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Racial disparities in cardiotoxicity after chemotherapy
a research review indicates.
“It’s important that both patients and clinicians be aware of these disparities so that more meaningful conversations around long-term cardiac health and cancer treatment can take place,” lead investigator Wondewossen Gebeyehu, with the University of Toronto, said in an interview.
However, patients “should not avoid chemotherapy, as the most important thing is making sure they get the best cancer treatment possible, and studies already show Black patients may get less optimal cancer treatments,” Mr. Gebeyehu added in a statement.
Ana Barac, MD, PHD, chair of cardio-oncology at Inova Schar Cancer Institute and Inova Heart and Vascular Institute, Fairfax, Va., who wasn’t involved in the study, agreed.
“The most important message is to look at preexisting cardiovascular disease, oncology diagnosis, and be aware of existing disparities in a specific cancer and CVD,” Barac said in an interview.
“What should NOT happen is to overinterpret this report of cardiotoxicity as an indication to modify/avoid planned cancer treatment to decrease cardiotoxicity. This approach could worsen oncology outcomes and lead to undertreatment of cancer, therefore posing real danger,” said Dr. Barac.
The study was presented at the American College of Cardiology Advancing the Cardiovascular Care of the Oncology Patient 2023 conference.
Causes unclear
Chemotherapy is known to increase the risk of cardiovascular heart failure and other forms of CVD, but less is known about racial disparities in the incidence of chemotherapy-induced cardiotoxicity.
Mr. Gebeyehu and colleagues conducted a systematic review and meta-analysis of the available literature to assess racial disparities in CV adverse effects among cancer patients who were treated with chemotherapeutic agents. They screened 7,057 studies, fully reviewed 57, and included 24 studies, representing 683,749 participants, in their analysis.
Breast cancer was the most commonly reported malignancy. Other common malignancies were prostate, kidney, and hematologic malignancies such as leukemia and lymphoma.
Chemotherapeutic agents included anthracyclines (doxorubicin, daunorubicin), trastuzumab, and hormonal therapies.
Black race or African ancestry was associated with increased odds of chemotherapy-associated cardiotoxicity (odds ratio, 1.71; 95% confidence interval, 1.40-2.10), as well as congestive heart failure (OR, 1.92; 95% CI, 1.68-2.19).
Mr. Gebeyehu said in an interview that it’s hard to speculate on causation with an analysis of preexisting data such as this. “Our initial analysis that we’ve reported on so far are unadjusted values, meaning they don’t adjust for those potential underlying factors,” he noted.
“However, some of the studies individually controlled for socioeconomic factors and still found increased vulnerability to chemotherapy-associated cardiotoxicity in patients of Black race or African ancestry,” Mr. Gebeyehu said.
“It’s certainly possible that a mix of both biological and socioeconomic factors are interacting to lead to these disparities. One example could be the underrepresentation of Black patients in clinical trials to develop drugs. These could lead to chemotherapeutic agents being poorly optimized in this population relative to other racial/ethnic groups,” he added.
Dr. Barac said this study adds to the growing body of evidence about the importance of racial disparities in CVD and cancer outcomes.
“It is important to note that only the unadjusted odds ratio was reported and that much more detail is needed to understand what may be underlying the disparities. It is critically important to await the adjusted analysis, as well as details of the type of cancers and treatment used, before clinical implications can be discussed,” said Dr. Barac, who served as codirector of the conference.
“The risk of cardiotoxicity needs to be presented in the context of the oncology and CV disease burden, as both can influence the risk, and there could be a synergistic effect of disparities,” Dr. Barac added.
The study had no specific funding. Mr. Gebeyehu and Dr. Barac disclosed no relevant conflicts of interest.
A version of this article originally appeared on Medscape.com.
a research review indicates.
“It’s important that both patients and clinicians be aware of these disparities so that more meaningful conversations around long-term cardiac health and cancer treatment can take place,” lead investigator Wondewossen Gebeyehu, with the University of Toronto, said in an interview.
However, patients “should not avoid chemotherapy, as the most important thing is making sure they get the best cancer treatment possible, and studies already show Black patients may get less optimal cancer treatments,” Mr. Gebeyehu added in a statement.
Ana Barac, MD, PHD, chair of cardio-oncology at Inova Schar Cancer Institute and Inova Heart and Vascular Institute, Fairfax, Va., who wasn’t involved in the study, agreed.
“The most important message is to look at preexisting cardiovascular disease, oncology diagnosis, and be aware of existing disparities in a specific cancer and CVD,” Barac said in an interview.
“What should NOT happen is to overinterpret this report of cardiotoxicity as an indication to modify/avoid planned cancer treatment to decrease cardiotoxicity. This approach could worsen oncology outcomes and lead to undertreatment of cancer, therefore posing real danger,” said Dr. Barac.
The study was presented at the American College of Cardiology Advancing the Cardiovascular Care of the Oncology Patient 2023 conference.
Causes unclear
Chemotherapy is known to increase the risk of cardiovascular heart failure and other forms of CVD, but less is known about racial disparities in the incidence of chemotherapy-induced cardiotoxicity.
