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Orthostatic hypotension no deterrent to hypertension treatment
TOPLINE:
Intensive antihypertensive treatment provides the same benefit with regard to cardiovascular disease (CVD) and all-cause mortality regardless of the presence or absence of orthostatic or standing hypotension, new research shows.
METHODOLOGY:
- In response to ongoing concern about the benefits of intensive versus standard blood pressure treatment for adults with orthostatic hypotension (OH), researchers conducted a meta-analysis of individual patient data from nine randomized clinical trials to see whether the benefit of antihypertensive treatment was diminished for patients who had OH at baseline. Benefit was defined as a reduction in nonfatal CVD events and all-cause mortality.
- The included trials assessed BP pharmacologic treatment (more intensive BP goal or active agent) and had data on OH.
TAKEAWAY:
- The nine trials included 29,235 participants (mean age, 69 years; 48% women) who were followed for a median of 4 years; 9% had OH and 5% had standing hypotension at baseline.
- Having OH at baseline was significantly associated with the composite of CVD or all-cause mortality (hazard ratio, 1.14; 95% confidence interval, 1.04-1.26) and with all-cause mortality (HR, 1.24; 95% CI, 1.09-1.41). The same was true for baseline standing hypotension (composite outcome: HR, 1.39; 95% CI, 1.24-1.57; all-cause mortality: HR, 1.38; 95% CI, 1.14-1.66).
- More intensive BP treatment or active therapy significantly and similarly lowered risk of CVD or all-cause mortality among adults who did not have OH at baseline (HR, 0.81; 95% CI, 0.76-0.86) as well as those with OH at baseline (HR, 0.83; 95% CI, 0.70-1.00).
- More intensive BP treatment or active therapy also significantly lowered risk of CVD or all-cause mortality among those without baseline standing hypotension (HR, 0.80; 95% CI, 0.75-0.85) and nonsignificantly lowered the risk among those with baseline standing hypotension (HR, 0.94; 95% CI, 0.75-1.18).
IN PRACTICE:
“These findings suggest that orthostatic hypotension alone (that is, without symptoms) and standing hypotension measured prior to intensification of BP treatment should not deter adoption of more intensive BP treatment in adults with hypertension,” the authors conclude.
The findings should “reassure clinicians that patients with OH (and perhaps standing hypotension) will derive the full expected benefits from antihypertensive therapy,” add the authors of an accompanying editorial. “This also applies to patients treated to lower BP goals, albeit with less certainty.”
SOURCE:
The study, with first author Stephen Juraschek, MD, PhD, Beth Israel Deaconess Medical Center/Harvard Medical School, Boston, and the accompanying editorial were published online in JAMA.
LIMITATIONS:
In the hypertension trials that were included in the analysis, the study populations differed, as did BP measurement procedures, interventions, duration, and CVD outcome ascertainment processes and definitions. Some trials excluded adults with low standing systolic BP, limiting the number of participants with standing hypotension. OH was determined on the basis of a seated-to-standing protocol; supine-to-standing protocols are more sensitive and may not be interchangeable. Medications used in the trials may not reflect current medicine practice, or the trials may not have included agents thought to be more likely to affect OH and falls.
DISCLOSURES:
The study had no specific funding. Dr. Juraschek has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
TOPLINE:
Intensive antihypertensive treatment provides the same benefit with regard to cardiovascular disease (CVD) and all-cause mortality regardless of the presence or absence of orthostatic or standing hypotension, new research shows.
METHODOLOGY:
- In response to ongoing concern about the benefits of intensive versus standard blood pressure treatment for adults with orthostatic hypotension (OH), researchers conducted a meta-analysis of individual patient data from nine randomized clinical trials to see whether the benefit of antihypertensive treatment was diminished for patients who had OH at baseline. Benefit was defined as a reduction in nonfatal CVD events and all-cause mortality.
- The included trials assessed BP pharmacologic treatment (more intensive BP goal or active agent) and had data on OH.
TAKEAWAY:
- The nine trials included 29,235 participants (mean age, 69 years; 48% women) who were followed for a median of 4 years; 9% had OH and 5% had standing hypotension at baseline.
- Having OH at baseline was significantly associated with the composite of CVD or all-cause mortality (hazard ratio, 1.14; 95% confidence interval, 1.04-1.26) and with all-cause mortality (HR, 1.24; 95% CI, 1.09-1.41). The same was true for baseline standing hypotension (composite outcome: HR, 1.39; 95% CI, 1.24-1.57; all-cause mortality: HR, 1.38; 95% CI, 1.14-1.66).
- More intensive BP treatment or active therapy significantly and similarly lowered risk of CVD or all-cause mortality among adults who did not have OH at baseline (HR, 0.81; 95% CI, 0.76-0.86) as well as those with OH at baseline (HR, 0.83; 95% CI, 0.70-1.00).
- More intensive BP treatment or active therapy also significantly lowered risk of CVD or all-cause mortality among those without baseline standing hypotension (HR, 0.80; 95% CI, 0.75-0.85) and nonsignificantly lowered the risk among those with baseline standing hypotension (HR, 0.94; 95% CI, 0.75-1.18).
IN PRACTICE:
“These findings suggest that orthostatic hypotension alone (that is, without symptoms) and standing hypotension measured prior to intensification of BP treatment should not deter adoption of more intensive BP treatment in adults with hypertension,” the authors conclude.
The findings should “reassure clinicians that patients with OH (and perhaps standing hypotension) will derive the full expected benefits from antihypertensive therapy,” add the authors of an accompanying editorial. “This also applies to patients treated to lower BP goals, albeit with less certainty.”
SOURCE:
The study, with first author Stephen Juraschek, MD, PhD, Beth Israel Deaconess Medical Center/Harvard Medical School, Boston, and the accompanying editorial were published online in JAMA.
LIMITATIONS:
In the hypertension trials that were included in the analysis, the study populations differed, as did BP measurement procedures, interventions, duration, and CVD outcome ascertainment processes and definitions. Some trials excluded adults with low standing systolic BP, limiting the number of participants with standing hypotension. OH was determined on the basis of a seated-to-standing protocol; supine-to-standing protocols are more sensitive and may not be interchangeable. Medications used in the trials may not reflect current medicine practice, or the trials may not have included agents thought to be more likely to affect OH and falls.
DISCLOSURES:
The study had no specific funding. Dr. Juraschek has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
TOPLINE:
Intensive antihypertensive treatment provides the same benefit with regard to cardiovascular disease (CVD) and all-cause mortality regardless of the presence or absence of orthostatic or standing hypotension, new research shows.
METHODOLOGY:
- In response to ongoing concern about the benefits of intensive versus standard blood pressure treatment for adults with orthostatic hypotension (OH), researchers conducted a meta-analysis of individual patient data from nine randomized clinical trials to see whether the benefit of antihypertensive treatment was diminished for patients who had OH at baseline. Benefit was defined as a reduction in nonfatal CVD events and all-cause mortality.
- The included trials assessed BP pharmacologic treatment (more intensive BP goal or active agent) and had data on OH.
TAKEAWAY:
- The nine trials included 29,235 participants (mean age, 69 years; 48% women) who were followed for a median of 4 years; 9% had OH and 5% had standing hypotension at baseline.
- Having OH at baseline was significantly associated with the composite of CVD or all-cause mortality (hazard ratio, 1.14; 95% confidence interval, 1.04-1.26) and with all-cause mortality (HR, 1.24; 95% CI, 1.09-1.41). The same was true for baseline standing hypotension (composite outcome: HR, 1.39; 95% CI, 1.24-1.57; all-cause mortality: HR, 1.38; 95% CI, 1.14-1.66).
- More intensive BP treatment or active therapy significantly and similarly lowered risk of CVD or all-cause mortality among adults who did not have OH at baseline (HR, 0.81; 95% CI, 0.76-0.86) as well as those with OH at baseline (HR, 0.83; 95% CI, 0.70-1.00).
- More intensive BP treatment or active therapy also significantly lowered risk of CVD or all-cause mortality among those without baseline standing hypotension (HR, 0.80; 95% CI, 0.75-0.85) and nonsignificantly lowered the risk among those with baseline standing hypotension (HR, 0.94; 95% CI, 0.75-1.18).
IN PRACTICE:
“These findings suggest that orthostatic hypotension alone (that is, without symptoms) and standing hypotension measured prior to intensification of BP treatment should not deter adoption of more intensive BP treatment in adults with hypertension,” the authors conclude.
The findings should “reassure clinicians that patients with OH (and perhaps standing hypotension) will derive the full expected benefits from antihypertensive therapy,” add the authors of an accompanying editorial. “This also applies to patients treated to lower BP goals, albeit with less certainty.”
SOURCE:
The study, with first author Stephen Juraschek, MD, PhD, Beth Israel Deaconess Medical Center/Harvard Medical School, Boston, and the accompanying editorial were published online in JAMA.
LIMITATIONS:
In the hypertension trials that were included in the analysis, the study populations differed, as did BP measurement procedures, interventions, duration, and CVD outcome ascertainment processes and definitions. Some trials excluded adults with low standing systolic BP, limiting the number of participants with standing hypotension. OH was determined on the basis of a seated-to-standing protocol; supine-to-standing protocols are more sensitive and may not be interchangeable. Medications used in the trials may not reflect current medicine practice, or the trials may not have included agents thought to be more likely to affect OH and falls.
DISCLOSURES:
The study had no specific funding. Dr. Juraschek has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
This drug works, but wait till you hear what’s in it
This transcript has been edited for clarity.
As some of you may know, I do a fair amount of clinical research developing and evaluating artificial intelligence (AI) models, particularly machine learning algorithms that predict certain outcomes.
A thorny issue that comes up as algorithms have gotten more complicated is “explainability.” The problem is that AI can be a black box. Even if you have a model that is very accurate at predicting death, clinicians don’t trust it unless you can explain how it makes its predictions – how it works. “It just works” is not good enough to build trust.
It’s easier to build trust when you’re talking about a medication rather than a computer program. When a new blood pressure drug comes out that lowers blood pressure, importantly, we know why it lowers blood pressure. Every drug has a mechanism of action and, for most of the drugs in our arsenal, we know what that mechanism is.
But what if there were a drug – or better yet, a treatment – that worked? And I can honestly say we have no idea how it works. That’s what came across my desk today in what I believe is the largest, most rigorous trial of a traditional Chinese medication in history.
“Traditional Chinese medicine” is an omnibus term that refers to a class of therapies and health practices that are fundamentally different from how we practice medicine in the West.
It’s a highly personalized practice, with practitioners using often esoteric means to choose what substance to give what patient. That personalization makes traditional Chinese medicine nearly impossible to study in the typical randomized trial framework because treatments are not chosen solely on the basis of disease states.
The lack of scientific rigor in traditional Chinese medicine means that it is rife with practices and beliefs that can legitimately be called pseudoscience. As a nephrologist who has treated someone for “Chinese herb nephropathy,” I can tell you that some of the practices may be actively harmful.
But that doesn’t mean there is nothing there. I do not subscribe to the “argument from antiquity” – the idea that because something has been done for a long time it must be correct. But at the same time, traditional and non–science-based medicine practices could still identify therapies that work.
And with that, let me introduce you to Tongxinluo. Tongxinluo literally means “to open the network of the heart,” and it is a substance that has been used for centuries by traditional Chinese medicine practitioners to treat angina but was approved by the Chinese state medicine agency for use in 1996.
