) and plaque burden has been seen previously in the literature in a very similar study but with only 1-year follow-up.

Similarly, registry data have suggested that Lp(a) is associated with worsening plaque progression over time.

“Here, with 10-year follow-up, [the study] is much more interesting,” due to its greater statistical power, he said in an interview. It is also “well-documented” and uses an “appropriate” methodology.

But Dr. Moulin underlined that the number of patients with high Lp(a) levels included in the study is relatively small.

Consequently, the researchers were not able to look at the level and rate of progression of atherosclerosis between different quartiles of Lp(a), “so you have no dose-response analysis.”

It also does not “establish causality,” as it remains an observational study, despite being longitudinal, “well done, and so on.”

Dr. Moulin added that the study nevertheless adds “one more stone” to the construct of the idea of high risk around high Lp(a) levels, and “prepares the ground” for the availability of two drugs to decrease Lp(a) levels, expected in 2026 and 2027.

These are expected to substantially reduce Lp(a) levels and achieve a reduction in cardiovascular risk of around 20%-40%, “which would be interesting,” especially as “we have patients who have Lp(a) levels four times above the upper normal value.”

Crucially, they may already have normal LDL cholesterol levels, meaning that, for some patients, “there is clearly a need for such treatment, as long as it is proven that it will decrease cardiovascular risk.”

For the moment, however, the strategy for managing patients with high Lp(a) remains to increase the dose of statin and to have more stringent targets, although Dr. Moulin pointed out that, “when you give statins, you raise slightly Lp(a) levels.”

Dr. Nurmohamed said in an interview that “we know from largely genetic and observational studies that Lp(a) is causally associated with atherosclerotic cardiovascular disease.”

What is less clear is the exact underlying mechanism, he said, noting that there have been several imaging studies in high and low Lp(a) patients that have yielded conflicting results in terms of the relationship with plaque burden.

To investigate the impact of Lp(a) levels on long-term coronary plaque progression, the team invited patients who had taken part in a previous CCTA study to undergo repeat CCTA, regardless of their underlying symptoms.

In all, 299 patients underwent follow-up imaging a median of 10.2 years after their original scan. Plaque volumes were quantified and adjusted for vessel volumes, and the patients were classified as having high (≥ 70 nmol/L) or low (< 70 nmol/L) Lp(a) levels.

After excluding patients who had undergone coronary artery bypass grafting, the team analyzed 274 patients with a mean age at baseline of 57 years. Of these, 159 (58%) were men. High Lp(a) levels were identified in 87 (32%) patients.

The team found that at baseline, patients with high Lp(a) levels had significantly larger percent atheroma volumes than those with low levels, at 3.92% versus 2.17%, or an absolute difference of 1.75% (P = .013).

The difference between the two groups was even greater at the follow-up, when percent atheroma volumes reached 8.75% in patients with high Lp(a) levels versus 3.90% for those with low levels, or an absolute difference of 4.85% (P = .005).

Similar findings were seen when looking separately at percentage of noncalcified and calcified plaque volumes as well as when analyzing for the presence of low-density plaques.

Multivariate analysis taking into account clinical risk factors, statin use, and CT tube voltage found that high Lp(a) levels were associated with a greater percent atheroma volume at baseline, at an odds ratio versus low Lp(a) of 1.83 (95% confidence interval, 0.12-3.54; P = .037).

High Lp(a) levels were also linked to a larger percent atheroma volume on follow-up imaging, at an odds ratio of 3.25 (95% CI, 0.80-5.71; P = .010), and a significantly greater change in atheroma volume from baseline to follow-up imaging, at an odds ratio of 1.86 (95% CI, 0.59-3.14; P = .005)

Finally, the team showed that, after adjusting for clinical risk factors, high baseline Lp(a) levels were associated with an increased risk of MACE during the follow-up period, at a hazard ratio versus low Lp(a) levels of 2.10 (95% CI, 1.01-4.29, P = .048).

No funding was declared. Dr. Nurmohamed is cofounder of Lipid Tools. Other authors declare relationships with Amgen, Novartis, Esperion, Sanofi-Regeneron, Ackee, Cleerly, GW Heart and Vascular Institute, Siemens Healthineers, and HeartFlow.

A version of this article first appeared on Medscape.com.

MANNHEIM, GERMANY – Patients with high lipoprotein(a) (Lp[a]) levels not only have an almost twofold higher coronary plaque burden than those with low levels but also a faster rate of plaque progression, an observational imaging study shows.

This could explain the greater risk for major adverse cardiovascular events seen in patients with high Lp(a) levels, suggests the research, presented during the annual European Atherosclerosis Society Congress.

The team performed follow-up coronary CT angiography (CCTA) on almost 275 patients who had undergone imaging approximately 10 years earlier, finding that almost one-third had high Lp(a) levels.

At baseline, per cent plaque volumes were 1.8 times greater in high Lp(a) patients versus those with low levels of the protein. After 10 years, plaque volumes were 3.3 times larger in patients with high Lp(a) levels.

Over this period, the rate of increase of plaque volume was 1.9 times greater in patients with high Lp(a) levels.

Study presenter Nick S. Nurmohamed, MD, PhD candidate, department of vascular medicine, Amsterdam University Medical Centers, also showed that high Lp(a) levels were associated with a 2.1-fold increase in rates of MACE.

He said in an interview that this finding could be related to Lp(a) increasing inflammatory signaling in the plaque, “making it more prone to rupture, and we saw that on the CCTA scans,” where high Lp(a) levels were associated with the presence of more high-risk plaques.

He added that in the absence of drugs that target Lp(a) levels directly, the results underline the need to focus on other means of lipid-lowering, as well as “creating awareness that Lp(a) is associated with plaque formation.”

Dr. Nurmohamed said that “for the moment, we have to treat patients with high Lp(a) with other risk-lowering therapies, such as low-density lipoprotein [LDL] cholesterol–lowering drugs, and the management of other risk factors.”

However, he noted that “there are a couple of Lp(a)-lowering medications in trials,” with results expected in the next 2-3 years.

“Then we will have the means to treat those patients, and with CCTA we can identify the patients with the biggest risk,” Dr. Nurmohamed added.
 

Plaque burden

Philippe Moulin, MD, PhD, head of endocrinology and professor of human nutrition at Faculté Lyon Est, Claude Bernard Lyon (France) 1 University, said that the association between Lp(a) and plaque burden has been seen previously in the literature in a very similar study but with only 1-year follow-up.

Similarly, registry data have suggested that Lp(a) is associated with worsening plaque progression over time.

“Here, with 10-year follow-up, [the study] is much more interesting,” due to its greater statistical power, he said in an interview. It is also “well-documented” and uses an “appropriate” methodology.

But Dr. Moulin underlined that the number of patients with high Lp(a) levels included in the study is relatively small.

Consequently, the researchers were not able to look at the level and rate of progression of atherosclerosis between different quartiles of Lp(a), “so you have no dose-response analysis.”

It also does not “establish causality,” as it remains an observational study, despite being longitudinal, “well done, and so on.”

Dr. Moulin added that the study nevertheless adds “one more stone” to the construct of the idea of high risk around high Lp(a) levels, and “prepares the ground” for the availability of two drugs to decrease Lp(a) levels, expected in 2026 and 2027.

These are expected to substantially reduce Lp(a) levels and achieve a reduction in cardiovascular risk of around 20%-40%, “which would be interesting,” especially as “we have patients who have Lp(a) levels four times above the upper normal value.”

Crucially, they may already have normal LDL cholesterol levels, meaning that, for some patients, “there is clearly a need for such treatment, as long as it is proven that it will decrease cardiovascular risk.”

For the moment, however, the strategy for managing patients with high Lp(a) remains to increase the dose of statin and to have more stringent targets, although Dr. Moulin pointed out that, “when you give statins, you raise slightly Lp(a) levels.”

Dr. Nurmohamed said in an interview that “we know from largely genetic and observational studies that Lp(a) is causally associated with atherosclerotic cardiovascular disease.”

What is less clear is the exact underlying mechanism, he said, noting that there have been several imaging studies in high and low Lp(a) patients that have yielded conflicting results in terms of the relationship with plaque burden.

To investigate the impact of Lp(a) levels on long-term coronary plaque progression, the team invited patients who had taken part in a previous CCTA study to undergo repeat CCTA, regardless of their underlying symptoms.

In all, 299 patients underwent follow-up imaging a median of 10.2 years after their original scan. Plaque volumes were quantified and adjusted for vessel volumes, and the patients were classified as having high (≥ 70 nmol/L) or low (< 70 nmol/L) Lp(a) levels.

After excluding patients who had undergone coronary artery bypass grafting, the team analyzed 274 patients with a mean age at baseline of 57 years. Of these, 159 (58%) were men. High Lp(a) levels were identified in 87 (32%) patients.

The team found that at baseline, patients with high Lp(a) levels had significantly larger percent atheroma volumes than those with low levels, at 3.92% versus 2.17%, or an absolute difference of 1.75% (P = .013).

The difference between the two groups was even greater at the follow-up, when percent atheroma volumes reached 8.75% in patients with high Lp(a) levels versus 3.90% for those with low levels, or an absolute difference of 4.85% (P = .005).

Similar findings were seen when looking separately at percentage of noncalcified and calcified plaque volumes as well as when analyzing for the presence of low-density plaques.

Multivariate analysis taking into account clinical risk factors, statin use, and CT tube voltage found that high Lp(a) levels were associated with a greater percent atheroma volume at baseline, at an odds ratio versus low Lp(a) of 1.83 (95% confidence interval, 0.12-3.54; P = .037).

High Lp(a) levels were also linked to a larger percent atheroma volume on follow-up imaging, at an odds ratio of 3.25 (95% CI, 0.80-5.71; P = .010), and a significantly greater change in atheroma volume from baseline to follow-up imaging, at an odds ratio of 1.86 (95% CI, 0.59-3.14; P = .005)

Finally, the team showed that, after adjusting for clinical risk factors, high baseline Lp(a) levels were associated with an increased risk of MACE during the follow-up period, at a hazard ratio versus low Lp(a) levels of 2.10 (95% CI, 1.01-4.29, P = .048).

No funding was declared. Dr. Nurmohamed is cofounder of Lipid Tools. Other authors declare relationships with Amgen, Novartis, Esperion, Sanofi-Regeneron, Ackee, Cleerly, GW Heart and Vascular Institute, Siemens Healthineers, and HeartFlow.

A version of this article first appeared on Medscape.com.

Nearly one in five U.S. adults with type 2 diabetes but without symptoms of cardiovascular disease (CVD) have a clinically meaningful elevation of a marker of cardiac damage – namely, high-sensitivity cardiac troponin T (hs-cTnT) – based on data from a representative sample of more than 10,000 U.S. adults.

The finding suggests hs-cTnT maybe a useful marker for adults with diabetes who could benefit from more aggressive CVD risk reduction despite having no clinical indications of CVD.

The results “highlight the substantial burden of subclinical CVD in persons with diabetes and emphasize the importance of early detection and treatment of CVD for this high-risk population,” say the authors of the research, published in the Journal of the American Heart Association.

Johns Hopkins University

“This is the first study to examine subclinical CVD, defined by elevated cardiac biomarkers, in a nationally representative population of adults with or without diabetes. It provides novel information on the high burden of subclinical CVD [in American adults with diabetes] and the potential utility of hs-cTnT for monitoring this risk in people with diabetes,” said Elizabeth Selvin, PhD, senior author and a professor of epidemiology at Johns Hopkins University, Baltimore.

“What we are seeing is that many people with type 2 diabetes who have not had a heart attack or a history of cardiovascular disease are at high risk for cardiovascular complications,” added Dr. Selvin in an AHA press release. “When we look at the whole population of people diagnosed with type 2 diabetes, about 27 million adults in the U.S., according to the [Centers for Disease Control and Prevention], some are at low risk and some are at high risk for cardiovascular disease, so the open question is: ‘Who is most at risk?’ These cardiac biomarkers give us a window into cardiovascular risk in people who otherwise might not be recognized as highest risk.”

“Our results provide evidence to support use of cardiac biomarkers for routine risk monitoring in high-risk populations such as people with diabetes,” Dr. Selvin noted in an interview.
 

Need for aggressive CVD risk reduction

The findings also indicate that people with diabetes and an elevated hs-cTnT “should be targeted for aggressive cardiovascular risk reduction, including lifestyle interventions, weight loss, and treatment with statins, blood pressure medications, and cardioprotective therapies such as sodium-glucose cotransporter 2 (SGLT-2) inhibitors and glucagonlike peptide-1 (GLP-1) receptor agonists,” Dr. Selvin added.

“Cholesterol is often the factor that we target to reduce the risk of cardiovascular disease in people with type 2 diabetes,” she observed. “However, type 2 diabetes may have a direct effect on the heart not related to cholesterol levels. If type 2 diabetes is directly causing damage to the small vessels in the heart unrelated to cholesterol plaque buildup, then cholesterol-lowering medications are not going to prevent cardiac damage,” Dr. Selvin explained. “Our research suggests that additional non–statin-related therapies are needed to lower the cardiovascular disease risk in people with type 2 diabetes.”

However, she noted that a necessary step prior to formally recommending such a strategy is to run clinical trials to assess the efficacy of specific treatments, such as SGLT-2 inhibitors and GLP-1 agonists, in people with diabetes and elevated hs-cTnT.

“Randomized controlled trials would be best to test the relevance of measuring these biomarkers to assess risk in asymptomatic people with diabetes,” as well as prospective study of the value of hs-cTnT to guide treatment, commented Robert H. Eckel, MD, an endocrinologist affiliated with the University of Colorado at Denver, Aurora.

“I doubt measurements [of hs-cTnT] would be reimbursed [by third-party payers] if carried out without such outcome data,” he added.

Dr. Eckel also highlights the need to further validate in additional cohorts the link between elevations in hs-cTnT and CVD events in adults with diabetes, and to confirm that elevated levels of another cardiac biomarker – N-terminal of the prohormone brain natriuretic peptide (NT-proBNP) – do not work as well as troponin as a risk marker for people with diabetes, another finding of the study.
 

ADA report already recommends testing these biomarkers for HF

However, a consensus report published in 2022 by the American Diabetes Association laid out the case for routinely and regularly measuring levels of both high sensitivity cardiac troponin and natriuretic peptides in people with diabetes for early identification of incident heart failure.

“Among individuals with diabetes, measurement of a natriuretic peptide or high-sensitivity cardiac troponin is recommended on at least a yearly basis to identify the earliest heart failure stages and implement strategies to prevent transition to symptomatic heart failure,” noted the ADA consensus report on heart failure.

The new study run by Dr. Selvin and coauthors used data collected by the National Health and Nutrition Examination Survey (NHANES) between 1999 and 2004 from U.S. adults who were at least 20 years old and had no history of CVD: myocardial infarction, stroke, coronary heart disease, or heart failure. This included 9,273 people without diabetes and 1,031 with diabetes, defined as a prior diagnosis or hemoglobin A1c of at least 6.5%.

“Cardiovascular risk varies substantially in adults with type 2 diabetes, highlighting the need for accurate risk stratification,” the authors observed.

All study participants had recorded measures of hs-cTnT and NT-proBNP.

The researchers considered an hs-cTnT level of greater than 14 ng/L and an NT-proBNP level of greater than 125 pg/mL as indicators of subclinical CVD.

The crude prevalence of elevated NT-proBNP was 33.4% among those with diabetes and 16.1% in those without diabetes. Elevated hs-cTnT occurred in 19% of those with diabetes and in 5% of those without diabetes. Elevated levels of both markers existed in 9% of those with diabetes and in 3% of those without diabetes.

“Approximately one in three adults with diabetes had subclinical CVD, with 19% having elevated levels of hs-cTnT, 23% having elevated NT-proBNP, and 9% having elevations in both cardiac biomarkers,” the researchers noted.
 

Diabetes linked with a doubled prevalence of elevated hs-cTnT 

After adjustment for several demographic variables as well as traditional CVD risk factors, people with diabetes had a significant 98% higher rate of elevated hs-cTnT, compared with those without diabetes. But after similar adjustments, the rate of elevated NT-proBNP was significantly lower among people with diabetes, compared with controls, by a relative reduction of 24%.

“Our findings suggest that, in people with diabetes, hs-cTnT may be more useful [than NT-proBNP] for general risk monitoring, as its interpretation is less complicated,” said Dr. Selvin, who explained that “NT-proBNP is affected by overweight and obesity.”

In people with diabetes, the age-adjusted prevalence of elevated hs-cTnT ran higher in those with longer duration diabetes, and in those with less well-controlled diabetes based on a higher level of A1c. Neither of these factors showed any significant relationship with measured levels of NT-proBNP.

