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Long-term use of ADHD meds and CVD risk: New data
results of a large Swedish nested case-control study suggest.
The increased risk was evident only for hypertension and arterial disease, was dose dependent, and was higher for stimulant than nonstimulant ADHD medications.
“Clinicians should be vigilant in monitoring signs and symptoms of cardiovascular diseases, particularly among those receiving higher doses,” Zheng Chang, PhD, principal researcher, department of medical epidemiology and biostatistics, Karolinska Institutet, Stockholm, said in an interview.
“Treatment decisions, as always, should be based on careful weighing of potential benefits and risks at individual patient level, rather than simple one-size-fits-all recommendations,” Dr. Chang added.
The study was published online in JAMA Psychiatry
Filling in the research gaps
The use of medications to treat ADHD has increased markedly over the past decades in both children and adults. The potential risk for CVD associated with long-term ADHD medication use remains unclear. Most “longitudinal” studies that have looked at the association have an average follow-up time of no more than 2 years, the authors note.
In contrast, the Swedish study assessed the association between cumulative use of ADHD medication in children and adults followed for up to 14 years and also looked at whether associations differ across types of medication and dosages, types of CVD, gender, and age.
Among 278,027 individuals aged 6-64 years diagnosed with ADHD or dispensed ADHD medication, 10,388 with CVD were identified and matched to 51,672 controls without CVD.
Longer cumulative duration of ADHD medication use was associated with a statistically significant increased risk for CVD, compared with no use.
When the risk for specific CVDs was examined, long-term use of ADHD medication (compared with no use) was associated with an increased risk for hypertension and arterial disease but not arrhythmias, heart failure, ischemic heart disease, thromboembolic disease, or cerebrovascular disease.
For hypertension, the adjusted odds ratio was 1.72 (95% confidence interval, 1.51-1.97) for 3 to ≤ 5 years and 1.80 (95% CI, 1.55-2.08) for > 5 years of medication use. For arterial disease, the AOR was 1.65 (95% CI, 1.11-2.45) for 3 to ≤ 5 years and 1.49 (95% CI, 0.96-2.32) for > 5 years of use.
Stimulants confer greatest risk
Across the 14-year follow-up period, each additional year of ADHD medication use was associated with an average 4% increased CVD risk, with a larger 8% increased risk in the first 3 years of cumulative use, followed by stable risk over the remaining follow-up.
Similar risks were observed in children and adults, as well as in females and males.
When focusing on specific ADHD medications, compared with no use, long-term use of the stimulant methylphenidate was associated with an increased risk for CVD (AOR, 1.20 [95% CI, 1.10-1.31] for 3 to ≤ 5 years and 1.19 [95% CI, 1.08-1.31] for > 5 years).
The same was true for long-term use of the stimulant lisdexamfetamine (AOR, 1.23 [95% CI, 1.05-1.44] for 2 to ≤ 3 years and 1.17 [95% CI, 0.98-1.40] for > 3 years).
In contrast, use of the nonstimulant atomoxetine was associated with elevated CVD risk only for the first year of use (AOR, 1.07; 95% CI, 1.01-1.13).
The increased risk for CVD occurred only above certain average daily doses: 45 mg for methylphenidate and lisdexamfetamine, 22.5 mg for amphetamines, and 120 mg for atomoxetine.
The authors note that, although they accounted for a wide range of potential confounding variables, considering the observational nature of the study and the possibility of residual confounding, they could not prove causality.
‘Tricky trade-offs’
The coauthors of an editorial in JAMA Psychiatry (2023 Nov 22. doi: 10.1001/jamapsychiatry.2023.4126) note that the study “should remind us that clinical decision-making is often based on tricky trade-offs that should be considered at the individual patient level.”
Given that hypertension is the leading cause of CV morbidity and mortality worldwide, the increased likelihood of hypertension with long-term use of ADHD medications “cannot be disregarded,” write Samuele Cortese, MD, PhD, and Cristiano Fava, MD, PhD, with University of Southampton (England).
“These findings are especially relevant given the reported association between ADHD and physical conditions, such as obesity, which further contribute to increased cardiovascular risk,” they add.
Dr. Cortese and Dr. Fava say that the increased CV risk – averaging 4% per year and stabilizing after 3 years of treatment – “should be carefully weighed against the established benefits, on a case-by-case basis.”
“Importantly,” they write, “large real-world self-controlled studies have shown that individuals with ADHD experience significantly fewer unintentional physical injuries, motor vehicle crashes, substance use disorders, and criminal acts, as well as improved academic functioning, during periods when they are taking, compared with periods when they are not taking, methylphenidate.”
The risk-benefit ratio, however, may be lower in people with preexisting heart conditions. However, more evidence and precise recommendations are needed in relation to the treatment of individuals with ADHD and preexisting CV conditions, the editorial writers say.
This study was supported by grants from the Swedish Research Council for Health, Working Life, and Welfare and the European Union’s Horizon 2020 research and innovation program. The authors and editorial writers have no relevant conflicts of interest.
A version of this article appeared on Medscape.com.
results of a large Swedish nested case-control study suggest.
The increased risk was evident only for hypertension and arterial disease, was dose dependent, and was higher for stimulant than nonstimulant ADHD medications.
“Clinicians should be vigilant in monitoring signs and symptoms of cardiovascular diseases, particularly among those receiving higher doses,” Zheng Chang, PhD, principal researcher, department of medical epidemiology and biostatistics, Karolinska Institutet, Stockholm, said in an interview.
“Treatment decisions, as always, should be based on careful weighing of potential benefits and risks at individual patient level, rather than simple one-size-fits-all recommendations,” Dr. Chang added.
The study was published online in JAMA Psychiatry
Filling in the research gaps
The use of medications to treat ADHD has increased markedly over the past decades in both children and adults. The potential risk for CVD associated with long-term ADHD medication use remains unclear. Most “longitudinal” studies that have looked at the association have an average follow-up time of no more than 2 years, the authors note.
In contrast, the Swedish study assessed the association between cumulative use of ADHD medication in children and adults followed for up to 14 years and also looked at whether associations differ across types of medication and dosages, types of CVD, gender, and age.
Among 278,027 individuals aged 6-64 years diagnosed with ADHD or dispensed ADHD medication, 10,388 with CVD were identified and matched to 51,672 controls without CVD.
Longer cumulative duration of ADHD medication use was associated with a statistically significant increased risk for CVD, compared with no use.
When the risk for specific CVDs was examined, long-term use of ADHD medication (compared with no use) was associated with an increased risk for hypertension and arterial disease but not arrhythmias, heart failure, ischemic heart disease, thromboembolic disease, or cerebrovascular disease.
For hypertension, the adjusted odds ratio was 1.72 (95% confidence interval, 1.51-1.97) for 3 to ≤ 5 years and 1.80 (95% CI, 1.55-2.08) for > 5 years of medication use. For arterial disease, the AOR was 1.65 (95% CI, 1.11-2.45) for 3 to ≤ 5 years and 1.49 (95% CI, 0.96-2.32) for > 5 years of use.
Stimulants confer greatest risk
Across the 14-year follow-up period, each additional year of ADHD medication use was associated with an average 4% increased CVD risk, with a larger 8% increased risk in the first 3 years of cumulative use, followed by stable risk over the remaining follow-up.
Similar risks were observed in children and adults, as well as in females and males.
When focusing on specific ADHD medications, compared with no use, long-term use of the stimulant methylphenidate was associated with an increased risk for CVD (AOR, 1.20 [95% CI, 1.10-1.31] for 3 to ≤ 5 years and 1.19 [95% CI, 1.08-1.31] for > 5 years).
The same was true for long-term use of the stimulant lisdexamfetamine (AOR, 1.23 [95% CI, 1.05-1.44] for 2 to ≤ 3 years and 1.17 [95% CI, 0.98-1.40] for > 3 years).
In contrast, use of the nonstimulant atomoxetine was associated with elevated CVD risk only for the first year of use (AOR, 1.07; 95% CI, 1.01-1.13).
The increased risk for CVD occurred only above certain average daily doses: 45 mg for methylphenidate and lisdexamfetamine, 22.5 mg for amphetamines, and 120 mg for atomoxetine.
The authors note that, although they accounted for a wide range of potential confounding variables, considering the observational nature of the study and the possibility of residual confounding, they could not prove causality.
‘Tricky trade-offs’
The coauthors of an editorial in JAMA Psychiatry (2023 Nov 22. doi: 10.1001/jamapsychiatry.2023.4126) note that the study “should remind us that clinical decision-making is often based on tricky trade-offs that should be considered at the individual patient level.”
Given that hypertension is the leading cause of CV morbidity and mortality worldwide, the increased likelihood of hypertension with long-term use of ADHD medications “cannot be disregarded,” write Samuele Cortese, MD, PhD, and Cristiano Fava, MD, PhD, with University of Southampton (England).
“These findings are especially relevant given the reported association between ADHD and physical conditions, such as obesity, which further contribute to increased cardiovascular risk,” they add.
Dr. Cortese and Dr. Fava say that the increased CV risk – averaging 4% per year and stabilizing after 3 years of treatment – “should be carefully weighed against the established benefits, on a case-by-case basis.”
“Importantly,” they write, “large real-world self-controlled studies have shown that individuals with ADHD experience significantly fewer unintentional physical injuries, motor vehicle crashes, substance use disorders, and criminal acts, as well as improved academic functioning, during periods when they are taking, compared with periods when they are not taking, methylphenidate.”
The risk-benefit ratio, however, may be lower in people with preexisting heart conditions. However, more evidence and precise recommendations are needed in relation to the treatment of individuals with ADHD and preexisting CV conditions, the editorial writers say.
This study was supported by grants from the Swedish Research Council for Health, Working Life, and Welfare and the European Union’s Horizon 2020 research and innovation program. The authors and editorial writers have no relevant conflicts of interest.
A version of this article appeared on Medscape.com.
results of a large Swedish nested case-control study suggest.
The increased risk was evident only for hypertension and arterial disease, was dose dependent, and was higher for stimulant than nonstimulant ADHD medications.
“Clinicians should be vigilant in monitoring signs and symptoms of cardiovascular diseases, particularly among those receiving higher doses,” Zheng Chang, PhD, principal researcher, department of medical epidemiology and biostatistics, Karolinska Institutet, Stockholm, said in an interview.
“Treatment decisions, as always, should be based on careful weighing of potential benefits and risks at individual patient level, rather than simple one-size-fits-all recommendations,” Dr. Chang added.
The study was published online in JAMA Psychiatry
Filling in the research gaps
The use of medications to treat ADHD has increased markedly over the past decades in both children and adults. The potential risk for CVD associated with long-term ADHD medication use remains unclear. Most “longitudinal” studies that have looked at the association have an average follow-up time of no more than 2 years, the authors note.
In contrast, the Swedish study assessed the association between cumulative use of ADHD medication in children and adults followed for up to 14 years and also looked at whether associations differ across types of medication and dosages, types of CVD, gender, and age.
Among 278,027 individuals aged 6-64 years diagnosed with ADHD or dispensed ADHD medication, 10,388 with CVD were identified and matched to 51,672 controls without CVD.
Longer cumulative duration of ADHD medication use was associated with a statistically significant increased risk for CVD, compared with no use.
When the risk for specific CVDs was examined, long-term use of ADHD medication (compared with no use) was associated with an increased risk for hypertension and arterial disease but not arrhythmias, heart failure, ischemic heart disease, thromboembolic disease, or cerebrovascular disease.
For hypertension, the adjusted odds ratio was 1.72 (95% confidence interval, 1.51-1.97) for 3 to ≤ 5 years and 1.80 (95% CI, 1.55-2.08) for > 5 years of medication use. For arterial disease, the AOR was 1.65 (95% CI, 1.11-2.45) for 3 to ≤ 5 years and 1.49 (95% CI, 0.96-2.32) for > 5 years of use.
Stimulants confer greatest risk
Across the 14-year follow-up period, each additional year of ADHD medication use was associated with an average 4% increased CVD risk, with a larger 8% increased risk in the first 3 years of cumulative use, followed by stable risk over the remaining follow-up.
Similar risks were observed in children and adults, as well as in females and males.
When focusing on specific ADHD medications, compared with no use, long-term use of the stimulant methylphenidate was associated with an increased risk for CVD (AOR, 1.20 [95% CI, 1.10-1.31] for 3 to ≤ 5 years and 1.19 [95% CI, 1.08-1.31] for > 5 years).
The same was true for long-term use of the stimulant lisdexamfetamine (AOR, 1.23 [95% CI, 1.05-1.44] for 2 to ≤ 3 years and 1.17 [95% CI, 0.98-1.40] for > 3 years).
In contrast, use of the nonstimulant atomoxetine was associated with elevated CVD risk only for the first year of use (AOR, 1.07; 95% CI, 1.01-1.13).
The increased risk for CVD occurred only above certain average daily doses: 45 mg for methylphenidate and lisdexamfetamine, 22.5 mg for amphetamines, and 120 mg for atomoxetine.
The authors note that, although they accounted for a wide range of potential confounding variables, considering the observational nature of the study and the possibility of residual confounding, they could not prove causality.
‘Tricky trade-offs’
The coauthors of an editorial in JAMA Psychiatry (2023 Nov 22. doi: 10.1001/jamapsychiatry.2023.4126) note that the study “should remind us that clinical decision-making is often based on tricky trade-offs that should be considered at the individual patient level.”
Given that hypertension is the leading cause of CV morbidity and mortality worldwide, the increased likelihood of hypertension with long-term use of ADHD medications “cannot be disregarded,” write Samuele Cortese, MD, PhD, and Cristiano Fava, MD, PhD, with University of Southampton (England).
“These findings are especially relevant given the reported association between ADHD and physical conditions, such as obesity, which further contribute to increased cardiovascular risk,” they add.
Dr. Cortese and Dr. Fava say that the increased CV risk – averaging 4% per year and stabilizing after 3 years of treatment – “should be carefully weighed against the established benefits, on a case-by-case basis.”
“Importantly,” they write, “large real-world self-controlled studies have shown that individuals with ADHD experience significantly fewer unintentional physical injuries, motor vehicle crashes, substance use disorders, and criminal acts, as well as improved academic functioning, during periods when they are taking, compared with periods when they are not taking, methylphenidate.”
The risk-benefit ratio, however, may be lower in people with preexisting heart conditions. However, more evidence and precise recommendations are needed in relation to the treatment of individuals with ADHD and preexisting CV conditions, the editorial writers say.
This study was supported by grants from the Swedish Research Council for Health, Working Life, and Welfare and the European Union’s Horizon 2020 research and innovation program. The authors and editorial writers have no relevant conflicts of interest.
A version of this article appeared on Medscape.com.
FROM JAMA PSYCHIATRY
AI interpretation of CCTA unlocks value of inflammation as CV risk factor
Risk calculations might be transformed
, according to a study that suggests this approach would change treatment about half the time.
In patients with nonobstructive CAD, CCTA measurement of inflammation on the basis of the Fat Attenuation Index (FAI) “predicts fatal and nonfatal cardiac events independently from clinical risk scores and routine CCTA interpretation,” reported Charalambos Antoniades, MD, PhD, professor of cardiology, Radcliffe Department of Medicine, Oxford, England.
This analysis was based on data from ORFAN, an ongoing study that expects to eventually collect data from 250,000 CCTA. There were multiple goals. The first was to evaluate whether there is a need and a role of CCTA to risk stratify patients without obstructive CAD. A second objective was to evaluate if the FAI inflammation score can quantify residual risk in these patients.
Based on the answers to these questions, the investigators then proceeded to determine if an AI risk model that combines data from the FAI score and risk factors is widely generalizable and, in addition, whether it reclassifies patients in a way meaningful to management.
CCTA-based inflammation is promising
The answers to all these questions were yes, according to data presented by Dr. Antoniades in a late-breaker at the American Heart Association scientific sessions.