Like many traditional Chinese medicine preparations, Tongxinluo is not a single chemical – far from it. It is a powder made from a variety of plant and insect parts, as you can see here.
I can’t imagine running a trial of this concoction in the United States; I just don’t see an institutional review board signing off, given the ingredient list.
But let’s set that aside and talk about the study itself.
While I don’t have access to any primary data, the write-up of the study suggests that it was highly rigorous. Chinese researchers randomized 3,797 patients with ST-elevation MI to take Tongxinluo – four capsules, three times a day for 12 months – or matching placebo. The placebo was designed to look just like the Tongxinluo capsules and, if the capsules were opened, to smell like them as well.
Researchers and participants were blinded, and the statistical analysis was done both by the primary team and an independent research agency, also in China.
And the results were pretty good. The primary outcome, 30-day major cardiovascular and cerebral events, were significantly lower in the intervention group than in the placebo group.
One-year outcomes were similarly good; 8.3% of the placebo group suffered a major cardiovascular or cerebral event in that time frame, compared with 5.3% of the Tongxinluo group. In short, if this were a pure chemical compound from a major pharmaceutical company, well, you might be seeing a new treatment for heart attack – and a boost in stock price.
But there are some issues here, generalizability being a big one. This study was done entirely in China, so its applicability to a more diverse population is unclear. Moreover, the quality of post-MI care in this study is quite a bit worse than what we’d see here in the United States, with just over 50% of patients being discharged on a beta-blocker, for example.
But issues of generalizability and potentially substandard supplementary treatments are the usual reasons we worry about new medication trials. And those concerns seem to pale before the big one I have here which is, you know – we don’t know why this works.
Is it the extract of leech in the preparation perhaps thinning the blood a bit? Or is it the antioxidants in the ginseng, or something from the Pacific centipede or the sandalwood?
This trial doesn’t read to me as a vindication of traditional Chinese medicine but rather as an example of missed opportunity. More rigorous scientific study over the centuries that Tongxinluo has been used could have identified one, or perhaps more, compounds with strong therapeutic potential.
Purity of medical substances is incredibly important. Pure substances have predictable effects and side effects. Pure substances interact with other treatments we give patients in predictable ways. Pure substances can be quantified for purity by third parties, they can be manufactured according to accepted standards, and they can be assessed for adulteration. In short, pure substances pose less risk.
Now, I know that may come off as particularly sterile. Some people will feel that a “natural” substance has some inherent benefit over pure compounds. And, of course, there is something soothing about imagining a traditional preparation handed down over centuries, being prepared with care by a single practitioner, in contrast to the sterile industrial processes of a for-profit pharmaceutical company. I get it. But natural is not the same as safe. I am glad I have access to purified aspirin and don’t have to chew willow bark. I like my pure penicillin and am glad I don’t have to make a mold slurry to treat a bacterial infection.
I applaud the researchers for subjecting Tongxinluo to the rigor of a well-designed trial. They have generated data that are incredibly exciting, but not because we have a new treatment for ST-elevation MI on our hands; it’s because we have a map to a new treatment. The next big thing in heart attack care is not the mixture that is Tongxinluo, but it might be in the mixture.
A version of this article first appeared on Medscape.com.
F. Perry Wilson, MD, MSCE, is an associate professor of medicine and public health and director of Yale’s Clinical and Translational Research Accelerator. His science communication work can be found in the Huffington Post, on NPR, and on Medscape. He tweets @fperrywilson and his new book, “How Medicine Works and When It Doesn’t,” is available now.
This transcript has been edited for clarity.
As some of you may know, I do a fair amount of clinical research developing and evaluating artificial intelligence (AI) models, particularly machine learning algorithms that predict certain outcomes.
A thorny issue that comes up as algorithms have gotten more complicated is “explainability.” The problem is that AI can be a black box. Even if you have a model that is very accurate at predicting death, clinicians don’t trust it unless you can explain how it makes its predictions – how it works. “It just works” is not good enough to build trust.
It’s easier to build trust when you’re talking about a medication rather than a computer program. When a new blood pressure drug comes out that lowers blood pressure, importantly, we know why it lowers blood pressure. Every drug has a mechanism of action and, for most of the drugs in our arsenal, we know what that mechanism is.
But what if there were a drug – or better yet, a treatment – that worked? And I can honestly say we have no idea how it works. That’s what came across my desk today in what I believe is the largest, most rigorous trial of a traditional Chinese medication in history.
“Traditional Chinese medicine” is an omnibus term that refers to a class of therapies and health practices that are fundamentally different from how we practice medicine in the West.
It’s a highly personalized practice, with practitioners using often esoteric means to choose what substance to give what patient. That personalization makes traditional Chinese medicine nearly impossible to study in the typical randomized trial framework because treatments are not chosen solely on the basis of disease states.
The lack of scientific rigor in traditional Chinese medicine means that it is rife with practices and beliefs that can legitimately be called pseudoscience. As a nephrologist who has treated someone for “Chinese herb nephropathy,” I can tell you that some of the practices may be actively harmful.
But that doesn’t mean there is nothing there. I do not subscribe to the “argument from antiquity” – the idea that because something has been done for a long time it must be correct. But at the same time, traditional and non–science-based medicine practices could still identify therapies that work.
And with that, let me introduce you to Tongxinluo. Tongxinluo literally means “to open the network of the heart,” and it is a substance that has been used for centuries by traditional Chinese medicine practitioners to treat angina but was approved by the Chinese state medicine agency for use in 1996.
Like many traditional Chinese medicine preparations, Tongxinluo is not a single chemical – far from it. It is a powder made from a variety of plant and insect parts, as you can see here.
I can’t imagine running a trial of this concoction in the United States; I just don’t see an institutional review board signing off, given the ingredient list.
But let’s set that aside and talk about the study itself.
While I don’t have access to any primary data, the write-up of the study suggests that it was highly rigorous. Chinese researchers randomized 3,797 patients with ST-elevation MI to take Tongxinluo – four capsules, three times a day for 12 months – or matching placebo. The placebo was designed to look just like the Tongxinluo capsules and, if the capsules were opened, to smell like them as well.
Researchers and participants were blinded, and the statistical analysis was done both by the primary team and an independent research agency, also in China.
And the results were pretty good. The primary outcome, 30-day major cardiovascular and cerebral events, were significantly lower in the intervention group than in the placebo group.
One-year outcomes were similarly good; 8.3% of the placebo group suffered a major cardiovascular or cerebral event in that time frame, compared with 5.3% of the Tongxinluo group. In short, if this were a pure chemical compound from a major pharmaceutical company, well, you might be seeing a new treatment for heart attack – and a boost in stock price.
But there are some issues here, generalizability being a big one. This study was done entirely in China, so its applicability to a more diverse population is unclear. Moreover, the quality of post-MI care in this study is quite a bit worse than what we’d see here in the United States, with just over 50% of patients being discharged on a beta-blocker, for example.
But issues of generalizability and potentially substandard supplementary treatments are the usual reasons we worry about new medication trials. And those concerns seem to pale before the big one I have here which is, you know – we don’t know why this works.
Is it the extract of leech in the preparation perhaps thinning the blood a bit? Or is it the antioxidants in the ginseng, or something from the Pacific centipede or the sandalwood?
This trial doesn’t read to me as a vindication of traditional Chinese medicine but rather as an example of missed opportunity. More rigorous scientific study over the centuries that Tongxinluo has been used could have identified one, or perhaps more, compounds with strong therapeutic potential.
Purity of medical substances is incredibly important. Pure substances have predictable effects and side effects. Pure substances interact with other treatments we give patients in predictable ways. Pure substances can be quantified for purity by third parties, they can be manufactured according to accepted standards, and they can be assessed for adulteration. In short, pure substances pose less risk.
Now, I know that may come off as particularly sterile. Some people will feel that a “natural” substance has some inherent benefit over pure compounds. And, of course, there is something soothing about imagining a traditional preparation handed down over centuries, being prepared with care by a single practitioner, in contrast to the sterile industrial processes of a for-profit pharmaceutical company. I get it. But natural is not the same as safe. I am glad I have access to purified aspirin and don’t have to chew willow bark. I like my pure penicillin and am glad I don’t have to make a mold slurry to treat a bacterial infection.
I applaud the researchers for subjecting Tongxinluo to the rigor of a well-designed trial. They have generated data that are incredibly exciting, but not because we have a new treatment for ST-elevation MI on our hands; it’s because we have a map to a new treatment. The next big thing in heart attack care is not the mixture that is Tongxinluo, but it might be in the mixture.
A version of this article first appeared on Medscape.com.
F. Perry Wilson, MD, MSCE, is an associate professor of medicine and public health and director of Yale’s Clinical and Translational Research Accelerator. His science communication work can be found in the Huffington Post, on NPR, and on Medscape. He tweets @fperrywilson and his new book, “How Medicine Works and When It Doesn’t,” is available now.
This transcript has been edited for clarity.
As some of you may know, I do a fair amount of clinical research developing and evaluating artificial intelligence (AI) models, particularly machine learning algorithms that predict certain outcomes.
A thorny issue that comes up as algorithms have gotten more complicated is “explainability.” The problem is that AI can be a black box. Even if you have a model that is very accurate at predicting death, clinicians don’t trust it unless you can explain how it makes its predictions – how it works. “It just works” is not good enough to build trust.
It’s easier to build trust when you’re talking about a medication rather than a computer program. When a new blood pressure drug comes out that lowers blood pressure, importantly, we know why it lowers blood pressure. Every drug has a mechanism of action and, for most of the drugs in our arsenal, we know what that mechanism is.
But what if there were a drug – or better yet, a treatment – that worked? And I can honestly say we have no idea how it works. That’s what came across my desk today in what I believe is the largest, most rigorous trial of a traditional Chinese medication in history.
“Traditional Chinese medicine” is an omnibus term that refers to a class of therapies and health practices that are fundamentally different from how we practice medicine in the West.
It’s a highly personalized practice, with practitioners using often esoteric means to choose what substance to give what patient. That personalization makes traditional Chinese medicine nearly impossible to study in the typical randomized trial framework because treatments are not chosen solely on the basis of disease states.
The lack of scientific rigor in traditional Chinese medicine means that it is rife with practices and beliefs that can legitimately be called pseudoscience. As a nephrologist who has treated someone for “Chinese herb nephropathy,” I can tell you that some of the practices may be actively harmful.
But that doesn’t mean there is nothing there. I do not subscribe to the “argument from antiquity” – the idea that because something has been done for a long time it must be correct. But at the same time, traditional and non–science-based medicine practices could still identify therapies that work.
And with that, let me introduce you to Tongxinluo. Tongxinluo literally means “to open the network of the heart,” and it is a substance that has been used for centuries by traditional Chinese medicine practitioners to treat angina but was approved by the Chinese state medicine agency for use in 1996.
Like many traditional Chinese medicine preparations, Tongxinluo is not a single chemical – far from it. It is a powder made from a variety of plant and insect parts, as you can see here.
I can’t imagine running a trial of this concoction in the United States; I just don’t see an institutional review board signing off, given the ingredient list.
But let’s set that aside and talk about the study itself.
While I don’t have access to any primary data, the write-up of the study suggests that it was highly rigorous. Chinese researchers randomized 3,797 patients with ST-elevation MI to take Tongxinluo – four capsules, three times a day for 12 months – or matching placebo. The placebo was designed to look just like the Tongxinluo capsules and, if the capsules were opened, to smell like them as well.