Further analysis linked the NHANES findings during 1999-2004 with U.S. national death records through the end of 2019. This showed that elevated levels of both hs-cTnT and NT-proBNP significantly linked with subsequently higher rates of all-cause mortality among people with diabetes. Elevated hs-cTnT linked with a 77% increased mortality and NT-proBNP linked with a 78% increased rate, compared with people with diabetes and no elevations in these markers, after adjustment for demographic variables and CVD risk factors.

However, for the outcome of cardiovascular death, elevated hs-cTnT linked with a nonsignificant 54% relative increase, while elevated NT-proBNP linked with a significant 2.46-fold relative increase.

The study “adds new data on biomarkers that are not routinely measured in asymptomatic people with or without diabetes” and the relationships of these markers to CVD mortality and all-cause mortality, Dr. Eckel concluded.

The study received no commercial funding, but used reagents donated by Abbott Laboratories, Ortho Clinical Diagnostics, Roche Diagnostics, and Siemens Healthcare Diagnostics. Dr. Selvin and Dr. Eckel had no disclosures.

A version of this article first appeared on Medscape.com.

Nearly one in five U.S. adults with type 2 diabetes but without symptoms of cardiovascular disease (CVD) have a clinically meaningful elevation of a marker of cardiac damage – namely, high-sensitivity cardiac troponin T (hs-cTnT) – based on data from a representative sample of more than 10,000 U.S. adults.

The finding suggests hs-cTnT maybe a useful marker for adults with diabetes who could benefit from more aggressive CVD risk reduction despite having no clinical indications of CVD.

The results “highlight the substantial burden of subclinical CVD in persons with diabetes and emphasize the importance of early detection and treatment of CVD for this high-risk population,” say the authors of the research, published in the Journal of the American Heart Association.

Johns Hopkins University

“This is the first study to examine subclinical CVD, defined by elevated cardiac biomarkers, in a nationally representative population of adults with or without diabetes. It provides novel information on the high burden of subclinical CVD [in American adults with diabetes] and the potential utility of hs-cTnT for monitoring this risk in people with diabetes,” said Elizabeth Selvin, PhD, senior author and a professor of epidemiology at Johns Hopkins University, Baltimore.

“What we are seeing is that many people with type 2 diabetes who have not had a heart attack or a history of cardiovascular disease are at high risk for cardiovascular complications,” added Dr. Selvin in an AHA press release. “When we look at the whole population of people diagnosed with type 2 diabetes, about 27 million adults in the U.S., according to the [Centers for Disease Control and Prevention], some are at low risk and some are at high risk for cardiovascular disease, so the open question is: ‘Who is most at risk?’ These cardiac biomarkers give us a window into cardiovascular risk in people who otherwise might not be recognized as highest risk.”

“Our results provide evidence to support use of cardiac biomarkers for routine risk monitoring in high-risk populations such as people with diabetes,” Dr. Selvin noted in an interview.
 

Need for aggressive CVD risk reduction

The findings also indicate that people with diabetes and an elevated hs-cTnT “should be targeted for aggressive cardiovascular risk reduction, including lifestyle interventions, weight loss, and treatment with statins, blood pressure medications, and cardioprotective therapies such as sodium-glucose cotransporter 2 (SGLT-2) inhibitors and glucagonlike peptide-1 (GLP-1) receptor agonists,” Dr. Selvin added.

“Cholesterol is often the factor that we target to reduce the risk of cardiovascular disease in people with type 2 diabetes,” she observed. “However, type 2 diabetes may have a direct effect on the heart not related to cholesterol levels. If type 2 diabetes is directly causing damage to the small vessels in the heart unrelated to cholesterol plaque buildup, then cholesterol-lowering medications are not going to prevent cardiac damage,” Dr. Selvin explained. “Our research suggests that additional non–statin-related therapies are needed to lower the cardiovascular disease risk in people with type 2 diabetes.”

However, she noted that a necessary step prior to formally recommending such a strategy is to run clinical trials to assess the efficacy of specific treatments, such as SGLT-2 inhibitors and GLP-1 agonists, in people with diabetes and elevated hs-cTnT.

“Randomized controlled trials would be best to test the relevance of measuring these biomarkers to assess risk in asymptomatic people with diabetes,” as well as prospective study of the value of hs-cTnT to guide treatment, commented Robert H. Eckel, MD, an endocrinologist affiliated with the University of Colorado at Denver, Aurora.

“I doubt measurements [of hs-cTnT] would be reimbursed [by third-party payers] if carried out without such outcome data,” he added.

Dr. Eckel also highlights the need to further validate in additional cohorts the link between elevations in hs-cTnT and CVD events in adults with diabetes, and to confirm that elevated levels of another cardiac biomarker – N-terminal of the prohormone brain natriuretic peptide (NT-proBNP) – do not work as well as troponin as a risk marker for people with diabetes, another finding of the study.
 

ADA report already recommends testing these biomarkers for HF

However, a consensus report published in 2022 by the American Diabetes Association laid out the case for routinely and regularly measuring levels of both high sensitivity cardiac troponin and natriuretic peptides in people with diabetes for early identification of incident heart failure.

“Among individuals with diabetes, measurement of a natriuretic peptide or high-sensitivity cardiac troponin is recommended on at least a yearly basis to identify the earliest heart failure stages and implement strategies to prevent transition to symptomatic heart failure,” noted the ADA consensus report on heart failure.

The new study run by Dr. Selvin and coauthors used data collected by the National Health and Nutrition Examination Survey (NHANES) between 1999 and 2004 from U.S. adults who were at least 20 years old and had no history of CVD: myocardial infarction, stroke, coronary heart disease, or heart failure. This included 9,273 people without diabetes and 1,031 with diabetes, defined as a prior diagnosis or hemoglobin A1c of at least 6.5%.

“Cardiovascular risk varies substantially in adults with type 2 diabetes, highlighting the need for accurate risk stratification,” the authors observed.

All study participants had recorded measures of hs-cTnT and NT-proBNP.

The researchers considered an hs-cTnT level of greater than 14 ng/L and an NT-proBNP level of greater than 125 pg/mL as indicators of subclinical CVD.

The crude prevalence of elevated NT-proBNP was 33.4% among those with diabetes and 16.1% in those without diabetes. Elevated hs-cTnT occurred in 19% of those with diabetes and in 5% of those without diabetes. Elevated levels of both markers existed in 9% of those with diabetes and in 3% of those without diabetes.

“Approximately one in three adults with diabetes had subclinical CVD, with 19% having elevated levels of hs-cTnT, 23% having elevated NT-proBNP, and 9% having elevations in both cardiac biomarkers,” the researchers noted.
 

Diabetes linked with a doubled prevalence of elevated hs-cTnT 

After adjustment for several demographic variables as well as traditional CVD risk factors, people with diabetes had a significant 98% higher rate of elevated hs-cTnT, compared with those without diabetes. But after similar adjustments, the rate of elevated NT-proBNP was significantly lower among people with diabetes, compared with controls, by a relative reduction of 24%.

“Our findings suggest that, in people with diabetes, hs-cTnT may be more useful [than NT-proBNP] for general risk monitoring, as its interpretation is less complicated,” said Dr. Selvin, who explained that “NT-proBNP is affected by overweight and obesity.”

In people with diabetes, the age-adjusted prevalence of elevated hs-cTnT ran higher in those with longer duration diabetes, and in those with less well-controlled diabetes based on a higher level of A1c. Neither of these factors showed any significant relationship with measured levels of NT-proBNP.

Further analysis linked the NHANES findings during 1999-2004 with U.S. national death records through the end of 2019. This showed that elevated levels of both hs-cTnT and NT-proBNP significantly linked with subsequently higher rates of all-cause mortality among people with diabetes. Elevated hs-cTnT linked with a 77% increased mortality and NT-proBNP linked with a 78% increased rate, compared with people with diabetes and no elevations in these markers, after adjustment for demographic variables and CVD risk factors.

However, for the outcome of cardiovascular death, elevated hs-cTnT linked with a nonsignificant 54% relative increase, while elevated NT-proBNP linked with a significant 2.46-fold relative increase.

The study “adds new data on biomarkers that are not routinely measured in asymptomatic people with or without diabetes” and the relationships of these markers to CVD mortality and all-cause mortality, Dr. Eckel concluded.

The study received no commercial funding, but used reagents donated by Abbott Laboratories, Ortho Clinical Diagnostics, Roche Diagnostics, and Siemens Healthcare Diagnostics. Dr. Selvin and Dr. Eckel had no disclosures.

A version of this article first appeared on Medscape.com.

Nearly one in five U.S. adults with type 2 diabetes but without symptoms of cardiovascular disease (CVD) have a clinically meaningful elevation of a marker of cardiac damage – namely, high-sensitivity cardiac troponin T (hs-cTnT) – based on data from a representative sample of more than 10,000 U.S. adults.

The finding suggests hs-cTnT maybe a useful marker for adults with diabetes who could benefit from more aggressive CVD risk reduction despite having no clinical indications of CVD.

The results “highlight the substantial burden of subclinical CVD in persons with diabetes and emphasize the importance of early detection and treatment of CVD for this high-risk population,” say the authors of the research, published in the Journal of the American Heart Association.

Johns Hopkins University

“This is the first study to examine subclinical CVD, defined by elevated cardiac biomarkers, in a nationally representative population of adults with or without diabetes. It provides novel information on the high burden of subclinical CVD [in American adults with diabetes] and the potential utility of hs-cTnT for monitoring this risk in people with diabetes,” said Elizabeth Selvin, PhD, senior author and a professor of epidemiology at Johns Hopkins University, Baltimore.

“What we are seeing is that many people with type 2 diabetes who have not had a heart attack or a history of cardiovascular disease are at high risk for cardiovascular complications,” added Dr. Selvin in an AHA press release. “When we look at the whole population of people diagnosed with type 2 diabetes, about 27 million adults in the U.S., according to the [Centers for Disease Control and Prevention], some are at low risk and some are at high risk for cardiovascular disease, so the open question is: ‘Who is most at risk?’ These cardiac biomarkers give us a window into cardiovascular risk in people who otherwise might not be recognized as highest risk.”

“Our results provide evidence to support use of cardiac biomarkers for routine risk monitoring in high-risk populations such as people with diabetes,” Dr. Selvin noted in an interview.
 

Need for aggressive CVD risk reduction

The findings also indicate that people with diabetes and an elevated hs-cTnT “should be targeted for aggressive cardiovascular risk reduction, including lifestyle interventions, weight loss, and treatment with statins, blood pressure medications, and cardioprotective therapies such as sodium-glucose cotransporter 2 (SGLT-2) inhibitors and glucagonlike peptide-1 (GLP-1) receptor agonists,” Dr. Selvin added.

“Cholesterol is often the factor that we target to reduce the risk of cardiovascular disease in people with type 2 diabetes,” she observed. “However, type 2 diabetes may have a direct effect on the heart not related to cholesterol levels. If type 2 diabetes is directly causing damage to the small vessels in the heart unrelated to cholesterol plaque buildup, then cholesterol-lowering medications are not going to prevent cardiac damage,” Dr. Selvin explained. “Our research suggests that additional non–statin-related therapies are needed to lower the cardiovascular disease risk in people with type 2 diabetes.”

However, she noted that a necessary step prior to formally recommending such a strategy is to run clinical trials to assess the efficacy of specific treatments, such as SGLT-2 inhibitors and GLP-1 agonists, in people with diabetes and elevated hs-cTnT.

“Randomized controlled trials would be best to test the relevance of measuring these biomarkers to assess risk in asymptomatic people with diabetes,” as well as prospective study of the value of hs-cTnT to guide treatment, commented Robert H. Eckel, MD, an endocrinologist affiliated with the University of Colorado at Denver, Aurora.

“I doubt measurements [of hs-cTnT] would be reimbursed [by third-party payers] if carried out without such outcome data,” he added.

Dr. Eckel also highlights the need to further validate in additional cohorts the link between elevations in hs-cTnT and CVD events in adults with diabetes, and to confirm that elevated levels of another cardiac biomarker – N-terminal of the prohormone brain natriuretic peptide (NT-proBNP) – do not work as well as troponin as a risk marker for people with diabetes, another finding of the study.
 

ADA report already recommends testing these biomarkers for HF

However, a consensus report published in 2022 by the American Diabetes Association laid out the case for routinely and regularly measuring levels of both high sensitivity cardiac troponin and natriuretic peptides in people with diabetes for early identification of incident heart failure.

“Among individuals with diabetes, measurement of a natriuretic peptide or high-sensitivity cardiac troponin is recommended on at least a yearly basis to identify the earliest heart failure stages and implement strategies to prevent transition to symptomatic heart failure,” noted the ADA consensus report on heart failure.

The new study run by Dr. Selvin and coauthors used data collected by the National Health and Nutrition Examination Survey (NHANES) between 1999 and 2004 from U.S. adults who were at least 20 years old and had no history of CVD: myocardial infarction, stroke, coronary heart disease, or heart failure. This included 9,273 people without diabetes and 1,031 with diabetes, defined as a prior diagnosis or hemoglobin A1c of at least 6.5%.

“Cardiovascular risk varies substantially in adults with type 2 diabetes, highlighting the need for accurate risk stratification,” the authors observed.

All study participants had recorded measures of hs-cTnT and NT-proBNP.

The researchers considered an hs-cTnT level of greater than 14 ng/L and an NT-proBNP level of greater than 125 pg/mL as indicators of subclinical CVD.

The crude prevalence of elevated NT-proBNP was 33.4% among those with diabetes and 16.1% in those without diabetes. Elevated hs-cTnT occurred in 19% of those with diabetes and in 5% of those without diabetes. Elevated levels of both markers existed in 9% of those with diabetes and in 3% of those without diabetes.

“Approximately one in three adults with diabetes had subclinical CVD, with 19% having elevated levels of hs-cTnT, 23% having elevated NT-proBNP, and 9% having elevations in both cardiac biomarkers,” the researchers noted.
 

Diabetes linked with a doubled prevalence of elevated hs-cTnT 

After adjustment for several demographic variables as well as traditional CVD risk factors, people with diabetes had a significant 98% higher rate of elevated hs-cTnT, compared with those without diabetes. But after similar adjustments, the rate of elevated NT-proBNP was significantly lower among people with diabetes, compared with controls, by a relative reduction of 24%.

“Our findings suggest that, in people with diabetes, hs-cTnT may be more useful [than NT-proBNP] for general risk monitoring, as its interpretation is less complicated,” said Dr. Selvin, who explained that “NT-proBNP is affected by overweight and obesity.”

In people with diabetes, the age-adjusted prevalence of elevated hs-cTnT ran higher in those with longer duration diabetes, and in those with less well-controlled diabetes based on a higher level of A1c. Neither of these factors showed any significant relationship with measured levels of NT-proBNP.

Further analysis linked the NHANES findings during 1999-2004 with U.S. national death records through the end of 2019. This showed that elevated levels of both hs-cTnT and NT-proBNP significantly linked with subsequently higher rates of all-cause mortality among people with diabetes. Elevated hs-cTnT linked with a 77% increased mortality and NT-proBNP linked with a 78% increased rate, compared with people with diabetes and no elevations in these markers, after adjustment for demographic variables and CVD risk factors.

However, for the outcome of cardiovascular death, elevated hs-cTnT linked with a nonsignificant 54% relative increase, while elevated NT-proBNP linked with a significant 2.46-fold relative increase.

The study “adds new data on biomarkers that are not routinely measured in asymptomatic people with or without diabetes” and the relationships of these markers to CVD mortality and all-cause mortality, Dr. Eckel concluded.

The study received no commercial funding, but used reagents donated by Abbott Laboratories, Ortho Clinical Diagnostics, Roche Diagnostics, and Siemens Healthcare Diagnostics. Dr. Selvin and Dr. Eckel had no disclosures.

A version of this article first appeared on Medscape.com.

MANNHEIM, GERMANY – Contrary to expectations, individuals with familial hypercholesterolemia (FH) have rates of overweight and obesity that mirror the general population – rates that appear to have a substantial impact on these patients’ already increased risk of coronary artery disease, a registry analysis suggests.

Data on almost 36,000 individuals with FH were collated from an international registry, revealing that 55% of adults and 25% of children and adolescents with the homozygous form of FH had overweight or obesity. The figures for heterozygous FH were 52% and 27%, respectively.

Crucially, overweight or obesity was associated with substantially increased rates of coronary artery disease, particularly in persons with heterozygous FH, among whom adults with obesity faced a twofold increased risk, rising to more than sixfold in children and adolescents.

Moreover, “obesity is associated with a worse lipid profile, even from childhood, regardless of whether a patient is on medication,” said study presenter Amany Elshorbagy, DPhil, Cardiovascular Epidemiologist, department of primary care and public health, Imperial College London.