So far, ORPHAN, which has multiple participating sites in the United Kingdom, Europe, United States, South America, Asia, and Australia, have data on more than 100,000 CCTAs. Approximately 40,000 have been processed. Of these, 82% have had nonobstructive CAD and the remaining obstructive disease.
In long-term follow-up, the numbers of major adverse cardiovascular events (MACE) and cardiac deaths were compared in these two groups. In absolute terms, the nonobstructive CAD group had about twice as many MACE (2,587 vs. 1,450) and cardiac deaths (1,118 vs. 636).
The rate of these events was much lower in the nonobstructive group , which had four times more patients than the obstructive group, but Dr. Antoniades said these data demonstrate substantial rates of events in the nonobstructive group as well as an unmet need to identify and treat risk associated with nonobstructive CAD.
When determining if coronary inflammation as measured with CCTA could be a means identifying risk independent of other factors, the FAI scores were evaluated by quartile in a nested cohort of 3,666 consecutive patients. FAI, which has been validated, is calculated with spatial changes in CCTA-measured perivascular fat composition after standardization for anatomy and other variables.
The discrimination for risk with FAI was impressive. When evaluated across all patients (obstructive or nonobstructive CAD), those in the highest FAI quartile had a hazard ratio (HR) for MACE that was more than six times higher (HR 6.76; P < .001) and a risk of cardiac mortality that was more than 20 times higher (HR 20.20; P < .001) than that of those in the first quartile.
“The prediction was independent of all other risk factors,” Dr. Antoniades reported.
Predictive value greater in nonobstructive CAD
When evaluated in nonobstructive disease, the predictive value of FAI was even greater. In obstructive CAD patients, the increased risk of MACE for the fourth relative to the first quartile was increased threefold (HR 3.15; P < .001), but it was increased almost fivefold among those with nonobstructive CAD (HR 4.77; P < .001). The increases for cardiac mortality were fivefold (HR 5.15; P < .001) and more than 10-fold (HR 10.49; P < .001) in these groups, respectively.
When a risk model based on AI that incorporated FAI plus other cardiovascular risk factors was applied retrospectively to the ORPHAN data, the predicted and actual event graph lines were nearly superimposable over a follow-up to 10 years at risk levels ranging from low to very high.
When this inflammation-based AI model was evaluated against standard risk prediction in patients with nonobstructive CAD, 30% of patients were reclassified to a higher risk category and 10% to a lower risk category.
When the AI-risk calculations were provided to clinicians at four hospitals over a recent 1-year period, it resulted “in changes of management in approximately half of patients,” Dr. Antoniades said.
Overall, Dr. Antoniades said these data provide evidence that coronary inflammation is an important driver of residual risk in patients who have nonobstructive CAD on CCTA, and he believes that the AI-enhanced interpretation of the FAI-based inflammatory burden has the potential to become an important management tool.
“AI-risk assessment may transform risk stratification and management of patients undergoing routine CCTA,” Dr. Antoniades said.
Imaging has potential for expanded risk assessment
The AHA-invited discussant, Viviany R. Taqueti, MD, director of the cardiac stress laboratory at Brigham and Women’s Hospital, Boston, agreed with the promise of evaluating inflammatory infiltrate in the coronary arteries as well as looking at fat in other tissues, such as skeletal muscle, to better risk stratify patients, but she cautioned about the limitations of conclusions based on observational data.
“A registry is not a randomized trial,” she said.
Characterizing AI as a “black box” in terms of understanding methodology, she also recommended further studies to validate the relative contribution of AI to inflammation alone in risk stratification.
Still, she believes that the “explosive growth” in imaging has created new opportunities for more precisely evaluating cardiovascular risk. She said these might be particularly helpful in the context of the “changing landscape” in CAD driven by less smoking, more obesity, and increased statin use. Overall, she endorsed the basic questions Dr. Antoniades is exploring.
“This is an incredibly intriguing idea that deserves continuing research,” she said.
Dr. Antoniades reported financial relationships with Amarin, AstraZeneca, Caristo Diagnostics, Covance, Mitsubishi Tanabe, MedImmune, Novo Nordisk, Sanofi, and Silence Therapeutics. Dr. Taqueti reported no potential conflicts of interest.
Risk calculations might be transformed
Risk calculations might be transformed
, according to a study that suggests this approach would change treatment about half the time.
In patients with nonobstructive CAD, CCTA measurement of inflammation on the basis of the Fat Attenuation Index (FAI) “predicts fatal and nonfatal cardiac events independently from clinical risk scores and routine CCTA interpretation,” reported Charalambos Antoniades, MD, PhD, professor of cardiology, Radcliffe Department of Medicine, Oxford, England.
This analysis was based on data from ORFAN, an ongoing study that expects to eventually collect data from 250,000 CCTA. There were multiple goals. The first was to evaluate whether there is a need and a role of CCTA to risk stratify patients without obstructive CAD. A second objective was to evaluate if the FAI inflammation score can quantify residual risk in these patients.
Based on the answers to these questions, the investigators then proceeded to determine if an AI risk model that combines data from the FAI score and risk factors is widely generalizable and, in addition, whether it reclassifies patients in a way meaningful to management.
CCTA-based inflammation is promising
The answers to all these questions were yes, according to data presented by Dr. Antoniades in a late-breaker at the American Heart Association scientific sessions.
So far, ORPHAN, which has multiple participating sites in the United Kingdom, Europe, United States, South America, Asia, and Australia, have data on more than 100,000 CCTAs. Approximately 40,000 have been processed. Of these, 82% have had nonobstructive CAD and the remaining obstructive disease.
In long-term follow-up, the numbers of major adverse cardiovascular events (MACE) and cardiac deaths were compared in these two groups. In absolute terms, the nonobstructive CAD group had about twice as many MACE (2,587 vs. 1,450) and cardiac deaths (1,118 vs. 636).
The rate of these events was much lower in the nonobstructive group , which had four times more patients than the obstructive group, but Dr. Antoniades said these data demonstrate substantial rates of events in the nonobstructive group as well as an unmet need to identify and treat risk associated with nonobstructive CAD.
When determining if coronary inflammation as measured with CCTA could be a means identifying risk independent of other factors, the FAI scores were evaluated by quartile in a nested cohort of 3,666 consecutive patients. FAI, which has been validated, is calculated with spatial changes in CCTA-measured perivascular fat composition after standardization for anatomy and other variables.
The discrimination for risk with FAI was impressive. When evaluated across all patients (obstructive or nonobstructive CAD), those in the highest FAI quartile had a hazard ratio (HR) for MACE that was more than six times higher (HR 6.76; P < .001) and a risk of cardiac mortality that was more than 20 times higher (HR 20.20; P < .001) than that of those in the first quartile.
“The prediction was independent of all other risk factors,” Dr. Antoniades reported.
Predictive value greater in nonobstructive CAD
When evaluated in nonobstructive disease, the predictive value of FAI was even greater. In obstructive CAD patients, the increased risk of MACE for the fourth relative to the first quartile was increased threefold (HR 3.15; P < .001), but it was increased almost fivefold among those with nonobstructive CAD (HR 4.77; P < .001). The increases for cardiac mortality were fivefold (HR 5.15; P < .001) and more than 10-fold (HR 10.49; P < .001) in these groups, respectively.
When a risk model based on AI that incorporated FAI plus other cardiovascular risk factors was applied retrospectively to the ORPHAN data, the predicted and actual event graph lines were nearly superimposable over a follow-up to 10 years at risk levels ranging from low to very high.
When this inflammation-based AI model was evaluated against standard risk prediction in patients with nonobstructive CAD, 30% of patients were reclassified to a higher risk category and 10% to a lower risk category.
When the AI-risk calculations were provided to clinicians at four hospitals over a recent 1-year period, it resulted “in changes of management in approximately half of patients,” Dr. Antoniades said.
Overall, Dr. Antoniades said these data provide evidence that coronary inflammation is an important driver of residual risk in patients who have nonobstructive CAD on CCTA, and he believes that the AI-enhanced interpretation of the FAI-based inflammatory burden has the potential to become an important management tool.
“AI-risk assessment may transform risk stratification and management of patients undergoing routine CCTA,” Dr. Antoniades said.
Imaging has potential for expanded risk assessment
The AHA-invited discussant, Viviany R. Taqueti, MD, director of the cardiac stress laboratory at Brigham and Women’s Hospital, Boston, agreed with the promise of evaluating inflammatory infiltrate in the coronary arteries as well as looking at fat in other tissues, such as skeletal muscle, to better risk stratify patients, but she cautioned about the limitations of conclusions based on observational data.
“A registry is not a randomized trial,” she said.
Characterizing AI as a “black box” in terms of understanding methodology, she also recommended further studies to validate the relative contribution of AI to inflammation alone in risk stratification.
Still, she believes that the “explosive growth” in imaging has created new opportunities for more precisely evaluating cardiovascular risk. She said these might be particularly helpful in the context of the “changing landscape” in CAD driven by less smoking, more obesity, and increased statin use. Overall, she endorsed the basic questions Dr. Antoniades is exploring.
“This is an incredibly intriguing idea that deserves continuing research,” she said.
Dr. Antoniades reported financial relationships with Amarin, AstraZeneca, Caristo Diagnostics, Covance, Mitsubishi Tanabe, MedImmune, Novo Nordisk, Sanofi, and Silence Therapeutics. Dr. Taqueti reported no potential conflicts of interest.
, according to a study that suggests this approach would change treatment about half the time.
In patients with nonobstructive CAD, CCTA measurement of inflammation on the basis of the Fat Attenuation Index (FAI) “predicts fatal and nonfatal cardiac events independently from clinical risk scores and routine CCTA interpretation,” reported Charalambos Antoniades, MD, PhD, professor of cardiology, Radcliffe Department of Medicine, Oxford, England.
This analysis was based on data from ORFAN, an ongoing study that expects to eventually collect data from 250,000 CCTA. There were multiple goals. The first was to evaluate whether there is a need and a role of CCTA to risk stratify patients without obstructive CAD. A second objective was to evaluate if the FAI inflammation score can quantify residual risk in these patients.
Based on the answers to these questions, the investigators then proceeded to determine if an AI risk model that combines data from the FAI score and risk factors is widely generalizable and, in addition, whether it reclassifies patients in a way meaningful to management.
CCTA-based inflammation is promising
The answers to all these questions were yes, according to data presented by Dr. Antoniades in a late-breaker at the American Heart Association scientific sessions.
So far, ORPHAN, which has multiple participating sites in the United Kingdom, Europe, United States, South America, Asia, and Australia, have data on more than 100,000 CCTAs. Approximately 40,000 have been processed. Of these, 82% have had nonobstructive CAD and the remaining obstructive disease.
In long-term follow-up, the numbers of major adverse cardiovascular events (MACE) and cardiac deaths were compared in these two groups. In absolute terms, the nonobstructive CAD group had about twice as many MACE (2,587 vs. 1,450) and cardiac deaths (1,118 vs. 636).
The rate of these events was much lower in the nonobstructive group , which had four times more patients than the obstructive group, but Dr. Antoniades said these data demonstrate substantial rates of events in the nonobstructive group as well as an unmet need to identify and treat risk associated with nonobstructive CAD.
When determining if coronary inflammation as measured with CCTA could be a means identifying risk independent of other factors, the FAI scores were evaluated by quartile in a nested cohort of 3,666 consecutive patients. FAI, which has been validated, is calculated with spatial changes in CCTA-measured perivascular fat composition after standardization for anatomy and other variables.
The discrimination for risk with FAI was impressive. When evaluated across all patients (obstructive or nonobstructive CAD), those in the highest FAI quartile had a hazard ratio (HR) for MACE that was more than six times higher (HR 6.76; P < .001) and a risk of cardiac mortality that was more than 20 times higher (HR 20.20; P < .001) than that of those in the first quartile.
“The prediction was independent of all other risk factors,” Dr. Antoniades reported.
Predictive value greater in nonobstructive CAD
When evaluated in nonobstructive disease, the predictive value of FAI was even greater. In obstructive CAD patients, the increased risk of MACE for the fourth relative to the first quartile was increased threefold (HR 3.15; P < .001), but it was increased almost fivefold among those with nonobstructive CAD (HR 4.77; P < .001). The increases for cardiac mortality were fivefold (HR 5.15; P < .001) and more than 10-fold (HR 10.49; P < .001) in these groups, respectively.
When a risk model based on AI that incorporated FAI plus other cardiovascular risk factors was applied retrospectively to the ORPHAN data, the predicted and actual event graph lines were nearly superimposable over a follow-up to 10 years at risk levels ranging from low to very high.
When this inflammation-based AI model was evaluated against standard risk prediction in patients with nonobstructive CAD, 30% of patients were reclassified to a higher risk category and 10% to a lower risk category.
When the AI-risk calculations were provided to clinicians at four hospitals over a recent 1-year period, it resulted “in changes of management in approximately half of patients,” Dr. Antoniades said.
Overall, Dr. Antoniades said these data provide evidence that coronary inflammation is an important driver of residual risk in patients who have nonobstructive CAD on CCTA, and he believes that the AI-enhanced interpretation of the FAI-based inflammatory burden has the potential to become an important management tool.
“AI-risk assessment may transform risk stratification and management of patients undergoing routine CCTA,” Dr. Antoniades said.
Imaging has potential for expanded risk assessment
The AHA-invited discussant, Viviany R. Taqueti, MD, director of the cardiac stress laboratory at Brigham and Women’s Hospital, Boston, agreed with the promise of evaluating inflammatory infiltrate in the coronary arteries as well as looking at fat in other tissues, such as skeletal muscle, to better risk stratify patients, but she cautioned about the limitations of conclusions based on observational data.
“A registry is not a randomized trial,” she said.
Characterizing AI as a “black box” in terms of understanding methodology, she also recommended further studies to validate the relative contribution of AI to inflammation alone in risk stratification.
Still, she believes that the “explosive growth” in imaging has created new opportunities for more precisely evaluating cardiovascular risk. She said these might be particularly helpful in the context of the “changing landscape” in CAD driven by less smoking, more obesity, and increased statin use. Overall, she endorsed the basic questions Dr. Antoniades is exploring.
“This is an incredibly intriguing idea that deserves continuing research,” she said.
Dr. Antoniades reported financial relationships with Amarin, AstraZeneca, Caristo Diagnostics, Covance, Mitsubishi Tanabe, MedImmune, Novo Nordisk, Sanofi, and Silence Therapeutics. Dr. Taqueti reported no potential conflicts of interest.
FROM AHA 2023
PREVENT: AHA’s new risk calculator incorporates CKM health
.
The new Predicting Risk of CVD Events (PREVENT) calculator is the first risk calculator that combines measures of cardiovascular, kidney, and metabolic health to estimate risk for CVD.
It follows an AHA presidential advisory and scientific statement published in October, formally defining cardiovascular-kidney-metabolic (CKM) syndrome.
The PREVENT calculator also “starts earlier and goes longer” than the pooled cohort equations (PCE), Sadiya Khan, MD, MSc, chair of the statement writing committee, told this news organization.
PREVENT is for use in adults aged 30-79 years and estimates the 10- and 30-year risk of total CVD including, for the first time, heart failure. The PCE were designed to assess 10-year risk of only myocardial infarction and stroke and only in adults aged 40-79 years.
“The new PREVENT equations are important for doctors because they allow us to start conversations earlier and more comprehensively and accurately calculate risk for our patients,” said Dr. Khan, preventive cardiologist at Northwestern Medicine and associate professor at Northwestern University in Chicago.
“We want to support clinicians in starting these conversations around optimizing CKM health earlier and begin to engage in discussions on ways to optimize health,” Dr. Khan added.
The AHA scientific statement on the PREVENT calculator, with Dr. Khan as lead author, was published online in Circulation, with an accompanying article that describes development and validation of the tool.
Going beyond the PCE
The new calculator was developed using health information from more than 6 million adults from diverse racial and ethnic, socioeconomic, and geographic backgrounds.
In addition to blood pressure and cholesterol levels, the PREVENT equations allow for inclusion of hemoglobin A1c, if necessary, to monitor metabolic health.