Researchers and participants were blinded, and the statistical analysis was done both by the primary team and an independent research agency, also in China.
And the results were pretty good. The primary outcome, 30-day major cardiovascular and cerebral events, were significantly lower in the intervention group than in the placebo group.
One-year outcomes were similarly good; 8.3% of the placebo group suffered a major cardiovascular or cerebral event in that time frame, compared with 5.3% of the Tongxinluo group. In short, if this were a pure chemical compound from a major pharmaceutical company, well, you might be seeing a new treatment for heart attack – and a boost in stock price.
But there are some issues here, generalizability being a big one. This study was done entirely in China, so its applicability to a more diverse population is unclear. Moreover, the quality of post-MI care in this study is quite a bit worse than what we’d see here in the United States, with just over 50% of patients being discharged on a beta-blocker, for example.
But issues of generalizability and potentially substandard supplementary treatments are the usual reasons we worry about new medication trials. And those concerns seem to pale before the big one I have here which is, you know – we don’t know why this works.
Is it the extract of leech in the preparation perhaps thinning the blood a bit? Or is it the antioxidants in the ginseng, or something from the Pacific centipede or the sandalwood?
This trial doesn’t read to me as a vindication of traditional Chinese medicine but rather as an example of missed opportunity. More rigorous scientific study over the centuries that Tongxinluo has been used could have identified one, or perhaps more, compounds with strong therapeutic potential.
Purity of medical substances is incredibly important. Pure substances have predictable effects and side effects. Pure substances interact with other treatments we give patients in predictable ways. Pure substances can be quantified for purity by third parties, they can be manufactured according to accepted standards, and they can be assessed for adulteration. In short, pure substances pose less risk.
Now, I know that may come off as particularly sterile. Some people will feel that a “natural” substance has some inherent benefit over pure compounds. And, of course, there is something soothing about imagining a traditional preparation handed down over centuries, being prepared with care by a single practitioner, in contrast to the sterile industrial processes of a for-profit pharmaceutical company. I get it. But natural is not the same as safe. I am glad I have access to purified aspirin and don’t have to chew willow bark. I like my pure penicillin and am glad I don’t have to make a mold slurry to treat a bacterial infection.
I applaud the researchers for subjecting Tongxinluo to the rigor of a well-designed trial. They have generated data that are incredibly exciting, but not because we have a new treatment for ST-elevation MI on our hands; it’s because we have a map to a new treatment. The next big thing in heart attack care is not the mixture that is Tongxinluo, but it might be in the mixture.
A version of this article first appeared on Medscape.com.
F. Perry Wilson, MD, MSCE, is an associate professor of medicine and public health and director of Yale’s Clinical and Translational Research Accelerator. His science communication work can be found in the Huffington Post, on NPR, and on Medscape. He tweets @fperrywilson and his new book, “How Medicine Works and When It Doesn’t,” is available now.
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
Common meds link to sudden cardiac arrest in type 2 diabetes
HAMBURG, Germany – , shows the first such analysis of real-world, primary care data.
People with type 2 diabetes who do not have a history of CVD have almost three times the risk of SCA if they take antipsychotic medications and nearly double the risk if they take certain antibiotics that prolong the QT interval, notably, macrolides and fluoroquinolones.
“These data show that commonly prescribed drugs - antipsychotic medications, used by about 3% of people with type 2 diabetes, and antibiotics, taken by 5% to 10%, convey an increased risk of sudden cardiac arrest in those without a history of cardiovascular disease,” said Peter Harms, MSc, who presented the study at the annual meeting of the European Association for the Study of Diabetes. Another drug associated with an increase in SCA among patients with diabetes was domperidone, an antinausea medication.
“Perhaps these drugs could be avoided in some cases, and GPs should be more aware of the possible consequences of their use,” he added. “If the patient has type 2 diabetes, then maybe it’s better to avoid some of these medications and try and cope without them, or at least find an alternative antibiotic.”
Mr. Harms, an epidemiologist from Amsterdam University Medical Centers, highlighted that their study was unique because the investigators drew upon primary care data. “These data are extensive, and we find a lot of associations which are very real.”
SCA is associated with 50% of all cardiac deaths and accounts for 20% of all mortality in high-income countries. Of those people who experience SCA, 80% of cases prove fatal.
“As the name suggests, it is difficult to predict because it is sudden, especially in people without a cardiovascular disease history,” Mr. Harms pointed out in an interview with this news organization. He highlighted that “around half of those who experience SCA, often between the ages of 40 and 60 years, have never seen a cardiologist, but many do have type 2 diabetes.
“We need to better understand how to recognize people at risk of SCA, know who to watch and how to prevent these events,” he emphasized.
Vladimira Fejfarova, MD, comoderated the session and commented on the study. “From the clinical point of view, it’s necessary to evaluate risk factors that can contribute to sudden cardiac arrest.”
Overall, the researchers found that, among people with type 2 diabetes who do not have a history of CVD, hypoglycemia, severe hypertension, dyslipidemia, and use of QTc-prolonging medications are associated with SCA risk. Among people with type 2 diabetes and CVD, albuminuria and heart failure are associated with SCA risk.
Dr. Fejfarova added: “With type 2 diabetes and also type 1, we need to look more at adverse events, especially when treating infections with macrolides, but also mycotic infections, because antimycotic drugs are known to influence QT intervals that could contribute to sudden cardiac arrest.
“We need to be more cautious with prescribing certain antibiotics that have these side effects in our patients with diabetes,” asserted Dr. Fejfarova, from the Diabetes Centre, Institute for Clinical and Experimental Medicine, Prague.
Type 2 diabetes doubles the risk of SCA
The researcher decided to investigate the population of people with type 2 diabetes because their risk of SCD is around twice that of those without type 2 diabetes. Because these patients have relatively frequent checkups with general practitioners, Mr. Harms turned to primary care databases that contained comprehensive and relatively routine information on risk indicators.
Longitudinal associations between clinical characteristics of 3,919 patients with type 2 diabetes – both those with and those without a history of CVD – and SCA (a total of 689 patients) were determined.
Cases were found in the AmsteRdam REsuscitation STtudies (ARREST) registry of out-of-hospital resuscitation attempts by emergency medical services in the Dutch region of Noord-Holland from 2010 to 2019. Case patients were matched with up to five control patients. The control group comprised people with type 2 diabetes who had not experienced an SCA. Control patients were sourced from the same primary care practices who were of similar age and sex. Clinical measurements, including blood pressure and blood glucose readings, medication use, and medical history for the 5 years leading up to an SCA, were obtained from general practice records. A multivariable analysis was performed, and results were stratified for people with and for those without a history of CVD.
Of particular interest were drugs that interfere with cardiac function, including some prokinetic, antibiotic, and antipsychotic medications. All of the drugs are known to be associated with a change in QTc prolongation. Examples include domperidone (QTc-prolonging prokinetic), macrolides and fluoroquinolones (QTc-prolonging antibiotics), and haloperidol (a QTc-prolonging antipsychotic).
Antibiotic and antipsychotic use might contribute to SCA in T2D
Case patients and control patients were similar in age, hemoglobin A1c level, and other characteristics with the exception that more patients with SCA had a history of CVD (40.0% vs. 29.4%).
“Looking at the associations in the overall population, insulin use was strongly associated with SCA risk [hazard ratio, 2.38] and perhaps this was an indicator of severity of type 2 diabetes,” remarked Mr. Harms. “Also, unsurprisingly, a history of arrhythmia [HR, 1.68] and, more surprisingly, prokinetic drug use [HR, 1.66; 95% confidence interval, 1.20-2.31], specifically those known for QTc-prolongation, were associated with SCA.”
Among people who had experienced an SCA and who did not have a history of CVD (337 case patients/2,023 control patients), QTc-prolonging antipsychotic medication use was associated with SCA at an HR of 2.87, and antibiotic medication use was associated with SCA at an HR of 1.66. A low fasting glucose level (< 4.5 mmol/mol) was associated with SCA at an HR of 2.5; severely high systolic blood pressure (> 180 mm Hg) was associated with SCA at an HR of 2.21; low HDL cholesterol level, with an HR of 1.35; and high LDL cholesterol level (> 2.6 mmol/L), with an HR of 1.64.
Among people with a history of CVD (352 case patients/1,207 control patients), associations between albuminuria and SCA were moderate (HR, 1.54) and severe (HR, 1.55); heart failure was associated with SCA at an HR of 1.85 (95% CI, 1.50-2.29).
Comoderator Dr. Fejfarova added that, in addition to the findings from Dr. Harms’ study, other research presented in the same session highlighted the importance of checking patients for the presence of arrhythmias that could lead to the development of atrioventricular blocks, sinus node diseases, and SCA.
Mr. Harms and Dr. Fejfarova have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
HAMBURG, Germany – , shows the first such analysis of real-world, primary care data.
People with type 2 diabetes who do not have a history of CVD have almost three times the risk of SCA if they take antipsychotic medications and nearly double the risk if they take certain antibiotics that prolong the QT interval, notably, macrolides and fluoroquinolones.
“These data show that commonly prescribed drugs - antipsychotic medications, used by about 3% of people with type 2 diabetes, and antibiotics, taken by 5% to 10%, convey an increased risk of sudden cardiac arrest in those without a history of cardiovascular disease,” said Peter Harms, MSc, who presented the study at the annual meeting of the European Association for the Study of Diabetes. Another drug associated with an increase in SCA among patients with diabetes was domperidone, an antinausea medication.
“Perhaps these drugs could be avoided in some cases, and GPs should be more aware of the possible consequences of their use,” he added. “If the patient has type 2 diabetes, then maybe it’s better to avoid some of these medications and try and cope without them, or at least find an alternative antibiotic.”
Mr. Harms, an epidemiologist from Amsterdam University Medical Centers, highlighted that their study was unique because the investigators drew upon primary care data. “These data are extensive, and we find a lot of associations which are very real.”
SCA is associated with 50% of all cardiac deaths and accounts for 20% of all mortality in high-income countries. Of those people who experience SCA, 80% of cases prove fatal.
“As the name suggests, it is difficult to predict because it is sudden, especially in people without a cardiovascular disease history,” Mr. Harms pointed out in an interview with this news organization. He highlighted that “around half of those who experience SCA, often between the ages of 40 and 60 years, have never seen a cardiologist, but many do have type 2 diabetes.
“We need to better understand how to recognize people at risk of SCA, know who to watch and how to prevent these events,” he emphasized.
Vladimira Fejfarova, MD, comoderated the session and commented on the study. “From the clinical point of view, it’s necessary to evaluate risk factors that can contribute to sudden cardiac arrest.”
Overall, the researchers found that, among people with type 2 diabetes who do not have a history of CVD, hypoglycemia, severe hypertension, dyslipidemia, and use of QTc-prolonging medications are associated with SCA risk. Among people with type 2 diabetes and CVD, albuminuria and heart failure are associated with SCA risk.
Dr. Fejfarova added: “With type 2 diabetes and also type 1, we need to look more at adverse events, especially when treating infections with macrolides, but also mycotic infections, because antimycotic drugs are known to influence QT intervals that could contribute to sudden cardiac arrest.