She added that, with the increased risk of coronary artery disease associated with heterozygous FH, the results showed that “together with lipid-lowering medication, weight management is needed.”

The research was presented at the annual meeting of the European Atherosclerosis Society.
 

Tended to be thin

Alberico L. Catapano, MD, PhD, director of cardiovascular research and of the Lipoproteins and Atherosclerosis Laboratory of IRCCS Multimedica, Milan, and past president of the EAS, said in an interview that, historically, few FH patients were overweight or obese; rather, they tended to be thin.

However, there is now “a trend for people with FH to show more diabetes and obesity,” with the “bottom line” being that, as they are already at increased risk of coronary artery disease, it pushes their risk up even further.

In other words, if a risk factor such as obesity is added “on top of the strongest risk factor, that is LDL cholesterol, it is not one plus one makes two, it is one plus one makes three,” he said.

As such, Dr. Catapano believes that the study is “very interesting,” because it further underlines the importance of weight management for individuals with increased LDL cholesterol, “especially when you have genetic forms, like FH.”

Dr. Catapano’s comments were echoed by session co-chair Ulrike Schatz, MD, leader of the lipidology specialty department at the University Hospital Carl Gustav Carus, Technical University of Dresden (Germany).

Indeed, she told Dr. Elshorbagy before her presentation that she finds “a lot of my FH patients have a tendency towards anorexia.”

In an interview, Dr. Elshorbagy said that that reaction was typical of “most of the clinicians” she had spoken to. Upon seeing her data, especially for homozygous FH patients, they say, “They are on the lean side.”

Consequently, the research team went into the study “with the expectation that they might have a lower prevalence of obesity and overweight than the general population,” but “that’s not what we’re seeing.”

Dr. Elshorbagy noted that it would be helpful to have longitudinal data to determine whether, 50 years ago, patients with HF “were leaner, along with the rest of the population.”

The registry data are cross-sectional, and the team is now reaching out to the respective national lead investigators to submit follow-up data on their patients, with the aim of looking at changes in body weight and the impact on outcomes over time.

Another key question for the researchers is in regard to fat distribution, as body mass index “is not the best predictor of heart disease,” Dr. Elshorbagy said, but is rather central obesity.

Although they have also asked investigators to share waist circumference data, she conceded that it is a measurement that “is a lot harder to standardize across centers and countries; it’s not like putting patients on a scale.”

Overall, Dr. Elshorbagy believes that her findings indicate that clinicians should take a broader, more holistic approach toward their patients – in other words, an approach in which lipid lowering medication is “key but is just one of several things we need to do to make sure the coronary event rate goes down.”
 

More with than without

Dr. Elshorbagy began her presentation by highlighting that the prevalence of overweight and obesity ranges from 50% to 70% and that it is “the only health condition where you’ve got more people worldwide with the condition than without.”

Crucially, overweight increases the risk of coronary artery disease by approximately 20%. Among patients with obesity, the risk rises to 50%.

Given that FH patients “already have a very high risk of cardiovascular disease from their high cholesterol levels,” the team set out to determine rates of obesity and overweight in this population and their impact on coronary artery disease risk.

They used cross-sectional data from the EAS FH Studies Collaboration Global Registry, which involves 29,262 adults aged greater than or equal to 18 years and 6,275 children and adolescents aged 5 to 17 years with heterozygous FH, and 325 adults and 57 children with homozygous FH.

Dividing the adults into standard BMI categories, they found that 16% of heterozygous and 23% of homozygous FH patients had obesity, while 52% and 55%, respectively, had overweight or obesity.

For children, the team used World Health Organization z score cutoffs, which indicated that 9% of patients with heterozygous FH and 7% of patients with homozygous FH had obesity. Rates of overweight or obesity were 27% and 25%, respectively.

Among patients with heterozygous FH, rates of overweight or obesity among adults were 50% in high-income countries and 63% in other countries; among children, the rates were and 27% and 29%, respectively.

Stratified by region, the team found that the lowest rate of overweight or obesity among adult patients with heterozygous FH was in Eastern Asia, at 27%, while the highest was in Northern Africa/Western Asia (the Middle East), at 82%.

In North America, 56% of adult patients had overweight or obesity. The prevalence of coronary artery disease rose with increasing BMI.

Among adult patients with heterozygous FH, 11.3% of those with normal weight had coronary artery disease; the percentage rose to 22.9% among those with overweight, and 30.9% among those with obesity. Among children, the corresponding figures were 0.1%, 0.2%, and 0.7%.

Putting adults and children with homozygous FH together, the researchers found that 29.0% of patients with normal weight had coronary artery disease, compared with 31.3% of those with overweight and 49.3% of those with obesity.

Moreover, the results showed that levels of LDL and remnant cholesterol were significantly associated with BMI in adults and children with heterozygous FH, even after adjusting for age, sex, and lipid-lowering medication (P < .001 for all).

Multivariate analysis that took into account age, sex, lipid-lowering medication, and LDL cholesterol revealed that having obesity, compared with not having obesity, was associated with a substantial increase in the risk of coronary artery disease among patients with heterozygous FH.

Among adults with the condition, the odds ratio was 2.16 (95% confidence interval, 1.97-2.36), while among children and adolescents, it was 6.87 (95% CI, 1.55-30.46).

The results remained similar after further adjustment for the presence of diabetes and when considering peripheral artery disease and stroke.

No funding for the study was declared. Dr. Elshorbagy has relationships with Amgen, Daiichi Sankyo, and Regeneron.

A version of this article first appeared on Medscape.com.

MANNHEIM, GERMANY – Contrary to expectations, individuals with familial hypercholesterolemia (FH) have rates of overweight and obesity that mirror the general population – rates that appear to have a substantial impact on these patients’ already increased risk of coronary artery disease, a registry analysis suggests.

Data on almost 36,000 individuals with FH were collated from an international registry, revealing that 55% of adults and 25% of children and adolescents with the homozygous form of FH had overweight or obesity. The figures for heterozygous FH were 52% and 27%, respectively.

Crucially, overweight or obesity was associated with substantially increased rates of coronary artery disease, particularly in persons with heterozygous FH, among whom adults with obesity faced a twofold increased risk, rising to more than sixfold in children and adolescents.

Moreover, “obesity is associated with a worse lipid profile, even from childhood, regardless of whether a patient is on medication,” said study presenter Amany Elshorbagy, DPhil, Cardiovascular Epidemiologist, department of primary care and public health, Imperial College London.

She added that, with the increased risk of coronary artery disease associated with heterozygous FH, the results showed that “together with lipid-lowering medication, weight management is needed.”

The research was presented at the annual meeting of the European Atherosclerosis Society.
 

Tended to be thin

Alberico L. Catapano, MD, PhD, director of cardiovascular research and of the Lipoproteins and Atherosclerosis Laboratory of IRCCS Multimedica, Milan, and past president of the EAS, said in an interview that, historically, few FH patients were overweight or obese; rather, they tended to be thin.

However, there is now “a trend for people with FH to show more diabetes and obesity,” with the “bottom line” being that, as they are already at increased risk of coronary artery disease, it pushes their risk up even further.

In other words, if a risk factor such as obesity is added “on top of the strongest risk factor, that is LDL cholesterol, it is not one plus one makes two, it is one plus one makes three,” he said.

As such, Dr. Catapano believes that the study is “very interesting,” because it further underlines the importance of weight management for individuals with increased LDL cholesterol, “especially when you have genetic forms, like FH.”

Dr. Catapano’s comments were echoed by session co-chair Ulrike Schatz, MD, leader of the lipidology specialty department at the University Hospital Carl Gustav Carus, Technical University of Dresden (Germany).

Indeed, she told Dr. Elshorbagy before her presentation that she finds “a lot of my FH patients have a tendency towards anorexia.”

In an interview, Dr. Elshorbagy said that that reaction was typical of “most of the clinicians” she had spoken to. Upon seeing her data, especially for homozygous FH patients, they say, “They are on the lean side.”

Consequently, the research team went into the study “with the expectation that they might have a lower prevalence of obesity and overweight than the general population,” but “that’s not what we’re seeing.”

Dr. Elshorbagy noted that it would be helpful to have longitudinal data to determine whether, 50 years ago, patients with HF “were leaner, along with the rest of the population.”

The registry data are cross-sectional, and the team is now reaching out to the respective national lead investigators to submit follow-up data on their patients, with the aim of looking at changes in body weight and the impact on outcomes over time.

Another key question for the researchers is in regard to fat distribution, as body mass index “is not the best predictor of heart disease,” Dr. Elshorbagy said, but is rather central obesity.

Although they have also asked investigators to share waist circumference data, she conceded that it is a measurement that “is a lot harder to standardize across centers and countries; it’s not like putting patients on a scale.”

Overall, Dr. Elshorbagy believes that her findings indicate that clinicians should take a broader, more holistic approach toward their patients – in other words, an approach in which lipid lowering medication is “key but is just one of several things we need to do to make sure the coronary event rate goes down.”
 

More with than without

Dr. Elshorbagy began her presentation by highlighting that the prevalence of overweight and obesity ranges from 50% to 70% and that it is “the only health condition where you’ve got more people worldwide with the condition than without.”

Crucially, overweight increases the risk of coronary artery disease by approximately 20%. Among patients with obesity, the risk rises to 50%.

Given that FH patients “already have a very high risk of cardiovascular disease from their high cholesterol levels,” the team set out to determine rates of obesity and overweight in this population and their impact on coronary artery disease risk.

They used cross-sectional data from the EAS FH Studies Collaboration Global Registry, which involves 29,262 adults aged greater than or equal to 18 years and 6,275 children and adolescents aged 5 to 17 years with heterozygous FH, and 325 adults and 57 children with homozygous FH.

Dividing the adults into standard BMI categories, they found that 16% of heterozygous and 23% of homozygous FH patients had obesity, while 52% and 55%, respectively, had overweight or obesity.

For children, the team used World Health Organization z score cutoffs, which indicated that 9% of patients with heterozygous FH and 7% of patients with homozygous FH had obesity. Rates of overweight or obesity were 27% and 25%, respectively.

Among patients with heterozygous FH, rates of overweight or obesity among adults were 50% in high-income countries and 63% in other countries; among children, the rates were and 27% and 29%, respectively.

Stratified by region, the team found that the lowest rate of overweight or obesity among adult patients with heterozygous FH was in Eastern Asia, at 27%, while the highest was in Northern Africa/Western Asia (the Middle East), at 82%.

In North America, 56% of adult patients had overweight or obesity. The prevalence of coronary artery disease rose with increasing BMI.

Among adult patients with heterozygous FH, 11.3% of those with normal weight had coronary artery disease; the percentage rose to 22.9% among those with overweight, and 30.9% among those with obesity. Among children, the corresponding figures were 0.1%, 0.2%, and 0.7%.

Putting adults and children with homozygous FH together, the researchers found that 29.0% of patients with normal weight had coronary artery disease, compared with 31.3% of those with overweight and 49.3% of those with obesity.

Moreover, the results showed that levels of LDL and remnant cholesterol were significantly associated with BMI in adults and children with heterozygous FH, even after adjusting for age, sex, and lipid-lowering medication (P < .001 for all).

Multivariate analysis that took into account age, sex, lipid-lowering medication, and LDL cholesterol revealed that having obesity, compared with not having obesity, was associated with a substantial increase in the risk of coronary artery disease among patients with heterozygous FH.

Among adults with the condition, the odds ratio was 2.16 (95% confidence interval, 1.97-2.36), while among children and adolescents, it was 6.87 (95% CI, 1.55-30.46).

The results remained similar after further adjustment for the presence of diabetes and when considering peripheral artery disease and stroke.

No funding for the study was declared. Dr. Elshorbagy has relationships with Amgen, Daiichi Sankyo, and Regeneron.

A version of this article first appeared on Medscape.com.

MANNHEIM, GERMANY – Contrary to expectations, individuals with familial hypercholesterolemia (FH) have rates of overweight and obesity that mirror the general population – rates that appear to have a substantial impact on these patients’ already increased risk of coronary artery disease, a registry analysis suggests.

Data on almost 36,000 individuals with FH were collated from an international registry, revealing that 55% of adults and 25% of children and adolescents with the homozygous form of FH had overweight or obesity. The figures for heterozygous FH were 52% and 27%, respectively.

Crucially, overweight or obesity was associated with substantially increased rates of coronary artery disease, particularly in persons with heterozygous FH, among whom adults with obesity faced a twofold increased risk, rising to more than sixfold in children and adolescents.

Moreover, “obesity is associated with a worse lipid profile, even from childhood, regardless of whether a patient is on medication,” said study presenter Amany Elshorbagy, DPhil, Cardiovascular Epidemiologist, department of primary care and public health, Imperial College London.

She added that, with the increased risk of coronary artery disease associated with heterozygous FH, the results showed that “together with lipid-lowering medication, weight management is needed.”

The research was presented at the annual meeting of the European Atherosclerosis Society.
 

Tended to be thin

Alberico L. Catapano, MD, PhD, director of cardiovascular research and of the Lipoproteins and Atherosclerosis Laboratory of IRCCS Multimedica, Milan, and past president of the EAS, said in an interview that, historically, few FH patients were overweight or obese; rather, they tended to be thin.

However, there is now “a trend for people with FH to show more diabetes and obesity,” with the “bottom line” being that, as they are already at increased risk of coronary artery disease, it pushes their risk up even further.

In other words, if a risk factor such as obesity is added “on top of the strongest risk factor, that is LDL cholesterol, it is not one plus one makes two, it is one plus one makes three,” he said.

As such, Dr. Catapano believes that the study is “very interesting,” because it further underlines the importance of weight management for individuals with increased LDL cholesterol, “especially when you have genetic forms, like FH.”

Dr. Catapano’s comments were echoed by session co-chair Ulrike Schatz, MD, leader of the lipidology specialty department at the University Hospital Carl Gustav Carus, Technical University of Dresden (Germany).

Indeed, she told Dr. Elshorbagy before her presentation that she finds “a lot of my FH patients have a tendency towards anorexia.”

In an interview, Dr. Elshorbagy said that that reaction was typical of “most of the clinicians” she had spoken to. Upon seeing her data, especially for homozygous FH patients, they say, “They are on the lean side.”

Consequently, the research team went into the study “with the expectation that they might have a lower prevalence of obesity and overweight than the general population,” but “that’s not what we’re seeing.”

Dr. Elshorbagy noted that it would be helpful to have longitudinal data to determine whether, 50 years ago, patients with HF “were leaner, along with the rest of the population.”

The registry data are cross-sectional, and the team is now reaching out to the respective national lead investigators to submit follow-up data on their patients, with the aim of looking at changes in body weight and the impact on outcomes over time.

Another key question for the researchers is in regard to fat distribution, as body mass index “is not the best predictor of heart disease,” Dr. Elshorbagy said, but is rather central obesity.

Although they have also asked investigators to share waist circumference data, she conceded that it is a measurement that “is a lot harder to standardize across centers and countries; it’s not like putting patients on a scale.”

Overall, Dr. Elshorbagy believes that her findings indicate that clinicians should take a broader, more holistic approach toward their patients – in other words, an approach in which lipid lowering medication is “key but is just one of several things we need to do to make sure the coronary event rate goes down.”
 

More with than without

Dr. Elshorbagy began her presentation by highlighting that the prevalence of overweight and obesity ranges from 50% to 70% and that it is “the only health condition where you’ve got more people worldwide with the condition than without.”

Crucially, overweight increases the risk of coronary artery disease by approximately 20%. Among patients with obesity, the risk rises to 50%.

Given that FH patients “already have a very high risk of cardiovascular disease from their high cholesterol levels,” the team set out to determine rates of obesity and overweight in this population and their impact on coronary artery disease risk.

They used cross-sectional data from the EAS FH Studies Collaboration Global Registry, which involves 29,262 adults aged greater than or equal to 18 years and 6,275 children and adolescents aged 5 to 17 years with heterozygous FH, and 325 adults and 57 children with homozygous FH.

Dividing the adults into standard BMI categories, they found that 16% of heterozygous and 23% of homozygous FH patients had obesity, while 52% and 55%, respectively, had overweight or obesity.

For children, the team used World Health Organization z score cutoffs, which indicated that 9% of patients with heterozygous FH and 7% of patients with homozygous FH had obesity. Rates of overweight or obesity were 27% and 25%, respectively.

Among patients with heterozygous FH, rates of overweight or obesity among adults were 50% in high-income countries and 63% in other countries; among children, the rates were and 27% and 29%, respectively.

Stratified by region, the team found that the lowest rate of overweight or obesity among adult patients with heterozygous FH was in Eastern Asia, at 27%, while the highest was in Northern Africa/Western Asia (the Middle East), at 82%.

In North America, 56% of adult patients had overweight or obesity. The prevalence of coronary artery disease rose with increasing BMI.