It also includes estimated glomerular filtration rate (eGFR), a measure of kidney function, and allows for use of albumin excretion to monitor kidney disease to further individualize risk assessment and help inform personalized treatment options.
The new calculator also asks about tobacco use and use of medications for CVD risk factors and factors in age and sex, and it removes race from the risk calculations.
“The inclusion of race in risk prediction may imply that differences by race are not modifiable and may reify race as a biological construct, which may worsen health disparities. Therefore, it was decided a priori not to include race as a predictor in the development of PREVENT,” the writing group said.
They emphasized that the PREVENT calculator has similar accuracy among varied racial and ethnic groups.
The equations include an option to use the Social Deprivation Index, which incorporates measures of adverse social determinants of health such as education, poverty, unemployment, and factors based on a person’s environment.
The PREVENT equations are a “critical first step” toward including CKM health and social factors in risk prediction for CVD, Dr. Khan said in a news release.
“We are working on finalizing the online tool and it should be available soon – hopefully in a few weeks,” Dr. Khan told this news organization.
Knowledge gaps
The scientific statement lists several knowledge gaps and areas for more research. These include:
- Incorporating “net benefit” to identify the expected benefit of treatment recommendations based on an individual’s level of risk.
- Collecting more data from people of diverse race and ethnic backgrounds to better represent the increasing diversity in the United States. The number of Hispanic and Asian people included in the PREVENT datasets is lower than national estimates in the general U.S. population, so risk estimations in these populations may be less precise.
- Expanding the collection, reporting, and standardization of social determinants of health data, such as individual information rather than neighborhood information.
- Expanding risk assessment and prevention to earlier in life (childhood and/or adolescence) and in key life periods, such as during the peripartum period, since adverse pregnancy outcomes are associated with increased CVD risk.
- Investigating whether predicting adverse kidney outcomes, particularly among people with and without type 2 diabetes, may further optimize cardiovascular risk prediction.
The scientific statement was prepared by the volunteer writing group on behalf of the AHA. Dr. Khan reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
.
The new Predicting Risk of CVD Events (PREVENT) calculator is the first risk calculator that combines measures of cardiovascular, kidney, and metabolic health to estimate risk for CVD.
It follows an AHA presidential advisory and scientific statement published in October, formally defining cardiovascular-kidney-metabolic (CKM) syndrome.
The PREVENT calculator also “starts earlier and goes longer” than the pooled cohort equations (PCE), Sadiya Khan, MD, MSc, chair of the statement writing committee, told this news organization.
PREVENT is for use in adults aged 30-79 years and estimates the 10- and 30-year risk of total CVD including, for the first time, heart failure. The PCE were designed to assess 10-year risk of only myocardial infarction and stroke and only in adults aged 40-79 years.
“The new PREVENT equations are important for doctors because they allow us to start conversations earlier and more comprehensively and accurately calculate risk for our patients,” said Dr. Khan, preventive cardiologist at Northwestern Medicine and associate professor at Northwestern University in Chicago.
“We want to support clinicians in starting these conversations around optimizing CKM health earlier and begin to engage in discussions on ways to optimize health,” Dr. Khan added.
The AHA scientific statement on the PREVENT calculator, with Dr. Khan as lead author, was published online in Circulation, with an accompanying article that describes development and validation of the tool.
Going beyond the PCE
The new calculator was developed using health information from more than 6 million adults from diverse racial and ethnic, socioeconomic, and geographic backgrounds.
In addition to blood pressure and cholesterol levels, the PREVENT equations allow for inclusion of hemoglobin A1c, if necessary, to monitor metabolic health.
It also includes estimated glomerular filtration rate (eGFR), a measure of kidney function, and allows for use of albumin excretion to monitor kidney disease to further individualize risk assessment and help inform personalized treatment options.
The new calculator also asks about tobacco use and use of medications for CVD risk factors and factors in age and sex, and it removes race from the risk calculations.
“The inclusion of race in risk prediction may imply that differences by race are not modifiable and may reify race as a biological construct, which may worsen health disparities. Therefore, it was decided a priori not to include race as a predictor in the development of PREVENT,” the writing group said.
They emphasized that the PREVENT calculator has similar accuracy among varied racial and ethnic groups.
The equations include an option to use the Social Deprivation Index, which incorporates measures of adverse social determinants of health such as education, poverty, unemployment, and factors based on a person’s environment.
The PREVENT equations are a “critical first step” toward including CKM health and social factors in risk prediction for CVD, Dr. Khan said in a news release.
“We are working on finalizing the online tool and it should be available soon – hopefully in a few weeks,” Dr. Khan told this news organization.
Knowledge gaps
The scientific statement lists several knowledge gaps and areas for more research. These include:
- Incorporating “net benefit” to identify the expected benefit of treatment recommendations based on an individual’s level of risk.
- Collecting more data from people of diverse race and ethnic backgrounds to better represent the increasing diversity in the United States. The number of Hispanic and Asian people included in the PREVENT datasets is lower than national estimates in the general U.S. population, so risk estimations in these populations may be less precise.
- Expanding the collection, reporting, and standardization of social determinants of health data, such as individual information rather than neighborhood information.
- Expanding risk assessment and prevention to earlier in life (childhood and/or adolescence) and in key life periods, such as during the peripartum period, since adverse pregnancy outcomes are associated with increased CVD risk.
- Investigating whether predicting adverse kidney outcomes, particularly among people with and without type 2 diabetes, may further optimize cardiovascular risk prediction.
The scientific statement was prepared by the volunteer writing group on behalf of the AHA. Dr. Khan reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
.
The new Predicting Risk of CVD Events (PREVENT) calculator is the first risk calculator that combines measures of cardiovascular, kidney, and metabolic health to estimate risk for CVD.
It follows an AHA presidential advisory and scientific statement published in October, formally defining cardiovascular-kidney-metabolic (CKM) syndrome.
The PREVENT calculator also “starts earlier and goes longer” than the pooled cohort equations (PCE), Sadiya Khan, MD, MSc, chair of the statement writing committee, told this news organization.
PREVENT is for use in adults aged 30-79 years and estimates the 10- and 30-year risk of total CVD including, for the first time, heart failure. The PCE were designed to assess 10-year risk of only myocardial infarction and stroke and only in adults aged 40-79 years.
“The new PREVENT equations are important for doctors because they allow us to start conversations earlier and more comprehensively and accurately calculate risk for our patients,” said Dr. Khan, preventive cardiologist at Northwestern Medicine and associate professor at Northwestern University in Chicago.
“We want to support clinicians in starting these conversations around optimizing CKM health earlier and begin to engage in discussions on ways to optimize health,” Dr. Khan added.
The AHA scientific statement on the PREVENT calculator, with Dr. Khan as lead author, was published online in Circulation, with an accompanying article that describes development and validation of the tool.
Going beyond the PCE
The new calculator was developed using health information from more than 6 million adults from diverse racial and ethnic, socioeconomic, and geographic backgrounds.
In addition to blood pressure and cholesterol levels, the PREVENT equations allow for inclusion of hemoglobin A1c, if necessary, to monitor metabolic health.
It also includes estimated glomerular filtration rate (eGFR), a measure of kidney function, and allows for use of albumin excretion to monitor kidney disease to further individualize risk assessment and help inform personalized treatment options.
The new calculator also asks about tobacco use and use of medications for CVD risk factors and factors in age and sex, and it removes race from the risk calculations.
“The inclusion of race in risk prediction may imply that differences by race are not modifiable and may reify race as a biological construct, which may worsen health disparities. Therefore, it was decided a priori not to include race as a predictor in the development of PREVENT,” the writing group said.
They emphasized that the PREVENT calculator has similar accuracy among varied racial and ethnic groups.
The equations include an option to use the Social Deprivation Index, which incorporates measures of adverse social determinants of health such as education, poverty, unemployment, and factors based on a person’s environment.
The PREVENT equations are a “critical first step” toward including CKM health and social factors in risk prediction for CVD, Dr. Khan said in a news release.
“We are working on finalizing the online tool and it should be available soon – hopefully in a few weeks,” Dr. Khan told this news organization.
Knowledge gaps
The scientific statement lists several knowledge gaps and areas for more research. These include:
- Incorporating “net benefit” to identify the expected benefit of treatment recommendations based on an individual’s level of risk.
- Collecting more data from people of diverse race and ethnic backgrounds to better represent the increasing diversity in the United States. The number of Hispanic and Asian people included in the PREVENT datasets is lower than national estimates in the general U.S. population, so risk estimations in these populations may be less precise.
- Expanding the collection, reporting, and standardization of social determinants of health data, such as individual information rather than neighborhood information.
- Expanding risk assessment and prevention to earlier in life (childhood and/or adolescence) and in key life periods, such as during the peripartum period, since adverse pregnancy outcomes are associated with increased CVD risk.
- Investigating whether predicting adverse kidney outcomes, particularly among people with and without type 2 diabetes, may further optimize cardiovascular risk prediction.
The scientific statement was prepared by the volunteer writing group on behalf of the AHA. Dr. Khan reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM CIRCULATION
‘Love more’: Why doctors should promote social connection
Those who embrace lifestyle medicine are familiar with the slogan Dean Ornish, MD, likes to use: Eat well, move more, stress less, love more.
That last one, love, was the renowned physician and author’s focus at the recent American College of Lifestyle Medicine Conference in Denver. That’s because love – essentially the support, connectedness, and caring that patients feel when they join a lifestyle-change program – is “where healing occurs at the deepest level.”
Indeed, social connectedness is emerging as a vital pillar in the burgeoning field of lifestyle medicine, a specialty that uses lifestyle interventions to treat chronic conditions. About 300 lifestyle medicine programs are now integrated into residencies in medical schools across the country, up from a handful just 5 years ago, said Meagan Grega, MD, the conference chair.
“The energy and growth in American lifestyle medicine is unparalleled by anything else I see in the health care world right now,” said Dr. Grega, a family physician for 25 years in eastern Pennsylvania.
The field applies volumes of research, from the 1990s to today, demonstrating the healing effects of lifestyle changes. Dr. Ornish’s Preventive Medicine Research Institute has published research on small changes (like pomegranate juice helping blood flow in the heart) and huge ones: Coronary heart patients reversed the narrowing of arteries without lipid-lowering drugs after 1 year of lifestyle changes, including a vegetarian diet, aerobic exercise, stress management, and group support.
Ranking alongside bedrocks such as healthy diet, sleep, exercise, and stress management is positive social connection. That part, the “love more” part, often draws skepticism but is vital, said Dr. Ornish, who is sometimes referred to as the father of lifestyle medicine.
It’s “invariably the part that’s the most meaningful – that sense of connection to community that can come when you bring total strangers together,” Dr. Ornish said. “The ‘love more’ part, in many ways, is not only as important, but in some ways even more because everything really flows from that.”
Patients in a support group, who can “let down their emotional defenses and talk openly and authentically,” are much more likely to make and maintain healthy changes, Dr. Ornish said.
Love as medicine
Mounting evidence links loneliness and isolation with a range of health issues, from mood disorders such as depression to chronic conditions such as cardiovascular disease. What’s more, data suggest that loneliness and social isolation in the United States are on the rise, and the COVID pandemic made that more clear. In May 2023, Surgeon General Vivek Murthy, MD, called loneliness, isolation, and lack of connection in the United States a “public health crisis.”
“Good relationships keep us happier and healthier,” said Robert Waldinger, MD, a psychiatrist at Massachusetts General Hospital, Boston.
Dr. Waldinger, who was not affiliated with the conference, is head of the Harvard Study of Adult Development, one of the longest studies of adult life. Beginning in 1938, the study has tracked 724 people plus more than 1,300 of their descendants and found that embracing community and close relationships helps us live longer and be happier.
In the study, the people who were most satisfied with their relationships at age 50 years were the healthiest at age 80 years. Knowing you have someone to rely on protects the brain: “Those people’s memories stay sharper longer,” Dr. Waldinger said.
He draws a distinction between connection and love. “Love is, I think, more of a feeling,” Dr. Waldinger noted. “Connection is a feeling, but it’s also an activity.”
One in five Americans say they’re lonely, he said, “and loneliness is a stressor.” People who are isolated don’t sleep as well, he added. Their health declines earlier in midlife, brain function slips sooner, and their lives are shorter.
“You don’t have anyone to complain to,” he said. If you do, “you can feel your body start to calm down.” Those without social connections may stay in a low-level “fight-or-flight mode.”
“What we think happens is that you have low levels of inflammation chronically, and those can gradually break down body systems.” Moreover, higher rates of cardiac reactivity, for instance, a racing heartbeat when upset, can lead to high blood pressure and lower immune function.
In his talk, Dr. Ornish said, “Anger is that one emotion that has consistently been shown to make heart disease worse.”
Helping people in those straits is gratifying, Dr. Ornish said. “If we can work with people as lifestyle medicine practitioners when they’re suffering, there’s an opportunity for transformation.”
Future
Of course, that can be easier said than done. Dr. Ornish relayed a patient’s typical reaction to a lifestyle program: “This is kind of weird stuff. Like, I get diet. But a plant-based diet, really? Meditation? Loving more? Really?”
He told the conference, “Part of our job as lifestyle medicine practitioners is to spend a little extra time with them. It doesn’t even take that much time. And to really help them understand what brings them a sense of hope and meaning and purpose.”
The results can be motivating. “Most people feel so much better so quickly,” Dr. Ornish said. “It reframes the reason for change from fear of dying to joy of living.”
Dr. Grega, for one, is optimistic for the future, citing survey results showing that 95% of medical students think that they›d be better counselors with lifestyle training. ‘They passionately want this type of thing,” she said.
A version of this article first appeared on Medscape.com.
Those who embrace lifestyle medicine are familiar with the slogan Dean Ornish, MD, likes to use: Eat well, move more, stress less, love more.
That last one, love, was the renowned physician and author’s focus at the recent American College of Lifestyle Medicine Conference in Denver. That’s because love – essentially the support, connectedness, and caring that patients feel when they join a lifestyle-change program – is “where healing occurs at the deepest level.”
Indeed, social connectedness is emerging as a vital pillar in the burgeoning field of lifestyle medicine, a specialty that uses lifestyle interventions to treat chronic conditions. About 300 lifestyle medicine programs are now integrated into residencies in medical schools across the country, up from a handful just 5 years ago, said Meagan Grega, MD, the conference chair.
“The energy and growth in American lifestyle medicine is unparalleled by anything else I see in the health care world right now,” said Dr. Grega, a family physician for 25 years in eastern Pennsylvania.
The field applies volumes of research, from the 1990s to today, demonstrating the healing effects of lifestyle changes. Dr. Ornish’s Preventive Medicine Research Institute has published research on small changes (like pomegranate juice helping blood flow in the heart) and huge ones: Coronary heart patients reversed the narrowing of arteries without lipid-lowering drugs after 1 year of lifestyle changes, including a vegetarian diet, aerobic exercise, stress management, and group support.
Ranking alongside bedrocks such as healthy diet, sleep, exercise, and stress management is positive social connection. That part, the “love more” part, often draws skepticism but is vital, said Dr. Ornish, who is sometimes referred to as the father of lifestyle medicine.
It’s “invariably the part that’s the most meaningful – that sense of connection to community that can come when you bring total strangers together,” Dr. Ornish said. “The ‘love more’ part, in many ways, is not only as important, but in some ways even more because everything really flows from that.”
Patients in a support group, who can “let down their emotional defenses and talk openly and authentically,” are much more likely to make and maintain healthy changes, Dr. Ornish said.
Love as medicine
Mounting evidence links loneliness and isolation with a range of health issues, from mood disorders such as depression to chronic conditions such as cardiovascular disease. What’s more, data suggest that loneliness and social isolation in the United States are on the rise, and the COVID pandemic made that more clear. In May 2023, Surgeon General Vivek Murthy, MD, called loneliness, isolation, and lack of connection in the United States a “public health crisis.”