Mr. Gebeyehu and colleagues conducted a systematic review and meta-analysis of the available literature to assess racial disparities in CV adverse effects among cancer patients who were treated with chemotherapeutic agents. They screened 7,057 studies, fully reviewed 57, and included 24 studies, representing 683,749 participants, in their analysis.
Breast cancer was the most commonly reported malignancy. Other common malignancies were prostate, kidney, and hematologic malignancies such as leukemia and lymphoma.
Chemotherapeutic agents included anthracyclines (doxorubicin, daunorubicin), trastuzumab, and hormonal therapies.
Black race or African ancestry was associated with increased odds of chemotherapy-associated cardiotoxicity (odds ratio, 1.71; 95% confidence interval, 1.40-2.10), as well as congestive heart failure (OR, 1.92; 95% CI, 1.68-2.19).
Mr. Gebeyehu said in an interview that it’s hard to speculate on causation with an analysis of preexisting data such as this. “Our initial analysis that we’ve reported on so far are unadjusted values, meaning they don’t adjust for those potential underlying factors,” he noted.
“However, some of the studies individually controlled for socioeconomic factors and still found increased vulnerability to chemotherapy-associated cardiotoxicity in patients of Black race or African ancestry,” Mr. Gebeyehu said.
“It’s certainly possible that a mix of both biological and socioeconomic factors are interacting to lead to these disparities. One example could be the underrepresentation of Black patients in clinical trials to develop drugs. These could lead to chemotherapeutic agents being poorly optimized in this population relative to other racial/ethnic groups,” he added.
Dr. Barac said this study adds to the growing body of evidence about the importance of racial disparities in CVD and cancer outcomes.
“It is important to note that only the unadjusted odds ratio was reported and that much more detail is needed to understand what may be underlying the disparities. It is critically important to await the adjusted analysis, as well as details of the type of cancers and treatment used, before clinical implications can be discussed,” said Dr. Barac, who served as codirector of the conference.
“The risk of cardiotoxicity needs to be presented in the context of the oncology and CV disease burden, as both can influence the risk, and there could be a synergistic effect of disparities,” Dr. Barac added.
The study had no specific funding. Mr. Gebeyehu and Dr. Barac disclosed no relevant conflicts of interest.
A version of this article originally appeared on Medscape.com.
a research review indicates.
“It’s important that both patients and clinicians be aware of these disparities so that more meaningful conversations around long-term cardiac health and cancer treatment can take place,” lead investigator Wondewossen Gebeyehu, with the University of Toronto, said in an interview.
However, patients “should not avoid chemotherapy, as the most important thing is making sure they get the best cancer treatment possible, and studies already show Black patients may get less optimal cancer treatments,” Mr. Gebeyehu added in a statement.
Ana Barac, MD, PHD, chair of cardio-oncology at Inova Schar Cancer Institute and Inova Heart and Vascular Institute, Fairfax, Va., who wasn’t involved in the study, agreed.
“The most important message is to look at preexisting cardiovascular disease, oncology diagnosis, and be aware of existing disparities in a specific cancer and CVD,” Barac said in an interview.
“What should NOT happen is to overinterpret this report of cardiotoxicity as an indication to modify/avoid planned cancer treatment to decrease cardiotoxicity. This approach could worsen oncology outcomes and lead to undertreatment of cancer, therefore posing real danger,” said Dr. Barac.
The study was presented at the American College of Cardiology Advancing the Cardiovascular Care of the Oncology Patient 2023 conference.
Causes unclear
Chemotherapy is known to increase the risk of cardiovascular heart failure and other forms of CVD, but less is known about racial disparities in the incidence of chemotherapy-induced cardiotoxicity.
Mr. Gebeyehu and colleagues conducted a systematic review and meta-analysis of the available literature to assess racial disparities in CV adverse effects among cancer patients who were treated with chemotherapeutic agents. They screened 7,057 studies, fully reviewed 57, and included 24 studies, representing 683,749 participants, in their analysis.
Breast cancer was the most commonly reported malignancy. Other common malignancies were prostate, kidney, and hematologic malignancies such as leukemia and lymphoma.
Chemotherapeutic agents included anthracyclines (doxorubicin, daunorubicin), trastuzumab, and hormonal therapies.
Black race or African ancestry was associated with increased odds of chemotherapy-associated cardiotoxicity (odds ratio, 1.71; 95% confidence interval, 1.40-2.10), as well as congestive heart failure (OR, 1.92; 95% CI, 1.68-2.19).
Mr. Gebeyehu said in an interview that it’s hard to speculate on causation with an analysis of preexisting data such as this. “Our initial analysis that we’ve reported on so far are unadjusted values, meaning they don’t adjust for those potential underlying factors,” he noted.
“However, some of the studies individually controlled for socioeconomic factors and still found increased vulnerability to chemotherapy-associated cardiotoxicity in patients of Black race or African ancestry,” Mr. Gebeyehu said.
“It’s certainly possible that a mix of both biological and socioeconomic factors are interacting to lead to these disparities. One example could be the underrepresentation of Black patients in clinical trials to develop drugs. These could lead to chemotherapeutic agents being poorly optimized in this population relative to other racial/ethnic groups,” he added.
Dr. Barac said this study adds to the growing body of evidence about the importance of racial disparities in CVD and cancer outcomes.