Among adult patients with heterozygous FH, 11.3% of those with normal weight had coronary artery disease; the percentage rose to 22.9% among those with overweight, and 30.9% among those with obesity. Among children, the corresponding figures were 0.1%, 0.2%, and 0.7%.

Putting adults and children with homozygous FH together, the researchers found that 29.0% of patients with normal weight had coronary artery disease, compared with 31.3% of those with overweight and 49.3% of those with obesity.

Moreover, the results showed that levels of LDL and remnant cholesterol were significantly associated with BMI in adults and children with heterozygous FH, even after adjusting for age, sex, and lipid-lowering medication (P < .001 for all).

Multivariate analysis that took into account age, sex, lipid-lowering medication, and LDL cholesterol revealed that having obesity, compared with not having obesity, was associated with a substantial increase in the risk of coronary artery disease among patients with heterozygous FH.

Among adults with the condition, the odds ratio was 2.16 (95% confidence interval, 1.97-2.36), while among children and adolescents, it was 6.87 (95% CI, 1.55-30.46).

The results remained similar after further adjustment for the presence of diabetes and when considering peripheral artery disease and stroke.

No funding for the study was declared. Dr. Elshorbagy has relationships with Amgen, Daiichi Sankyo, and Regeneron.

A version of this article first appeared on Medscape.com.

As a predictor of coronary heart disease (CHD) events, the coronary artery calcium (CAC) score on computed tomography had better risk discrimination than the polygenic risk score, a binational study found. And when added to classic cardiovascular risk factors, the CAC score significantly improved risk classification while the polygenic risk factor score did not.

Sadiya S. Khan

These findings emerged from two large cohorts of middle-aged and older White adults from the United States and the Netherlands in the first head-to-head comparison of these two approaches. Led by Sadiya S. Kahn, MD, MSc, an assistant professor of medicine (cardiology) and preventive medicine (epidemiology) at Northwestern University, Chicago, the study was published online in JAMA.

There has been much interest in using both genetic factors and CT imaging to better identify individuals at risk for heart disease. “Each approach has advantages and disadvantages, and we wanted to better understand the comparative predictive utility to provide support for what the preferred approach should be,” Dr. Kahn said in an interview. “We focused on middle-aged to older adults for whom current risk prediction equations are relevant in estimating risk with the Pooled Cohort Equation, or PCE.”

The superiority of the CT-imaged coronary artery risk score may be because of its direct visualization of calcification in the arteries and the subclinical disease burden rather than a focus on common genetic variants, Dr. Kahn explained. “In addition, prior studies have demonstrated that genetics, or inherited risk, is not destiny, so this score may not perform as well for risk discrimination as the traditional risk factors themselves along with CT.”
 

The study

Study participants came from the U.S. Multi-Ethnic Study of Atherosclerosis (MESA, n = 1,991) and the Dutch Rotterdam Study (RS, n = 1,217). Ages ranged from 45 to 79, with the medians in the two cohorts 61 and 68 years, respectively. Slightly more than half of participants in both groups were female.

Traditional risk factors were used to calculate CHD risk with pooled cohort equations, while computed tomography was used to determine the CAC score and genotyped samples for a validated polygenic risk score.

Both scores were significantly associated with 10-year risk of incident CHD.

The median predicted atherosclerotic disease risk based on traditional risk factors was 6.99% in MESA and 5.93% in RS. During the total available follow-up in MESA (median, 16.0 years) and RS (median, 14.2 years), incident CHD occurred in 187 participants (9.4%) and 98 participants (8.1%), respectively.

C (concordance) statistics for the two scores showed the superiority of the CAC. This statistic measures a model’s ability to rank patients from high to low risk, with a value of 1 being perfect risk fit or concordance and 0.70 or more indicating good concordance and risk discrimination. The CAC score had a C statistic of 0.76 (95% confidence interval, 0.71-0.79) vs. 0.69 for the polygenic risk score (95% CI, 0.63-0.71).

When each score was added to PCEs, the C statistics changed as follows: CAC score, 0.09 (95% CI, 0.06-0.13); polygenic risk score, 0.02 (95% CI, 0.00-0.04); and 0.10 (95% CI, 0.07-0.14) for both.

Net reclassification significantly improved with the CAC plus PCEs by the following values: 0.19 (95% CI, 0.06-0.28). The change was not significant, however, with the polygenic risk score plus PCEs: 0.04 (95% CI, –0.05-0.10).

In the clinical setting, Dr. Kahn said, “The use of CT in patients who are at intermediate risk for heart disease can be helpful in refining risk estimation and guiding recommendations for lipid-lowering therapy. Polygenic risk scores are not helpful in middle-aged to older adults above and beyond traditional risk factors for predicting risk of heart disease.”

This study was supported by the National Heart, Lung, and Blood Institute. MESA is supported by the NHLBI. The Rotterdam Study is funded by Erasmus Medical Center and Erasmus University Rotterdam; the Netherlands Organization for Scientific Research; the Netherlands Organization for Health Research and Development; the Research Institute for Diseases in the Elderly; the Netherlands Genomics Initiative; the Ministry of Education, Culture and Science, the Ministry of Health, Welfare and Sports; the European Commission (DG XII); and the Municipality of Rotterdam. Dr. Khan reported grants from the NHLBI and the NIH during the study and outside of the submitted work. Several coauthors reported grant support from, variously, the NIH, the NHLBI, and the American Heart Association.
 

As a predictor of coronary heart disease (CHD) events, the coronary artery calcium (CAC) score on computed tomography had better risk discrimination than the polygenic risk score, a binational study found. And when added to classic cardiovascular risk factors, the CAC score significantly improved risk classification while the polygenic risk factor score did not.

Sadiya S. Khan

These findings emerged from two large cohorts of middle-aged and older White adults from the United States and the Netherlands in the first head-to-head comparison of these two approaches. Led by Sadiya S. Kahn, MD, MSc, an assistant professor of medicine (cardiology) and preventive medicine (epidemiology) at Northwestern University, Chicago, the study was published online in JAMA.

There has been much interest in using both genetic factors and CT imaging to better identify individuals at risk for heart disease. “Each approach has advantages and disadvantages, and we wanted to better understand the comparative predictive utility to provide support for what the preferred approach should be,” Dr. Kahn said in an interview. “We focused on middle-aged to older adults for whom current risk prediction equations are relevant in estimating risk with the Pooled Cohort Equation, or PCE.”

The superiority of the CT-imaged coronary artery risk score may be because of its direct visualization of calcification in the arteries and the subclinical disease burden rather than a focus on common genetic variants, Dr. Kahn explained. “In addition, prior studies have demonstrated that genetics, or inherited risk, is not destiny, so this score may not perform as well for risk discrimination as the traditional risk factors themselves along with CT.”
 

The study

Study participants came from the U.S. Multi-Ethnic Study of Atherosclerosis (MESA, n = 1,991) and the Dutch Rotterdam Study (RS, n = 1,217). Ages ranged from 45 to 79, with the medians in the two cohorts 61 and 68 years, respectively. Slightly more than half of participants in both groups were female.

Traditional risk factors were used to calculate CHD risk with pooled cohort equations, while computed tomography was used to determine the CAC score and genotyped samples for a validated polygenic risk score.

Both scores were significantly associated with 10-year risk of incident CHD.

The median predicted atherosclerotic disease risk based on traditional risk factors was 6.99% in MESA and 5.93% in RS. During the total available follow-up in MESA (median, 16.0 years) and RS (median, 14.2 years), incident CHD occurred in 187 participants (9.4%) and 98 participants (8.1%), respectively.

C (concordance) statistics for the two scores showed the superiority of the CAC. This statistic measures a model’s ability to rank patients from high to low risk, with a value of 1 being perfect risk fit or concordance and 0.70 or more indicating good concordance and risk discrimination. The CAC score had a C statistic of 0.76 (95% confidence interval, 0.71-0.79) vs. 0.69 for the polygenic risk score (95% CI, 0.63-0.71).

When each score was added to PCEs, the C statistics changed as follows: CAC score, 0.09 (95% CI, 0.06-0.13); polygenic risk score, 0.02 (95% CI, 0.00-0.04); and 0.10 (95% CI, 0.07-0.14) for both.

Net reclassification significantly improved with the CAC plus PCEs by the following values: 0.19 (95% CI, 0.06-0.28). The change was not significant, however, with the polygenic risk score plus PCEs: 0.04 (95% CI, –0.05-0.10).

In the clinical setting, Dr. Kahn said, “The use of CT in patients who are at intermediate risk for heart disease can be helpful in refining risk estimation and guiding recommendations for lipid-lowering therapy. Polygenic risk scores are not helpful in middle-aged to older adults above and beyond traditional risk factors for predicting risk of heart disease.”

This study was supported by the National Heart, Lung, and Blood Institute. MESA is supported by the NHLBI. The Rotterdam Study is funded by Erasmus Medical Center and Erasmus University Rotterdam; the Netherlands Organization for Scientific Research; the Netherlands Organization for Health Research and Development; the Research Institute for Diseases in the Elderly; the Netherlands Genomics Initiative; the Ministry of Education, Culture and Science, the Ministry of Health, Welfare and Sports; the European Commission (DG XII); and the Municipality of Rotterdam. Dr. Khan reported grants from the NHLBI and the NIH during the study and outside of the submitted work. Several coauthors reported grant support from, variously, the NIH, the NHLBI, and the American Heart Association.
 

As a predictor of coronary heart disease (CHD) events, the coronary artery calcium (CAC) score on computed tomography had better risk discrimination than the polygenic risk score, a binational study found. And when added to classic cardiovascular risk factors, the CAC score significantly improved risk classification while the polygenic risk factor score did not.

Sadiya S. Khan

These findings emerged from two large cohorts of middle-aged and older White adults from the United States and the Netherlands in the first head-to-head comparison of these two approaches. Led by Sadiya S. Kahn, MD, MSc, an assistant professor of medicine (cardiology) and preventive medicine (epidemiology) at Northwestern University, Chicago, the study was published online in JAMA.

There has been much interest in using both genetic factors and CT imaging to better identify individuals at risk for heart disease. “Each approach has advantages and disadvantages, and we wanted to better understand the comparative predictive utility to provide support for what the preferred approach should be,” Dr. Kahn said in an interview. “We focused on middle-aged to older adults for whom current risk prediction equations are relevant in estimating risk with the Pooled Cohort Equation, or PCE.”

The superiority of the CT-imaged coronary artery risk score may be because of its direct visualization of calcification in the arteries and the subclinical disease burden rather than a focus on common genetic variants, Dr. Kahn explained. “In addition, prior studies have demonstrated that genetics, or inherited risk, is not destiny, so this score may not perform as well for risk discrimination as the traditional risk factors themselves along with CT.”
 

The study

Study participants came from the U.S. Multi-Ethnic Study of Atherosclerosis (MESA, n = 1,991) and the Dutch Rotterdam Study (RS, n = 1,217). Ages ranged from 45 to 79, with the medians in the two cohorts 61 and 68 years, respectively. Slightly more than half of participants in both groups were female.

Traditional risk factors were used to calculate CHD risk with pooled cohort equations, while computed tomography was used to determine the CAC score and genotyped samples for a validated polygenic risk score.

Both scores were significantly associated with 10-year risk of incident CHD.

The median predicted atherosclerotic disease risk based on traditional risk factors was 6.99% in MESA and 5.93% in RS. During the total available follow-up in MESA (median, 16.0 years) and RS (median, 14.2 years), incident CHD occurred in 187 participants (9.4%) and 98 participants (8.1%), respectively.

C (concordance) statistics for the two scores showed the superiority of the CAC. This statistic measures a model’s ability to rank patients from high to low risk, with a value of 1 being perfect risk fit or concordance and 0.70 or more indicating good concordance and risk discrimination. The CAC score had a C statistic of 0.76 (95% confidence interval, 0.71-0.79) vs. 0.69 for the polygenic risk score (95% CI, 0.63-0.71).

When each score was added to PCEs, the C statistics changed as follows: CAC score, 0.09 (95% CI, 0.06-0.13); polygenic risk score, 0.02 (95% CI, 0.00-0.04); and 0.10 (95% CI, 0.07-0.14) for both.

Net reclassification significantly improved with the CAC plus PCEs by the following values: 0.19 (95% CI, 0.06-0.28). The change was not significant, however, with the polygenic risk score plus PCEs: 0.04 (95% CI, –0.05-0.10).

In the clinical setting, Dr. Kahn said, “The use of CT in patients who are at intermediate risk for heart disease can be helpful in refining risk estimation and guiding recommendations for lipid-lowering therapy. Polygenic risk scores are not helpful in middle-aged to older adults above and beyond traditional risk factors for predicting risk of heart disease.”

This study was supported by the National Heart, Lung, and Blood Institute. MESA is supported by the NHLBI. The Rotterdam Study is funded by Erasmus Medical Center and Erasmus University Rotterdam; the Netherlands Organization for Scientific Research; the Netherlands Organization for Health Research and Development; the Research Institute for Diseases in the Elderly; the Netherlands Genomics Initiative; the Ministry of Education, Culture and Science, the Ministry of Health, Welfare and Sports; the European Commission (DG XII); and the Municipality of Rotterdam. Dr. Khan reported grants from the NHLBI and the NIH during the study and outside of the submitted work. Several coauthors reported grant support from, variously, the NIH, the NHLBI, and the American Heart Association.
 

For patients with chronic, limb-threatening ischemia due to atherosclerosis that affects the arteries below the knee, a revascularization strategy using endovascular treatment as the first option was superior to one that prioritized vein bypass surgery in a new randomized trial.

In the Bypass Versus Angioplasty in Severe Ischaemia of the Leg (BASIL-2) trial, patients who received vein bypass as the first approach were more likely to require a major amputation or to die during follow-up than patients who were randomly assigned to the endovascular approach as first strategy.

iStock/Getty Images

“Our findings suggest that a best endovascular treatment first revascularization strategy is associated with a better amputation-free survival. This is mainly because the best endovascular treatment first revascularization strategy resulted in fewer deaths. Limb-related outcomes were similar between groups,” the authors stated.

“The BASIL-2 trial has produced a statistically robust and clinically meaningful result that is likely to have an influence on the management of chronic limb-threatening ischemia worldwide,” added the study’s chief investigator, Andrew Bradbury, MD, professor of vascular surgery at the University of Birmingham (England).

However, the results of the BASIL-2 trial conflict with those from two previous studies – BASIL-1 and BEST-CLI, which both suggested that a surgical approach for chronic limb-threatening ischemia may be most appropriate.

The BASIL-2 study was published online in The Lancet.

The authors explained that chronic limb-threatening ischemia, previously known as critical limb ischemia and severe ischemia of the leg, is the most severe form of peripheral arterial disease caused by atherosclerosis. Patients present with ischemic rest pain and tissue loss (ulceration, gangrene, or both) that usually affects the foot.

Mainly because of tobacco smoking and the growing prevalence of type 2 diabetes, chronic limb-threatening ischemia represents a growing burden on health care and social care services around the world.

Unless the blood supply to the affected limb is restored, patients with chronic limb-threatening ischemia are at high risk for amputation or death. Although it is universally agreed that – in addition to best medical therapy – virtually all patients with chronic limb-threatening ischemia should at least be considered for revascularization, there is continuing debate as to whether conducting vein bypass surgery, preferably using a vein taken from the patient’s own leg, or endovascular treatment (balloon angioplasty with or without stents) is preferable.

“BASIL-2 is the only randomized trial to specifically compare a vein bypass first with best endovascular treatment first revascularisation strategy in patients with chronic limb-threatening ischemia who required an infrapopliteal (with or without an additional more proximal infrainguinal) revascularization procedure to restore limb perfusion,” the authors noted.

For the trial, which was conducted at 41 vascular surgery units in the United Kingdom, Sweden, and Denmark, 345 patients with chronic limb-threatening ischemia who required an infrapopliteal revascularization procedure to restore limb perfusion were randomly assigned to receive either vein bypass or best endovascular treatment as their first revascularization procedure.

Most vein bypasses used the great saphenous vein and originated from the common or superficial femoral arteries. Most endovascular interventions comprised plain balloon angioplasty with selective use of plain or drug-eluting stents. Participants were followed up for a minimum of 2 years.

The primary outcome was amputation-free survival, defined as time to first major (above the ankle) amputation or death from any cause measured in the intention-to-treat population.

Results showed that major amputation or death occurred in 63% of patients in the vein bypass group and in 53% of those in the best endovascular treatment group (adjusted hazard ratio, 1.35; P = .037).

The results were driven by a higher death rate in the vein bypass group (53% vs. 45%; aHR, 1.37).

In both groups, the most common causes of morbidity and death, including death occurring within 30 days of first revascularization, were cardiovascular and respiratory events.