“Good relationships keep us happier and healthier,” said Robert Waldinger, MD, a psychiatrist at Massachusetts General Hospital, Boston.
Dr. Waldinger, who was not affiliated with the conference, is head of the Harvard Study of Adult Development, one of the longest studies of adult life. Beginning in 1938, the study has tracked 724 people plus more than 1,300 of their descendants and found that embracing community and close relationships helps us live longer and be happier.
In the study, the people who were most satisfied with their relationships at age 50 years were the healthiest at age 80 years. Knowing you have someone to rely on protects the brain: “Those people’s memories stay sharper longer,” Dr. Waldinger said.
He draws a distinction between connection and love. “Love is, I think, more of a feeling,” Dr. Waldinger noted. “Connection is a feeling, but it’s also an activity.”
One in five Americans say they’re lonely, he said, “and loneliness is a stressor.” People who are isolated don’t sleep as well, he added. Their health declines earlier in midlife, brain function slips sooner, and their lives are shorter.
“You don’t have anyone to complain to,” he said. If you do, “you can feel your body start to calm down.” Those without social connections may stay in a low-level “fight-or-flight mode.”
“What we think happens is that you have low levels of inflammation chronically, and those can gradually break down body systems.” Moreover, higher rates of cardiac reactivity, for instance, a racing heartbeat when upset, can lead to high blood pressure and lower immune function.
In his talk, Dr. Ornish said, “Anger is that one emotion that has consistently been shown to make heart disease worse.”
Helping people in those straits is gratifying, Dr. Ornish said. “If we can work with people as lifestyle medicine practitioners when they’re suffering, there’s an opportunity for transformation.”
Future
Of course, that can be easier said than done. Dr. Ornish relayed a patient’s typical reaction to a lifestyle program: “This is kind of weird stuff. Like, I get diet. But a plant-based diet, really? Meditation? Loving more? Really?”
He told the conference, “Part of our job as lifestyle medicine practitioners is to spend a little extra time with them. It doesn’t even take that much time. And to really help them understand what brings them a sense of hope and meaning and purpose.”
The results can be motivating. “Most people feel so much better so quickly,” Dr. Ornish said. “It reframes the reason for change from fear of dying to joy of living.”
Dr. Grega, for one, is optimistic for the future, citing survey results showing that 95% of medical students think that they›d be better counselors with lifestyle training. ‘They passionately want this type of thing,” she said.
A version of this article first appeared on Medscape.com.
Those who embrace lifestyle medicine are familiar with the slogan Dean Ornish, MD, likes to use: Eat well, move more, stress less, love more.
That last one, love, was the renowned physician and author’s focus at the recent American College of Lifestyle Medicine Conference in Denver. That’s because love – essentially the support, connectedness, and caring that patients feel when they join a lifestyle-change program – is “where healing occurs at the deepest level.”
Indeed, social connectedness is emerging as a vital pillar in the burgeoning field of lifestyle medicine, a specialty that uses lifestyle interventions to treat chronic conditions. About 300 lifestyle medicine programs are now integrated into residencies in medical schools across the country, up from a handful just 5 years ago, said Meagan Grega, MD, the conference chair.
“The energy and growth in American lifestyle medicine is unparalleled by anything else I see in the health care world right now,” said Dr. Grega, a family physician for 25 years in eastern Pennsylvania.
The field applies volumes of research, from the 1990s to today, demonstrating the healing effects of lifestyle changes. Dr. Ornish’s Preventive Medicine Research Institute has published research on small changes (like pomegranate juice helping blood flow in the heart) and huge ones: Coronary heart patients reversed the narrowing of arteries without lipid-lowering drugs after 1 year of lifestyle changes, including a vegetarian diet, aerobic exercise, stress management, and group support.
Ranking alongside bedrocks such as healthy diet, sleep, exercise, and stress management is positive social connection. That part, the “love more” part, often draws skepticism but is vital, said Dr. Ornish, who is sometimes referred to as the father of lifestyle medicine.
It’s “invariably the part that’s the most meaningful – that sense of connection to community that can come when you bring total strangers together,” Dr. Ornish said. “The ‘love more’ part, in many ways, is not only as important, but in some ways even more because everything really flows from that.”
Patients in a support group, who can “let down their emotional defenses and talk openly and authentically,” are much more likely to make and maintain healthy changes, Dr. Ornish said.
Love as medicine
Mounting evidence links loneliness and isolation with a range of health issues, from mood disorders such as depression to chronic conditions such as cardiovascular disease. What’s more, data suggest that loneliness and social isolation in the United States are on the rise, and the COVID pandemic made that more clear. In May 2023, Surgeon General Vivek Murthy, MD, called loneliness, isolation, and lack of connection in the United States a “public health crisis.”
“Good relationships keep us happier and healthier,” said Robert Waldinger, MD, a psychiatrist at Massachusetts General Hospital, Boston.
Dr. Waldinger, who was not affiliated with the conference, is head of the Harvard Study of Adult Development, one of the longest studies of adult life. Beginning in 1938, the study has tracked 724 people plus more than 1,300 of their descendants and found that embracing community and close relationships helps us live longer and be happier.
In the study, the people who were most satisfied with their relationships at age 50 years were the healthiest at age 80 years. Knowing you have someone to rely on protects the brain: “Those people’s memories stay sharper longer,” Dr. Waldinger said.
He draws a distinction between connection and love. “Love is, I think, more of a feeling,” Dr. Waldinger noted. “Connection is a feeling, but it’s also an activity.”
One in five Americans say they’re lonely, he said, “and loneliness is a stressor.” People who are isolated don’t sleep as well, he added. Their health declines earlier in midlife, brain function slips sooner, and their lives are shorter.
“You don’t have anyone to complain to,” he said. If you do, “you can feel your body start to calm down.” Those without social connections may stay in a low-level “fight-or-flight mode.”
“What we think happens is that you have low levels of inflammation chronically, and those can gradually break down body systems.” Moreover, higher rates of cardiac reactivity, for instance, a racing heartbeat when upset, can lead to high blood pressure and lower immune function.
In his talk, Dr. Ornish said, “Anger is that one emotion that has consistently been shown to make heart disease worse.”
Helping people in those straits is gratifying, Dr. Ornish said. “If we can work with people as lifestyle medicine practitioners when they’re suffering, there’s an opportunity for transformation.”
Future
Of course, that can be easier said than done. Dr. Ornish relayed a patient’s typical reaction to a lifestyle program: “This is kind of weird stuff. Like, I get diet. But a plant-based diet, really? Meditation? Loving more? Really?”
He told the conference, “Part of our job as lifestyle medicine practitioners is to spend a little extra time with them. It doesn’t even take that much time. And to really help them understand what brings them a sense of hope and meaning and purpose.”
The results can be motivating. “Most people feel so much better so quickly,” Dr. Ornish said. “It reframes the reason for change from fear of dying to joy of living.”
Dr. Grega, for one, is optimistic for the future, citing survey results showing that 95% of medical students think that they›d be better counselors with lifestyle training. ‘They passionately want this type of thing,” she said.
A version of this article first appeared on Medscape.com.
Study takes fine-grained look at MACE risk with glucocorticoids in RA
SAN DIEGO – Even when taken at low doses and over short periods, glucocorticoids (GCs) were linked to a higher risk of major adverse cardiovascular events (MACE) over the long term in a Veterans Affairs population of older, mostly male patients with rheumatoid arthritis, a new retrospective cohort study has found.
The analysis of nearly 19,000 patients, presented by rheumatologist Beth Wallace, MD, MSc, at the annual meeting of the American College of Rheumatology, showed that the level of risk for MACE rose with the dose, duration, and recency of GC use, in which risk increased significantly at prednisone-equivalent doses as low as 5 mg/day, durations as short as 30 days, and with last use as long as 1 year before MACE.
“Up to half of RA patients in the United States use long-term glucocorticoids despite previous work suggesting they increase MACE in a dose-dependent way,” said Dr. Wallace, assistant professor of medicine at the University of Michigan, Ann Arbor, and a rheumatologist at the VA Ann Arbor Healthcare Center. “Our group previously presented work suggesting that less than 14 days of glucocorticoid use in a 6-month period is associated with a two-thirds increase in odds of MACE over the following 6 months, with 90 days of use associated with more than twofold increase.”
In recent years, researchers such as Dr. Wallace have focused attention on the risks of GCs in RA. The American College of Rheumatology and the European Alliance of Associations for Rheumatology emphasize avoiding long-term use of GCs in RA and keeping doses as small and over the shortest amount of time as possible.
When Dr. Wallace and colleagues looked at the clinical pattern of GC use for patients with RA during the past 2 years, those who took 5 mg, 7.5 mg, and 10 mg daily doses for 30 days and had stopped at least a year before had risk for MACE that rose significantly by 3%, 5%, and 7%, respectively, compared with those who didn’t take GCs in the past 2 years.
While those increases were small, risk for MACE rose even more for those who took the same daily doses for 90 days, increasing 10%, 15%, and 21%, respectively. Researchers linked current ongoing use of GCs for the past 90 days to a 13%, 19%, and 27% higher risk for MACE at those respective doses.
The findings “add to the literature suggesting that there is some risk even with low-dose steroids,” said Michael George, MD, assistant professor of rheumatology and epidemiology at the University of Pennsylvania, Philadelphia, who did not take part in the research but is familiar with the findings.
“We can see that even glucocorticoids taken several years ago may affect cardiovascular risk but that recent use has a bigger effect on risk,” Dr. George said in an interview. “This study also suggests that very low-dose use affects risk.”
For the new study, Dr. Wallace and colleagues examined a Veterans Affairs database and identified 18,882 patients with RA (mean age, 62.5 years; 84% male; 66% GC users) who met the criteria of being > 40 and < 90 years old. The subjects had an initial VA rheumatology visit during 2010-2018 and were excluded if they had a non-RA rheumatologic disorder, prior MACE, or heart failure. MACE was defined as MI, stroke/TIA, cardiac arrest, coronary revascularization, or death from CV cause.
A total of 16% of the cohort had the largest exposure to GCs, defined as use for 90 days or more; 23% had exposure of 14-89 days, and 14% had exposure of 1-13 days.
The median 5-year MACE risk at baseline was 5.3%, and 3,754 patients (19.9%) had high baseline MACE risk. Incident MACE occurred in 4.1% of patients, and the median time to MACE was 2.67 years (interquartile ratio, 1.26-4.45 years).
Covariates included factors such as age, race, sex, body mass index, smoking status, adjusted Elixhauser index, VA risk score for cardiovascular disease, cancer, hospitalization for infection, number of rheumatology clinic visits, and use of lipid-lowering drugs, opioids, methotrexate, biologics, and hydroxychloroquine.
Dr. Wallace noted limitations including the possibility of residual confounding and the influence of background cardiovascular risk. The study didn’t examine the clinical value of taking GCs or compare that to the potential risk. Nor did it examine cost or the risks and benefits of alternative therapeutic options.
A study released earlier this year suggested that patients taking daily prednisolone doses under 5 mg do not have a higher risk of MACE. Previous studies had reached conflicting results.
“Glucocorticoids can provide major benefits to patients, but these benefits must be balanced with the potential risks,” Dr. George said. At low doses, these risks may be small, but they are present. In many cases, escalating DMARD [disease-modifying antirheumatic drug] therapy may be safer than continuing glucocorticoids.”
He added that the risks of GCs may be especially high in older patients and in those who have cardiovascular risk factors: “Often biologics are avoided in these higher-risk patients. But in fact, in many cases biologics may be the safer choice.”
No study funding was reported. Dr. Wallace reported no relevant financial relationships, and some of the other authors reported various ties with industry. Dr. George reported research funding from GlaxoSmithKline and Janssen and consulting fees from AbbVie.
SAN DIEGO – Even when taken at low doses and over short periods, glucocorticoids (GCs) were linked to a higher risk of major adverse cardiovascular events (MACE) over the long term in a Veterans Affairs population of older, mostly male patients with rheumatoid arthritis, a new retrospective cohort study has found.
The analysis of nearly 19,000 patients, presented by rheumatologist Beth Wallace, MD, MSc, at the annual meeting of the American College of Rheumatology, showed that the level of risk for MACE rose with the dose, duration, and recency of GC use, in which risk increased significantly at prednisone-equivalent doses as low as 5 mg/day, durations as short as 30 days, and with last use as long as 1 year before MACE.
“Up to half of RA patients in the United States use long-term glucocorticoids despite previous work suggesting they increase MACE in a dose-dependent way,” said Dr. Wallace, assistant professor of medicine at the University of Michigan, Ann Arbor, and a rheumatologist at the VA Ann Arbor Healthcare Center. “Our group previously presented work suggesting that less than 14 days of glucocorticoid use in a 6-month period is associated with a two-thirds increase in odds of MACE over the following 6 months, with 90 days of use associated with more than twofold increase.”
In recent years, researchers such as Dr. Wallace have focused attention on the risks of GCs in RA. The American College of Rheumatology and the European Alliance of Associations for Rheumatology emphasize avoiding long-term use of GCs in RA and keeping doses as small and over the shortest amount of time as possible.
When Dr. Wallace and colleagues looked at the clinical pattern of GC use for patients with RA during the past 2 years, those who took 5 mg, 7.5 mg, and 10 mg daily doses for 30 days and had stopped at least a year before had risk for MACE that rose significantly by 3%, 5%, and 7%, respectively, compared with those who didn’t take GCs in the past 2 years.
While those increases were small, risk for MACE rose even more for those who took the same daily doses for 90 days, increasing 10%, 15%, and 21%, respectively. Researchers linked current ongoing use of GCs for the past 90 days to a 13%, 19%, and 27% higher risk for MACE at those respective doses.
The findings “add to the literature suggesting that there is some risk even with low-dose steroids,” said Michael George, MD, assistant professor of rheumatology and epidemiology at the University of Pennsylvania, Philadelphia, who did not take part in the research but is familiar with the findings.
“We can see that even glucocorticoids taken several years ago may affect cardiovascular risk but that recent use has a bigger effect on risk,” Dr. George said in an interview. “This study also suggests that very low-dose use affects risk.”
For the new study, Dr. Wallace and colleagues examined a Veterans Affairs database and identified 18,882 patients with RA (mean age, 62.5 years; 84% male; 66% GC users) who met the criteria of being > 40 and < 90 years old. The subjects had an initial VA rheumatology visit during 2010-2018 and were excluded if they had a non-RA rheumatologic disorder, prior MACE, or heart failure. MACE was defined as MI, stroke/TIA, cardiac arrest, coronary revascularization, or death from CV cause.
A total of 16% of the cohort had the largest exposure to GCs, defined as use for 90 days or more; 23% had exposure of 14-89 days, and 14% had exposure of 1-13 days.
The median 5-year MACE risk at baseline was 5.3%, and 3,754 patients (19.9%) had high baseline MACE risk. Incident MACE occurred in 4.1% of patients, and the median time to MACE was 2.67 years (interquartile ratio, 1.26-4.45 years).
Covariates included factors such as age, race, sex, body mass index, smoking status, adjusted Elixhauser index, VA risk score for cardiovascular disease, cancer, hospitalization for infection, number of rheumatology clinic visits, and use of lipid-lowering drugs, opioids, methotrexate, biologics, and hydroxychloroquine.
Dr. Wallace noted limitations including the possibility of residual confounding and the influence of background cardiovascular risk. The study didn’t examine the clinical value of taking GCs or compare that to the potential risk. Nor did it examine cost or the risks and benefits of alternative therapeutic options.
A study released earlier this year suggested that patients taking daily prednisolone doses under 5 mg do not have a higher risk of MACE. Previous studies had reached conflicting results.
“Glucocorticoids can provide major benefits to patients, but these benefits must be balanced with the potential risks,” Dr. George said. At low doses, these risks may be small, but they are present. In many cases, escalating DMARD [disease-modifying antirheumatic drug] therapy may be safer than continuing glucocorticoids.”