“It is important to note that only the unadjusted odds ratio was reported and that much more detail is needed to understand what may be underlying the disparities. It is critically important to await the adjusted analysis, as well as details of the type of cancers and treatment used, before clinical implications can be discussed,” said Dr. Barac, who served as codirector of the conference.
“The risk of cardiotoxicity needs to be presented in the context of the oncology and CV disease burden, as both can influence the risk, and there could be a synergistic effect of disparities,” Dr. Barac added.
The study had no specific funding. Mr. Gebeyehu and Dr. Barac disclosed no relevant conflicts of interest.
A version of this article originally appeared on Medscape.com.
Green Mediterranean diet may relieve aortic stiffness
A green adaptation to the traditional Mediterranean diet improves proximal aortic stiffness (PAS), a distinct marker of vascular aging and increased cardiovascular risk, according to an exploratory post hoc analysis of the DIRECT-PLUS randomized clinical trial.
The green Mediterranean diet is distinct from the traditional Mediterranean diet because of its more abundant dietary polyphenols, from green tea and a Wolffia globosa (Mankai) plant green shake, and lower intake of red or processed meat.
Independent of weight loss, the modified green Mediterranean diet regressed PAS by 15%, the traditional Mediterranean diet by 7.3%, and the healthy dietary guideline–based diet by 4.8%, the study team observed.
“The DIRECT-PLUS trial research team was the first to introduce the concept of the green-Mediterranean/high polyphenols diet,” lead researcher Iris Shai, RD, PhD, with Ben-Gurion University of the Negev, Be’er-Sheva, Israel, told this news organization.
This diet promoted “dramatic proximal aortic de-stiffening” as assessed by MRI over 18 months in roughly 300 participants with abdominal obesity/dyslipidemia. “To date, no dietary strategies have been shown to impact vascular aging physiology,” Dr. Shai said.
The analysis was published online in the Journal of the American College of Cardiology.
Not all healthy diets are equal
Of the 294 participants, 281 had valid PAS measurements at baseline. The baseline PAS (6.1 m/s) was similar across intervention groups (P = .20). Increased PAS was associated with aging, hypertension, dyslipidemia, diabetes, and visceral adiposity (P < .05).
After 18 months’ intervention (retention rate 89.8%), all diet groups showed significant PAS reductions: –0.05 m/s with the standard healthy diet (4.8%), –0.08 m/s with the traditional Mediterranean diet (7.3%) and –0.15 the green Mediterranean diet (15%).
In the multivariable model, the green Mediterranean dieters had greater PAS reduction than did the healthy-diet and Mediterranean dieters (P = .003 and P = .032, respectively).
The researchers caution that DIRECT-PLUS had multiple endpoints and this exploratory post hoc analysis might be sensitive to type I statistical error and should be considered “hypothesis-generating.”
High-quality study, believable results
Reached for comment on the study, Deepak L. Bhatt, MD, MPH, director of Mount Sinai Heart in New York, said, “There is not a lot of high-quality research on diet, and I would call this high-quality research in as much as they used randomization which most dietary studies don’t do.
“The greener Mediterranean diet seemed to be the best one on the surrogate marker of MRI-defined aortic stiffness,” Dr. Bhatt, professor of cardiovascular medicine, Icahn School of Medicine at Mount Sinai, who wasn’t involved in the study, told this news organization.
“It makes sense that a diet that has more green in it, more polyphenols, would be healthier. This has been shown in some other studies, that these plant-based polyphenols might have various cardiovascular protective aspects to them,” Dr. Bhatt said.
Overall, he said the results are “quite believable, with the caveat that it would be nice to see the results reproduced in a more diverse and larger sample.”
“There is emerging evidence that diets that are higher in fresh fruits and vegetables and whole grains and lower in overall caloric intake, in general, seem to be good diets to reduce cardiovascular risk factors and maybe even reduce actual cardiovascular risk,” Dr. Bhatt added.
The study was funded by grants from the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation), the Rosetrees Trust, Israel Ministry of Health, Israel Ministry of Science and Technology, and the California Walnuts Commission. Dr. Shai and Dr. Bhatt have no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
A green adaptation to the traditional Mediterranean diet improves proximal aortic stiffness (PAS), a distinct marker of vascular aging and increased cardiovascular risk, according to an exploratory post hoc analysis of the DIRECT-PLUS randomized clinical trial.
The green Mediterranean diet is distinct from the traditional Mediterranean diet because of its more abundant dietary polyphenols, from green tea and a Wolffia globosa (Mankai) plant green shake, and lower intake of red or processed meat.
Independent of weight loss, the modified green Mediterranean diet regressed PAS by 15%, the traditional Mediterranean diet by 7.3%, and the healthy dietary guideline–based diet by 4.8%, the study team observed.
“The DIRECT-PLUS trial research team was the first to introduce the concept of the green-Mediterranean/high polyphenols diet,” lead researcher Iris Shai, RD, PhD, with Ben-Gurion University of the Negev, Be’er-Sheva, Israel, told this news organization.
This diet promoted “dramatic proximal aortic de-stiffening” as assessed by MRI over 18 months in roughly 300 participants with abdominal obesity/dyslipidemia. “To date, no dietary strategies have been shown to impact vascular aging physiology,” Dr. Shai said.
The analysis was published online in the Journal of the American College of Cardiology.