“We need to be more cautious with prescribing certain antibiotics that have these side effects in our patients with diabetes,” asserted Dr. Fejfarova, from the Diabetes Centre, Institute for Clinical and Experimental Medicine, Prague.
Type 2 diabetes doubles the risk of SCA
The researcher decided to investigate the population of people with type 2 diabetes because their risk of SCD is around twice that of those without type 2 diabetes. Because these patients have relatively frequent checkups with general practitioners, Mr. Harms turned to primary care databases that contained comprehensive and relatively routine information on risk indicators.
Longitudinal associations between clinical characteristics of 3,919 patients with type 2 diabetes – both those with and those without a history of CVD – and SCA (a total of 689 patients) were determined.
Cases were found in the AmsteRdam REsuscitation STtudies (ARREST) registry of out-of-hospital resuscitation attempts by emergency medical services in the Dutch region of Noord-Holland from 2010 to 2019. Case patients were matched with up to five control patients. The control group comprised people with type 2 diabetes who had not experienced an SCA. Control patients were sourced from the same primary care practices who were of similar age and sex. Clinical measurements, including blood pressure and blood glucose readings, medication use, and medical history for the 5 years leading up to an SCA, were obtained from general practice records. A multivariable analysis was performed, and results were stratified for people with and for those without a history of CVD.
Of particular interest were drugs that interfere with cardiac function, including some prokinetic, antibiotic, and antipsychotic medications. All of the drugs are known to be associated with a change in QTc prolongation. Examples include domperidone (QTc-prolonging prokinetic), macrolides and fluoroquinolones (QTc-prolonging antibiotics), and haloperidol (a QTc-prolonging antipsychotic).
Antibiotic and antipsychotic use might contribute to SCA in T2D
Case patients and control patients were similar in age, hemoglobin A1c level, and other characteristics with the exception that more patients with SCA had a history of CVD (40.0% vs. 29.4%).
“Looking at the associations in the overall population, insulin use was strongly associated with SCA risk [hazard ratio, 2.38] and perhaps this was an indicator of severity of type 2 diabetes,” remarked Mr. Harms. “Also, unsurprisingly, a history of arrhythmia [HR, 1.68] and, more surprisingly, prokinetic drug use [HR, 1.66; 95% confidence interval, 1.20-2.31], specifically those known for QTc-prolongation, were associated with SCA.”
Among people who had experienced an SCA and who did not have a history of CVD (337 case patients/2,023 control patients), QTc-prolonging antipsychotic medication use was associated with SCA at an HR of 2.87, and antibiotic medication use was associated with SCA at an HR of 1.66. A low fasting glucose level (< 4.5 mmol/mol) was associated with SCA at an HR of 2.5; severely high systolic blood pressure (> 180 mm Hg) was associated with SCA at an HR of 2.21; low HDL cholesterol level, with an HR of 1.35; and high LDL cholesterol level (> 2.6 mmol/L), with an HR of 1.64.
Among people with a history of CVD (352 case patients/1,207 control patients), associations between albuminuria and SCA were moderate (HR, 1.54) and severe (HR, 1.55); heart failure was associated with SCA at an HR of 1.85 (95% CI, 1.50-2.29).
Comoderator Dr. Fejfarova added that, in addition to the findings from Dr. Harms’ study, other research presented in the same session highlighted the importance of checking patients for the presence of arrhythmias that could lead to the development of atrioventricular blocks, sinus node diseases, and SCA.
Mr. Harms and Dr. Fejfarova have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
HAMBURG, Germany – , shows the first such analysis of real-world, primary care data.
People with type 2 diabetes who do not have a history of CVD have almost three times the risk of SCA if they take antipsychotic medications and nearly double the risk if they take certain antibiotics that prolong the QT interval, notably, macrolides and fluoroquinolones.
“These data show that commonly prescribed drugs - antipsychotic medications, used by about 3% of people with type 2 diabetes, and antibiotics, taken by 5% to 10%, convey an increased risk of sudden cardiac arrest in those without a history of cardiovascular disease,” said Peter Harms, MSc, who presented the study at the annual meeting of the European Association for the Study of Diabetes. Another drug associated with an increase in SCA among patients with diabetes was domperidone, an antinausea medication.
“Perhaps these drugs could be avoided in some cases, and GPs should be more aware of the possible consequences of their use,” he added. “If the patient has type 2 diabetes, then maybe it’s better to avoid some of these medications and try and cope without them, or at least find an alternative antibiotic.”
Mr. Harms, an epidemiologist from Amsterdam University Medical Centers, highlighted that their study was unique because the investigators drew upon primary care data. “These data are extensive, and we find a lot of associations which are very real.”
SCA is associated with 50% of all cardiac deaths and accounts for 20% of all mortality in high-income countries. Of those people who experience SCA, 80% of cases prove fatal.
“As the name suggests, it is difficult to predict because it is sudden, especially in people without a cardiovascular disease history,” Mr. Harms pointed out in an interview with this news organization. He highlighted that “around half of those who experience SCA, often between the ages of 40 and 60 years, have never seen a cardiologist, but many do have type 2 diabetes.
“We need to better understand how to recognize people at risk of SCA, know who to watch and how to prevent these events,” he emphasized.
Vladimira Fejfarova, MD, comoderated the session and commented on the study. “From the clinical point of view, it’s necessary to evaluate risk factors that can contribute to sudden cardiac arrest.”
Overall, the researchers found that, among people with type 2 diabetes who do not have a history of CVD, hypoglycemia, severe hypertension, dyslipidemia, and use of QTc-prolonging medications are associated with SCA risk. Among people with type 2 diabetes and CVD, albuminuria and heart failure are associated with SCA risk.
Dr. Fejfarova added: “With type 2 diabetes and also type 1, we need to look more at adverse events, especially when treating infections with macrolides, but also mycotic infections, because antimycotic drugs are known to influence QT intervals that could contribute to sudden cardiac arrest.
“We need to be more cautious with prescribing certain antibiotics that have these side effects in our patients with diabetes,” asserted Dr. Fejfarova, from the Diabetes Centre, Institute for Clinical and Experimental Medicine, Prague.
Type 2 diabetes doubles the risk of SCA
The researcher decided to investigate the population of people with type 2 diabetes because their risk of SCD is around twice that of those without type 2 diabetes. Because these patients have relatively frequent checkups with general practitioners, Mr. Harms turned to primary care databases that contained comprehensive and relatively routine information on risk indicators.
Longitudinal associations between clinical characteristics of 3,919 patients with type 2 diabetes – both those with and those without a history of CVD – and SCA (a total of 689 patients) were determined.
Cases were found in the AmsteRdam REsuscitation STtudies (ARREST) registry of out-of-hospital resuscitation attempts by emergency medical services in the Dutch region of Noord-Holland from 2010 to 2019. Case patients were matched with up to five control patients. The control group comprised people with type 2 diabetes who had not experienced an SCA. Control patients were sourced from the same primary care practices who were of similar age and sex. Clinical measurements, including blood pressure and blood glucose readings, medication use, and medical history for the 5 years leading up to an SCA, were obtained from general practice records. A multivariable analysis was performed, and results were stratified for people with and for those without a history of CVD.
Of particular interest were drugs that interfere with cardiac function, including some prokinetic, antibiotic, and antipsychotic medications. All of the drugs are known to be associated with a change in QTc prolongation. Examples include domperidone (QTc-prolonging prokinetic), macrolides and fluoroquinolones (QTc-prolonging antibiotics), and haloperidol (a QTc-prolonging antipsychotic).
Antibiotic and antipsychotic use might contribute to SCA in T2D
Case patients and control patients were similar in age, hemoglobin A1c level, and other characteristics with the exception that more patients with SCA had a history of CVD (40.0% vs. 29.4%).
“Looking at the associations in the overall population, insulin use was strongly associated with SCA risk [hazard ratio, 2.38] and perhaps this was an indicator of severity of type 2 diabetes,” remarked Mr. Harms. “Also, unsurprisingly, a history of arrhythmia [HR, 1.68] and, more surprisingly, prokinetic drug use [HR, 1.66; 95% confidence interval, 1.20-2.31], specifically those known for QTc-prolongation, were associated with SCA.”
Among people who had experienced an SCA and who did not have a history of CVD (337 case patients/2,023 control patients), QTc-prolonging antipsychotic medication use was associated with SCA at an HR of 2.87, and antibiotic medication use was associated with SCA at an HR of 1.66. A low fasting glucose level (< 4.5 mmol/mol) was associated with SCA at an HR of 2.5; severely high systolic blood pressure (> 180 mm Hg) was associated with SCA at an HR of 2.21; low HDL cholesterol level, with an HR of 1.35; and high LDL cholesterol level (> 2.6 mmol/L), with an HR of 1.64.
Among people with a history of CVD (352 case patients/1,207 control patients), associations between albuminuria and SCA were moderate (HR, 1.54) and severe (HR, 1.55); heart failure was associated with SCA at an HR of 1.85 (95% CI, 1.50-2.29).
Comoderator Dr. Fejfarova added that, in addition to the findings from Dr. Harms’ study, other research presented in the same session highlighted the importance of checking patients for the presence of arrhythmias that could lead to the development of atrioventricular blocks, sinus node diseases, and SCA.
Mr. Harms and Dr. Fejfarova have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
AT EASD 2023
CMS ‘million hearts’ CVD risk reduction model works
TOPLINE:
The Million Hearts Model, a U.S. Centers for Medicare & Medicaid Services (CMS) initiative that encouraged and paid health care organizations to assess and reduce cardiovascular disease (CVD) risk, reduced first-time myocardial infarction (MI) and strokes among Medicare beneficiaries without significant changes in Medicare spending, a randomized trial finds.
METHODOLOGY:
- Researchers assessed the Million Hearts CVD Risk Reduction Model in a pragmatic, cluster-randomized trial among 342 health care organizations – half in the intervention group and half in the standard care control group.
- Among 218,684 medium- or high-risk Medicare beneficiaries (median age, 72 years), 130,578 were in the intervention group in which Medicare paid for guideline-concordant care including routine CVD risk assessment, and 88,286 were in the standard care group.
- Outcomes included first time CVD events (for instance, MI, stroke, transient ischemic attack), combined first-time CVD events and CVD deaths, and Medicare spending.
TAKEAWAY:
- Over a median follow-up of 4.3 years, the intervention group had a 3.3% lower rate of CVD events than the control group (adjusted hazard ratio, 0.97; 90% confidence interval, 0.93-1.00; P = .09) and a 4.2% lower rate of combined first-time CVD events and CVD deaths (HR, 0.96; 90% CI, 0.93-0.99; P = .02).
- These relative effects represent an absolute re.duction of 0.3 percentage points in the probability of a CVD event over 5 years (7.8% intervention vs 8.1%) and 0.4 percentage points in the probability of a CVD event or CVD death over 5 years (9.3% intervention vs. 9.7% control).
- The intervention group also had a 4.3% lower death rate (HR, 0.96; 90% CI, 0.93-0.98; P = .01; absolute reduction of 0.5 percentage points over 5 years).
- Analyses by cause of death showed the largest relative declines (10.6%) among deaths due to coronary heart disease and CVD.
- There was no significant between-group difference in Medicare spending on CVD events or in overall Medicare Parts A and B spending.
IN PRACTICE:
“The model was unique in paying for overall CVD risk reduction, measured by a novel, longitudinal risk calculator, rather than tying performance-based payments to control of individual risk factors,” the authors write.