He added that the risks of GCs may be especially high in older patients and in those who have cardiovascular risk factors: “Often biologics are avoided in these higher-risk patients. But in fact, in many cases biologics may be the safer choice.”
No study funding was reported. Dr. Wallace reported no relevant financial relationships, and some of the other authors reported various ties with industry. Dr. George reported research funding from GlaxoSmithKline and Janssen and consulting fees from AbbVie.
SAN DIEGO – Even when taken at low doses and over short periods, glucocorticoids (GCs) were linked to a higher risk of major adverse cardiovascular events (MACE) over the long term in a Veterans Affairs population of older, mostly male patients with rheumatoid arthritis, a new retrospective cohort study has found.
The analysis of nearly 19,000 patients, presented by rheumatologist Beth Wallace, MD, MSc, at the annual meeting of the American College of Rheumatology, showed that the level of risk for MACE rose with the dose, duration, and recency of GC use, in which risk increased significantly at prednisone-equivalent doses as low as 5 mg/day, durations as short as 30 days, and with last use as long as 1 year before MACE.
“Up to half of RA patients in the United States use long-term glucocorticoids despite previous work suggesting they increase MACE in a dose-dependent way,” said Dr. Wallace, assistant professor of medicine at the University of Michigan, Ann Arbor, and a rheumatologist at the VA Ann Arbor Healthcare Center. “Our group previously presented work suggesting that less than 14 days of glucocorticoid use in a 6-month period is associated with a two-thirds increase in odds of MACE over the following 6 months, with 90 days of use associated with more than twofold increase.”
In recent years, researchers such as Dr. Wallace have focused attention on the risks of GCs in RA. The American College of Rheumatology and the European Alliance of Associations for Rheumatology emphasize avoiding long-term use of GCs in RA and keeping doses as small and over the shortest amount of time as possible.
When Dr. Wallace and colleagues looked at the clinical pattern of GC use for patients with RA during the past 2 years, those who took 5 mg, 7.5 mg, and 10 mg daily doses for 30 days and had stopped at least a year before had risk for MACE that rose significantly by 3%, 5%, and 7%, respectively, compared with those who didn’t take GCs in the past 2 years.
While those increases were small, risk for MACE rose even more for those who took the same daily doses for 90 days, increasing 10%, 15%, and 21%, respectively. Researchers linked current ongoing use of GCs for the past 90 days to a 13%, 19%, and 27% higher risk for MACE at those respective doses.
The findings “add to the literature suggesting that there is some risk even with low-dose steroids,” said Michael George, MD, assistant professor of rheumatology and epidemiology at the University of Pennsylvania, Philadelphia, who did not take part in the research but is familiar with the findings.
“We can see that even glucocorticoids taken several years ago may affect cardiovascular risk but that recent use has a bigger effect on risk,” Dr. George said in an interview. “This study also suggests that very low-dose use affects risk.”
For the new study, Dr. Wallace and colleagues examined a Veterans Affairs database and identified 18,882 patients with RA (mean age, 62.5 years; 84% male; 66% GC users) who met the criteria of being > 40 and < 90 years old. The subjects had an initial VA rheumatology visit during 2010-2018 and were excluded if they had a non-RA rheumatologic disorder, prior MACE, or heart failure. MACE was defined as MI, stroke/TIA, cardiac arrest, coronary revascularization, or death from CV cause.
A total of 16% of the cohort had the largest exposure to GCs, defined as use for 90 days or more; 23% had exposure of 14-89 days, and 14% had exposure of 1-13 days.
The median 5-year MACE risk at baseline was 5.3%, and 3,754 patients (19.9%) had high baseline MACE risk. Incident MACE occurred in 4.1% of patients, and the median time to MACE was 2.67 years (interquartile ratio, 1.26-4.45 years).
Covariates included factors such as age, race, sex, body mass index, smoking status, adjusted Elixhauser index, VA risk score for cardiovascular disease, cancer, hospitalization for infection, number of rheumatology clinic visits, and use of lipid-lowering drugs, opioids, methotrexate, biologics, and hydroxychloroquine.
Dr. Wallace noted limitations including the possibility of residual confounding and the influence of background cardiovascular risk. The study didn’t examine the clinical value of taking GCs or compare that to the potential risk. Nor did it examine cost or the risks and benefits of alternative therapeutic options.
A study released earlier this year suggested that patients taking daily prednisolone doses under 5 mg do not have a higher risk of MACE. Previous studies had reached conflicting results.
“Glucocorticoids can provide major benefits to patients, but these benefits must be balanced with the potential risks,” Dr. George said. At low doses, these risks may be small, but they are present. In many cases, escalating DMARD [disease-modifying antirheumatic drug] therapy may be safer than continuing glucocorticoids.”
He added that the risks of GCs may be especially high in older patients and in those who have cardiovascular risk factors: “Often biologics are avoided in these higher-risk patients. But in fact, in many cases biologics may be the safer choice.”
No study funding was reported. Dr. Wallace reported no relevant financial relationships, and some of the other authors reported various ties with industry. Dr. George reported research funding from GlaxoSmithKline and Janssen and consulting fees from AbbVie.
AT ACR 2023
Marijuana use dramatically increases risk of heart problems, stroke
Regularly using marijuana can significantly increase a person’s risk of heart attack, heart failure, and stroke, according to a pair of new studies that will be presented at a major upcoming medical conference.
People who use marijuana daily have a 34% increased risk of heart failure, compared with people who don’t use the drug, according to one of the new studies.
The new findings leverage health data from 157,000 people in the National Institutes of Health “All of Us” research program. Researchers analyzed whether marijuana users were more likely to experience heart failure than nonusers over the course of nearly 4 years. The results indicated that coronary artery disease was behind marijuana users’ increased risk. (Coronary artery disease is the buildup of plaque on the walls of the arteries that supply blood to the heart.)
The research was conducted by a team at Medstar Health, a large Maryland health care system that operates 10 hospitals plus hundreds of clinics. The findings will be presented at the American Heart Association’s Scientific Sessions 2023 in Philadelphia.
“Our results should encourage more researchers to study the use of marijuana to better understand its health implications, especially on cardiovascular risk,” said researcher Yakubu Bene-Alhasan, MD, MPH, a doctor at Medstar Health in Baltimore. “We want to provide the population with high-quality information on marijuana use and to help inform policy decisions at the state level, to educate patients, and to guide health care professionals.”
About one in five people in the United States use marijuana, according to the Centers for Disease Control and Prevention. The majority of U.S. states allow marijuana to be used legally for medical purposes, and more than 20 states have legalized recreational marijuana, a tracker from the National Conference of State Legislatures shows.
A second study that will be presented at the conference shows that older people with any combination of type 2 diabetes, high blood pressure, and high cholesterol who use marijuana have an increased risk for a major heart or brain event, compared with people who never used the drug.
The researchers analyzed data for more than 28,000 people age 65 and older who had health conditions that put them at risk for heart problems and whose medical records showed they were marijuana users but not tobacco users. The results showed at least a 20% increased risk of heart attack, stroke, cardiac arrest, or arrhythmia (irregular heartbeat).
The findings are significant because medical professionals have long said that research on the long-term health effects of using marijuana are limited.
“The latest research about cannabis use indicates that smoking and inhaling cannabis increases concentrations of blood carboxyhemoglobin (carbon monoxide, a poisonous gas), tar (partly burned combustible matter) similar to the effects of inhaling a tobacco cigarette, both of which have been linked to heart muscle disease, chest pain, heart rhythm disturbances, heart attacks and other serious conditions,” said Robert L. Page II, PharmD, MSPH, chair of the volunteer writing group for the 2020 American Heart Association Scientific Statement: Medical Marijuana, Recreational Cannabis, and Cardiovascular Health, in a statement. “Together with the results of these two research studies, the cardiovascular risks of cannabis use are becoming clearer and should be carefully considered and monitored by health care professionals and the public.”
A version of this article first appeared on WebMD.com.
Regularly using marijuana can significantly increase a person’s risk of heart attack, heart failure, and stroke, according to a pair of new studies that will be presented at a major upcoming medical conference.
People who use marijuana daily have a 34% increased risk of heart failure, compared with people who don’t use the drug, according to one of the new studies.
The new findings leverage health data from 157,000 people in the National Institutes of Health “All of Us” research program. Researchers analyzed whether marijuana users were more likely to experience heart failure than nonusers over the course of nearly 4 years. The results indicated that coronary artery disease was behind marijuana users’ increased risk. (Coronary artery disease is the buildup of plaque on the walls of the arteries that supply blood to the heart.)
The research was conducted by a team at Medstar Health, a large Maryland health care system that operates 10 hospitals plus hundreds of clinics. The findings will be presented at the American Heart Association’s Scientific Sessions 2023 in Philadelphia.
“Our results should encourage more researchers to study the use of marijuana to better understand its health implications, especially on cardiovascular risk,” said researcher Yakubu Bene-Alhasan, MD, MPH, a doctor at Medstar Health in Baltimore. “We want to provide the population with high-quality information on marijuana use and to help inform policy decisions at the state level, to educate patients, and to guide health care professionals.”
About one in five people in the United States use marijuana, according to the Centers for Disease Control and Prevention. The majority of U.S. states allow marijuana to be used legally for medical purposes, and more than 20 states have legalized recreational marijuana, a tracker from the National Conference of State Legislatures shows.
A second study that will be presented at the conference shows that older people with any combination of type 2 diabetes, high blood pressure, and high cholesterol who use marijuana have an increased risk for a major heart or brain event, compared with people who never used the drug.
The researchers analyzed data for more than 28,000 people age 65 and older who had health conditions that put them at risk for heart problems and whose medical records showed they were marijuana users but not tobacco users. The results showed at least a 20% increased risk of heart attack, stroke, cardiac arrest, or arrhythmia (irregular heartbeat).
The findings are significant because medical professionals have long said that research on the long-term health effects of using marijuana are limited.
“The latest research about cannabis use indicates that smoking and inhaling cannabis increases concentrations of blood carboxyhemoglobin (carbon monoxide, a poisonous gas), tar (partly burned combustible matter) similar to the effects of inhaling a tobacco cigarette, both of which have been linked to heart muscle disease, chest pain, heart rhythm disturbances, heart attacks and other serious conditions,” said Robert L. Page II, PharmD, MSPH, chair of the volunteer writing group for the 2020 American Heart Association Scientific Statement: Medical Marijuana, Recreational Cannabis, and Cardiovascular Health, in a statement. “Together with the results of these two research studies, the cardiovascular risks of cannabis use are becoming clearer and should be carefully considered and monitored by health care professionals and the public.”
A version of this article first appeared on WebMD.com.
Regularly using marijuana can significantly increase a person’s risk of heart attack, heart failure, and stroke, according to a pair of new studies that will be presented at a major upcoming medical conference.
People who use marijuana daily have a 34% increased risk of heart failure, compared with people who don’t use the drug, according to one of the new studies.
The new findings leverage health data from 157,000 people in the National Institutes of Health “All of Us” research program. Researchers analyzed whether marijuana users were more likely to experience heart failure than nonusers over the course of nearly 4 years. The results indicated that coronary artery disease was behind marijuana users’ increased risk. (Coronary artery disease is the buildup of plaque on the walls of the arteries that supply blood to the heart.)
The research was conducted by a team at Medstar Health, a large Maryland health care system that operates 10 hospitals plus hundreds of clinics. The findings will be presented at the American Heart Association’s Scientific Sessions 2023 in Philadelphia.
“Our results should encourage more researchers to study the use of marijuana to better understand its health implications, especially on cardiovascular risk,” said researcher Yakubu Bene-Alhasan, MD, MPH, a doctor at Medstar Health in Baltimore. “We want to provide the population with high-quality information on marijuana use and to help inform policy decisions at the state level, to educate patients, and to guide health care professionals.”
About one in five people in the United States use marijuana, according to the Centers for Disease Control and Prevention. The majority of U.S. states allow marijuana to be used legally for medical purposes, and more than 20 states have legalized recreational marijuana, a tracker from the National Conference of State Legislatures shows.
A second study that will be presented at the conference shows that older people with any combination of type 2 diabetes, high blood pressure, and high cholesterol who use marijuana have an increased risk for a major heart or brain event, compared with people who never used the drug.
The researchers analyzed data for more than 28,000 people age 65 and older who had health conditions that put them at risk for heart problems and whose medical records showed they were marijuana users but not tobacco users. The results showed at least a 20% increased risk of heart attack, stroke, cardiac arrest, or arrhythmia (irregular heartbeat).
The findings are significant because medical professionals have long said that research on the long-term health effects of using marijuana are limited.
“The latest research about cannabis use indicates that smoking and inhaling cannabis increases concentrations of blood carboxyhemoglobin (carbon monoxide, a poisonous gas), tar (partly burned combustible matter) similar to the effects of inhaling a tobacco cigarette, both of which have been linked to heart muscle disease, chest pain, heart rhythm disturbances, heart attacks and other serious conditions,” said Robert L. Page II, PharmD, MSPH, chair of the volunteer writing group for the 2020 American Heart Association Scientific Statement: Medical Marijuana, Recreational Cannabis, and Cardiovascular Health, in a statement. “Together with the results of these two research studies, the cardiovascular risks of cannabis use are becoming clearer and should be carefully considered and monitored by health care professionals and the public.”
A version of this article first appeared on WebMD.com.
FROM AHA 2023
Review finds no CV or VTE risk signal with use of JAK inhibitors for skin indications
, results from a systematic literature review, and meta-analysis showed.
“There remains a knowledge gap regarding the risk of JAK inhibitor use and VTE and/or MACE in the dermatologic population,” researchers led by Michael S. Garshick, MD, a cardiologist at New York University Langone Health, wrote in their study, which was published online in JAMA Dermatology . “Pooled safety studies suggest that the risk of MACE and VTE may be lower in patients treated with JAK inhibitors for a dermatologic indication than the risk observed in the ORAL Surveillance study, which may be related to the younger age and better health status of those enrolled in trials for dermatologic indications.” The results of that study, which included patients with rheumatoid arthritis only, resulted in the addition of a boxed warning in the labels for topical and oral JAK inhibitors regarding the increased risk of MACE, VTE, serious infections, malignancies, and death .
For the review – thought to be the first to specifically evaluate these risks for dermatologic indications – the researchers searched PubMed and ClinicalTrials.gov from inception through April 1, 2023, for phase 3 dermatology randomized clinical trials (RCTs) to evaluate the risk of MACE, VTE, and all-cause mortality with JAK inhibitors, compared with placebo or an active comparator in the treatment of immune-mediated inflammatory skin diseases. They followed Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guidelines and used a random-effects model and the DerSimonian-Laird method to calculate adverse events with odds ratios.
The database search yielded 35 RCTs with a total of 20,651 patients. Their mean age was 38.5 years, 54% were male, and the mean follow-up time was 4.9 months. Of the 35 trials, most (21) involved patients with atopic dermatitis, followed by psoriasis/psoriatic arthritis (9 trials), alopecia areata (3 trials) and vitiligo (2 trials).
The researchers found no significant difference between JAK inhibitors and placebo/active comparator in composite MACE and all-cause mortality (odds ratio, 0.83; 95% confidence interval, 0.44-1.57) or in VTE (OR, 0.52; 95% CI, 0.26-1.04).
In a secondary analysis, which included additional psoriatic arthritis RCTs, no significant differences between the treatment and placebo/active comparator groups were observed. Similarly, subgroup analyses of oral versus topical JAK inhibitors and a sensitivity analysis that excluded pediatric trials showed no significant differences between patients exposed to JAK inhibitors and those not exposed.
The researchers acknowledged certain limitations of the review, including the lack of access to patient-level data, the fact that most trials only included short-term follow-up, and that the findings have limited generalizability to an older patient population. “It remains unclear if the cardiovascular risks of JAK inhibitors are primarily due to patient level cardiovascular risk factors or are drug mediated,” they concluded. “Dermatologists should carefully select patients and assess baseline cardiovascular risk factors when considering JAK therapy. Cardiovascular risk assessment should continue for the duration of treatment.”