Not all healthy diets are equal
Of the 294 participants, 281 had valid PAS measurements at baseline. The baseline PAS (6.1 m/s) was similar across intervention groups (P = .20). Increased PAS was associated with aging, hypertension, dyslipidemia, diabetes, and visceral adiposity (P < .05).
After 18 months’ intervention (retention rate 89.8%), all diet groups showed significant PAS reductions: –0.05 m/s with the standard healthy diet (4.8%), –0.08 m/s with the traditional Mediterranean diet (7.3%) and –0.15 the green Mediterranean diet (15%).
In the multivariable model, the green Mediterranean dieters had greater PAS reduction than did the healthy-diet and Mediterranean dieters (P = .003 and P = .032, respectively).
The researchers caution that DIRECT-PLUS had multiple endpoints and this exploratory post hoc analysis might be sensitive to type I statistical error and should be considered “hypothesis-generating.”
High-quality study, believable results
Reached for comment on the study, Deepak L. Bhatt, MD, MPH, director of Mount Sinai Heart in New York, said, “There is not a lot of high-quality research on diet, and I would call this high-quality research in as much as they used randomization which most dietary studies don’t do.
“The greener Mediterranean diet seemed to be the best one on the surrogate marker of MRI-defined aortic stiffness,” Dr. Bhatt, professor of cardiovascular medicine, Icahn School of Medicine at Mount Sinai, who wasn’t involved in the study, told this news organization.
“It makes sense that a diet that has more green in it, more polyphenols, would be healthier. This has been shown in some other studies, that these plant-based polyphenols might have various cardiovascular protective aspects to them,” Dr. Bhatt said.
Overall, he said the results are “quite believable, with the caveat that it would be nice to see the results reproduced in a more diverse and larger sample.”
“There is emerging evidence that diets that are higher in fresh fruits and vegetables and whole grains and lower in overall caloric intake, in general, seem to be good diets to reduce cardiovascular risk factors and maybe even reduce actual cardiovascular risk,” Dr. Bhatt added.
The study was funded by grants from the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation), the Rosetrees Trust, Israel Ministry of Health, Israel Ministry of Science and Technology, and the California Walnuts Commission. Dr. Shai and Dr. Bhatt have no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
A green adaptation to the traditional Mediterranean diet improves proximal aortic stiffness (PAS), a distinct marker of vascular aging and increased cardiovascular risk, according to an exploratory post hoc analysis of the DIRECT-PLUS randomized clinical trial.
The green Mediterranean diet is distinct from the traditional Mediterranean diet because of its more abundant dietary polyphenols, from green tea and a Wolffia globosa (Mankai) plant green shake, and lower intake of red or processed meat.
Independent of weight loss, the modified green Mediterranean diet regressed PAS by 15%, the traditional Mediterranean diet by 7.3%, and the healthy dietary guideline–based diet by 4.8%, the study team observed.
“The DIRECT-PLUS trial research team was the first to introduce the concept of the green-Mediterranean/high polyphenols diet,” lead researcher Iris Shai, RD, PhD, with Ben-Gurion University of the Negev, Be’er-Sheva, Israel, told this news organization.
This diet promoted “dramatic proximal aortic de-stiffening” as assessed by MRI over 18 months in roughly 300 participants with abdominal obesity/dyslipidemia. “To date, no dietary strategies have been shown to impact vascular aging physiology,” Dr. Shai said.
The analysis was published online in the Journal of the American College of Cardiology.
Not all healthy diets are equal
Of the 294 participants, 281 had valid PAS measurements at baseline. The baseline PAS (6.1 m/s) was similar across intervention groups (P = .20). Increased PAS was associated with aging, hypertension, dyslipidemia, diabetes, and visceral adiposity (P < .05).
After 18 months’ intervention (retention rate 89.8%), all diet groups showed significant PAS reductions: –0.05 m/s with the standard healthy diet (4.8%), –0.08 m/s with the traditional Mediterranean diet (7.3%) and –0.15 the green Mediterranean diet (15%).
In the multivariable model, the green Mediterranean dieters had greater PAS reduction than did the healthy-diet and Mediterranean dieters (P = .003 and P = .032, respectively).
The researchers caution that DIRECT-PLUS had multiple endpoints and this exploratory post hoc analysis might be sensitive to type I statistical error and should be considered “hypothesis-generating.”
High-quality study, believable results
Reached for comment on the study, Deepak L. Bhatt, MD, MPH, director of Mount Sinai Heart in New York, said, “There is not a lot of high-quality research on diet, and I would call this high-quality research in as much as they used randomization which most dietary studies don’t do.
“The greener Mediterranean diet seemed to be the best one on the surrogate marker of MRI-defined aortic stiffness,” Dr. Bhatt, professor of cardiovascular medicine, Icahn School of Medicine at Mount Sinai, who wasn’t involved in the study, told this news organization.
“It makes sense that a diet that has more green in it, more polyphenols, would be healthier. This has been shown in some other studies, that these plant-based polyphenols might have various cardiovascular protective aspects to them,” Dr. Bhatt said.
Overall, he said the results are “quite believable, with the caveat that it would be nice to see the results reproduced in a more diverse and larger sample.”