“The encouraging findings from the Million Hearts Model suggest that modernized payment models may be an affirmative strategy to [incentivize guideline-concordant CVD preventive care and improve outcomes], though further work is needed to ensure that these models are patient-centric, optimally deployed, and equity-enhancing,” add the editorial writers.
SOURCE:
The study, with first author Laura Blue, PhD, Mathematica, Washington, was published online in JAMA, with an accompanying editorial.
LIMITATIONS:
The main limitation is nonparticipation of many of the organizations (516 were randomly assigned to one of the study groups, 342 participated) and incomplete entry of beneficiary data into the registry, which could have led to systematic differences between the two groups. Bias due to the selective participation of organizations and beneficiaries cannot be ruled out.
DISCLOSURES:
Funding for the study was provided by CMS, Department of Health & Human Services. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
TOPLINE:
The Million Hearts Model, a U.S. Centers for Medicare & Medicaid Services (CMS) initiative that encouraged and paid health care organizations to assess and reduce cardiovascular disease (CVD) risk, reduced first-time myocardial infarction (MI) and strokes among Medicare beneficiaries without significant changes in Medicare spending, a randomized trial finds.
METHODOLOGY:
- Researchers assessed the Million Hearts CVD Risk Reduction Model in a pragmatic, cluster-randomized trial among 342 health care organizations – half in the intervention group and half in the standard care control group.
- Among 218,684 medium- or high-risk Medicare beneficiaries (median age, 72 years), 130,578 were in the intervention group in which Medicare paid for guideline-concordant care including routine CVD risk assessment, and 88,286 were in the standard care group.
- Outcomes included first time CVD events (for instance, MI, stroke, transient ischemic attack), combined first-time CVD events and CVD deaths, and Medicare spending.
TAKEAWAY:
- Over a median follow-up of 4.3 years, the intervention group had a 3.3% lower rate of CVD events than the control group (adjusted hazard ratio, 0.97; 90% confidence interval, 0.93-1.00; P = .09) and a 4.2% lower rate of combined first-time CVD events and CVD deaths (HR, 0.96; 90% CI, 0.93-0.99; P = .02).
- These relative effects represent an absolute re.duction of 0.3 percentage points in the probability of a CVD event over 5 years (7.8% intervention vs 8.1%) and 0.4 percentage points in the probability of a CVD event or CVD death over 5 years (9.3% intervention vs. 9.7% control).
- The intervention group also had a 4.3% lower death rate (HR, 0.96; 90% CI, 0.93-0.98; P = .01; absolute reduction of 0.5 percentage points over 5 years).
- Analyses by cause of death showed the largest relative declines (10.6%) among deaths due to coronary heart disease and CVD.
- There was no significant between-group difference in Medicare spending on CVD events or in overall Medicare Parts A and B spending.
IN PRACTICE:
“The model was unique in paying for overall CVD risk reduction, measured by a novel, longitudinal risk calculator, rather than tying performance-based payments to control of individual risk factors,” the authors write.
“The encouraging findings from the Million Hearts Model suggest that modernized payment models may be an affirmative strategy to [incentivize guideline-concordant CVD preventive care and improve outcomes], though further work is needed to ensure that these models are patient-centric, optimally deployed, and equity-enhancing,” add the editorial writers.
SOURCE:
The study, with first author Laura Blue, PhD, Mathematica, Washington, was published online in JAMA, with an accompanying editorial.
LIMITATIONS:
The main limitation is nonparticipation of many of the organizations (516 were randomly assigned to one of the study groups, 342 participated) and incomplete entry of beneficiary data into the registry, which could have led to systematic differences between the two groups. Bias due to the selective participation of organizations and beneficiaries cannot be ruled out.
DISCLOSURES:
Funding for the study was provided by CMS, Department of Health & Human Services. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
TOPLINE:
The Million Hearts Model, a U.S. Centers for Medicare & Medicaid Services (CMS) initiative that encouraged and paid health care organizations to assess and reduce cardiovascular disease (CVD) risk, reduced first-time myocardial infarction (MI) and strokes among Medicare beneficiaries without significant changes in Medicare spending, a randomized trial finds.
METHODOLOGY:
- Researchers assessed the Million Hearts CVD Risk Reduction Model in a pragmatic, cluster-randomized trial among 342 health care organizations – half in the intervention group and half in the standard care control group.
- Among 218,684 medium- or high-risk Medicare beneficiaries (median age, 72 years), 130,578 were in the intervention group in which Medicare paid for guideline-concordant care including routine CVD risk assessment, and 88,286 were in the standard care group.
- Outcomes included first time CVD events (for instance, MI, stroke, transient ischemic attack), combined first-time CVD events and CVD deaths, and Medicare spending.
TAKEAWAY:
- Over a median follow-up of 4.3 years, the intervention group had a 3.3% lower rate of CVD events than the control group (adjusted hazard ratio, 0.97; 90% confidence interval, 0.93-1.00; P = .09) and a 4.2% lower rate of combined first-time CVD events and CVD deaths (HR, 0.96; 90% CI, 0.93-0.99; P = .02).
- These relative effects represent an absolute re.duction of 0.3 percentage points in the probability of a CVD event over 5 years (7.8% intervention vs 8.1%) and 0.4 percentage points in the probability of a CVD event or CVD death over 5 years (9.3% intervention vs. 9.7% control).
- The intervention group also had a 4.3% lower death rate (HR, 0.96; 90% CI, 0.93-0.98; P = .01; absolute reduction of 0.5 percentage points over 5 years).
- Analyses by cause of death showed the largest relative declines (10.6%) among deaths due to coronary heart disease and CVD.
- There was no significant between-group difference in Medicare spending on CVD events or in overall Medicare Parts A and B spending.
IN PRACTICE:
“The model was unique in paying for overall CVD risk reduction, measured by a novel, longitudinal risk calculator, rather than tying performance-based payments to control of individual risk factors,” the authors write.
“The encouraging findings from the Million Hearts Model suggest that modernized payment models may be an affirmative strategy to [incentivize guideline-concordant CVD preventive care and improve outcomes], though further work is needed to ensure that these models are patient-centric, optimally deployed, and equity-enhancing,” add the editorial writers.
SOURCE:
The study, with first author Laura Blue, PhD, Mathematica, Washington, was published online in JAMA, with an accompanying editorial.
LIMITATIONS:
The main limitation is nonparticipation of many of the organizations (516 were randomly assigned to one of the study groups, 342 participated) and incomplete entry of beneficiary data into the registry, which could have led to systematic differences between the two groups. Bias due to the selective participation of organizations and beneficiaries cannot be ruled out.
DISCLOSURES:
Funding for the study was provided by CMS, Department of Health & Human Services. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
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.
‘Diagnosis creep’: Are some AFib patients overtreated?
without those treatments having been validated in those particular groups.
This concern has been highlighted recently in the atrial fibrillation (AF) field, with the recent change in the definition of hypertension in the United States at lower levels of blood pressure causing a lot more patients to become eligible for oral anticoagulation at an earlier stage in their AF course.
U.S. researchers analyzed data from 316,388 patients with AF from the National Cardiovascular Data Registry Practice Innovation and Clinical Excellence outpatient quality improvement registry, and found that at 36 months’ follow-up, 83.5% of patients met the new 130/80 mm Hg definition of hypertension, while only 53.3% met the previous 140/90 mm Hg definition.
The diagnosis of hypertension gives 1 point in the CHA2DS2-VASc score, which is used to determine risk in AF patients, those with scores of 2 or more being eligible for oral anticoagulation.
The researchers report that in patients with an index CHA2DS2-VASc score of 1 (before the hypertension diagnosis), at 36 months, 83% fulfilled the 130/80 mm Hg definition of hypertension while the 140/90 mm Hg definition was met by only 50%, giving a large increase in the number of patients who could qualify for oral anticoagulation therapy.
“While the definition of hypertension has changed in response to landmark clinical trials, CHA2DS2-VASc was validated using an older hypertension definition, with limited ambulatory blood pressure monitoring and higher blood pressure goals for treatment,” the authors state.
“Now, patients with AF will meet the CHA2DS2-VASc threshold for oral anticoagulation earlier in their disease course. However, it is not known if patients with scores of 1 or 2 using the new hypertension definition have sufficient stroke risk to offset the bleeding risk of oral anticoagulation and will receive net clinical benefit,” they point out.
This study was published online as a research letter in JAMA Network Open.
Senior author of the report, Mintu Turakhia, MD, Stanford (Calif.) University/iRhythm Technologies Inc., said AF is a good example of how “diagnosis creep” may lead to patients receiving inappropriate treatment.
“Risk scores derived when risk variables were described in one way are starting to be applied based on a diagnosis made in a totally different way,” he said in an interview. “Diagnosis creep is a problem everywhere in medicine. The goal of this study was to quantify what this means for the new definition of hypertension in the context of risk scoring AF patients for anticoagulation treatment. We are calling attention to this issue so clinicians are aware of possible implications.”
Dr. Turakhia explained that the CHA2DS2-VASc score was formulated based on claims data so there was a record of hypertension on the clinical encounter. That hypertension diagnosis would have been based on the old definition of 140/90 mm Hg.
“But now we apply a label of hypertension in the office every time someone has a measurement of elevated blood pressure – treated or untreated – and the blood pressure threshold for a hypertension diagnosis has changed to 130/80 mm Hg,” he said. “We are asking what this means for risk stratification scores such as CHA2DS2-VASc, and how do we quantify what that means for anticoagulation eligibility?”
He said that while identifying hypertension at lower blood pressures may be beneficial with regard to starting antihypertensive treatment earlier with a consequent reduction in cardiovascular outcomes, when this also affects risk scores that determine treatment for other conditions, as is the case for AF, the case is not so clear.
Dr. Turakhia pointed out that with AF, there are additional factors causing diagnosis creep, including earlier detection of AF and identification of shorter episodes due to the use of higher sensitivity tools to detect abnormal rhythms.
“What about the patient who has been identified as having AF based on just a few seconds found on monitoring and who is aged 65 (so just over the age threshold for 1 point on the CHA2DS2-VASc score)?” he asked. “Now we’re going to throw in hypertension with a blood pressure measurement just over 130/80 mm Hg, and they will be eligible for anticoagulation.”
Dr. Turakhia noted that in addition to earlier classification of hypertension, other conditions contributing to the CHA2DS2-VASc score are also being detected earlier, including diabetes and reduced ejection fractions that are considered heart failure.
“I worry about the sum of the parts. We don’t know if the risk score performs equally well when we’re using these different thresholds. We have to be careful that we are not exposing patients to the bleeding risks of anticoagulation unnecessarily. There is a clear issue here,” he said.
What should clinicians do?
In a comment, Gregory Lip, MD, chair of cardiovascular medicine at the University of Liverpool, England, who helped develop the CHA2DS2-VASc score, said clinicians needed to think more broadly when considering hypertension as a risk factor for the score.
He points out that if a patient had a history of hypertension but is now controlled to below 130/80 mm Hg, they would still be considered to be at risk per the CHA2DS2-VASc score.
And for patients without a history of hypertension, and who have a current blood pressure measurement of around 130/80 mm Hg, Dr. Lip advises that it would be premature to diagnose hypertension immediately.
“Hypertension is not a yes/no diagnosis. If you look at the relationship between blood pressure and risk of stroke, it is like a continual dose-response. It doesn’t mean that at 129/79 there is no stroke risk but that at 130/80 there is a stroke risk. It’s not like that,” he said.