Raj Chovatiya, MD, PhD, assistant professor of dermatology and director of the center for eczema and itch at Northwestern University, Chicago, who was asked to comment on the study results, characterized the findings as reassuring to dermatologists who may be reluctant to initiate therapy with JAK inhibitors based on concerns about safety signals for MACE, VTE, and all-cause mortality.
“These data systematically show that across medications and across conditions, there doesn’t appear to be an increased signal for these events during the short-term, placebo-controlled period which generally spans a few months in most studies,” he told this news organization. The findings, he added, “align well with our clinical experience to date for JAK inhibitor use in inflammatory skin disease. Short-term safety, particularly in relation to boxed warning events such MACE, VTE, and all-cause mortality, have generally been favorable with real-world use. It’s good to have a rigorous statistical analysis to refer to when setting patient expectations.”
However, he noted that these data only examined short-term safety during the placebo or active comparator-controlled periods. “Considering that events like MACE or VTE may take many months or years to manifest, continued long-term data generation is needed to fully answer the question of risk,” he said.
Dr. Garshick disclosed that he received grants from Pfizer and personal fees from Bristol Myers Squibb during the conduct of the study and personal fees from Kiniksa Pharmaceuticals outside the submitted work. Several other coauthors reported having advisory board roles and/or having received funding or support from several pharmaceutical companies. Dr. Chovatiya disclosed that he is a consultant to, a speaker for, investigator, and/or a member of the advisory board for several pharmaceutical companies, including those that develop JAK inhibitors.
, results from a systematic literature review, and meta-analysis showed.
“There remains a knowledge gap regarding the risk of JAK inhibitor use and VTE and/or MACE in the dermatologic population,” researchers led by Michael S. Garshick, MD, a cardiologist at New York University Langone Health, wrote in their study, which was published online in JAMA Dermatology . “Pooled safety studies suggest that the risk of MACE and VTE may be lower in patients treated with JAK inhibitors for a dermatologic indication than the risk observed in the ORAL Surveillance study, which may be related to the younger age and better health status of those enrolled in trials for dermatologic indications.” The results of that study, which included patients with rheumatoid arthritis only, resulted in the addition of a boxed warning in the labels for topical and oral JAK inhibitors regarding the increased risk of MACE, VTE, serious infections, malignancies, and death .
For the review – thought to be the first to specifically evaluate these risks for dermatologic indications – the researchers searched PubMed and ClinicalTrials.gov from inception through April 1, 2023, for phase 3 dermatology randomized clinical trials (RCTs) to evaluate the risk of MACE, VTE, and all-cause mortality with JAK inhibitors, compared with placebo or an active comparator in the treatment of immune-mediated inflammatory skin diseases. They followed Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guidelines and used a random-effects model and the DerSimonian-Laird method to calculate adverse events with odds ratios.
The database search yielded 35 RCTs with a total of 20,651 patients. Their mean age was 38.5 years, 54% were male, and the mean follow-up time was 4.9 months. Of the 35 trials, most (21) involved patients with atopic dermatitis, followed by psoriasis/psoriatic arthritis (9 trials), alopecia areata (3 trials) and vitiligo (2 trials).
The researchers found no significant difference between JAK inhibitors and placebo/active comparator in composite MACE and all-cause mortality (odds ratio, 0.83; 95% confidence interval, 0.44-1.57) or in VTE (OR, 0.52; 95% CI, 0.26-1.04).
In a secondary analysis, which included additional psoriatic arthritis RCTs, no significant differences between the treatment and placebo/active comparator groups were observed. Similarly, subgroup analyses of oral versus topical JAK inhibitors and a sensitivity analysis that excluded pediatric trials showed no significant differences between patients exposed to JAK inhibitors and those not exposed.
The researchers acknowledged certain limitations of the review, including the lack of access to patient-level data, the fact that most trials only included short-term follow-up, and that the findings have limited generalizability to an older patient population. “It remains unclear if the cardiovascular risks of JAK inhibitors are primarily due to patient level cardiovascular risk factors or are drug mediated,” they concluded. “Dermatologists should carefully select patients and assess baseline cardiovascular risk factors when considering JAK therapy. Cardiovascular risk assessment should continue for the duration of treatment.”
Raj Chovatiya, MD, PhD, assistant professor of dermatology and director of the center for eczema and itch at Northwestern University, Chicago, who was asked to comment on the study results, characterized the findings as reassuring to dermatologists who may be reluctant to initiate therapy with JAK inhibitors based on concerns about safety signals for MACE, VTE, and all-cause mortality.
“These data systematically show that across medications and across conditions, there doesn’t appear to be an increased signal for these events during the short-term, placebo-controlled period which generally spans a few months in most studies,” he told this news organization. The findings, he added, “align well with our clinical experience to date for JAK inhibitor use in inflammatory skin disease. Short-term safety, particularly in relation to boxed warning events such MACE, VTE, and all-cause mortality, have generally been favorable with real-world use. It’s good to have a rigorous statistical analysis to refer to when setting patient expectations.”
However, he noted that these data only examined short-term safety during the placebo or active comparator-controlled periods. “Considering that events like MACE or VTE may take many months or years to manifest, continued long-term data generation is needed to fully answer the question of risk,” he said.
Dr. Garshick disclosed that he received grants from Pfizer and personal fees from Bristol Myers Squibb during the conduct of the study and personal fees from Kiniksa Pharmaceuticals outside the submitted work. Several other coauthors reported having advisory board roles and/or having received funding or support from several pharmaceutical companies. Dr. Chovatiya disclosed that he is a consultant to, a speaker for, investigator, and/or a member of the advisory board for several pharmaceutical companies, including those that develop JAK inhibitors.
, results from a systematic literature review, and meta-analysis showed.
“There remains a knowledge gap regarding the risk of JAK inhibitor use and VTE and/or MACE in the dermatologic population,” researchers led by Michael S. Garshick, MD, a cardiologist at New York University Langone Health, wrote in their study, which was published online in JAMA Dermatology . “Pooled safety studies suggest that the risk of MACE and VTE may be lower in patients treated with JAK inhibitors for a dermatologic indication than the risk observed in the ORAL Surveillance study, which may be related to the younger age and better health status of those enrolled in trials for dermatologic indications.” The results of that study, which included patients with rheumatoid arthritis only, resulted in the addition of a boxed warning in the labels for topical and oral JAK inhibitors regarding the increased risk of MACE, VTE, serious infections, malignancies, and death .
For the review – thought to be the first to specifically evaluate these risks for dermatologic indications – the researchers searched PubMed and ClinicalTrials.gov from inception through April 1, 2023, for phase 3 dermatology randomized clinical trials (RCTs) to evaluate the risk of MACE, VTE, and all-cause mortality with JAK inhibitors, compared with placebo or an active comparator in the treatment of immune-mediated inflammatory skin diseases. They followed Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guidelines and used a random-effects model and the DerSimonian-Laird method to calculate adverse events with odds ratios.
The database search yielded 35 RCTs with a total of 20,651 patients. Their mean age was 38.5 years, 54% were male, and the mean follow-up time was 4.9 months. Of the 35 trials, most (21) involved patients with atopic dermatitis, followed by psoriasis/psoriatic arthritis (9 trials), alopecia areata (3 trials) and vitiligo (2 trials).
The researchers found no significant difference between JAK inhibitors and placebo/active comparator in composite MACE and all-cause mortality (odds ratio, 0.83; 95% confidence interval, 0.44-1.57) or in VTE (OR, 0.52; 95% CI, 0.26-1.04).
In a secondary analysis, which included additional psoriatic arthritis RCTs, no significant differences between the treatment and placebo/active comparator groups were observed. Similarly, subgroup analyses of oral versus topical JAK inhibitors and a sensitivity analysis that excluded pediatric trials showed no significant differences between patients exposed to JAK inhibitors and those not exposed.
The researchers acknowledged certain limitations of the review, including the lack of access to patient-level data, the fact that most trials only included short-term follow-up, and that the findings have limited generalizability to an older patient population. “It remains unclear if the cardiovascular risks of JAK inhibitors are primarily due to patient level cardiovascular risk factors or are drug mediated,” they concluded. “Dermatologists should carefully select patients and assess baseline cardiovascular risk factors when considering JAK therapy. Cardiovascular risk assessment should continue for the duration of treatment.”
Raj Chovatiya, MD, PhD, assistant professor of dermatology and director of the center for eczema and itch at Northwestern University, Chicago, who was asked to comment on the study results, characterized the findings as reassuring to dermatologists who may be reluctant to initiate therapy with JAK inhibitors based on concerns about safety signals for MACE, VTE, and all-cause mortality.
“These data systematically show that across medications and across conditions, there doesn’t appear to be an increased signal for these events during the short-term, placebo-controlled period which generally spans a few months in most studies,” he told this news organization. The findings, he added, “align well with our clinical experience to date for JAK inhibitor use in inflammatory skin disease. Short-term safety, particularly in relation to boxed warning events such MACE, VTE, and all-cause mortality, have generally been favorable with real-world use. It’s good to have a rigorous statistical analysis to refer to when setting patient expectations.”
However, he noted that these data only examined short-term safety during the placebo or active comparator-controlled periods. “Considering that events like MACE or VTE may take many months or years to manifest, continued long-term data generation is needed to fully answer the question of risk,” he said.
Dr. Garshick disclosed that he received grants from Pfizer and personal fees from Bristol Myers Squibb during the conduct of the study and personal fees from Kiniksa Pharmaceuticals outside the submitted work. Several other coauthors reported having advisory board roles and/or having received funding or support from several pharmaceutical companies. Dr. Chovatiya disclosed that he is a consultant to, a speaker for, investigator, and/or a member of the advisory board for several pharmaceutical companies, including those that develop JAK inhibitors.
FROM JAMA DERMATOLOGY
COVID coronary plaque infection confirms CV risk
The findings may not only explain the link between COVID and the increased risk of cardiovascular events but mark a starting point for new therapeutic approaches.
“Our study shows there is persistence of viral debris in the artery,” senior investigator Chiara Giannarelli, MD, associate professor of medicine and pathology at NYU Langone Health, New York, said in an interview. “There is an important inflammatory response. We can now look at ways to control this inflammation,” she said.
Dr. Giannarelli says COVID is more than a respiratory virus and that it can affect the whole body. “Our study shows a remarkable ability of the virus to hijack the immune system,” she points out. “Our findings may explain how that happens.”
Dr. Giannarelli says it’s important for doctors and patients to be aware of an increased cardiovascular risk after a SARS-CoV-2 infection and to pay extra attention to traditional risk factors, such as blood pressure and cholesterol.
“This study showing that severe acute respiratory syndrome coronavirus directly infects coronary artery plaques, producing inflammatory substances, really joins the dots and helps our understanding on why we’re seeing so much heart disease in COVID patients,” Peter Hotez, MD, professor of molecular virology and microbiology at Baylor College of Medicine, Houston, said in an interview.
Asked whether this direct infection of vascular plaques was unique to SARS-CoV-2 or whether this may also occur with other viruses, both Dr. Giannarelli and Dr. Hotez said they believe this may be a specific COVID effect.
“I wouldn’t say it is likely that other viruses infect coronary arteries in this way, but I suppose it is possible,” Dr. Giannarelli said.
Dr. Hotez pointed out that other viruses can cause inflammation in the heart, such as myocarditis. “But I can’t think of another virus that stimulates the sequence of events in coronary artery inflammation like we’re seeing here.”
Dr. Giannarelli noted that influenza is also associated with an increased risk of cardiovascular events, but there has been no evidence to date that it directly affects coronary arteries.
Dr. Hotez added that the increased risk of cardiovascular events with influenza has also been reported to be prolonged after the acute infection. “These new findings with SARS-CoV-2 could stimulate a redoubling of efforts to look at this possibility with influenza,” he suggested.
Heart disease after COVID
In a recent article published online in Nature Cardiovascular Research, Dr. Giannarelli and colleagues analyzed human autopsy tissue samples from coronary arterial walls of patients who had died from COVID in the early stages of the pandemic in New York.
They found an accumulation of viral RNA in atherosclerotic plaques in the coronary arteries, which was particularly concentrated in lipid-rich macrophage foam cells present within the plaques.
“Our data conclusively demonstrate that severe acute respiratory syndrome coronavirus is capable of infecting and replicating in macrophages within the coronary vasculature,” the researchers report.
The virus preferentially replicates in foam cells, in comparison with other macrophages, they add, suggesting that these cells might act as a reservoir of viral debris in atherosclerotic plaque.
“We have shown that the virus is targeting lipid-rich macrophages in atherosclerotic lesions. This is the first time this has been shown, and we think this is a very important finding,” Dr. Giannarelli said in an interview.
“We also found that the virus persists in these foam cells that could be responsible for long-term, low-grade inflammation in the vasculature that could contribute to the long-term cardiovascular manifestations in patients who have recovered from COVID,” she said.
Viral reservoirs
Macrophages residing in vascular tissue can undergo self-renewal and can remain in the tissue for many years, the investigators point out. They suggest that these macrophages may act as viral reservoirs of SARS-CoV-2 RNA in atherosclerotic plaques.
Using an ex vivo model, the researchers also found that atherosclerotic tissue could be directly infected by the virus. And just as was seen in cultured macrophages and foam cells, infection of vascular tissue triggered an inflammatory response. That response induced the secretion of key proatherogenic cytokines, such as interleukin-6 and interleukin-1 beta, which have been implicated in the pathogenesis of atherosclerosis and in an increased risk of cardiovascular events.
“Considering that plaque inflammation promotes disease progression and contributes to plaque rupture, our results provide a molecular basis for how infection of coronary lesions can contribute to the acute cardiovascular manifestations of COVID-19, such as myocardial infarction,” the researchers report.
Another interesting finding was a higher accumulation of viral RNA in the coronary vasculature of the three patients with acute ischemic cardiovascular manifestations, which they say adds to evidence that infection may increase cardiovascular risk.
Dr. Giannarelli points out that the patients in their study died in New York early in the pandemic, before vaccines were available. “They were unvaccinated and likely had little immunity against initial viral strains.”
Dr. Hotez says that when COVID-19 first emerged, many in the medical and scientific communities thought it would closely resemble the original SARS viral infection, which was primarily a respiratory pathogen.
“But it became pretty clear early on this virus was causing a lot of cardiovascular and thromboembolic disease,” he says. “This study provides an insight into the mechanisms involved here.”
Affecting more than lungs
Dr. Hotez pointed out that a recent study reported a 5% increase in cardiovascular deaths during the years 2020-2022, compared with before the pandemic.
“Those peaks of cardiovascular deaths corresponded with specific waves of COVID – the first happening at the time of the initial wave with the original virus and second during the Delta wave. So, there’s no question that this virus is contributing to excess cardiovascular mortality, and this paper appears to explain the mechanism.”
Dr. Hotez pointed out that the new findings suggest the cardiovascular risk may be prolonged well after the acute infection resolves.
“In long COVID, a lot of people focus on the neurological effects – brain fog and depression. But cardiac insufficiency and other cardiovascular events can also be considered another element of long COVID,” he said.
Dr. Giannarelli says her group is now studying whether patients with long COVID have virus in their coronary arteries. She points out that the current studies were a result of a team effort between experts in cardiovascular disease and virology and infectious disease. “We need to collaborate more like this to understand better the impact of viral infection in patients and the clinical manifestations,” she said.
Dr. Hotez says he believes these new findings will have implications for the future.
“COVID hasn’t gone away. The numbers have been going up again steadily in the U.S. in the last few months. There are still a significant number of hospitalizations,” he said.
While it would be unwieldy to ask for a cardiology consult for every COVID patient, he acknowledged, “there is probably a subset of people – possibly those of older age and who have had a severe case of COVID – who we suspect are now going to be more prone to cardiovascular disease because of having COVID.
“We should be vigilant in looking for cardiovascular disease in these patients,” Dr. Hotez said, “and perhaps be a bit more aggressive about controlling their cardiovascular risk factors.”