The authors noted that outcomes for the patients in the BASIL-2 trial were poor (median amputation-free survival was 3.8 years, and half the patients died within 5 years).

They pointed out that severe, multilevel atherosclerotic disease that causes chronic limb-threatening ischemia develops over many years, but at baseline in this study, around 20% of patients said they were still smoking, and around 70% of patients had diabetes, of whom around 50% required insulin. In addition, around 90% of the participants often had quite extensive tissue loss.

“These baseline data suggest that there might still be missed opportunities in public health and primary care to prevent chronic limb-threatening ischemia through medical therapy and lifestyle interventions and missed opportunities to refer patients to secondary care earlier once chronic limb-threatening ischemia begins to develop,” they suggested.

“Better prevention and timely referral are important: the BASIL-2 trial shows that, by the time patients present to vascular and endovascular surgeons and interventional radiologists with established chronic limb-threatening ischemia, their prognosis is often poor regardless of what form of revascularization they are offered,” they added.
 

Conflicting results

In an accompanying comment, Ankur Kalra, MD, Franciscan Health, Lafayette, Ind., and Ashish Kumar, MD, Cleveland Clinic Akron (Ohio) General, noted that atherosclerotic lower-extremity peripheral artery disease affects more than 230 million people worldwide, and prevalence is increasing. Chronic limb-threatening ischemia is a severe form of peripheral artery disease that affects 11% of patients with peripheral artery disease and is associated with significant cardiovascular morbidity and death.

Furthermore, amputation rates of 10%-40% during a 6-month follow-up of patients with chronic limb-threatening ischemia who were unable to undergo revascularization have been reported, highlighting the severity of atherosclerotic burden and the need for improved treatment strategies.

Dr. Kalra and Dr. Kumar pointed out that two previous randomized clinical trials compared surgical vein graft bypass with endovascular treatment for patients with chronic limb-threatening ischemia – the BASIL-1 trial, and the BEST-CLI trial.

In the BASIL-1 trial, vein bypass was associated with improved overall survival and amputation-free survival for patients who survived at least 2 years. The BEST-CLI trial also reported a lower risk of a composite of major adverse limb events or death among patients undergoing a surgery-first strategy, compared with endovascular therapy, mostly in patients with suitable single segment of great saphenous vein.

Dr. Kalra and Dr. Kumar said the findings of the BASIL-2 trial should be put in context with these previous studies, which report a positive or equivocal effect of surgery. The results of the BEST-CLI trial were driven by fewer major reinterventions and above-ankle amputations in the surgical group, whereas the results of the BASIL-2 trial were driven by fewer deaths in the best endovascular treatment group, “which potentially points towards a difference in the characteristics of the patients randomly assigned in the two trials.”

They concluded: “Considering the results of the BASIL-2 trial and the BEST-CLI trial, choice of intervention should be based on shared decision making between interventional cardiology, vascular surgery, and the patient, until more evidence is accrued.”

The BASIL-2 trial was funded by the U.K. National Institute of Health Research.

A version of this article first appeared on Medscape.com.

For patients with chronic, limb-threatening ischemia due to atherosclerosis that affects the arteries below the knee, a revascularization strategy using endovascular treatment as the first option was superior to one that prioritized vein bypass surgery in a new randomized trial.

In the Bypass Versus Angioplasty in Severe Ischaemia of the Leg (BASIL-2) trial, patients who received vein bypass as the first approach were more likely to require a major amputation or to die during follow-up than patients who were randomly assigned to the endovascular approach as first strategy.

iStock/Getty Images

“Our findings suggest that a best endovascular treatment first revascularization strategy is associated with a better amputation-free survival. This is mainly because the best endovascular treatment first revascularization strategy resulted in fewer deaths. Limb-related outcomes were similar between groups,” the authors stated.

“The BASIL-2 trial has produced a statistically robust and clinically meaningful result that is likely to have an influence on the management of chronic limb-threatening ischemia worldwide,” added the study’s chief investigator, Andrew Bradbury, MD, professor of vascular surgery at the University of Birmingham (England).

However, the results of the BASIL-2 trial conflict with those from two previous studies – BASIL-1 and BEST-CLI, which both suggested that a surgical approach for chronic limb-threatening ischemia may be most appropriate.

The BASIL-2 study was published online in The Lancet.

The authors explained that chronic limb-threatening ischemia, previously known as critical limb ischemia and severe ischemia of the leg, is the most severe form of peripheral arterial disease caused by atherosclerosis. Patients present with ischemic rest pain and tissue loss (ulceration, gangrene, or both) that usually affects the foot.

Mainly because of tobacco smoking and the growing prevalence of type 2 diabetes, chronic limb-threatening ischemia represents a growing burden on health care and social care services around the world.

Unless the blood supply to the affected limb is restored, patients with chronic limb-threatening ischemia are at high risk for amputation or death. Although it is universally agreed that – in addition to best medical therapy – virtually all patients with chronic limb-threatening ischemia should at least be considered for revascularization, there is continuing debate as to whether conducting vein bypass surgery, preferably using a vein taken from the patient’s own leg, or endovascular treatment (balloon angioplasty with or without stents) is preferable.

“BASIL-2 is the only randomized trial to specifically compare a vein bypass first with best endovascular treatment first revascularisation strategy in patients with chronic limb-threatening ischemia who required an infrapopliteal (with or without an additional more proximal infrainguinal) revascularization procedure to restore limb perfusion,” the authors noted.

For the trial, which was conducted at 41 vascular surgery units in the United Kingdom, Sweden, and Denmark, 345 patients with chronic limb-threatening ischemia who required an infrapopliteal revascularization procedure to restore limb perfusion were randomly assigned to receive either vein bypass or best endovascular treatment as their first revascularization procedure.

Most vein bypasses used the great saphenous vein and originated from the common or superficial femoral arteries. Most endovascular interventions comprised plain balloon angioplasty with selective use of plain or drug-eluting stents. Participants were followed up for a minimum of 2 years.

The primary outcome was amputation-free survival, defined as time to first major (above the ankle) amputation or death from any cause measured in the intention-to-treat population.

Results showed that major amputation or death occurred in 63% of patients in the vein bypass group and in 53% of those in the best endovascular treatment group (adjusted hazard ratio, 1.35; P = .037).

The results were driven by a higher death rate in the vein bypass group (53% vs. 45%; aHR, 1.37).

In both groups, the most common causes of morbidity and death, including death occurring within 30 days of first revascularization, were cardiovascular and respiratory events.

The authors noted that outcomes for the patients in the BASIL-2 trial were poor (median amputation-free survival was 3.8 years, and half the patients died within 5 years).

They pointed out that severe, multilevel atherosclerotic disease that causes chronic limb-threatening ischemia develops over many years, but at baseline in this study, around 20% of patients said they were still smoking, and around 70% of patients had diabetes, of whom around 50% required insulin. In addition, around 90% of the participants often had quite extensive tissue loss.

“These baseline data suggest that there might still be missed opportunities in public health and primary care to prevent chronic limb-threatening ischemia through medical therapy and lifestyle interventions and missed opportunities to refer patients to secondary care earlier once chronic limb-threatening ischemia begins to develop,” they suggested.

“Better prevention and timely referral are important: the BASIL-2 trial shows that, by the time patients present to vascular and endovascular surgeons and interventional radiologists with established chronic limb-threatening ischemia, their prognosis is often poor regardless of what form of revascularization they are offered,” they added.
 

Conflicting results

In an accompanying comment, Ankur Kalra, MD, Franciscan Health, Lafayette, Ind., and Ashish Kumar, MD, Cleveland Clinic Akron (Ohio) General, noted that atherosclerotic lower-extremity peripheral artery disease affects more than 230 million people worldwide, and prevalence is increasing. Chronic limb-threatening ischemia is a severe form of peripheral artery disease that affects 11% of patients with peripheral artery disease and is associated with significant cardiovascular morbidity and death.

Furthermore, amputation rates of 10%-40% during a 6-month follow-up of patients with chronic limb-threatening ischemia who were unable to undergo revascularization have been reported, highlighting the severity of atherosclerotic burden and the need for improved treatment strategies.

Dr. Kalra and Dr. Kumar pointed out that two previous randomized clinical trials compared surgical vein graft bypass with endovascular treatment for patients with chronic limb-threatening ischemia – the BASIL-1 trial, and the BEST-CLI trial.

In the BASIL-1 trial, vein bypass was associated with improved overall survival and amputation-free survival for patients who survived at least 2 years. The BEST-CLI trial also reported a lower risk of a composite of major adverse limb events or death among patients undergoing a surgery-first strategy, compared with endovascular therapy, mostly in patients with suitable single segment of great saphenous vein.

Dr. Kalra and Dr. Kumar said the findings of the BASIL-2 trial should be put in context with these previous studies, which report a positive or equivocal effect of surgery. The results of the BEST-CLI trial were driven by fewer major reinterventions and above-ankle amputations in the surgical group, whereas the results of the BASIL-2 trial were driven by fewer deaths in the best endovascular treatment group, “which potentially points towards a difference in the characteristics of the patients randomly assigned in the two trials.”

They concluded: “Considering the results of the BASIL-2 trial and the BEST-CLI trial, choice of intervention should be based on shared decision making between interventional cardiology, vascular surgery, and the patient, until more evidence is accrued.”

The BASIL-2 trial was funded by the U.K. National Institute of Health Research.

A version of this article first appeared on Medscape.com.

For patients with chronic, limb-threatening ischemia due to atherosclerosis that affects the arteries below the knee, a revascularization strategy using endovascular treatment as the first option was superior to one that prioritized vein bypass surgery in a new randomized trial.

In the Bypass Versus Angioplasty in Severe Ischaemia of the Leg (BASIL-2) trial, patients who received vein bypass as the first approach were more likely to require a major amputation or to die during follow-up than patients who were randomly assigned to the endovascular approach as first strategy.

iStock/Getty Images

“Our findings suggest that a best endovascular treatment first revascularization strategy is associated with a better amputation-free survival. This is mainly because the best endovascular treatment first revascularization strategy resulted in fewer deaths. Limb-related outcomes were similar between groups,” the authors stated.

“The BASIL-2 trial has produced a statistically robust and clinically meaningful result that is likely to have an influence on the management of chronic limb-threatening ischemia worldwide,” added the study’s chief investigator, Andrew Bradbury, MD, professor of vascular surgery at the University of Birmingham (England).

However, the results of the BASIL-2 trial conflict with those from two previous studies – BASIL-1 and BEST-CLI, which both suggested that a surgical approach for chronic limb-threatening ischemia may be most appropriate.

The BASIL-2 study was published online in The Lancet.

The authors explained that chronic limb-threatening ischemia, previously known as critical limb ischemia and severe ischemia of the leg, is the most severe form of peripheral arterial disease caused by atherosclerosis. Patients present with ischemic rest pain and tissue loss (ulceration, gangrene, or both) that usually affects the foot.

Mainly because of tobacco smoking and the growing prevalence of type 2 diabetes, chronic limb-threatening ischemia represents a growing burden on health care and social care services around the world.

Unless the blood supply to the affected limb is restored, patients with chronic limb-threatening ischemia are at high risk for amputation or death. Although it is universally agreed that – in addition to best medical therapy – virtually all patients with chronic limb-threatening ischemia should at least be considered for revascularization, there is continuing debate as to whether conducting vein bypass surgery, preferably using a vein taken from the patient’s own leg, or endovascular treatment (balloon angioplasty with or without stents) is preferable.

“BASIL-2 is the only randomized trial to specifically compare a vein bypass first with best endovascular treatment first revascularisation strategy in patients with chronic limb-threatening ischemia who required an infrapopliteal (with or without an additional more proximal infrainguinal) revascularization procedure to restore limb perfusion,” the authors noted.

For the trial, which was conducted at 41 vascular surgery units in the United Kingdom, Sweden, and Denmark, 345 patients with chronic limb-threatening ischemia who required an infrapopliteal revascularization procedure to restore limb perfusion were randomly assigned to receive either vein bypass or best endovascular treatment as their first revascularization procedure.

Most vein bypasses used the great saphenous vein and originated from the common or superficial femoral arteries. Most endovascular interventions comprised plain balloon angioplasty with selective use of plain or drug-eluting stents. Participants were followed up for a minimum of 2 years.

The primary outcome was amputation-free survival, defined as time to first major (above the ankle) amputation or death from any cause measured in the intention-to-treat population.

Results showed that major amputation or death occurred in 63% of patients in the vein bypass group and in 53% of those in the best endovascular treatment group (adjusted hazard ratio, 1.35; P = .037).

The results were driven by a higher death rate in the vein bypass group (53% vs. 45%; aHR, 1.37).

In both groups, the most common causes of morbidity and death, including death occurring within 30 days of first revascularization, were cardiovascular and respiratory events.

The authors noted that outcomes for the patients in the BASIL-2 trial were poor (median amputation-free survival was 3.8 years, and half the patients died within 5 years).

They pointed out that severe, multilevel atherosclerotic disease that causes chronic limb-threatening ischemia develops over many years, but at baseline in this study, around 20% of patients said they were still smoking, and around 70% of patients had diabetes, of whom around 50% required insulin. In addition, around 90% of the participants often had quite extensive tissue loss.

“These baseline data suggest that there might still be missed opportunities in public health and primary care to prevent chronic limb-threatening ischemia through medical therapy and lifestyle interventions and missed opportunities to refer patients to secondary care earlier once chronic limb-threatening ischemia begins to develop,” they suggested.

“Better prevention and timely referral are important: the BASIL-2 trial shows that, by the time patients present to vascular and endovascular surgeons and interventional radiologists with established chronic limb-threatening ischemia, their prognosis is often poor regardless of what form of revascularization they are offered,” they added.
 

Conflicting results

In an accompanying comment, Ankur Kalra, MD, Franciscan Health, Lafayette, Ind., and Ashish Kumar, MD, Cleveland Clinic Akron (Ohio) General, noted that atherosclerotic lower-extremity peripheral artery disease affects more than 230 million people worldwide, and prevalence is increasing. Chronic limb-threatening ischemia is a severe form of peripheral artery disease that affects 11% of patients with peripheral artery disease and is associated with significant cardiovascular morbidity and death.

Furthermore, amputation rates of 10%-40% during a 6-month follow-up of patients with chronic limb-threatening ischemia who were unable to undergo revascularization have been reported, highlighting the severity of atherosclerotic burden and the need for improved treatment strategies.

Dr. Kalra and Dr. Kumar pointed out that two previous randomized clinical trials compared surgical vein graft bypass with endovascular treatment for patients with chronic limb-threatening ischemia – the BASIL-1 trial, and the BEST-CLI trial.

In the BASIL-1 trial, vein bypass was associated with improved overall survival and amputation-free survival for patients who survived at least 2 years. The BEST-CLI trial also reported a lower risk of a composite of major adverse limb events or death among patients undergoing a surgery-first strategy, compared with endovascular therapy, mostly in patients with suitable single segment of great saphenous vein.

Dr. Kalra and Dr. Kumar said the findings of the BASIL-2 trial should be put in context with these previous studies, which report a positive or equivocal effect of surgery. The results of the BEST-CLI trial were driven by fewer major reinterventions and above-ankle amputations in the surgical group, whereas the results of the BASIL-2 trial were driven by fewer deaths in the best endovascular treatment group, “which potentially points towards a difference in the characteristics of the patients randomly assigned in the two trials.”

They concluded: “Considering the results of the BASIL-2 trial and the BEST-CLI trial, choice of intervention should be based on shared decision making between interventional cardiology, vascular surgery, and the patient, until more evidence is accrued.”

The BASIL-2 trial was funded by the U.K. National Institute of Health Research.

A version of this article first appeared on Medscape.com.

LONG BEACH, CALIF. – For years, clinicians have debated whether prescribing statins to patients older than 75 for the prevention of cardiovascular events is appropriate.

In 2022, the U.S. Preventive Services Task Force concluded that scientific evidence was insufficient to assess the balance between the benefits and harms of the therapy for this older population.

At a session of the annual meeting of the American Geriatrics Society, experts laid out new preliminary recommendations of the AGS and the National Lipid Association on assessing risk and deciding on treatment.

The group concluded that LDL cholesterol levels are associated with incident arteriosclerotic cardiovascular disease (ASCVD), that the coronary artery calcium (CAC) score can be a valuable measure, and that statins may be reasonable to prescribe, even given the risks that have been linked to statins, such as that for muscle pain. Final recommendations are expected by fall 2023.

“This is still a work in progress,” said Daniel E. Forman, MD, professor of medicine and chair of geriatric cardiology at the University of Pittsburgh.