“There is emerging evidence that diets that are higher in fresh fruits and vegetables and whole grains and lower in overall caloric intake, in general, seem to be good diets to reduce cardiovascular risk factors and maybe even reduce actual cardiovascular risk,” Dr. Bhatt added.
The study was funded by grants from the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation), the Rosetrees Trust, Israel Ministry of Health, Israel Ministry of Science and Technology, and the California Walnuts Commission. Dr. Shai and Dr. Bhatt have no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
Napping and AFib risk: The long and the short of it
Napping for more than half an hour during the day was associated with a 90% increased risk of atrial fibrillation (AFib), but shorter naps were linked to a reduced risk, based on data from more than 20,000 individuals.
“Short daytime napping is a common, healthy habit, especially in Mediterranean countries,” Jesus Diaz-Gutierrez, MD, of Juan Ramon Jimenez University Hospital, Huelva, Spain, said in a presentation at the annual congress of the European Association of Preventive Cardiology (EAPC).
Previous studies have shown a potential link between sleep patterns and AFib risk, but the association between specific duration of daytime naps and AFib risk has not been explored, he said.
Dr. Diaz-Gutierrez and colleagues used data from the University of Navarra Follow-up (SUN) Project, a prospective cohort of Spanish university graduates, to explore the possible link between naps and AFib. The study population included 20,348 individuals without AFib at baseline who were followed for a median of 13.8 years. The average age of participants at baseline was 38 years; 61% were women.
Daytime napping patterns were assessed at baseline, and participants were divided into nap groups of short nappers (defined as less than 30 minutes per day), and longer nappers (30 minutes or more per day), and those who reported no napping.
The researchers identified 131 incident cases of AFib during the follow-up period. Overall, the relative risk of incident AFib was significantly higher for the long nappers (adjusted hazard ratio 1.90) compared with short nappers in a multivariate analysis, while no significant risk appeared among non-nappers compared to short nappers (aHR 1.26).
The researchers then excluded the non-nappers in a secondary analysis to explore the impact of more specific daily nap duration on AFib risk. In a multivariate analysis, they found a 42% reduced risk of AF among those who napped for less than 15 minutes, and a 56% reduced risk for those who napped for 15-30 minutes, compared with those who napped for more than 30 minutes (aHR 0.56 and 0.42, respectively).
Potential explanations for the associations include the role of circadian rhythms, Dr. Diaz-Gutierrez said in a press release accompanying the presentation at the meeting. “Long daytime naps may disrupt the body’s internal clock (circadian rhythm), leading to shorter nighttime sleep, more nocturnal awakening, and reduced physical activity. In contrast, short daytime napping may improve circadian rhythm, lower blood pressure levels, and reduce stress.” More research is needed to validate the findings and the optimum nap duration, and whether a short nap is more advantageous than not napping in terms of AFib risk reduction, he said.
The study results suggest that naps of 15-30 minutes represent “a potential novel healthy lifestyle habit in the primary prevention of AFib,” Dr. Diaz-Gutierrez said in his presentation. However, the results also suggest that daily naps be limited to less than 30 minutes, he concluded.
Sleep habits may serve as red flag
“As we age, most if not all of us will develop sleep disturbances, such as insomnia, obstructive sleep apnea (OSA), and other sleep issues,” Lawrence S. Rosenthal, MD, of the University of Massachusetts, Worcester, said in an interview.
Therefore, “this study is near and dear to most people, and most would agree that poor sleeping habits affect our health.” In particular, OSA has been linked to AFib, although that was not measured in the current study, he added.
Dr. Rosenthal said he was not surprised by the current study findings. “It seems that a quick recharge of your ‘battery’ during the day is healthier than a long, deep sleep daytime nap,” he said. In addition, “Longer naps may be a marker of OSA,” he noted.
For clinicians, the take-home message of the current study is the need to consider underlying medical conditions in patients who regularly take long afternoon naps, and to consider these longer naps as a potential marker for AFib, said Dr. Rosenthal.
Looking ahead, a “deeper dive into the makeup of the populations studied” would be useful as a foundation for additional research, he said.
The SUN Project disclosed funding from the Spanish Government-Instituto de Salud Carlos III and the European Regional Development Fund (FEDER), the Navarra Regional Government, Plan Nacional Sobre Drogas, the University of Navarra, and the European Research Council. The researchers, and Dr. Rosenthal, had no financial conflicts to disclose.
Napping for more than half an hour during the day was associated with a 90% increased risk of atrial fibrillation (AFib), but shorter naps were linked to a reduced risk, based on data from more than 20,000 individuals.
“Short daytime napping is a common, healthy habit, especially in Mediterranean countries,” Jesus Diaz-Gutierrez, MD, of Juan Ramon Jimenez University Hospital, Huelva, Spain, said in a presentation at the annual congress of the European Association of Preventive Cardiology (EAPC).
Previous studies have shown a potential link between sleep patterns and AFib risk, but the association between specific duration of daytime naps and AFib risk has not been explored, he said.
Dr. Diaz-Gutierrez and colleagues used data from the University of Navarra Follow-up (SUN) Project, a prospective cohort of Spanish university graduates, to explore the possible link between naps and AFib. The study population included 20,348 individuals without AFib at baseline who were followed for a median of 13.8 years. The average age of participants at baseline was 38 years; 61% were women.