“I wouldn’t make a diagnosis on a one-off blood pressure measurement. I would want to monitor that patient and get them to do home measurements,” he commented. “If someone constantly has levels around that 130/80 mm Hg, I don’t necessarily rush in with a definite diagnosis of hypertension and start drug treatment. I would look at lifestyle first. And in such patients, I wouldn’t give them the 1 point for hypertension on the CHA2DS2-VASc score.”
Dr. Lip points out that a hypertension diagnosis is not just about blood pressure numbers. “We have to assess the patients much more completely before giving them a diagnosis and consider factors such as whether there is evidence of hypertension-related end-organ damage, and if lifestyle issues have been addressed.”
Are new risk scores needed?
Dr. Turakhia agreed that clinicians need to look at the bigger picture, but he also suggested that new risk scores may need to be developed.
“All of us in the medical community need to think about whether we should be recalibrating risk prediction with more contemporary evidence – based on our ability to detect disease now,” he commented.
“This could even be a different risk score altogether, possibly incorporating a wider range of parameters or perhaps incorporating machine learning. That’s really the question we need to be asking ourselves,” Dr. Turakhia added.
Dr. Lip noted that there are many stroke risk factors and only those that are most common and have been well validated go into clinical risk scores such as CHA2DS2-VASc.
“These risks scores are by design simplifications, and only have modest predictive value for identifying patients at high risk of stroke. You can always improve on clinical risk scores by adding in other variables,” he said. “There are some risk scores in AF with 26 variables. But the practical application of these more complex scores can be difficult in clinical practice. These risks scores are meant to be simple so that they can be used by busy clinicians in the outpatient clinic or on a ward round. It is not easy to input 26 different variables.”
He also noted that many guidelines are now veering away from categorizing patients at high, medium, or low risk of stroke, which he refers to as “artificial” classifications. “There is now more of a default position that patients should receive stroke prevention normally with a DOAC [direct oral anticoagulant] unless they are low risk.”
Dr. Turakhia agreed that it is imperative to look at the bigger picture when identifying AF patients for anticoagulation. “We have to be careful not to take things at face value. It is more important than ever to use clinical judgment to avoid overtreatment in borderline situations,” he concluded.
This study was supported by the American College of Cardiology Foundation’s National Cardiovascular Data Registry. Dr. Turakhia reported employment from iRhythm Technologies; equity from AliveCor, Connect America, Evidently, and Forward; grants from U.S. Food and Drug Administration, American Heart Association, Bayer, Sanofi, Gilead, and Bristol Myers Squibb; and personal fees from Pfizer and JAMA Cardiology (prior associate editor) outside the submitted work. Dr. Lip has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
without those treatments having been validated in those particular groups.
This concern has been highlighted recently in the atrial fibrillation (AF) field, with the recent change in the definition of hypertension in the United States at lower levels of blood pressure causing a lot more patients to become eligible for oral anticoagulation at an earlier stage in their AF course.
U.S. researchers analyzed data from 316,388 patients with AF from the National Cardiovascular Data Registry Practice Innovation and Clinical Excellence outpatient quality improvement registry, and found that at 36 months’ follow-up, 83.5% of patients met the new 130/80 mm Hg definition of hypertension, while only 53.3% met the previous 140/90 mm Hg definition.
The diagnosis of hypertension gives 1 point in the CHA2DS2-VASc score, which is used to determine risk in AF patients, those with scores of 2 or more being eligible for oral anticoagulation.
The researchers report that in patients with an index CHA2DS2-VASc score of 1 (before the hypertension diagnosis), at 36 months, 83% fulfilled the 130/80 mm Hg definition of hypertension while the 140/90 mm Hg definition was met by only 50%, giving a large increase in the number of patients who could qualify for oral anticoagulation therapy.
“While the definition of hypertension has changed in response to landmark clinical trials, CHA2DS2-VASc was validated using an older hypertension definition, with limited ambulatory blood pressure monitoring and higher blood pressure goals for treatment,” the authors state.
“Now, patients with AF will meet the CHA2DS2-VASc threshold for oral anticoagulation earlier in their disease course. However, it is not known if patients with scores of 1 or 2 using the new hypertension definition have sufficient stroke risk to offset the bleeding risk of oral anticoagulation and will receive net clinical benefit,” they point out.
This study was published online as a research letter in JAMA Network Open.
Senior author of the report, Mintu Turakhia, MD, Stanford (Calif.) University/iRhythm Technologies Inc., said AF is a good example of how “diagnosis creep” may lead to patients receiving inappropriate treatment.
“Risk scores derived when risk variables were described in one way are starting to be applied based on a diagnosis made in a totally different way,” he said in an interview. “Diagnosis creep is a problem everywhere in medicine. The goal of this study was to quantify what this means for the new definition of hypertension in the context of risk scoring AF patients for anticoagulation treatment. We are calling attention to this issue so clinicians are aware of possible implications.”
Dr. Turakhia explained that the CHA2DS2-VASc score was formulated based on claims data so there was a record of hypertension on the clinical encounter. That hypertension diagnosis would have been based on the old definition of 140/90 mm Hg.
“But now we apply a label of hypertension in the office every time someone has a measurement of elevated blood pressure – treated or untreated – and the blood pressure threshold for a hypertension diagnosis has changed to 130/80 mm Hg,” he said. “We are asking what this means for risk stratification scores such as CHA2DS2-VASc, and how do we quantify what that means for anticoagulation eligibility?”
He said that while identifying hypertension at lower blood pressures may be beneficial with regard to starting antihypertensive treatment earlier with a consequent reduction in cardiovascular outcomes, when this also affects risk scores that determine treatment for other conditions, as is the case for AF, the case is not so clear.
Dr. Turakhia pointed out that with AF, there are additional factors causing diagnosis creep, including earlier detection of AF and identification of shorter episodes due to the use of higher sensitivity tools to detect abnormal rhythms.
“What about the patient who has been identified as having AF based on just a few seconds found on monitoring and who is aged 65 (so just over the age threshold for 1 point on the CHA2DS2-VASc score)?” he asked. “Now we’re going to throw in hypertension with a blood pressure measurement just over 130/80 mm Hg, and they will be eligible for anticoagulation.”
Dr. Turakhia noted that in addition to earlier classification of hypertension, other conditions contributing to the CHA2DS2-VASc score are also being detected earlier, including diabetes and reduced ejection fractions that are considered heart failure.
“I worry about the sum of the parts. We don’t know if the risk score performs equally well when we’re using these different thresholds. We have to be careful that we are not exposing patients to the bleeding risks of anticoagulation unnecessarily. There is a clear issue here,” he said.
What should clinicians do?
In a comment, Gregory Lip, MD, chair of cardiovascular medicine at the University of Liverpool, England, who helped develop the CHA2DS2-VASc score, said clinicians needed to think more broadly when considering hypertension as a risk factor for the score.
He points out that if a patient had a history of hypertension but is now controlled to below 130/80 mm Hg, they would still be considered to be at risk per the CHA2DS2-VASc score.
And for patients without a history of hypertension, and who have a current blood pressure measurement of around 130/80 mm Hg, Dr. Lip advises that it would be premature to diagnose hypertension immediately.
“Hypertension is not a yes/no diagnosis. If you look at the relationship between blood pressure and risk of stroke, it is like a continual dose-response. It doesn’t mean that at 129/79 there is no stroke risk but that at 130/80 there is a stroke risk. It’s not like that,” he said.
“I wouldn’t make a diagnosis on a one-off blood pressure measurement. I would want to monitor that patient and get them to do home measurements,” he commented. “If someone constantly has levels around that 130/80 mm Hg, I don’t necessarily rush in with a definite diagnosis of hypertension and start drug treatment. I would look at lifestyle first. And in such patients, I wouldn’t give them the 1 point for hypertension on the CHA2DS2-VASc score.”
Dr. Lip points out that a hypertension diagnosis is not just about blood pressure numbers. “We have to assess the patients much more completely before giving them a diagnosis and consider factors such as whether there is evidence of hypertension-related end-organ damage, and if lifestyle issues have been addressed.”
Are new risk scores needed?
Dr. Turakhia agreed that clinicians need to look at the bigger picture, but he also suggested that new risk scores may need to be developed.
“All of us in the medical community need to think about whether we should be recalibrating risk prediction with more contemporary evidence – based on our ability to detect disease now,” he commented.
“This could even be a different risk score altogether, possibly incorporating a wider range of parameters or perhaps incorporating machine learning. That’s really the question we need to be asking ourselves,” Dr. Turakhia added.
Dr. Lip noted that there are many stroke risk factors and only those that are most common and have been well validated go into clinical risk scores such as CHA2DS2-VASc.
“These risks scores are by design simplifications, and only have modest predictive value for identifying patients at high risk of stroke. You can always improve on clinical risk scores by adding in other variables,” he said. “There are some risk scores in AF with 26 variables. But the practical application of these more complex scores can be difficult in clinical practice. These risks scores are meant to be simple so that they can be used by busy clinicians in the outpatient clinic or on a ward round. It is not easy to input 26 different variables.”
He also noted that many guidelines are now veering away from categorizing patients at high, medium, or low risk of stroke, which he refers to as “artificial” classifications. “There is now more of a default position that patients should receive stroke prevention normally with a DOAC [direct oral anticoagulant] unless they are low risk.”
Dr. Turakhia agreed that it is imperative to look at the bigger picture when identifying AF patients for anticoagulation. “We have to be careful not to take things at face value. It is more important than ever to use clinical judgment to avoid overtreatment in borderline situations,” he concluded.
This study was supported by the American College of Cardiology Foundation’s National Cardiovascular Data Registry. Dr. Turakhia reported employment from iRhythm Technologies; equity from AliveCor, Connect America, Evidently, and Forward; grants from U.S. Food and Drug Administration, American Heart Association, Bayer, Sanofi, Gilead, and Bristol Myers Squibb; and personal fees from Pfizer and JAMA Cardiology (prior associate editor) outside the submitted work. Dr. Lip has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
without those treatments having been validated in those particular groups.
This concern has been highlighted recently in the atrial fibrillation (AF) field, with the recent change in the definition of hypertension in the United States at lower levels of blood pressure causing a lot more patients to become eligible for oral anticoagulation at an earlier stage in their AF course.
U.S. researchers analyzed data from 316,388 patients with AF from the National Cardiovascular Data Registry Practice Innovation and Clinical Excellence outpatient quality improvement registry, and found that at 36 months’ follow-up, 83.5% of patients met the new 130/80 mm Hg definition of hypertension, while only 53.3% met the previous 140/90 mm Hg definition.
The diagnosis of hypertension gives 1 point in the CHA2DS2-VASc score, which is used to determine risk in AF patients, those with scores of 2 or more being eligible for oral anticoagulation.
The researchers report that in patients with an index CHA2DS2-VASc score of 1 (before the hypertension diagnosis), at 36 months, 83% fulfilled the 130/80 mm Hg definition of hypertension while the 140/90 mm Hg definition was met by only 50%, giving a large increase in the number of patients who could qualify for oral anticoagulation therapy.
“While the definition of hypertension has changed in response to landmark clinical trials, CHA2DS2-VASc was validated using an older hypertension definition, with limited ambulatory blood pressure monitoring and higher blood pressure goals for treatment,” the authors state.