The AGS-NLA panel concluded that, for those aged 75 or older without established ASCVD, LDL cholesterol is associated with incident ASCVD, the only recommendation to be given a class I (strong) rating; others were classed as moderate or weak.

Dr. Forman reviewed the evidence for lowering LDL cholesterol to decrease ASCVD, citing a 2018 study that concluded, “Reverse causation may contribute to the association of lower TC with higher mortality in nonrandomized studies.”

However, research overall shows that, as LDL cholesterol levels increase, patients are more likely to experience a heart event.

Dr. Forman noted that the utility of equations for assessing 5- or 10-year risk of ASCVD is uncertain. However, he said, traditional risk factors, such as family history and ethnicity, still have value.

Assessing risk “has been enriched in the past few years by the introduction of the coronary artery calcium [CAC] score,” he said.

Lower scores predict lower rates of CVD events, Forman said. The AGS-NLA recommends measuring CAC if clinical uncertainty exists about the value of statins.

“It’s reasonable to measure CAC and to withhold statins when the CAC is zero,” Dr. Forman said. “When the CAC score is zero ... the risk of having a cardiovascular event is really next to nil. Patients are happy to know they have a CAC of zero.”

Likewise, patients appreciate knowing whether their score is high, which would indicate increased risk. He said the CAC score is underused by geriatric physicians.

The group also determined, after reviewing the research, that starting treatment is reasonable for patients with an LDL cholesterol level of 70-189 if they have no life-limiting illness and their life expectancy is over 5 years.

Other preliminary recommendations include the use of statins for those aged 75 and older, irrespective of risk for statin-associated muscle symptoms, type 2 diabetes, or impaired cognition. These associations are often weak, Dr. Forman added.
 

Focusing on person-centered decisions

Ariel Green, MD, MPH, PhD, associate professor of medicine at Johns Hopkins University, Baltimore, said statin therapy “should be individualized” to weigh benefits, noncardiac risks, and other considerations.

Clinicians can incorporate life expectancy into prevention decisions using tools such as ePrognosis, from the University of California, San Francisco, Dr. Green said.

If life expectancy is greater than the time to benefit, statin therapy may help. Dr. Green cited research that showed that 2.5 years of statin therapy was needed to prevent one major adverse cardiovascular event (MACE) per 100 patients in a population aged 50-75. Other data show reductions in MACE for those older than 75, but overall, the data are limited in this population.

The proposed recommendation is to use tools such as life tables that include comorbid conditions and functional status to guide clinical decisions.

“Another aspect of assessing net benefits of statin therapy is to consider competing health risks,” Dr. Green said.

The group recommends considering using competing risk-adjusted CVD models, though these are not widely used.

The group also recommends integrating screenings for frailty (Clinical Frailty Scale), dementia (Mini-Cog), and functional status (Vulnerable Elders Scale–13) into assessments.

“The presence of these syndromes should prompt elicitation of patient values and preferences related to prevention and medication use,” Dr. Green said.

Clinicians can use decision aids, but these are not always practical, owing to obstacles such as patients’ cognitive problems, Dr. Green said.

“Another approach is asking people to prioritize a set of universal health outcomes that apply across health conditions, such as maintaining independence, staying alive, reducing, or eliminating symptoms and focusing on comfort,” Dr. Green said.

She addressed the evidence about deprescribing statins, with a focus on those with a life expectancy of less than a year. Researchers have found an increase in quality of life and no increases in cardiovascular events or death when statins were deprescribed.
 

A welcome framework

Cory Krueger, MD, an internal medicine and geriatric physician in Cornville, Ariz., who attended the talk, said he welcomed the presentation, in which preliminary recommendations were explained.

“This has been a controversial area in geriatrics,” Dr. Krueger said. “At least this gave me a framework for discussing this with my patients in a reasonable way.”

Dr. Forman and Dr. Krueger disclosed no relevant financial relationships. Dr. Green receives funding from the National Institute of Aging and Impact Collaboratory.

A version of this article first appeared on Medscape.com.

LONG BEACH, CALIF. – For years, clinicians have debated whether prescribing statins to patients older than 75 for the prevention of cardiovascular events is appropriate.

In 2022, the U.S. Preventive Services Task Force concluded that scientific evidence was insufficient to assess the balance between the benefits and harms of the therapy for this older population.

At a session of the annual meeting of the American Geriatrics Society, experts laid out new preliminary recommendations of the AGS and the National Lipid Association on assessing risk and deciding on treatment.

The group concluded that LDL cholesterol levels are associated with incident arteriosclerotic cardiovascular disease (ASCVD), that the coronary artery calcium (CAC) score can be a valuable measure, and that statins may be reasonable to prescribe, even given the risks that have been linked to statins, such as that for muscle pain. Final recommendations are expected by fall 2023.

“This is still a work in progress,” said Daniel E. Forman, MD, professor of medicine and chair of geriatric cardiology at the University of Pittsburgh.

The AGS-NLA panel concluded that, for those aged 75 or older without established ASCVD, LDL cholesterol is associated with incident ASCVD, the only recommendation to be given a class I (strong) rating; others were classed as moderate or weak.

Dr. Forman reviewed the evidence for lowering LDL cholesterol to decrease ASCVD, citing a 2018 study that concluded, “Reverse causation may contribute to the association of lower TC with higher mortality in nonrandomized studies.”

However, research overall shows that, as LDL cholesterol levels increase, patients are more likely to experience a heart event.

Dr. Forman noted that the utility of equations for assessing 5- or 10-year risk of ASCVD is uncertain. However, he said, traditional risk factors, such as family history and ethnicity, still have value.

Assessing risk “has been enriched in the past few years by the introduction of the coronary artery calcium [CAC] score,” he said.

Lower scores predict lower rates of CVD events, Forman said. The AGS-NLA recommends measuring CAC if clinical uncertainty exists about the value of statins.

“It’s reasonable to measure CAC and to withhold statins when the CAC is zero,” Dr. Forman said. “When the CAC score is zero ... the risk of having a cardiovascular event is really next to nil. Patients are happy to know they have a CAC of zero.”

Likewise, patients appreciate knowing whether their score is high, which would indicate increased risk. He said the CAC score is underused by geriatric physicians.

The group also determined, after reviewing the research, that starting treatment is reasonable for patients with an LDL cholesterol level of 70-189 if they have no life-limiting illness and their life expectancy is over 5 years.

Other preliminary recommendations include the use of statins for those aged 75 and older, irrespective of risk for statin-associated muscle symptoms, type 2 diabetes, or impaired cognition. These associations are often weak, Dr. Forman added.
 

Focusing on person-centered decisions

Ariel Green, MD, MPH, PhD, associate professor of medicine at Johns Hopkins University, Baltimore, said statin therapy “should be individualized” to weigh benefits, noncardiac risks, and other considerations.

Clinicians can incorporate life expectancy into prevention decisions using tools such as ePrognosis, from the University of California, San Francisco, Dr. Green said.

If life expectancy is greater than the time to benefit, statin therapy may help. Dr. Green cited research that showed that 2.5 years of statin therapy was needed to prevent one major adverse cardiovascular event (MACE) per 100 patients in a population aged 50-75. Other data show reductions in MACE for those older than 75, but overall, the data are limited in this population.

The proposed recommendation is to use tools such as life tables that include comorbid conditions and functional status to guide clinical decisions.

“Another aspect of assessing net benefits of statin therapy is to consider competing health risks,” Dr. Green said.

The group recommends considering using competing risk-adjusted CVD models, though these are not widely used.

The group also recommends integrating screenings for frailty (Clinical Frailty Scale), dementia (Mini-Cog), and functional status (Vulnerable Elders Scale–13) into assessments.

“The presence of these syndromes should prompt elicitation of patient values and preferences related to prevention and medication use,” Dr. Green said.

Clinicians can use decision aids, but these are not always practical, owing to obstacles such as patients’ cognitive problems, Dr. Green said.

“Another approach is asking people to prioritize a set of universal health outcomes that apply across health conditions, such as maintaining independence, staying alive, reducing, or eliminating symptoms and focusing on comfort,” Dr. Green said.

She addressed the evidence about deprescribing statins, with a focus on those with a life expectancy of less than a year. Researchers have found an increase in quality of life and no increases in cardiovascular events or death when statins were deprescribed.
 

A welcome framework

Cory Krueger, MD, an internal medicine and geriatric physician in Cornville, Ariz., who attended the talk, said he welcomed the presentation, in which preliminary recommendations were explained.

“This has been a controversial area in geriatrics,” Dr. Krueger said. “At least this gave me a framework for discussing this with my patients in a reasonable way.”

Dr. Forman and Dr. Krueger disclosed no relevant financial relationships. Dr. Green receives funding from the National Institute of Aging and Impact Collaboratory.

A version of this article first appeared on Medscape.com.

LONG BEACH, CALIF. – For years, clinicians have debated whether prescribing statins to patients older than 75 for the prevention of cardiovascular events is appropriate.

In 2022, the U.S. Preventive Services Task Force concluded that scientific evidence was insufficient to assess the balance between the benefits and harms of the therapy for this older population.

At a session of the annual meeting of the American Geriatrics Society, experts laid out new preliminary recommendations of the AGS and the National Lipid Association on assessing risk and deciding on treatment.

The group concluded that LDL cholesterol levels are associated with incident arteriosclerotic cardiovascular disease (ASCVD), that the coronary artery calcium (CAC) score can be a valuable measure, and that statins may be reasonable to prescribe, even given the risks that have been linked to statins, such as that for muscle pain. Final recommendations are expected by fall 2023.

“This is still a work in progress,” said Daniel E. Forman, MD, professor of medicine and chair of geriatric cardiology at the University of Pittsburgh.

The AGS-NLA panel concluded that, for those aged 75 or older without established ASCVD, LDL cholesterol is associated with incident ASCVD, the only recommendation to be given a class I (strong) rating; others were classed as moderate or weak.

Dr. Forman reviewed the evidence for lowering LDL cholesterol to decrease ASCVD, citing a 2018 study that concluded, “Reverse causation may contribute to the association of lower TC with higher mortality in nonrandomized studies.”

However, research overall shows that, as LDL cholesterol levels increase, patients are more likely to experience a heart event.

Dr. Forman noted that the utility of equations for assessing 5- or 10-year risk of ASCVD is uncertain. However, he said, traditional risk factors, such as family history and ethnicity, still have value.

Assessing risk “has been enriched in the past few years by the introduction of the coronary artery calcium [CAC] score,” he said.

Lower scores predict lower rates of CVD events, Forman said. The AGS-NLA recommends measuring CAC if clinical uncertainty exists about the value of statins.

“It’s reasonable to measure CAC and to withhold statins when the CAC is zero,” Dr. Forman said. “When the CAC score is zero ... the risk of having a cardiovascular event is really next to nil. Patients are happy to know they have a CAC of zero.”

Likewise, patients appreciate knowing whether their score is high, which would indicate increased risk. He said the CAC score is underused by geriatric physicians.

The group also determined, after reviewing the research, that starting treatment is reasonable for patients with an LDL cholesterol level of 70-189 if they have no life-limiting illness and their life expectancy is over 5 years.

Other preliminary recommendations include the use of statins for those aged 75 and older, irrespective of risk for statin-associated muscle symptoms, type 2 diabetes, or impaired cognition. These associations are often weak, Dr. Forman added.
 

Focusing on person-centered decisions

Ariel Green, MD, MPH, PhD, associate professor of medicine at Johns Hopkins University, Baltimore, said statin therapy “should be individualized” to weigh benefits, noncardiac risks, and other considerations.

Clinicians can incorporate life expectancy into prevention decisions using tools such as ePrognosis, from the University of California, San Francisco, Dr. Green said.

If life expectancy is greater than the time to benefit, statin therapy may help. Dr. Green cited research that showed that 2.5 years of statin therapy was needed to prevent one major adverse cardiovascular event (MACE) per 100 patients in a population aged 50-75. Other data show reductions in MACE for those older than 75, but overall, the data are limited in this population.

The proposed recommendation is to use tools such as life tables that include comorbid conditions and functional status to guide clinical decisions.

“Another aspect of assessing net benefits of statin therapy is to consider competing health risks,” Dr. Green said.

The group recommends considering using competing risk-adjusted CVD models, though these are not widely used.

The group also recommends integrating screenings for frailty (Clinical Frailty Scale), dementia (Mini-Cog), and functional status (Vulnerable Elders Scale–13) into assessments.

“The presence of these syndromes should prompt elicitation of patient values and preferences related to prevention and medication use,” Dr. Green said.

Clinicians can use decision aids, but these are not always practical, owing to obstacles such as patients’ cognitive problems, Dr. Green said.

“Another approach is asking people to prioritize a set of universal health outcomes that apply across health conditions, such as maintaining independence, staying alive, reducing, or eliminating symptoms and focusing on comfort,” Dr. Green said.

She addressed the evidence about deprescribing statins, with a focus on those with a life expectancy of less than a year. Researchers have found an increase in quality of life and no increases in cardiovascular events or death when statins were deprescribed.
 

A welcome framework

Cory Krueger, MD, an internal medicine and geriatric physician in Cornville, Ariz., who attended the talk, said he welcomed the presentation, in which preliminary recommendations were explained.

“This has been a controversial area in geriatrics,” Dr. Krueger said. “At least this gave me a framework for discussing this with my patients in a reasonable way.”

Dr. Forman and Dr. Krueger disclosed no relevant financial relationships. Dr. Green receives funding from the National Institute of Aging and Impact Collaboratory.

A version of this article first appeared on Medscape.com.

WASHINGTON – A bundled intervention combining point-of-care testing, electronic medical record support, and provider education significantly improved lipid screening rates in children aged 9-11 years, according to data from approximately 100 monthly visits over a 3-year period.

Guidelines from the National Heart, Lung, and Blood Institute currently recommend universal lipid screening for children aged 9-11 years, but screening rates in clinical practice remain low, according to Ruth E. Gardner, MD, of Penn State University, Hershey, and colleagues.

In a poster presented at the Pediatric Academic Societies annual meeting, Dr. Gardner and colleagues shared results of the implementation of a bundled testing protocol designed to improve screening.

The researchers reviewed data on lipid testing within 30 days for all 9- to 11-year-old well child visits at a single center between May 2019 and February 2022. The bundled intervention was introduced in May 2021.

The bundled protocol included in-office capillary testing and provider education. In addition, electronic medical record templates were modified to include prompts for lipid screening at relevant ages, and EMR orders were adjusted to include lipid testing. The researchers also collected targeted provider feedback on individualized screening rates in February 2022.

Screening rates were plotted monthly. For the period from May 2019 through May 2021, the rates averaged 6.5%. However, after the introduction of the bundled intervention, the rate increased to 29.9%. Following targeted provider feedback in February 2022, the researchers found an additional shift to 52.1% through March and April 2022.

The findings were limited by the use of data from a single center, and the researchers used an extended study period to account for disruptions to well-child care in the spring of 2020 related to the COVID-19 pandemic.

However, the results support the effectiveness of a bundled intervention for improving lipid screening rates in children aged 9-11 years, the researchers said, and targeted provider feedback and education could yield additional improvements, they concluded.
 

Preteen years are an optimal time for screening

“The current study is important because atherosclerosis begins in childhood, and screening at ages 9-11 is an optimal time to begin lifestyle changes to improve overall health and reduce risks of heart disease,” said Margaret Thew, DNP, FNP-BC, of the Medical College of Wisconsin, Milwaukee, in an interview.

Ms. Thew, who was not involved in the study, said, “The number of recommended and required screening items needed in pediatrics is vast, so many providers have to select which items to focus on for their health screenings with these ages.”

Overall, “I was impressed with the improvements that were made in this quality improvement study,” said Ms. Thew.

Barriers to lipid screening in this population include the reduced number of health screenings and immunizations recommended for this age group; the consequence is that access is limited to discuss preventive care opportunities, said Ms. Thew in an interview. Steps to overcome these barriers could include the use of many of the screening tools introduced in the current study, such as point-of-care testing in the office, use of the EMR to remind providers of testing, which can be done during well visits or school physicals, and educating providers about the current guidelines, she noted.

Other strategies to increase screening include moving the immunization series to provide more frequent appointments to children aged 9-11 years to offer education and preventive care, Ms. Thew added.

The study received no outside funding. The researchers had no financial conflicts to disclose. Ms. Thew had no financial conflicts to disclose and serves on the Editorial Advisory Board of Pediatric News.
 

WASHINGTON – A bundled intervention combining point-of-care testing, electronic medical record support, and provider education significantly improved lipid screening rates in children aged 9-11 years, according to data from approximately 100 monthly visits over a 3-year period.

Guidelines from the National Heart, Lung, and Blood Institute currently recommend universal lipid screening for children aged 9-11 years, but screening rates in clinical practice remain low, according to Ruth E. Gardner, MD, of Penn State University, Hershey, and colleagues.