Daytime napping patterns were assessed at baseline, and participants were divided into nap groups of short nappers (defined as less than 30 minutes per day), and longer nappers (30 minutes or more per day), and those who reported no napping.
The researchers identified 131 incident cases of AFib during the follow-up period. Overall, the relative risk of incident AFib was significantly higher for the long nappers (adjusted hazard ratio 1.90) compared with short nappers in a multivariate analysis, while no significant risk appeared among non-nappers compared to short nappers (aHR 1.26).
The researchers then excluded the non-nappers in a secondary analysis to explore the impact of more specific daily nap duration on AFib risk. In a multivariate analysis, they found a 42% reduced risk of AF among those who napped for less than 15 minutes, and a 56% reduced risk for those who napped for 15-30 minutes, compared with those who napped for more than 30 minutes (aHR 0.56 and 0.42, respectively).
Potential explanations for the associations include the role of circadian rhythms, Dr. Diaz-Gutierrez said in a press release accompanying the presentation at the meeting. “Long daytime naps may disrupt the body’s internal clock (circadian rhythm), leading to shorter nighttime sleep, more nocturnal awakening, and reduced physical activity. In contrast, short daytime napping may improve circadian rhythm, lower blood pressure levels, and reduce stress.” More research is needed to validate the findings and the optimum nap duration, and whether a short nap is more advantageous than not napping in terms of AFib risk reduction, he said.
The study results suggest that naps of 15-30 minutes represent “a potential novel healthy lifestyle habit in the primary prevention of AFib,” Dr. Diaz-Gutierrez said in his presentation. However, the results also suggest that daily naps be limited to less than 30 minutes, he concluded.
Sleep habits may serve as red flag
“As we age, most if not all of us will develop sleep disturbances, such as insomnia, obstructive sleep apnea (OSA), and other sleep issues,” Lawrence S. Rosenthal, MD, of the University of Massachusetts, Worcester, said in an interview.
Therefore, “this study is near and dear to most people, and most would agree that poor sleeping habits affect our health.” In particular, OSA has been linked to AFib, although that was not measured in the current study, he added.
Dr. Rosenthal said he was not surprised by the current study findings. “It seems that a quick recharge of your ‘battery’ during the day is healthier than a long, deep sleep daytime nap,” he said. In addition, “Longer naps may be a marker of OSA,” he noted.
For clinicians, the take-home message of the current study is the need to consider underlying medical conditions in patients who regularly take long afternoon naps, and to consider these longer naps as a potential marker for AFib, said Dr. Rosenthal.
Looking ahead, a “deeper dive into the makeup of the populations studied” would be useful as a foundation for additional research, he said.
The SUN Project disclosed funding from the Spanish Government-Instituto de Salud Carlos III and the European Regional Development Fund (FEDER), the Navarra Regional Government, Plan Nacional Sobre Drogas, the University of Navarra, and the European Research Council. The researchers, and Dr. Rosenthal, had no financial conflicts to disclose.
Napping for more than half an hour during the day was associated with a 90% increased risk of atrial fibrillation (AFib), but shorter naps were linked to a reduced risk, based on data from more than 20,000 individuals.
“Short daytime napping is a common, healthy habit, especially in Mediterranean countries,” Jesus Diaz-Gutierrez, MD, of Juan Ramon Jimenez University Hospital, Huelva, Spain, said in a presentation at the annual congress of the European Association of Preventive Cardiology (EAPC).
Previous studies have shown a potential link between sleep patterns and AFib risk, but the association between specific duration of daytime naps and AFib risk has not been explored, he said.
Dr. Diaz-Gutierrez and colleagues used data from the University of Navarra Follow-up (SUN) Project, a prospective cohort of Spanish university graduates, to explore the possible link between naps and AFib. The study population included 20,348 individuals without AFib at baseline who were followed for a median of 13.8 years. The average age of participants at baseline was 38 years; 61% were women.
Daytime napping patterns were assessed at baseline, and participants were divided into nap groups of short nappers (defined as less than 30 minutes per day), and longer nappers (30 minutes or more per day), and those who reported no napping.
The researchers identified 131 incident cases of AFib during the follow-up period. Overall, the relative risk of incident AFib was significantly higher for the long nappers (adjusted hazard ratio 1.90) compared with short nappers in a multivariate analysis, while no significant risk appeared among non-nappers compared to short nappers (aHR 1.26).
The researchers then excluded the non-nappers in a secondary analysis to explore the impact of more specific daily nap duration on AFib risk. In a multivariate analysis, they found a 42% reduced risk of AF among those who napped for less than 15 minutes, and a 56% reduced risk for those who napped for 15-30 minutes, compared with those who napped for more than 30 minutes (aHR 0.56 and 0.42, respectively).
Potential explanations for the associations include the role of circadian rhythms, Dr. Diaz-Gutierrez said in a press release accompanying the presentation at the meeting. “Long daytime naps may disrupt the body’s internal clock (circadian rhythm), leading to shorter nighttime sleep, more nocturnal awakening, and reduced physical activity. In contrast, short daytime napping may improve circadian rhythm, lower blood pressure levels, and reduce stress.” More research is needed to validate the findings and the optimum nap duration, and whether a short nap is more advantageous than not napping in terms of AFib risk reduction, he said.