The study was funded by the U.S. National Institutes of Health, the American Heart Association, and the Chan Zuckerberg Initiative.
A version of this article first appeared on Medscape.com .
The findings may not only explain the link between COVID and the increased risk of cardiovascular events but mark a starting point for new therapeutic approaches.
“Our study shows there is persistence of viral debris in the artery,” senior investigator Chiara Giannarelli, MD, associate professor of medicine and pathology at NYU Langone Health, New York, said in an interview. “There is an important inflammatory response. We can now look at ways to control this inflammation,” she said.
Dr. Giannarelli says COVID is more than a respiratory virus and that it can affect the whole body. “Our study shows a remarkable ability of the virus to hijack the immune system,” she points out. “Our findings may explain how that happens.”
Dr. Giannarelli says it’s important for doctors and patients to be aware of an increased cardiovascular risk after a SARS-CoV-2 infection and to pay extra attention to traditional risk factors, such as blood pressure and cholesterol.
“This study showing that severe acute respiratory syndrome coronavirus directly infects coronary artery plaques, producing inflammatory substances, really joins the dots and helps our understanding on why we’re seeing so much heart disease in COVID patients,” Peter Hotez, MD, professor of molecular virology and microbiology at Baylor College of Medicine, Houston, said in an interview.
Asked whether this direct infection of vascular plaques was unique to SARS-CoV-2 or whether this may also occur with other viruses, both Dr. Giannarelli and Dr. Hotez said they believe this may be a specific COVID effect.
“I wouldn’t say it is likely that other viruses infect coronary arteries in this way, but I suppose it is possible,” Dr. Giannarelli said.
Dr. Hotez pointed out that other viruses can cause inflammation in the heart, such as myocarditis. “But I can’t think of another virus that stimulates the sequence of events in coronary artery inflammation like we’re seeing here.”
Dr. Giannarelli noted that influenza is also associated with an increased risk of cardiovascular events, but there has been no evidence to date that it directly affects coronary arteries.
Dr. Hotez added that the increased risk of cardiovascular events with influenza has also been reported to be prolonged after the acute infection. “These new findings with SARS-CoV-2 could stimulate a redoubling of efforts to look at this possibility with influenza,” he suggested.
Heart disease after COVID
In a recent article published online in Nature Cardiovascular Research, Dr. Giannarelli and colleagues analyzed human autopsy tissue samples from coronary arterial walls of patients who had died from COVID in the early stages of the pandemic in New York.
They found an accumulation of viral RNA in atherosclerotic plaques in the coronary arteries, which was particularly concentrated in lipid-rich macrophage foam cells present within the plaques.
“Our data conclusively demonstrate that severe acute respiratory syndrome coronavirus is capable of infecting and replicating in macrophages within the coronary vasculature,” the researchers report.
The virus preferentially replicates in foam cells, in comparison with other macrophages, they add, suggesting that these cells might act as a reservoir of viral debris in atherosclerotic plaque.
“We have shown that the virus is targeting lipid-rich macrophages in atherosclerotic lesions. This is the first time this has been shown, and we think this is a very important finding,” Dr. Giannarelli said in an interview.
“We also found that the virus persists in these foam cells that could be responsible for long-term, low-grade inflammation in the vasculature that could contribute to the long-term cardiovascular manifestations in patients who have recovered from COVID,” she said.
Viral reservoirs
Macrophages residing in vascular tissue can undergo self-renewal and can remain in the tissue for many years, the investigators point out. They suggest that these macrophages may act as viral reservoirs of SARS-CoV-2 RNA in atherosclerotic plaques.
Using an ex vivo model, the researchers also found that atherosclerotic tissue could be directly infected by the virus. And just as was seen in cultured macrophages and foam cells, infection of vascular tissue triggered an inflammatory response. That response induced the secretion of key proatherogenic cytokines, such as interleukin-6 and interleukin-1 beta, which have been implicated in the pathogenesis of atherosclerosis and in an increased risk of cardiovascular events.
“Considering that plaque inflammation promotes disease progression and contributes to plaque rupture, our results provide a molecular basis for how infection of coronary lesions can contribute to the acute cardiovascular manifestations of COVID-19, such as myocardial infarction,” the researchers report.
Another interesting finding was a higher accumulation of viral RNA in the coronary vasculature of the three patients with acute ischemic cardiovascular manifestations, which they say adds to evidence that infection may increase cardiovascular risk.
Dr. Giannarelli points out that the patients in their study died in New York early in the pandemic, before vaccines were available. “They were unvaccinated and likely had little immunity against initial viral strains.”
Dr. Hotez says that when COVID-19 first emerged, many in the medical and scientific communities thought it would closely resemble the original SARS viral infection, which was primarily a respiratory pathogen.
“But it became pretty clear early on this virus was causing a lot of cardiovascular and thromboembolic disease,” he says. “This study provides an insight into the mechanisms involved here.”
Affecting more than lungs
Dr. Hotez pointed out that a recent study reported a 5% increase in cardiovascular deaths during the years 2020-2022, compared with before the pandemic.
“Those peaks of cardiovascular deaths corresponded with specific waves of COVID – the first happening at the time of the initial wave with the original virus and second during the Delta wave. So, there’s no question that this virus is contributing to excess cardiovascular mortality, and this paper appears to explain the mechanism.”
Dr. Hotez pointed out that the new findings suggest the cardiovascular risk may be prolonged well after the acute infection resolves.
“In long COVID, a lot of people focus on the neurological effects – brain fog and depression. But cardiac insufficiency and other cardiovascular events can also be considered another element of long COVID,” he said.
Dr. Giannarelli says her group is now studying whether patients with long COVID have virus in their coronary arteries. She points out that the current studies were a result of a team effort between experts in cardiovascular disease and virology and infectious disease. “We need to collaborate more like this to understand better the impact of viral infection in patients and the clinical manifestations,” she said.
Dr. Hotez says he believes these new findings will have implications for the future.
“COVID hasn’t gone away. The numbers have been going up again steadily in the U.S. in the last few months. There are still a significant number of hospitalizations,” he said.
While it would be unwieldy to ask for a cardiology consult for every COVID patient, he acknowledged, “there is probably a subset of people – possibly those of older age and who have had a severe case of COVID – who we suspect are now going to be more prone to cardiovascular disease because of having COVID.
“We should be vigilant in looking for cardiovascular disease in these patients,” Dr. Hotez said, “and perhaps be a bit more aggressive about controlling their cardiovascular risk factors.”
The study was funded by the U.S. National Institutes of Health, the American Heart Association, and the Chan Zuckerberg Initiative.
A version of this article first appeared on Medscape.com .
The findings may not only explain the link between COVID and the increased risk of cardiovascular events but mark a starting point for new therapeutic approaches.
“Our study shows there is persistence of viral debris in the artery,” senior investigator Chiara Giannarelli, MD, associate professor of medicine and pathology at NYU Langone Health, New York, said in an interview. “There is an important inflammatory response. We can now look at ways to control this inflammation,” she said.
Dr. Giannarelli says COVID is more than a respiratory virus and that it can affect the whole body. “Our study shows a remarkable ability of the virus to hijack the immune system,” she points out. “Our findings may explain how that happens.”
Dr. Giannarelli says it’s important for doctors and patients to be aware of an increased cardiovascular risk after a SARS-CoV-2 infection and to pay extra attention to traditional risk factors, such as blood pressure and cholesterol.
“This study showing that severe acute respiratory syndrome coronavirus directly infects coronary artery plaques, producing inflammatory substances, really joins the dots and helps our understanding on why we’re seeing so much heart disease in COVID patients,” Peter Hotez, MD, professor of molecular virology and microbiology at Baylor College of Medicine, Houston, said in an interview.
Asked whether this direct infection of vascular plaques was unique to SARS-CoV-2 or whether this may also occur with other viruses, both Dr. Giannarelli and Dr. Hotez said they believe this may be a specific COVID effect.
“I wouldn’t say it is likely that other viruses infect coronary arteries in this way, but I suppose it is possible,” Dr. Giannarelli said.
Dr. Hotez pointed out that other viruses can cause inflammation in the heart, such as myocarditis. “But I can’t think of another virus that stimulates the sequence of events in coronary artery inflammation like we’re seeing here.”
Dr. Giannarelli noted that influenza is also associated with an increased risk of cardiovascular events, but there has been no evidence to date that it directly affects coronary arteries.
Dr. Hotez added that the increased risk of cardiovascular events with influenza has also been reported to be prolonged after the acute infection. “These new findings with SARS-CoV-2 could stimulate a redoubling of efforts to look at this possibility with influenza,” he suggested.
Heart disease after COVID
In a recent article published online in Nature Cardiovascular Research, Dr. Giannarelli and colleagues analyzed human autopsy tissue samples from coronary arterial walls of patients who had died from COVID in the early stages of the pandemic in New York.
They found an accumulation of viral RNA in atherosclerotic plaques in the coronary arteries, which was particularly concentrated in lipid-rich macrophage foam cells present within the plaques.
“Our data conclusively demonstrate that severe acute respiratory syndrome coronavirus is capable of infecting and replicating in macrophages within the coronary vasculature,” the researchers report.
The virus preferentially replicates in foam cells, in comparison with other macrophages, they add, suggesting that these cells might act as a reservoir of viral debris in atherosclerotic plaque.
“We have shown that the virus is targeting lipid-rich macrophages in atherosclerotic lesions. This is the first time this has been shown, and we think this is a very important finding,” Dr. Giannarelli said in an interview.
“We also found that the virus persists in these foam cells that could be responsible for long-term, low-grade inflammation in the vasculature that could contribute to the long-term cardiovascular manifestations in patients who have recovered from COVID,” she said.
Viral reservoirs
Macrophages residing in vascular tissue can undergo self-renewal and can remain in the tissue for many years, the investigators point out. They suggest that these macrophages may act as viral reservoirs of SARS-CoV-2 RNA in atherosclerotic plaques.
Using an ex vivo model, the researchers also found that atherosclerotic tissue could be directly infected by the virus. And just as was seen in cultured macrophages and foam cells, infection of vascular tissue triggered an inflammatory response. That response induced the secretion of key proatherogenic cytokines, such as interleukin-6 and interleukin-1 beta, which have been implicated in the pathogenesis of atherosclerosis and in an increased risk of cardiovascular events.
“Considering that plaque inflammation promotes disease progression and contributes to plaque rupture, our results provide a molecular basis for how infection of coronary lesions can contribute to the acute cardiovascular manifestations of COVID-19, such as myocardial infarction,” the researchers report.
Another interesting finding was a higher accumulation of viral RNA in the coronary vasculature of the three patients with acute ischemic cardiovascular manifestations, which they say adds to evidence that infection may increase cardiovascular risk.
Dr. Giannarelli points out that the patients in their study died in New York early in the pandemic, before vaccines were available. “They were unvaccinated and likely had little immunity against initial viral strains.”
Dr. Hotez says that when COVID-19 first emerged, many in the medical and scientific communities thought it would closely resemble the original SARS viral infection, which was primarily a respiratory pathogen.
“But it became pretty clear early on this virus was causing a lot of cardiovascular and thromboembolic disease,” he says. “This study provides an insight into the mechanisms involved here.”
Affecting more than lungs
Dr. Hotez pointed out that a recent study reported a 5% increase in cardiovascular deaths during the years 2020-2022, compared with before the pandemic.
“Those peaks of cardiovascular deaths corresponded with specific waves of COVID – the first happening at the time of the initial wave with the original virus and second during the Delta wave. So, there’s no question that this virus is contributing to excess cardiovascular mortality, and this paper appears to explain the mechanism.”
Dr. Hotez pointed out that the new findings suggest the cardiovascular risk may be prolonged well after the acute infection resolves.
“In long COVID, a lot of people focus on the neurological effects – brain fog and depression. But cardiac insufficiency and other cardiovascular events can also be considered another element of long COVID,” he said.
Dr. Giannarelli says her group is now studying whether patients with long COVID have virus in their coronary arteries. She points out that the current studies were a result of a team effort between experts in cardiovascular disease and virology and infectious disease. “We need to collaborate more like this to understand better the impact of viral infection in patients and the clinical manifestations,” she said.
Dr. Hotez says he believes these new findings will have implications for the future.
“COVID hasn’t gone away. The numbers have been going up again steadily in the U.S. in the last few months. There are still a significant number of hospitalizations,” he said.
While it would be unwieldy to ask for a cardiology consult for every COVID patient, he acknowledged, “there is probably a subset of people – possibly those of older age and who have had a severe case of COVID – who we suspect are now going to be more prone to cardiovascular disease because of having COVID.
“We should be vigilant in looking for cardiovascular disease in these patients,” Dr. Hotez said, “and perhaps be a bit more aggressive about controlling their cardiovascular risk factors.”
The study was funded by the U.S. National Institutes of Health, the American Heart Association, and the Chan Zuckerberg Initiative.
A version of this article first appeared on Medscape.com .
FROM NATURE CARDIOVASCULAR RESEARCH
Stair climbing tied to reduced risk for heart disease
TOPLINE:
new observational data suggest.
METHODOLOGY:
- The prospective cohort study used data from 458,860 adults in the UK Biobank cohort who were 38-73 years old at baseline (2006-2010).
- Information about stair climbing, sociodemographic, and lifestyle factors was collected at baseline and 5 years later.
- Cases of ASCVD – defined as coronary artery disease (CAD), ischemic stroke, or acute complications – were identified via hospital records and death registry.
- Associations between stair climbing and ASCVD were examined as hazard ratios from Cox proportional hazards model. Analyses were stratified by susceptibility to ASCVD based on family history, genetic risk, and established risk factors.
TAKEAWAY:
- A total of 39,043 ASCVD, 30,718 CAD, and 10,521 ischemic stroke cases were recorded during a median follow-up of 12.5 years.
- Compared with no-stair climbing, climbing 6-10 flights of stairs daily was associated with a 7% lower ASCVD risk (multivariable-adjusted HR, 0.93; 95% confidence interval, 0.90-0.96) and climbing 16-20 flights daily was associated with a 10% lower risk (HR, 0.90; 95% CI, 0.85-0.94).
- The benefits plateaued at 20 flights daily; comparable results were obtained for CAD and ischemic stroke; the protective effect of stair climbing was attenuated by increasing levels of disease susceptibility.
- Adults who stopped climbing stairs daily during the study had a 32% higher risk of ASCVD (HR, 1.32; 95% CI,1.06-1.65), compared with peers who never reported stair climbing.
IN PRACTICE:
“These findings highlight the potential advantages of stair climbing as a primary preventive measure for ASCVD in the general population. Short bursts of high-intensity stair climbing are a time-efficient way to improve cardiorespiratory fitness and lipid profile, especially among those unable to achieve the current physical activity recommendations,” study author Lu Qi, with Tulane University, New Orleans, said in a news release.
SOURCE:
The study was published online in Atherosclerosis.
LIMITATIONS:
The observational design limits causal inferences. Stair climbing was self-reported via questionnaires and recall bias is a possibility. The UK Biobank participants do not represent the entire population of the country, with a healthy volunteer selection bias previously reported.
DISCLOSURES:
The study was supported by grants from the National Key R&D Program of China. The authors disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
TOPLINE:
new observational data suggest.
METHODOLOGY:
- The prospective cohort study used data from 458,860 adults in the UK Biobank cohort who were 38-73 years old at baseline (2006-2010).
- Information about stair climbing, sociodemographic, and lifestyle factors was collected at baseline and 5 years later.
- Cases of ASCVD – defined as coronary artery disease (CAD), ischemic stroke, or acute complications – were identified via hospital records and death registry.
- Associations between stair climbing and ASCVD were examined as hazard ratios from Cox proportional hazards model. Analyses were stratified by susceptibility to ASCVD based on family history, genetic risk, and established risk factors.
TAKEAWAY:
- A total of 39,043 ASCVD, 30,718 CAD, and 10,521 ischemic stroke cases were recorded during a median follow-up of 12.5 years.