In a poster presented at the Pediatric Academic Societies annual meeting, Dr. Gardner and colleagues shared results of the implementation of a bundled testing protocol designed to improve screening.

The researchers reviewed data on lipid testing within 30 days for all 9- to 11-year-old well child visits at a single center between May 2019 and February 2022. The bundled intervention was introduced in May 2021.

The bundled protocol included in-office capillary testing and provider education. In addition, electronic medical record templates were modified to include prompts for lipid screening at relevant ages, and EMR orders were adjusted to include lipid testing. The researchers also collected targeted provider feedback on individualized screening rates in February 2022.

Screening rates were plotted monthly. For the period from May 2019 through May 2021, the rates averaged 6.5%. However, after the introduction of the bundled intervention, the rate increased to 29.9%. Following targeted provider feedback in February 2022, the researchers found an additional shift to 52.1% through March and April 2022.

The findings were limited by the use of data from a single center, and the researchers used an extended study period to account for disruptions to well-child care in the spring of 2020 related to the COVID-19 pandemic.

However, the results support the effectiveness of a bundled intervention for improving lipid screening rates in children aged 9-11 years, the researchers said, and targeted provider feedback and education could yield additional improvements, they concluded.
 

Preteen years are an optimal time for screening

“The current study is important because atherosclerosis begins in childhood, and screening at ages 9-11 is an optimal time to begin lifestyle changes to improve overall health and reduce risks of heart disease,” said Margaret Thew, DNP, FNP-BC, of the Medical College of Wisconsin, Milwaukee, in an interview.

Ms. Thew, who was not involved in the study, said, “The number of recommended and required screening items needed in pediatrics is vast, so many providers have to select which items to focus on for their health screenings with these ages.”

Overall, “I was impressed with the improvements that were made in this quality improvement study,” said Ms. Thew.

Barriers to lipid screening in this population include the reduced number of health screenings and immunizations recommended for this age group; the consequence is that access is limited to discuss preventive care opportunities, said Ms. Thew in an interview. Steps to overcome these barriers could include the use of many of the screening tools introduced in the current study, such as point-of-care testing in the office, use of the EMR to remind providers of testing, which can be done during well visits or school physicals, and educating providers about the current guidelines, she noted.

Other strategies to increase screening include moving the immunization series to provide more frequent appointments to children aged 9-11 years to offer education and preventive care, Ms. Thew added.

The study received no outside funding. The researchers had no financial conflicts to disclose. Ms. Thew had no financial conflicts to disclose and serves on the Editorial Advisory Board of Pediatric News.
 

WASHINGTON – A bundled intervention combining point-of-care testing, electronic medical record support, and provider education significantly improved lipid screening rates in children aged 9-11 years, according to data from approximately 100 monthly visits over a 3-year period.

Guidelines from the National Heart, Lung, and Blood Institute currently recommend universal lipid screening for children aged 9-11 years, but screening rates in clinical practice remain low, according to Ruth E. Gardner, MD, of Penn State University, Hershey, and colleagues.

In a poster presented at the Pediatric Academic Societies annual meeting, Dr. Gardner and colleagues shared results of the implementation of a bundled testing protocol designed to improve screening.

The researchers reviewed data on lipid testing within 30 days for all 9- to 11-year-old well child visits at a single center between May 2019 and February 2022. The bundled intervention was introduced in May 2021.

The bundled protocol included in-office capillary testing and provider education. In addition, electronic medical record templates were modified to include prompts for lipid screening at relevant ages, and EMR orders were adjusted to include lipid testing. The researchers also collected targeted provider feedback on individualized screening rates in February 2022.

Screening rates were plotted monthly. For the period from May 2019 through May 2021, the rates averaged 6.5%. However, after the introduction of the bundled intervention, the rate increased to 29.9%. Following targeted provider feedback in February 2022, the researchers found an additional shift to 52.1% through March and April 2022.

The findings were limited by the use of data from a single center, and the researchers used an extended study period to account for disruptions to well-child care in the spring of 2020 related to the COVID-19 pandemic.

However, the results support the effectiveness of a bundled intervention for improving lipid screening rates in children aged 9-11 years, the researchers said, and targeted provider feedback and education could yield additional improvements, they concluded.
 

Preteen years are an optimal time for screening

“The current study is important because atherosclerosis begins in childhood, and screening at ages 9-11 is an optimal time to begin lifestyle changes to improve overall health and reduce risks of heart disease,” said Margaret Thew, DNP, FNP-BC, of the Medical College of Wisconsin, Milwaukee, in an interview.

Ms. Thew, who was not involved in the study, said, “The number of recommended and required screening items needed in pediatrics is vast, so many providers have to select which items to focus on for their health screenings with these ages.”

Overall, “I was impressed with the improvements that were made in this quality improvement study,” said Ms. Thew.

Barriers to lipid screening in this population include the reduced number of health screenings and immunizations recommended for this age group; the consequence is that access is limited to discuss preventive care opportunities, said Ms. Thew in an interview. Steps to overcome these barriers could include the use of many of the screening tools introduced in the current study, such as point-of-care testing in the office, use of the EMR to remind providers of testing, which can be done during well visits or school physicals, and educating providers about the current guidelines, she noted.

Other strategies to increase screening include moving the immunization series to provide more frequent appointments to children aged 9-11 years to offer education and preventive care, Ms. Thew added.

The study received no outside funding. The researchers had no financial conflicts to disclose. Ms. Thew had no financial conflicts to disclose and serves on the Editorial Advisory Board of Pediatric News.
 

In a new scientific statement, the American Heart Association highlighted the need to assess Asian American subgroups individually to get a more accurate picture of their risk for diabetes and heart disease.

Asian Americans have significant differences in genetics, socioeconomic factors, culture, diet, lifestyle, and acculturation levels based on the Asian region of their ancestry that likely have unique effects on their risk for type 2 diabetes and heart disease, the statement noted.

“Examining Asian subgroups separately is crucial to better understand the distinctions among them, how these differences translate into their risk of type 2 diabetes and atherosclerotic disease, and how health care professionals may provide care and support in a culturally appropriate manner,” writing group chair Tak W. Kwan, MD, chief of cardiology, Lenox Health Greenwich Village, and clinical professor of medicine, Northwell Health, New York City, said in a news release.

The statement was published online in the journal Circulation.
 

Impact on health outcomes

Asian American subgroups are broadly categorized by the geographic region of Asian descent and include South Asia (India, Pakistan, Sri Lanka, Bangladesh, Nepal, or Bhutan); East Asia (Japan, China, or Korea); Southeast Asia (Philippines, Vietnam, Thailand, Cambodia, Laos, Indonesia, Malaysia, Singapore, Hmong); and Native Hawaiian/Pacific Islander (Hawaii, Guam, Samoa, or other Pacific islands).

Asian Americans make up the fastest growing racial and ethnic group in the United States. Together, type 2 diabetes (T2D) and atherosclerotic cardiovascular disease (ASCVD) are the leading causes of illness and death among Asian American adults.

Yet, there is significant variability in prevalence and risk factors within the different subgroups, the writing group pointed out.

For example, based on available data, rates of coronary artery disease (CAD) among Asian Americans indicate an overall prevalence of 8% in men and about 3% in women.

However, available data for subgroups suggest higher CAD rates among Asian Indian Americans (13% for men and 4.4% for women) and Filipino Americans (about 9% and 4%, respectively).

Available data on T2D among Asian American subgroups also show varied prevalence and risk.

A study from California found overall, Asian American adults had higher rates of T2D (range of 15.6%-34.5%) compared with non-Hispanic White adults (12.8%). Among Chinese Americans, the rate was 15.8%. Among Korean and Japanese Americans, rates were about 18% and among Americans with Filipino ancestry, the rate was nearly 32%.

Yet most studies to date aggregate Asian Americans in a single group and do not examine the subgroups individually, which is a challenge to providing evidence-based recommendations, the writing group said.

“Particular attention should focus on the T2D and ASCVD risk differences among the different Asian American subgroups because they may affect the precision in clinical and health outcomes,” the group suggested.

“Culturally specific recommendations and interventions across the different Asian American subgroups related to T2D and ASCVD will help improve primary and secondary prevention and health outcomes in this population,” they added.

The writing group noted that existing CVD risk calculators, which are based on data validated in non-Hispanic Black adults and non-Hispanic White adults and less extensively studied in Asian Americans, may underestimate the risk of T2D and heart disease in South Asian adults, those of lower socioeconomic status, or those with chronic inflammatory diseases.

On the other hand, these tools may overestimate CVD risk among East Asians, those with higher socioeconomic status or those who are already participating in preventive healthcare services.

Advances in epidemiology and data analysis and the availability of larger, representative cohorts will allow for refinement of pooled cohort equations to better gauge ASCVD risk in Asian American subgroups, the group said.
 

Filling in the gaps

The writing group outlined several key areas to consider for strengthening the data about Asian American adults. Chief among them is the need to include disaggregated data on Asian American subgroups in clinical trials and government-sponsored studies.

Another is to standardize ways of collecting ethnic and subgroup data for Asian Americans for national health systems, surveys, and registries. National surveillance surveys should consider oversampling Asian Americans to increase representation for the various subgroups, the writing group suggested.

“All of us – health care professionals, policymakers, community leaders and patients – must advocate for more health research funding for Asian Americans and demand inclusion of Asian American subgroup information in clinical trials and government-sponsored research,” Dr. Kwan said.

“Having a platform to share and disseminate data on Asian Americans for the scientific and research community would also be an asset for the health care professionals who care for this population,” Dr. Kwan added.

The new scientific statement is a follow-up to a 2010 AHA “call to action” to seek data on health disparities among Asian American subgroups and a 2018 scientific statement addressing CVD risk in South Asians (Asian Indian, Pakistani, Sri Lankan, Bangladeshi, Nepali, or Bhutanese).

This scientific statement was prepared by the volunteer writing group on behalf of the AHA Council on Epidemiology and Prevention; the Council on Lifestyle and Cardiometabolic Health; the Council on Arteriosclerosis, Thrombosis and Vascular Biology; the Council on Clinical Cardiology; the Council on Cardiovascular and Stroke Nursing; and the Council on Genomic and Precision Medicine.
 

A version of this article first appeared on Medscape.com.

In a new scientific statement, the American Heart Association highlighted the need to assess Asian American subgroups individually to get a more accurate picture of their risk for diabetes and heart disease.

Asian Americans have significant differences in genetics, socioeconomic factors, culture, diet, lifestyle, and acculturation levels based on the Asian region of their ancestry that likely have unique effects on their risk for type 2 diabetes and heart disease, the statement noted.

“Examining Asian subgroups separately is crucial to better understand the distinctions among them, how these differences translate into their risk of type 2 diabetes and atherosclerotic disease, and how health care professionals may provide care and support in a culturally appropriate manner,” writing group chair Tak W. Kwan, MD, chief of cardiology, Lenox Health Greenwich Village, and clinical professor of medicine, Northwell Health, New York City, said in a news release.

The statement was published online in the journal Circulation.
 

Impact on health outcomes

Asian American subgroups are broadly categorized by the geographic region of Asian descent and include South Asia (India, Pakistan, Sri Lanka, Bangladesh, Nepal, or Bhutan); East Asia (Japan, China, or Korea); Southeast Asia (Philippines, Vietnam, Thailand, Cambodia, Laos, Indonesia, Malaysia, Singapore, Hmong); and Native Hawaiian/Pacific Islander (Hawaii, Guam, Samoa, or other Pacific islands).

Asian Americans make up the fastest growing racial and ethnic group in the United States. Together, type 2 diabetes (T2D) and atherosclerotic cardiovascular disease (ASCVD) are the leading causes of illness and death among Asian American adults.

Yet, there is significant variability in prevalence and risk factors within the different subgroups, the writing group pointed out.

For example, based on available data, rates of coronary artery disease (CAD) among Asian Americans indicate an overall prevalence of 8% in men and about 3% in women.

However, available data for subgroups suggest higher CAD rates among Asian Indian Americans (13% for men and 4.4% for women) and Filipino Americans (about 9% and 4%, respectively).

Available data on T2D among Asian American subgroups also show varied prevalence and risk.

A study from California found overall, Asian American adults had higher rates of T2D (range of 15.6%-34.5%) compared with non-Hispanic White adults (12.8%). Among Chinese Americans, the rate was 15.8%. Among Korean and Japanese Americans, rates were about 18% and among Americans with Filipino ancestry, the rate was nearly 32%.

Yet most studies to date aggregate Asian Americans in a single group and do not examine the subgroups individually, which is a challenge to providing evidence-based recommendations, the writing group said.

“Particular attention should focus on the T2D and ASCVD risk differences among the different Asian American subgroups because they may affect the precision in clinical and health outcomes,” the group suggested.

“Culturally specific recommendations and interventions across the different Asian American subgroups related to T2D and ASCVD will help improve primary and secondary prevention and health outcomes in this population,” they added.

The writing group noted that existing CVD risk calculators, which are based on data validated in non-Hispanic Black adults and non-Hispanic White adults and less extensively studied in Asian Americans, may underestimate the risk of T2D and heart disease in South Asian adults, those of lower socioeconomic status, or those with chronic inflammatory diseases.

On the other hand, these tools may overestimate CVD risk among East Asians, those with higher socioeconomic status or those who are already participating in preventive healthcare services.

Advances in epidemiology and data analysis and the availability of larger, representative cohorts will allow for refinement of pooled cohort equations to better gauge ASCVD risk in Asian American subgroups, the group said.
 

Filling in the gaps

The writing group outlined several key areas to consider for strengthening the data about Asian American adults. Chief among them is the need to include disaggregated data on Asian American subgroups in clinical trials and government-sponsored studies.

Another is to standardize ways of collecting ethnic and subgroup data for Asian Americans for national health systems, surveys, and registries. National surveillance surveys should consider oversampling Asian Americans to increase representation for the various subgroups, the writing group suggested.

“All of us – health care professionals, policymakers, community leaders and patients – must advocate for more health research funding for Asian Americans and demand inclusion of Asian American subgroup information in clinical trials and government-sponsored research,” Dr. Kwan said.

“Having a platform to share and disseminate data on Asian Americans for the scientific and research community would also be an asset for the health care professionals who care for this population,” Dr. Kwan added.

The new scientific statement is a follow-up to a 2010 AHA “call to action” to seek data on health disparities among Asian American subgroups and a 2018 scientific statement addressing CVD risk in South Asians (Asian Indian, Pakistani, Sri Lankan, Bangladeshi, Nepali, or Bhutanese).

This scientific statement was prepared by the volunteer writing group on behalf of the AHA Council on Epidemiology and Prevention; the Council on Lifestyle and Cardiometabolic Health; the Council on Arteriosclerosis, Thrombosis and Vascular Biology; the Council on Clinical Cardiology; the Council on Cardiovascular and Stroke Nursing; and the Council on Genomic and Precision Medicine.
 

A version of this article first appeared on Medscape.com.

In a new scientific statement, the American Heart Association highlighted the need to assess Asian American subgroups individually to get a more accurate picture of their risk for diabetes and heart disease.

Asian Americans have significant differences in genetics, socioeconomic factors, culture, diet, lifestyle, and acculturation levels based on the Asian region of their ancestry that likely have unique effects on their risk for type 2 diabetes and heart disease, the statement noted.

“Examining Asian subgroups separately is crucial to better understand the distinctions among them, how these differences translate into their risk of type 2 diabetes and atherosclerotic disease, and how health care professionals may provide care and support in a culturally appropriate manner,” writing group chair Tak W. Kwan, MD, chief of cardiology, Lenox Health Greenwich Village, and clinical professor of medicine, Northwell Health, New York City, said in a news release.

The statement was published online in the journal Circulation.
 

Impact on health outcomes

Asian American subgroups are broadly categorized by the geographic region of Asian descent and include South Asia (India, Pakistan, Sri Lanka, Bangladesh, Nepal, or Bhutan); East Asia (Japan, China, or Korea); Southeast Asia (Philippines, Vietnam, Thailand, Cambodia, Laos, Indonesia, Malaysia, Singapore, Hmong); and Native Hawaiian/Pacific Islander (Hawaii, Guam, Samoa, or other Pacific islands).

Asian Americans make up the fastest growing racial and ethnic group in the United States. Together, type 2 diabetes (T2D) and atherosclerotic cardiovascular disease (ASCVD) are the leading causes of illness and death among Asian American adults.

Yet, there is significant variability in prevalence and risk factors within the different subgroups, the writing group pointed out.

For example, based on available data, rates of coronary artery disease (CAD) among Asian Americans indicate an overall prevalence of 8% in men and about 3% in women.

However, available data for subgroups suggest higher CAD rates among Asian Indian Americans (13% for men and 4.4% for women) and Filipino Americans (about 9% and 4%, respectively).