The study results suggest that naps of 15-30 minutes represent “a potential novel healthy lifestyle habit in the primary prevention of AFib,” Dr. Diaz-Gutierrez said in his presentation. However, the results also suggest that daily naps be limited to less than 30 minutes, he concluded.
Sleep habits may serve as red flag
“As we age, most if not all of us will develop sleep disturbances, such as insomnia, obstructive sleep apnea (OSA), and other sleep issues,” Lawrence S. Rosenthal, MD, of the University of Massachusetts, Worcester, said in an interview.
Therefore, “this study is near and dear to most people, and most would agree that poor sleeping habits affect our health.” In particular, OSA has been linked to AFib, although that was not measured in the current study, he added.
Dr. Rosenthal said he was not surprised by the current study findings. “It seems that a quick recharge of your ‘battery’ during the day is healthier than a long, deep sleep daytime nap,” he said. In addition, “Longer naps may be a marker of OSA,” he noted.
For clinicians, the take-home message of the current study is the need to consider underlying medical conditions in patients who regularly take long afternoon naps, and to consider these longer naps as a potential marker for AFib, said Dr. Rosenthal.
Looking ahead, a “deeper dive into the makeup of the populations studied” would be useful as a foundation for additional research, he said.
The SUN Project disclosed funding from the Spanish Government-Instituto de Salud Carlos III and the European Regional Development Fund (FEDER), the Navarra Regional Government, Plan Nacional Sobre Drogas, the University of Navarra, and the European Research Council. The researchers, and Dr. Rosenthal, had no financial conflicts to disclose.
FROM ESC PREVENTIVE CARDIOLOGY 2023
Cardiovascular disease deaths rise on and after high-pollution days
Cardiovascular disease deaths were significantly more common on days of high pollution and for the following 2 days, compared with other days, based on data from nearly 88,000 deaths over a 5-year period.
Previous research has shown the harmful effect of air pollution on human health in highly polluted areas, but Eastern Poland, a region with so-called “Polish smog” has exceptionally high levels of pollution. However, the specific impact of Polish smog, caused primarily by burning coal, on cardiovascular disease (CVD) mortality has not been well studied, said Michal Swieczkowski, MD, of the Medical University of Bialystok (Poland) in a presentation at the annual congress of the European Association of Preventive Cardiology.
Dr. Swieczkowski and colleagues reviewed all-cause deaths from five main cities in Eastern Poland during 2016-2020 for associations with pollution levels and days when deaths occurred. Mortality data were obtained from the Central Statistical Office. Air pollution concentrations for two types of particulate matter (PM2.5, PM10) and nitrogen oxide were collected from the Voivodeship Inspectorate for Environmental Protection. The main sources of the pollutants were road traffic and household heaters using coal or wood.
The final analysis included nearly 6 million person-years of follow-up. The researchers used a time-stratified case-crossover design. For each participant, the researchers compared levels of each pollutant on the day of the week a death occurred (such as a Wednesday) with pollutant levels on the same day of the week without any deaths in the same month (the remaining Wednesdays of that month). This design eliminated the potential confounding effects of participant characteristics, including other cardiovascular risk factors such as smoking and hyperlipidemia, and time trends. Essentially, participants “served as their own controls,” Dr. Swieczkowski said. The researchers conducted similar analyses for pollution levels 1 day and 2 days before a death occurred.
Overall, 87,990 deaths were identified during the study period; of these, 34,907 were from CVD, 9,688 from acute coronary syndromes, and 3,776 from ischemic stroke.
“Exposure to PM2.5 and PM10 was associated with increased mortality on the day of exposure, the next day, and up to 2 days after exposure,” said Dr. Swieczkowski.
Overall, an increase of 10 mcg/m3 in the three pollutants was significantly associated with increase in CVD mortality on the day of exposure to the increased pollution levels, with odds ratios of 1.034, 1.033, and 1.083 for PM2.5, PM10, and NO2, respectively (all P < .001).
The risks of dying from CVD were similar 1 and 2 days after the polluted day.
An increase in PM levels, but not NO2, was significantly associated with acute coronary syndrome (ACS) on the day of exposure to increased pollutants (ORs, 1.029 for PM2.5 [P = .002] and 1.015 [P = .049] for PM10). Both ischemic stroke and ACS mortality were significantly higher at 1 day after exposure, compared with other days. Ischemic stroke was associated with increases in PM2.5 and PM10, while ACS was associated with increases in PM2.5, PM10, and NO2.
When stratified by gender, the effects were more noticeable in women, Dr. Swieczkowski said. “Exposure to both types of particulate caused increased mortality due to acute coronary syndrome as well as ischemic stroke.” Among men, only death from acute coronary syndrome was significantly associated with exposure to increased particulate matter.
In a head-to-head comparison, women were more vulnerable to air pollution by up to 2.5%, he added.
When stratified by age, the effects of all three pollutants were associated with increased risk of death from ischemic stroke and ACS in participants older than 65 years. For those aged 65 years and younger, the only significant association was between ACS-associated mortality and ischemic stroke.