“Now, patients with AF will meet the CHA2DS2-VASc threshold for oral anticoagulation earlier in their disease course. However, it is not known if patients with scores of 1 or 2 using the new hypertension definition have sufficient stroke risk to offset the bleeding risk of oral anticoagulation and will receive net clinical benefit,” they point out.
This study was published online as a research letter in JAMA Network Open.
Senior author of the report, Mintu Turakhia, MD, Stanford (Calif.) University/iRhythm Technologies Inc., said AF is a good example of how “diagnosis creep” may lead to patients receiving inappropriate treatment.
“Risk scores derived when risk variables were described in one way are starting to be applied based on a diagnosis made in a totally different way,” he said in an interview. “Diagnosis creep is a problem everywhere in medicine. The goal of this study was to quantify what this means for the new definition of hypertension in the context of risk scoring AF patients for anticoagulation treatment. We are calling attention to this issue so clinicians are aware of possible implications.”
Dr. Turakhia explained that the CHA2DS2-VASc score was formulated based on claims data so there was a record of hypertension on the clinical encounter. That hypertension diagnosis would have been based on the old definition of 140/90 mm Hg.
“But now we apply a label of hypertension in the office every time someone has a measurement of elevated blood pressure – treated or untreated – and the blood pressure threshold for a hypertension diagnosis has changed to 130/80 mm Hg,” he said. “We are asking what this means for risk stratification scores such as CHA2DS2-VASc, and how do we quantify what that means for anticoagulation eligibility?”
He said that while identifying hypertension at lower blood pressures may be beneficial with regard to starting antihypertensive treatment earlier with a consequent reduction in cardiovascular outcomes, when this also affects risk scores that determine treatment for other conditions, as is the case for AF, the case is not so clear.
Dr. Turakhia pointed out that with AF, there are additional factors causing diagnosis creep, including earlier detection of AF and identification of shorter episodes due to the use of higher sensitivity tools to detect abnormal rhythms.
“What about the patient who has been identified as having AF based on just a few seconds found on monitoring and who is aged 65 (so just over the age threshold for 1 point on the CHA2DS2-VASc score)?” he asked. “Now we’re going to throw in hypertension with a blood pressure measurement just over 130/80 mm Hg, and they will be eligible for anticoagulation.”
Dr. Turakhia noted that in addition to earlier classification of hypertension, other conditions contributing to the CHA2DS2-VASc score are also being detected earlier, including diabetes and reduced ejection fractions that are considered heart failure.
“I worry about the sum of the parts. We don’t know if the risk score performs equally well when we’re using these different thresholds. We have to be careful that we are not exposing patients to the bleeding risks of anticoagulation unnecessarily. There is a clear issue here,” he said.
What should clinicians do?
In a comment, Gregory Lip, MD, chair of cardiovascular medicine at the University of Liverpool, England, who helped develop the CHA2DS2-VASc score, said clinicians needed to think more broadly when considering hypertension as a risk factor for the score.
He points out that if a patient had a history of hypertension but is now controlled to below 130/80 mm Hg, they would still be considered to be at risk per the CHA2DS2-VASc score.
And for patients without a history of hypertension, and who have a current blood pressure measurement of around 130/80 mm Hg, Dr. Lip advises that it would be premature to diagnose hypertension immediately.
“Hypertension is not a yes/no diagnosis. If you look at the relationship between blood pressure and risk of stroke, it is like a continual dose-response. It doesn’t mean that at 129/79 there is no stroke risk but that at 130/80 there is a stroke risk. It’s not like that,” he said.
“I wouldn’t make a diagnosis on a one-off blood pressure measurement. I would want to monitor that patient and get them to do home measurements,” he commented. “If someone constantly has levels around that 130/80 mm Hg, I don’t necessarily rush in with a definite diagnosis of hypertension and start drug treatment. I would look at lifestyle first. And in such patients, I wouldn’t give them the 1 point for hypertension on the CHA2DS2-VASc score.”
Dr. Lip points out that a hypertension diagnosis is not just about blood pressure numbers. “We have to assess the patients much more completely before giving them a diagnosis and consider factors such as whether there is evidence of hypertension-related end-organ damage, and if lifestyle issues have been addressed.”
Are new risk scores needed?
Dr. Turakhia agreed that clinicians need to look at the bigger picture, but he also suggested that new risk scores may need to be developed.
“All of us in the medical community need to think about whether we should be recalibrating risk prediction with more contemporary evidence – based on our ability to detect disease now,” he commented.
“This could even be a different risk score altogether, possibly incorporating a wider range of parameters or perhaps incorporating machine learning. That’s really the question we need to be asking ourselves,” Dr. Turakhia added.
Dr. Lip noted that there are many stroke risk factors and only those that are most common and have been well validated go into clinical risk scores such as CHA2DS2-VASc.
“These risks scores are by design simplifications, and only have modest predictive value for identifying patients at high risk of stroke. You can always improve on clinical risk scores by adding in other variables,” he said. “There are some risk scores in AF with 26 variables. But the practical application of these more complex scores can be difficult in clinical practice. These risks scores are meant to be simple so that they can be used by busy clinicians in the outpatient clinic or on a ward round. It is not easy to input 26 different variables.”
He also noted that many guidelines are now veering away from categorizing patients at high, medium, or low risk of stroke, which he refers to as “artificial” classifications. “There is now more of a default position that patients should receive stroke prevention normally with a DOAC [direct oral anticoagulant] unless they are low risk.”
Dr. Turakhia agreed that it is imperative to look at the bigger picture when identifying AF patients for anticoagulation. “We have to be careful not to take things at face value. It is more important than ever to use clinical judgment to avoid overtreatment in borderline situations,” he concluded.
This study was supported by the American College of Cardiology Foundation’s National Cardiovascular Data Registry. Dr. Turakhia reported employment from iRhythm Technologies; equity from AliveCor, Connect America, Evidently, and Forward; grants from U.S. Food and Drug Administration, American Heart Association, Bayer, Sanofi, Gilead, and Bristol Myers Squibb; and personal fees from Pfizer and JAMA Cardiology (prior associate editor) outside the submitted work. Dr. Lip has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM JAMA NETWORK OPEN
CKD linked to cardiac arrest in Hispanic, Latinx patients
TOPLINE:
new data show, suggesting early identification of CKD may provide an opportunity to reduce the risk in these groups. Other predictors included heavy drinking, atrial fibrillation, coronary artery disease, heart failure and diabetes.
METHODOLOGY:
- The study included 295 Hispanic or Latinx patients with out-of-hospital SCA from the PRESTO study in Ventura County, California, and 590 frequency-matched controls from the San Diego site of the population-based HCHS/SOL (Hispanic Community Health Survey/Study of Latinos); in both cohorts, men made up 70% of participants, and the median age was about 63 years.
- Researchers collected data on demographics, medical history, and current health conditions. Of note, 51.2% of SCA cases and 8.8% of control participants had CKD, and 20.0% of cases and 0.7% of the control group were on dialysis.
- Pre-SCA echocardiograms were available for 48% of SCA cases and baseline echocardiograms for more than 99% of control participants.
TAKEAWAY:
- In analyses adjusted for age, sex, and clinical variables, predictors significantly associated with higher odds of SCA included: CKD (odds ratio, 7.3; 95% confidence interval, 3.8-14.3; P < .001), heavy drinking (OR, 4.5), stroke (OR, 3.1), atrial fibrillation (OR, 3.7), coronary artery disease (OR, 2.9), heart failure (OR, 2.5), and diabetes (OR, 1.5).
- Hypertension, hyperlipemia, body mass index, and current smoking status were not significantly associated with SCA.
- In adjusted analyses, heart rate (OR, 1.8 per one standard deviation [1-SD] increase), QTc interval (OR, 2.5 per 1-SD increase) and left ventricular ejection fraction (OR, 4.4 per 1-SD decrease) were significantly associated with SCA, suggesting echocardiogram evaluations could help identify Hispanic or Latinx individuals at increased risk for SCA, wrote the authors.
IN PRACTICE:
“Our study, the first to include feasible numbers of Hispanic or Latino individuals, highlights the importance of renal dysfunction as a risk factor for SCA in the community,” the authors wrote, adding that early identification and management of chronic kidney disease could reduce risk for SCA in this population.
SOURCE:
The study was conducted by Kyndaron Reinier, PhD, MPH, Cedars-Sinai Health System, Los Angeles, and colleagues. It was published online in the Journal of the American Heart Association.
LIMITATIONS:
Most participants from the HCHS/SOL study were born outside the United States, compared with about half the SCA cases, which could have influenced cardiovascular disease risk, although results did not change considerably when models were adjusted for place of birth. Study participants were predominantly of Mexican heritage, so results may not be generalizable to Hispanic or Latinx individuals from other regions. As medical history was assessed differently in the two studies, there could be some error in estimating the strength of associations. Results from echocardiographic data should be viewed as hypothesis generating because of the potential for residual bias.
DISCLOSURES:
The Ventura PRESTO study was funded, in part, by the National Institutes of Health, and National Heart, Lung, and Blood Institute. The HCHS/SOL was carried out as a collaborative study supported by contracts from the NHLBI.
A version of this article first appeared on Medscape.com.
TOPLINE:
new data show, suggesting early identification of CKD may provide an opportunity to reduce the risk in these groups. Other predictors included heavy drinking, atrial fibrillation, coronary artery disease, heart failure and diabetes.
METHODOLOGY:
- The study included 295 Hispanic or Latinx patients with out-of-hospital SCA from the PRESTO study in Ventura County, California, and 590 frequency-matched controls from the San Diego site of the population-based HCHS/SOL (Hispanic Community Health Survey/Study of Latinos); in both cohorts, men made up 70% of participants, and the median age was about 63 years.
- Researchers collected data on demographics, medical history, and current health conditions. Of note, 51.2% of SCA cases and 8.8% of control participants had CKD, and 20.0% of cases and 0.7% of the control group were on dialysis.
- Pre-SCA echocardiograms were available for 48% of SCA cases and baseline echocardiograms for more than 99% of control participants.
TAKEAWAY:
- In analyses adjusted for age, sex, and clinical variables, predictors significantly associated with higher odds of SCA included: CKD (odds ratio, 7.3; 95% confidence interval, 3.8-14.3; P < .001), heavy drinking (OR, 4.5), stroke (OR, 3.1), atrial fibrillation (OR, 3.7), coronary artery disease (OR, 2.9), heart failure (OR, 2.5), and diabetes (OR, 1.5).
- Hypertension, hyperlipemia, body mass index, and current smoking status were not significantly associated with SCA.
- In adjusted analyses, heart rate (OR, 1.8 per one standard deviation [1-SD] increase), QTc interval (OR, 2.5 per 1-SD increase) and left ventricular ejection fraction (OR, 4.4 per 1-SD decrease) were significantly associated with SCA, suggesting echocardiogram evaluations could help identify Hispanic or Latinx individuals at increased risk for SCA, wrote the authors.
IN PRACTICE:
“Our study, the first to include feasible numbers of Hispanic or Latino individuals, highlights the importance of renal dysfunction as a risk factor for SCA in the community,” the authors wrote, adding that early identification and management of chronic kidney disease could reduce risk for SCA in this population.
SOURCE:
The study was conducted by Kyndaron Reinier, PhD, MPH, Cedars-Sinai Health System, Los Angeles, and colleagues. It was published online in the Journal of the American Heart Association.