Available data on T2D among Asian American subgroups also show varied prevalence and risk.

A study from California found overall, Asian American adults had higher rates of T2D (range of 15.6%-34.5%) compared with non-Hispanic White adults (12.8%). Among Chinese Americans, the rate was 15.8%. Among Korean and Japanese Americans, rates were about 18% and among Americans with Filipino ancestry, the rate was nearly 32%.

Yet most studies to date aggregate Asian Americans in a single group and do not examine the subgroups individually, which is a challenge to providing evidence-based recommendations, the writing group said.

“Particular attention should focus on the T2D and ASCVD risk differences among the different Asian American subgroups because they may affect the precision in clinical and health outcomes,” the group suggested.

“Culturally specific recommendations and interventions across the different Asian American subgroups related to T2D and ASCVD will help improve primary and secondary prevention and health outcomes in this population,” they added.

The writing group noted that existing CVD risk calculators, which are based on data validated in non-Hispanic Black adults and non-Hispanic White adults and less extensively studied in Asian Americans, may underestimate the risk of T2D and heart disease in South Asian adults, those of lower socioeconomic status, or those with chronic inflammatory diseases.

On the other hand, these tools may overestimate CVD risk among East Asians, those with higher socioeconomic status or those who are already participating in preventive healthcare services.

Advances in epidemiology and data analysis and the availability of larger, representative cohorts will allow for refinement of pooled cohort equations to better gauge ASCVD risk in Asian American subgroups, the group said.
 

Filling in the gaps

The writing group outlined several key areas to consider for strengthening the data about Asian American adults. Chief among them is the need to include disaggregated data on Asian American subgroups in clinical trials and government-sponsored studies.

Another is to standardize ways of collecting ethnic and subgroup data for Asian Americans for national health systems, surveys, and registries. National surveillance surveys should consider oversampling Asian Americans to increase representation for the various subgroups, the writing group suggested.

“All of us – health care professionals, policymakers, community leaders and patients – must advocate for more health research funding for Asian Americans and demand inclusion of Asian American subgroup information in clinical trials and government-sponsored research,” Dr. Kwan said.

“Having a platform to share and disseminate data on Asian Americans for the scientific and research community would also be an asset for the health care professionals who care for this population,” Dr. Kwan added.

The new scientific statement is a follow-up to a 2010 AHA “call to action” to seek data on health disparities among Asian American subgroups and a 2018 scientific statement addressing CVD risk in South Asians (Asian Indian, Pakistani, Sri Lankan, Bangladeshi, Nepali, or Bhutanese).

This scientific statement was prepared by the volunteer writing group on behalf of the AHA Council on Epidemiology and Prevention; the Council on Lifestyle and Cardiometabolic Health; the Council on Arteriosclerosis, Thrombosis and Vascular Biology; the Council on Clinical Cardiology; the Council on Cardiovascular and Stroke Nursing; and the Council on Genomic and Precision Medicine.
 

A version of this article first appeared on Medscape.com.

The time has come to rethink the conventional primary endpoints investigators use in coronary revascularization trials – a composite of major adverse cardiovascular events (MACE), death or MI, and other endpoints – and shift toward greater emphasis on quality of life, two clinical trial investigators say.

Gregg Stone, MD, and Mario Gaudino, MD, MSCE, PhD, made their case in the Journal of the American College of Cardiology, writing: “The classic academic exercise of comparing revascularization modalities in an elusive search for a clear ‘winner’ has failed.” Dr. Stone was the principal investigator of the landmark EXCEL trial and an investigator for the ISCHEMIA trial, the latter of which Dr. Gaudino was also an investigator. Both trials evaluated percutaneous coronary intervention (PCI) and coronary artery bypass surgery (CABG) as treatments for coronary artery disease.

In an interview, Dr. Stone, a cardiologist at the Icahn School of Medicine at Mount Sinai, New York, said: “We’re proposing a new endpoint called a composite endpoint measured in a hierarchical fashion of death or quality of life [QOL].” Dr. Gaudino is a cardiac surgeon at Weill Cornell Medicine, New York.
 

Quality of life as a validation tool

As a measure of revascularization after PCI or CABG, Dr. Stone said, QOL is ready for prime time. “Over the last 20 years there’s been a very rich literature of science developed linking certain quality of life instruments to improved outcomes, in particularly health but also heart failure.”

Those instruments include the Seattle Angina Questionnaire, the Minnesota Living with Heart Failure Questionnaire and the Kansas City Cardiomyopathy questionnaire. “All of these are sufficiently validated that the [Food and Drug Administration] considers them ‘validated tools’ for use in clinical trials.” Dr. Stone also noted that substudies of three landmark trials comparing PCI and CABG – EXCEL, SYNTAX, and FREEDOM – used those instruments to evaluate QOL as an endpoint alongside “hard” outcomes such as death, MI or stroke. “So quality of life already is being used and it is already widely accepted. What we’re saying is, when you think about the information you need for medical studies, we believe it’s time to elevate that from secondary supportive information to primary.”

He and Dr. Gaudino are putting their money where their mouths are. They’ve applied for a grant through the Patient-Centered Outcomes Research Institute to use QOL as an outcomes measure in a trial of revascularization strategies in women and minority patients.
 

Shortcomings with traditional endpoints

Dr. Stone explained some of the shortcomings with the traditional endpoints revascularization studies have used. “Everybody agrees that mortality or survival is the most important endpoint, but studies can never be large enough to be powered for that. So we always end up combining them with myocardial infarction, stroke, and often with repeat revascularization” into one MACE endpoint.

But those four types of events are “very, very different,” Dr. Stone said. The severity of MIs and strokes can range from minor, almost inconsequential events to major, debilitating events. “Some strokes resolve in a few days but we count them all the same.”

He ticked off a list of the other outcomes the traditional endpoints don’t account for: atrial fibrillation, kidney dysfunction, musculoskeletal disorders, depression, cognitive changes, and vascular complications. They all can all have a significant impact on a patient’s QOL, Dr. Stone said.

“We’ve now entered an era that is much more patient centered,” Dr. Stone said. “My goal as a physician is to try to impart my knowledge of the evidence that’s out there so that the patient can make the decision that gives them the best chance of meeting their life goals and objectives. When you ask patients what they want, they all want to live longer and they want to live better.”

Mass General

MACE as a composite endpoint has its shortcomings, but using QOL can also be fraught with problems, said Suzanne Baron, MD, director of interventional cardiology research at Massachusetts General Hospital, Boston.

With regards to MACE, she echoed some of Dr. Stone’s concerns. “Patients and clinicians likely would not consider a repeat stenting procedure to be the same as having a stroke, and so weighting these two outcomes equally within a composite endpoint can potentially result in a skewed trial conclusion.”

One potential issue with QOL as an endpoint is that it can vary from day to day. “If quality of life is only measured at a few time points, such as annually, it is possible that those measurements may only reflect a small portion of the patient’s overall quality of life,” she said. “Accordingly, I think that it will be important to incorporate frequent assessments of a patient’s quality of life if these measures will be used as a primary endpoint in cardiac revascularization trials.”

And, in a cost-conscious health care system, quantity (length) of life tends to carry more weight than QOL, she said. “So it will be important that a trial using quality-of-life improvement as a primary endpoint mandates that the degree of improvement be large enough to ensure that the treatment remains high-value from a health economics standpoint.”

Dr. Stone disclosed financial relationships with numerous pharmaceutical companies. Dr. Baron reported financial relationships with Abiomed, Acarix, Boston Scientific, Medtronic, Zoll Medical, Biotronik, Edwards Lifesciences, and Janssen.
 

The time has come to rethink the conventional primary endpoints investigators use in coronary revascularization trials – a composite of major adverse cardiovascular events (MACE), death or MI, and other endpoints – and shift toward greater emphasis on quality of life, two clinical trial investigators say.

Gregg Stone, MD, and Mario Gaudino, MD, MSCE, PhD, made their case in the Journal of the American College of Cardiology, writing: “The classic academic exercise of comparing revascularization modalities in an elusive search for a clear ‘winner’ has failed.” Dr. Stone was the principal investigator of the landmark EXCEL trial and an investigator for the ISCHEMIA trial, the latter of which Dr. Gaudino was also an investigator. Both trials evaluated percutaneous coronary intervention (PCI) and coronary artery bypass surgery (CABG) as treatments for coronary artery disease.

In an interview, Dr. Stone, a cardiologist at the Icahn School of Medicine at Mount Sinai, New York, said: “We’re proposing a new endpoint called a composite endpoint measured in a hierarchical fashion of death or quality of life [QOL].” Dr. Gaudino is a cardiac surgeon at Weill Cornell Medicine, New York.
 

Quality of life as a validation tool

As a measure of revascularization after PCI or CABG, Dr. Stone said, QOL is ready for prime time. “Over the last 20 years there’s been a very rich literature of science developed linking certain quality of life instruments to improved outcomes, in particularly health but also heart failure.”

Those instruments include the Seattle Angina Questionnaire, the Minnesota Living with Heart Failure Questionnaire and the Kansas City Cardiomyopathy questionnaire. “All of these are sufficiently validated that the [Food and Drug Administration] considers them ‘validated tools’ for use in clinical trials.” Dr. Stone also noted that substudies of three landmark trials comparing PCI and CABG – EXCEL, SYNTAX, and FREEDOM – used those instruments to evaluate QOL as an endpoint alongside “hard” outcomes such as death, MI or stroke. “So quality of life already is being used and it is already widely accepted. What we’re saying is, when you think about the information you need for medical studies, we believe it’s time to elevate that from secondary supportive information to primary.”

He and Dr. Gaudino are putting their money where their mouths are. They’ve applied for a grant through the Patient-Centered Outcomes Research Institute to use QOL as an outcomes measure in a trial of revascularization strategies in women and minority patients.
 

Shortcomings with traditional endpoints

Dr. Stone explained some of the shortcomings with the traditional endpoints revascularization studies have used. “Everybody agrees that mortality or survival is the most important endpoint, but studies can never be large enough to be powered for that. So we always end up combining them with myocardial infarction, stroke, and often with repeat revascularization” into one MACE endpoint.

But those four types of events are “very, very different,” Dr. Stone said. The severity of MIs and strokes can range from minor, almost inconsequential events to major, debilitating events. “Some strokes resolve in a few days but we count them all the same.”

He ticked off a list of the other outcomes the traditional endpoints don’t account for: atrial fibrillation, kidney dysfunction, musculoskeletal disorders, depression, cognitive changes, and vascular complications. They all can all have a significant impact on a patient’s QOL, Dr. Stone said.

“We’ve now entered an era that is much more patient centered,” Dr. Stone said. “My goal as a physician is to try to impart my knowledge of the evidence that’s out there so that the patient can make the decision that gives them the best chance of meeting their life goals and objectives. When you ask patients what they want, they all want to live longer and they want to live better.”

Mass General

MACE as a composite endpoint has its shortcomings, but using QOL can also be fraught with problems, said Suzanne Baron, MD, director of interventional cardiology research at Massachusetts General Hospital, Boston.

With regards to MACE, she echoed some of Dr. Stone’s concerns. “Patients and clinicians likely would not consider a repeat stenting procedure to be the same as having a stroke, and so weighting these two outcomes equally within a composite endpoint can potentially result in a skewed trial conclusion.”

One potential issue with QOL as an endpoint is that it can vary from day to day. “If quality of life is only measured at a few time points, such as annually, it is possible that those measurements may only reflect a small portion of the patient’s overall quality of life,” she said. “Accordingly, I think that it will be important to incorporate frequent assessments of a patient’s quality of life if these measures will be used as a primary endpoint in cardiac revascularization trials.”

And, in a cost-conscious health care system, quantity (length) of life tends to carry more weight than QOL, she said. “So it will be important that a trial using quality-of-life improvement as a primary endpoint mandates that the degree of improvement be large enough to ensure that the treatment remains high-value from a health economics standpoint.”

Dr. Stone disclosed financial relationships with numerous pharmaceutical companies. Dr. Baron reported financial relationships with Abiomed, Acarix, Boston Scientific, Medtronic, Zoll Medical, Biotronik, Edwards Lifesciences, and Janssen.
 

The time has come to rethink the conventional primary endpoints investigators use in coronary revascularization trials – a composite of major adverse cardiovascular events (MACE), death or MI, and other endpoints – and shift toward greater emphasis on quality of life, two clinical trial investigators say.

Gregg Stone, MD, and Mario Gaudino, MD, MSCE, PhD, made their case in the Journal of the American College of Cardiology, writing: “The classic academic exercise of comparing revascularization modalities in an elusive search for a clear ‘winner’ has failed.” Dr. Stone was the principal investigator of the landmark EXCEL trial and an investigator for the ISCHEMIA trial, the latter of which Dr. Gaudino was also an investigator. Both trials evaluated percutaneous coronary intervention (PCI) and coronary artery bypass surgery (CABG) as treatments for coronary artery disease.

In an interview, Dr. Stone, a cardiologist at the Icahn School of Medicine at Mount Sinai, New York, said: “We’re proposing a new endpoint called a composite endpoint measured in a hierarchical fashion of death or quality of life [QOL].” Dr. Gaudino is a cardiac surgeon at Weill Cornell Medicine, New York.
 

Quality of life as a validation tool

As a measure of revascularization after PCI or CABG, Dr. Stone said, QOL is ready for prime time. “Over the last 20 years there’s been a very rich literature of science developed linking certain quality of life instruments to improved outcomes, in particularly health but also heart failure.”

Those instruments include the Seattle Angina Questionnaire, the Minnesota Living with Heart Failure Questionnaire and the Kansas City Cardiomyopathy questionnaire. “All of these are sufficiently validated that the [Food and Drug Administration] considers them ‘validated tools’ for use in clinical trials.” Dr. Stone also noted that substudies of three landmark trials comparing PCI and CABG – EXCEL, SYNTAX, and FREEDOM – used those instruments to evaluate QOL as an endpoint alongside “hard” outcomes such as death, MI or stroke. “So quality of life already is being used and it is already widely accepted. What we’re saying is, when you think about the information you need for medical studies, we believe it’s time to elevate that from secondary supportive information to primary.”

He and Dr. Gaudino are putting their money where their mouths are. They’ve applied for a grant through the Patient-Centered Outcomes Research Institute to use QOL as an outcomes measure in a trial of revascularization strategies in women and minority patients.
 

Shortcomings with traditional endpoints

Dr. Stone explained some of the shortcomings with the traditional endpoints revascularization studies have used. “Everybody agrees that mortality or survival is the most important endpoint, but studies can never be large enough to be powered for that. So we always end up combining them with myocardial infarction, stroke, and often with repeat revascularization” into one MACE endpoint.

But those four types of events are “very, very different,” Dr. Stone said. The severity of MIs and strokes can range from minor, almost inconsequential events to major, debilitating events. “Some strokes resolve in a few days but we count them all the same.”

He ticked off a list of the other outcomes the traditional endpoints don’t account for: atrial fibrillation, kidney dysfunction, musculoskeletal disorders, depression, cognitive changes, and vascular complications. They all can all have a significant impact on a patient’s QOL, Dr. Stone said.

“We’ve now entered an era that is much more patient centered,” Dr. Stone said. “My goal as a physician is to try to impart my knowledge of the evidence that’s out there so that the patient can make the decision that gives them the best chance of meeting their life goals and objectives. When you ask patients what they want, they all want to live longer and they want to live better.”

Mass General

MACE as a composite endpoint has its shortcomings, but using QOL can also be fraught with problems, said Suzanne Baron, MD, director of interventional cardiology research at Massachusetts General Hospital, Boston.

With regards to MACE, she echoed some of Dr. Stone’s concerns. “Patients and clinicians likely would not consider a repeat stenting procedure to be the same as having a stroke, and so weighting these two outcomes equally within a composite endpoint can potentially result in a skewed trial conclusion.”

One potential issue with QOL as an endpoint is that it can vary from day to day. “If quality of life is only measured at a few time points, such as annually, it is possible that those measurements may only reflect a small portion of the patient’s overall quality of life,” she said. “Accordingly, I think that it will be important to incorporate frequent assessments of a patient’s quality of life if these measures will be used as a primary endpoint in cardiac revascularization trials.”

And, in a cost-conscious health care system, quantity (length) of life tends to carry more weight than QOL, she said. “So it will be important that a trial using quality-of-life improvement as a primary endpoint mandates that the degree of improvement be large enough to ensure that the treatment remains high-value from a health economics standpoint.”

Dr. Stone disclosed financial relationships with numerous pharmaceutical companies. Dr. Baron reported financial relationships with Abiomed, Acarix, Boston Scientific, Medtronic, Zoll Medical, Biotronik, Edwards Lifesciences, and Janssen.