- Compared with no-stair climbing, climbing 6-10 flights of stairs daily was associated with a 7% lower ASCVD risk (multivariable-adjusted HR, 0.93; 95% confidence interval, 0.90-0.96) and climbing 16-20 flights daily was associated with a 10% lower risk (HR, 0.90; 95% CI, 0.85-0.94).
- The benefits plateaued at 20 flights daily; comparable results were obtained for CAD and ischemic stroke; the protective effect of stair climbing was attenuated by increasing levels of disease susceptibility.
- Adults who stopped climbing stairs daily during the study had a 32% higher risk of ASCVD (HR, 1.32; 95% CI,1.06-1.65), compared with peers who never reported stair climbing.
IN PRACTICE:
“These findings highlight the potential advantages of stair climbing as a primary preventive measure for ASCVD in the general population. Short bursts of high-intensity stair climbing are a time-efficient way to improve cardiorespiratory fitness and lipid profile, especially among those unable to achieve the current physical activity recommendations,” study author Lu Qi, with Tulane University, New Orleans, said in a news release.
SOURCE:
The study was published online in Atherosclerosis.
LIMITATIONS:
The observational design limits causal inferences. Stair climbing was self-reported via questionnaires and recall bias is a possibility. The UK Biobank participants do not represent the entire population of the country, with a healthy volunteer selection bias previously reported.
DISCLOSURES:
The study was supported by grants from the National Key R&D Program of China. The authors disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
TOPLINE:
new observational data suggest.
METHODOLOGY:
- The prospective cohort study used data from 458,860 adults in the UK Biobank cohort who were 38-73 years old at baseline (2006-2010).
- Information about stair climbing, sociodemographic, and lifestyle factors was collected at baseline and 5 years later.
- Cases of ASCVD – defined as coronary artery disease (CAD), ischemic stroke, or acute complications – were identified via hospital records and death registry.
- Associations between stair climbing and ASCVD were examined as hazard ratios from Cox proportional hazards model. Analyses were stratified by susceptibility to ASCVD based on family history, genetic risk, and established risk factors.
TAKEAWAY:
- A total of 39,043 ASCVD, 30,718 CAD, and 10,521 ischemic stroke cases were recorded during a median follow-up of 12.5 years.
- Compared with no-stair climbing, climbing 6-10 flights of stairs daily was associated with a 7% lower ASCVD risk (multivariable-adjusted HR, 0.93; 95% confidence interval, 0.90-0.96) and climbing 16-20 flights daily was associated with a 10% lower risk (HR, 0.90; 95% CI, 0.85-0.94).
- The benefits plateaued at 20 flights daily; comparable results were obtained for CAD and ischemic stroke; the protective effect of stair climbing was attenuated by increasing levels of disease susceptibility.
- Adults who stopped climbing stairs daily during the study had a 32% higher risk of ASCVD (HR, 1.32; 95% CI,1.06-1.65), compared with peers who never reported stair climbing.
IN PRACTICE:
“These findings highlight the potential advantages of stair climbing as a primary preventive measure for ASCVD in the general population. Short bursts of high-intensity stair climbing are a time-efficient way to improve cardiorespiratory fitness and lipid profile, especially among those unable to achieve the current physical activity recommendations,” study author Lu Qi, with Tulane University, New Orleans, said in a news release.
SOURCE:
The study was published online in Atherosclerosis.
LIMITATIONS:
The observational design limits causal inferences. Stair climbing was self-reported via questionnaires and recall bias is a possibility. The UK Biobank participants do not represent the entire population of the country, with a healthy volunteer selection bias previously reported.
DISCLOSURES:
The study was supported by grants from the National Key R&D Program of China. The authors disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Redefining CVD risk: Cardiovascular-kidney-metabolic (CKM) syndrome
“This work was prompted by the fact that CKM syndrome leads to premature morbidity and mortality, primarily because of a higher burden of CVD,” writing committee chair Chiadi Ndumele, MD, PhD, said in an interview.
“While CKM syndrome is a public health emergency, there is also great potential for improving CKM health in the population, with an increasing number of therapies that favorably impact metabolic risk factors, risk for adverse kidney events, or both, which also protect against CVD,” added Dr. Ndumele, director of obesity and cardiometabolic research in the division of cardiology at Johns Hopkins University, Baltimore.
The AHA presidential advisory and accompanying scientific statement, which provides a synopsis of evidence for the science and clinical management of CKM, were published online in the journal Circulation.
CKM syndrome staging
According to the AHA, one in three U.S. adults have three or more risk factors that contribute to CVD, metabolic disorders, and/or kidney disease.
In addition to defining CKM syndrome, the advisory provides a “staging construct, to be used in both adults and youth, that reflects the progressive pathophysiology and risk within CKM syndrome, with therapeutic guidance tied to CKM stages,” Dr. Ndumele told this news organization.
The AHA outlines four stages of CKM syndrome:
Stage 0: At this stage, no CKM risk factors are present, and the goal is to prevent CKM syndrome (particularly unhealthy weight gain) by achieving and maintaining ideal health based on the AHA’s Life’s Essential 8 recommendations. Adults in this stage should be screened every 3-5 years to assess lipids, blood pressure, and blood sugar.
Stage 1: At this stage, excess weight, abdominal obesity, or dysfunctional adipose tissue (clinically manifest as impaired glucose tolerance or prediabetes) is present without other metabolic risk factors or CVD. Management includes providing support for healthy lifestyle changes (healthy eating and regular physical activity), with a goal of at least 5% weight loss and addressing glucose intolerance if needed. Screening adults with stage 1 CKM every 2-3 years is advised to assess blood pressure, triglycerides, cholesterol, and blood sugar.
Stage 2: At this stage, metabolic risk factors (hypertriglyceridemia, hypertension, metabolic syndrome, diabetes) and kidney disease are present. The goal is to address risk factors to prevent progression to CVD and kidney failure. Screening for stage 2 CKM syndrome aligns with AHA/ACC guidelines, which include yearly assessment of blood pressure, triglycerides, cholesterol, blood sugar, and kidney function. More frequent kidney screening is recommended for individuals with increased risk of kidney failure based on kidney function assessments.
Stage 3: This stage describes individuals with subclinical CVD with metabolic risk factors or kidney disease or those at high predicted risk for CVD. The goal is to intensify efforts to prevent progression to symptomatic CVD and kidney failure. This may involve increasing or changing medications, and additional focus on lifestyle changes. Coronary artery calcium (CAC) measurement in some adults is recommended to assess narrowing of the arteries when treatment decisions are unclear.
Stage 4: Individuals with stage 4 CKM syndrome have symptomatic CVD, excess body fat, metabolic risk factors, or kidney disease. Stage 4 CKM syndrome is divided into two subcategories: (4a) no kidney failure and (4b) kidney failure. In this stage, patients may have already had a myocardial infarction (MI) or stroke or may already have heart failure. They also may have additional CV conditions such as peripheral artery disease or atrial fibrillation. The goal of care is individualized treatment for CVD with consideration for CKM syndrome conditions.
The advisory also describes CKM syndrome regression, “an important concept and public health message in which people making healthy lifestyle changes and achieving weight loss may regress to lower CKM syndrome stages and a better state of health,” the AHA says in a news release.
They note that a “critical” next step is to update the pooled cohort equation (PCE) risk prediction algorithm to include measures of kidney function, type 2 diabetes control, and social determinants of health for a more comprehensive risk estimate.
The advisory also recommends risk calculator updates be expanded to assess risk in people as young as age 30 and to calculate both 10- and 30-year CVD risk.
“Clearly defining the patient with CKM syndrome, and providing new approaches for CKM syndrome staging and risk prediction, will help health care professionals to identify these individuals earlier and to provide timely, holistic, and patient-centered care,” Dr. Ndumele said.
This presidential advisory was prepared by the volunteer writing group on behalf of the AHA . The authors have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
“This work was prompted by the fact that CKM syndrome leads to premature morbidity and mortality, primarily because of a higher burden of CVD,” writing committee chair Chiadi Ndumele, MD, PhD, said in an interview.
“While CKM syndrome is a public health emergency, there is also great potential for improving CKM health in the population, with an increasing number of therapies that favorably impact metabolic risk factors, risk for adverse kidney events, or both, which also protect against CVD,” added Dr. Ndumele, director of obesity and cardiometabolic research in the division of cardiology at Johns Hopkins University, Baltimore.
The AHA presidential advisory and accompanying scientific statement, which provides a synopsis of evidence for the science and clinical management of CKM, were published online in the journal Circulation.
CKM syndrome staging
According to the AHA, one in three U.S. adults have three or more risk factors that contribute to CVD, metabolic disorders, and/or kidney disease.
In addition to defining CKM syndrome, the advisory provides a “staging construct, to be used in both adults and youth, that reflects the progressive pathophysiology and risk within CKM syndrome, with therapeutic guidance tied to CKM stages,” Dr. Ndumele told this news organization.
The AHA outlines four stages of CKM syndrome:
Stage 0: At this stage, no CKM risk factors are present, and the goal is to prevent CKM syndrome (particularly unhealthy weight gain) by achieving and maintaining ideal health based on the AHA’s Life’s Essential 8 recommendations. Adults in this stage should be screened every 3-5 years to assess lipids, blood pressure, and blood sugar.
Stage 1: At this stage, excess weight, abdominal obesity, or dysfunctional adipose tissue (clinically manifest as impaired glucose tolerance or prediabetes) is present without other metabolic risk factors or CVD. Management includes providing support for healthy lifestyle changes (healthy eating and regular physical activity), with a goal of at least 5% weight loss and addressing glucose intolerance if needed. Screening adults with stage 1 CKM every 2-3 years is advised to assess blood pressure, triglycerides, cholesterol, and blood sugar.
Stage 2: At this stage, metabolic risk factors (hypertriglyceridemia, hypertension, metabolic syndrome, diabetes) and kidney disease are present. The goal is to address risk factors to prevent progression to CVD and kidney failure. Screening for stage 2 CKM syndrome aligns with AHA/ACC guidelines, which include yearly assessment of blood pressure, triglycerides, cholesterol, blood sugar, and kidney function. More frequent kidney screening is recommended for individuals with increased risk of kidney failure based on kidney function assessments.
Stage 3: This stage describes individuals with subclinical CVD with metabolic risk factors or kidney disease or those at high predicted risk for CVD. The goal is to intensify efforts to prevent progression to symptomatic CVD and kidney failure. This may involve increasing or changing medications, and additional focus on lifestyle changes. Coronary artery calcium (CAC) measurement in some adults is recommended to assess narrowing of the arteries when treatment decisions are unclear.
Stage 4: Individuals with stage 4 CKM syndrome have symptomatic CVD, excess body fat, metabolic risk factors, or kidney disease. Stage 4 CKM syndrome is divided into two subcategories: (4a) no kidney failure and (4b) kidney failure. In this stage, patients may have already had a myocardial infarction (MI) or stroke or may already have heart failure. They also may have additional CV conditions such as peripheral artery disease or atrial fibrillation. The goal of care is individualized treatment for CVD with consideration for CKM syndrome conditions.
The advisory also describes CKM syndrome regression, “an important concept and public health message in which people making healthy lifestyle changes and achieving weight loss may regress to lower CKM syndrome stages and a better state of health,” the AHA says in a news release.
They note that a “critical” next step is to update the pooled cohort equation (PCE) risk prediction algorithm to include measures of kidney function, type 2 diabetes control, and social determinants of health for a more comprehensive risk estimate.
The advisory also recommends risk calculator updates be expanded to assess risk in people as young as age 30 and to calculate both 10- and 30-year CVD risk.
“Clearly defining the patient with CKM syndrome, and providing new approaches for CKM syndrome staging and risk prediction, will help health care professionals to identify these individuals earlier and to provide timely, holistic, and patient-centered care,” Dr. Ndumele said.
This presidential advisory was prepared by the volunteer writing group on behalf of the AHA . The authors have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
“This work was prompted by the fact that CKM syndrome leads to premature morbidity and mortality, primarily because of a higher burden of CVD,” writing committee chair Chiadi Ndumele, MD, PhD, said in an interview.
“While CKM syndrome is a public health emergency, there is also great potential for improving CKM health in the population, with an increasing number of therapies that favorably impact metabolic risk factors, risk for adverse kidney events, or both, which also protect against CVD,” added Dr. Ndumele, director of obesity and cardiometabolic research in the division of cardiology at Johns Hopkins University, Baltimore.
The AHA presidential advisory and accompanying scientific statement, which provides a synopsis of evidence for the science and clinical management of CKM, were published online in the journal Circulation.
CKM syndrome staging
According to the AHA, one in three U.S. adults have three or more risk factors that contribute to CVD, metabolic disorders, and/or kidney disease.
In addition to defining CKM syndrome, the advisory provides a “staging construct, to be used in both adults and youth, that reflects the progressive pathophysiology and risk within CKM syndrome, with therapeutic guidance tied to CKM stages,” Dr. Ndumele told this news organization.
The AHA outlines four stages of CKM syndrome:
Stage 0: At this stage, no CKM risk factors are present, and the goal is to prevent CKM syndrome (particularly unhealthy weight gain) by achieving and maintaining ideal health based on the AHA’s Life’s Essential 8 recommendations. Adults in this stage should be screened every 3-5 years to assess lipids, blood pressure, and blood sugar.
Stage 1: At this stage, excess weight, abdominal obesity, or dysfunctional adipose tissue (clinically manifest as impaired glucose tolerance or prediabetes) is present without other metabolic risk factors or CVD. Management includes providing support for healthy lifestyle changes (healthy eating and regular physical activity), with a goal of at least 5% weight loss and addressing glucose intolerance if needed. Screening adults with stage 1 CKM every 2-3 years is advised to assess blood pressure, triglycerides, cholesterol, and blood sugar.
Stage 2: At this stage, metabolic risk factors (hypertriglyceridemia, hypertension, metabolic syndrome, diabetes) and kidney disease are present. The goal is to address risk factors to prevent progression to CVD and kidney failure. Screening for stage 2 CKM syndrome aligns with AHA/ACC guidelines, which include yearly assessment of blood pressure, triglycerides, cholesterol, blood sugar, and kidney function. More frequent kidney screening is recommended for individuals with increased risk of kidney failure based on kidney function assessments.
Stage 3: This stage describes individuals with subclinical CVD with metabolic risk factors or kidney disease or those at high predicted risk for CVD. The goal is to intensify efforts to prevent progression to symptomatic CVD and kidney failure. This may involve increasing or changing medications, and additional focus on lifestyle changes. Coronary artery calcium (CAC) measurement in some adults is recommended to assess narrowing of the arteries when treatment decisions are unclear.
Stage 4: Individuals with stage 4 CKM syndrome have symptomatic CVD, excess body fat, metabolic risk factors, or kidney disease. Stage 4 CKM syndrome is divided into two subcategories: (4a) no kidney failure and (4b) kidney failure. In this stage, patients may have already had a myocardial infarction (MI) or stroke or may already have heart failure. They also may have additional CV conditions such as peripheral artery disease or atrial fibrillation. The goal of care is individualized treatment for CVD with consideration for CKM syndrome conditions.
The advisory also describes CKM syndrome regression, “an important concept and public health message in which people making healthy lifestyle changes and achieving weight loss may regress to lower CKM syndrome stages and a better state of health,” the AHA says in a news release.
They note that a “critical” next step is to update the pooled cohort equation (PCE) risk prediction algorithm to include measures of kidney function, type 2 diabetes control, and social determinants of health for a more comprehensive risk estimate.
The advisory also recommends risk calculator updates be expanded to assess risk in people as young as age 30 and to calculate both 10- and 30-year CVD risk.
“Clearly defining the patient with CKM syndrome, and providing new approaches for CKM syndrome staging and risk prediction, will help health care professionals to identify these individuals earlier and to provide timely, holistic, and patient-centered care,” Dr. Ndumele said.
This presidential advisory was prepared by the volunteer writing group on behalf of the AHA . The authors have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM CIRCULATION