LIMITATIONS:
Most participants from the HCHS/SOL study were born outside the United States, compared with about half the SCA cases, which could have influenced cardiovascular disease risk, although results did not change considerably when models were adjusted for place of birth. Study participants were predominantly of Mexican heritage, so results may not be generalizable to Hispanic or Latinx individuals from other regions. As medical history was assessed differently in the two studies, there could be some error in estimating the strength of associations. Results from echocardiographic data should be viewed as hypothesis generating because of the potential for residual bias.
DISCLOSURES:
The Ventura PRESTO study was funded, in part, by the National Institutes of Health, and National Heart, Lung, and Blood Institute. The HCHS/SOL was carried out as a collaborative study supported by contracts from the NHLBI.
A version of this article first appeared on Medscape.com.
TOPLINE:
new data show, suggesting early identification of CKD may provide an opportunity to reduce the risk in these groups. Other predictors included heavy drinking, atrial fibrillation, coronary artery disease, heart failure and diabetes.
METHODOLOGY:
- The study included 295 Hispanic or Latinx patients with out-of-hospital SCA from the PRESTO study in Ventura County, California, and 590 frequency-matched controls from the San Diego site of the population-based HCHS/SOL (Hispanic Community Health Survey/Study of Latinos); in both cohorts, men made up 70% of participants, and the median age was about 63 years.
- Researchers collected data on demographics, medical history, and current health conditions. Of note, 51.2% of SCA cases and 8.8% of control participants had CKD, and 20.0% of cases and 0.7% of the control group were on dialysis.
- Pre-SCA echocardiograms were available for 48% of SCA cases and baseline echocardiograms for more than 99% of control participants.
TAKEAWAY:
- In analyses adjusted for age, sex, and clinical variables, predictors significantly associated with higher odds of SCA included: CKD (odds ratio, 7.3; 95% confidence interval, 3.8-14.3; P < .001), heavy drinking (OR, 4.5), stroke (OR, 3.1), atrial fibrillation (OR, 3.7), coronary artery disease (OR, 2.9), heart failure (OR, 2.5), and diabetes (OR, 1.5).
- Hypertension, hyperlipemia, body mass index, and current smoking status were not significantly associated with SCA.
- In adjusted analyses, heart rate (OR, 1.8 per one standard deviation [1-SD] increase), QTc interval (OR, 2.5 per 1-SD increase) and left ventricular ejection fraction (OR, 4.4 per 1-SD decrease) were significantly associated with SCA, suggesting echocardiogram evaluations could help identify Hispanic or Latinx individuals at increased risk for SCA, wrote the authors.
IN PRACTICE:
“Our study, the first to include feasible numbers of Hispanic or Latino individuals, highlights the importance of renal dysfunction as a risk factor for SCA in the community,” the authors wrote, adding that early identification and management of chronic kidney disease could reduce risk for SCA in this population.
SOURCE:
The study was conducted by Kyndaron Reinier, PhD, MPH, Cedars-Sinai Health System, Los Angeles, and colleagues. It was published online in the Journal of the American Heart Association.
LIMITATIONS:
Most participants from the HCHS/SOL study were born outside the United States, compared with about half the SCA cases, which could have influenced cardiovascular disease risk, although results did not change considerably when models were adjusted for place of birth. Study participants were predominantly of Mexican heritage, so results may not be generalizable to Hispanic or Latinx individuals from other regions. As medical history was assessed differently in the two studies, there could be some error in estimating the strength of associations. Results from echocardiographic data should be viewed as hypothesis generating because of the potential for residual bias.
DISCLOSURES:
The Ventura PRESTO study was funded, in part, by the National Institutes of Health, and National Heart, Lung, and Blood Institute. The HCHS/SOL was carried out as a collaborative study supported by contracts from the NHLBI.
A version of this article first appeared on Medscape.com.
EMA warns that omega-3-acid ethyl esters may cause AFib
In its September meeting, the Should atrial fibrillation develop, intake of the medication must be stopped permanently.
Omega-3-acid ethyl esters are used to treat hypertriglyceridemia if lifestyle changes, particularly those related to nutrition, have not been sufficient to lower the blood triglyceride level. Hypertriglyceridemia is a risk factor for coronary heart disease.
During a Periodic Safety Update Single Assessment Procedure, the EMA safety committee analyzed systematic overviews and meta-analyses of randomized, controlled clinical studies. Experts found a dose-dependent increase in the risk for atrial fibrillation in patients with cardiovascular diseases or cardiovascular risk factors who were being treated with omega-3-acid ethyl esters, compared with those treated with placebo. The observed risk was at its highest at a dose of 4 g/d.
The PRAC will recommend an update to the Summary of Product Characteristics for preparations that contain omega-3-acid ethyl esters. The aim is to inform physicians, pharmacists, and patients of the risk for atrial fibrillation. A notification will be sent to health care professionals soon to inform them of further details.
This article was translated from the Medscape German Edition. A version appeared on Medscape.com.
In its September meeting, the Should atrial fibrillation develop, intake of the medication must be stopped permanently.
Omega-3-acid ethyl esters are used to treat hypertriglyceridemia if lifestyle changes, particularly those related to nutrition, have not been sufficient to lower the blood triglyceride level. Hypertriglyceridemia is a risk factor for coronary heart disease.
During a Periodic Safety Update Single Assessment Procedure, the EMA safety committee analyzed systematic overviews and meta-analyses of randomized, controlled clinical studies. Experts found a dose-dependent increase in the risk for atrial fibrillation in patients with cardiovascular diseases or cardiovascular risk factors who were being treated with omega-3-acid ethyl esters, compared with those treated with placebo. The observed risk was at its highest at a dose of 4 g/d.
The PRAC will recommend an update to the Summary of Product Characteristics for preparations that contain omega-3-acid ethyl esters. The aim is to inform physicians, pharmacists, and patients of the risk for atrial fibrillation. A notification will be sent to health care professionals soon to inform them of further details.
This article was translated from the Medscape German Edition. A version appeared on Medscape.com.
In its September meeting, the Should atrial fibrillation develop, intake of the medication must be stopped permanently.
Omega-3-acid ethyl esters are used to treat hypertriglyceridemia if lifestyle changes, particularly those related to nutrition, have not been sufficient to lower the blood triglyceride level. Hypertriglyceridemia is a risk factor for coronary heart disease.
During a Periodic Safety Update Single Assessment Procedure, the EMA safety committee analyzed systematic overviews and meta-analyses of randomized, controlled clinical studies. Experts found a dose-dependent increase in the risk for atrial fibrillation in patients with cardiovascular diseases or cardiovascular risk factors who were being treated with omega-3-acid ethyl esters, compared with those treated with placebo. The observed risk was at its highest at a dose of 4 g/d.
The PRAC will recommend an update to the Summary of Product Characteristics for preparations that contain omega-3-acid ethyl esters. The aim is to inform physicians, pharmacists, and patients of the risk for atrial fibrillation. A notification will be sent to health care professionals soon to inform them of further details.
This article was translated from the Medscape German Edition. A version appeared on Medscape.com.
High and low HDL cholesterol levels linked to dementia risk
TOPLINE:
High and low levels of HDL cholesterol but not levels of LDL cholesterol are associated with an increased risk for dementia in older adults, a new study found.
METHODOLOGY:
- Electronic health record and survey data on 184,367 Kaiser Permanente Northern California participants (median age, 69.5 years) with no history of dementia were taken.
- Cholesterol levels were measured within 2 years of survey completion.
TAKEAWAY:
- There were 25,214 incident cases of dementia reported over an average follow-up of 8.77 years.
- Dementia risk was significantly higher in people with low HDL cholesterol (11-41 mg/dL; adjusted hazard ratio, 1.07; 95% confidence interval, 1.03-1.11) and high HDL cholesterol (> 65 mg/dL; aHR, 1.15; 95% CI, 1.11-1.20).
- The study demonstrates an association between low and high levels of “good” cholesterol but not a causal link.
- There was no significant association between LDL cholesterol and dementia risk.
IN PRACTICE:
“These results support the conclusion that some lipoproteins may be modifiable risk factors for dementia, even in late life,” the authors wrote.
SOURCE:
The study was conducted by Erin L. Ferguson, MPH, department of epidemiology & biostatistics, University of California, San Francisco, and was funded by the National Institutes of Health. It was published online in Neurology.
LIMITATIONS:
There were no adjustments for apo E status and confounding and selection bias.
DISCLOSURES:
The authors report no relevant disclosures.
A version of this article first appeared on Medscape.com.
TOPLINE:
High and low levels of HDL cholesterol but not levels of LDL cholesterol are associated with an increased risk for dementia in older adults, a new study found.
METHODOLOGY:
- Electronic health record and survey data on 184,367 Kaiser Permanente Northern California participants (median age, 69.5 years) with no history of dementia were taken.
- Cholesterol levels were measured within 2 years of survey completion.
TAKEAWAY:
- There were 25,214 incident cases of dementia reported over an average follow-up of 8.77 years.
- Dementia risk was significantly higher in people with low HDL cholesterol (11-41 mg/dL; adjusted hazard ratio, 1.07; 95% confidence interval, 1.03-1.11) and high HDL cholesterol (> 65 mg/dL; aHR, 1.15; 95% CI, 1.11-1.20).
- The study demonstrates an association between low and high levels of “good” cholesterol but not a causal link.
- There was no significant association between LDL cholesterol and dementia risk.
IN PRACTICE:
“These results support the conclusion that some lipoproteins may be modifiable risk factors for dementia, even in late life,” the authors wrote.
SOURCE:
The study was conducted by Erin L. Ferguson, MPH, department of epidemiology & biostatistics, University of California, San Francisco, and was funded by the National Institutes of Health. It was published online in Neurology.
LIMITATIONS:
There were no adjustments for apo E status and confounding and selection bias.
DISCLOSURES:
The authors report no relevant disclosures.
A version of this article first appeared on Medscape.com.
TOPLINE:
High and low levels of HDL cholesterol but not levels of LDL cholesterol are associated with an increased risk for dementia in older adults, a new study found.
METHODOLOGY:
- Electronic health record and survey data on 184,367 Kaiser Permanente Northern California participants (median age, 69.5 years) with no history of dementia were taken.
- Cholesterol levels were measured within 2 years of survey completion.
TAKEAWAY:
- There were 25,214 incident cases of dementia reported over an average follow-up of 8.77 years.
- Dementia risk was significantly higher in people with low HDL cholesterol (11-41 mg/dL; adjusted hazard ratio, 1.07; 95% confidence interval, 1.03-1.11) and high HDL cholesterol (> 65 mg/dL; aHR, 1.15; 95% CI, 1.11-1.20).
- The study demonstrates an association between low and high levels of “good” cholesterol but not a causal link.
- There was no significant association between LDL cholesterol and dementia risk.
IN PRACTICE:
“These results support the conclusion that some lipoproteins may be modifiable risk factors for dementia, even in late life,” the authors wrote.
SOURCE:
The study was conducted by Erin L. Ferguson, MPH, department of epidemiology & biostatistics, University of California, San Francisco, and was funded by the National Institutes of Health. It was published online in Neurology.
LIMITATIONS:
There were no adjustments for apo E status and confounding and selection bias.
DISCLOSURES:
The authors report no relevant disclosures.
A version of this article first appeared on Medscape.com.