The results suggest “a special need for developing calculators to estimate the risk of CVD incidence depending on the place of residence that could be used for everyday practice,” said Dr. Swieczkowski. “Systemic changes should become a priority for policy makers, and, simultaneously, we as physicians should educate and protect our patients, especially those with high risk of cardiovascular disease,” he said.
Gender differences rooted in anatomy
When asked for an explanation of the difference in the impact of pollution on mortality between men and women, Dr. Swieczkowski explained that women are likely more vulnerable because of differences in anatomy of the pharynx and larynx, and breathing patterns. Previous studies have shown that air pollution causes more oxidative stress in women. Also, in the current study, the mean age of the women was 8 to 9 years older, he said.
The study design was an “elegant way to take away the impact of other cardiovascular risk factors,” noted session moderator Maryam Kavousi, MD, of Erasmus University Medical Center, Rotterdam, the Netherlands.
The study was supported by the National Science Centre, Poland. The researchers had no financial conflicts to disclose.
Cardiovascular disease deaths were significantly more common on days of high pollution and for the following 2 days, compared with other days, based on data from nearly 88,000 deaths over a 5-year period.
Previous research has shown the harmful effect of air pollution on human health in highly polluted areas, but Eastern Poland, a region with so-called “Polish smog” has exceptionally high levels of pollution. However, the specific impact of Polish smog, caused primarily by burning coal, on cardiovascular disease (CVD) mortality has not been well studied, said Michal Swieczkowski, MD, of the Medical University of Bialystok (Poland) in a presentation at the annual congress of the European Association of Preventive Cardiology.
Dr. Swieczkowski and colleagues reviewed all-cause deaths from five main cities in Eastern Poland during 2016-2020 for associations with pollution levels and days when deaths occurred. Mortality data were obtained from the Central Statistical Office. Air pollution concentrations for two types of particulate matter (PM2.5, PM10) and nitrogen oxide were collected from the Voivodeship Inspectorate for Environmental Protection. The main sources of the pollutants were road traffic and household heaters using coal or wood.
The final analysis included nearly 6 million person-years of follow-up. The researchers used a time-stratified case-crossover design. For each participant, the researchers compared levels of each pollutant on the day of the week a death occurred (such as a Wednesday) with pollutant levels on the same day of the week without any deaths in the same month (the remaining Wednesdays of that month). This design eliminated the potential confounding effects of participant characteristics, including other cardiovascular risk factors such as smoking and hyperlipidemia, and time trends. Essentially, participants “served as their own controls,” Dr. Swieczkowski said. The researchers conducted similar analyses for pollution levels 1 day and 2 days before a death occurred.
Overall, 87,990 deaths were identified during the study period; of these, 34,907 were from CVD, 9,688 from acute coronary syndromes, and 3,776 from ischemic stroke.
“Exposure to PM2.5 and PM10 was associated with increased mortality on the day of exposure, the next day, and up to 2 days after exposure,” said Dr. Swieczkowski.
Overall, an increase of 10 mcg/m3 in the three pollutants was significantly associated with increase in CVD mortality on the day of exposure to the increased pollution levels, with odds ratios of 1.034, 1.033, and 1.083 for PM2.5, PM10, and NO2, respectively (all P < .001).
The risks of dying from CVD were similar 1 and 2 days after the polluted day.
An increase in PM levels, but not NO2, was significantly associated with acute coronary syndrome (ACS) on the day of exposure to increased pollutants (ORs, 1.029 for PM2.5 [P = .002] and 1.015 [P = .049] for PM10). Both ischemic stroke and ACS mortality were significantly higher at 1 day after exposure, compared with other days. Ischemic stroke was associated with increases in PM2.5 and PM10, while ACS was associated with increases in PM2.5, PM10, and NO2.
When stratified by gender, the effects were more noticeable in women, Dr. Swieczkowski said. “Exposure to both types of particulate caused increased mortality due to acute coronary syndrome as well as ischemic stroke.” Among men, only death from acute coronary syndrome was significantly associated with exposure to increased particulate matter.
In a head-to-head comparison, women were more vulnerable to air pollution by up to 2.5%, he added.
When stratified by age, the effects of all three pollutants were associated with increased risk of death from ischemic stroke and ACS in participants older than 65 years. For those aged 65 years and younger, the only significant association was between ACS-associated mortality and ischemic stroke.
The results suggest “a special need for developing calculators to estimate the risk of CVD incidence depending on the place of residence that could be used for everyday practice,” said Dr. Swieczkowski. “Systemic changes should become a priority for policy makers, and, simultaneously, we as physicians should educate and protect our patients, especially those with high risk of cardiovascular disease,” he said.
Gender differences rooted in anatomy
When asked for an explanation of the difference in the impact of pollution on mortality between men and women, Dr. Swieczkowski explained that women are likely more vulnerable because of differences in anatomy of the pharynx and larynx, and breathing patterns. Previous studies have shown that air pollution causes more oxidative stress in women. Also, in the current study, the mean age of the women was 8 to 9 years older, he said.
The study design was an “elegant way to take away the impact of other cardiovascular risk factors,” noted session moderator Maryam Kavousi, MD, of Erasmus University Medical Center, Rotterdam, the Netherlands.
The study was supported by the National Science Centre, Poland. The researchers had no financial conflicts to disclose.
Cardiovascular disease deaths were significantly more common on days of high pollution and for the following 2 days, compared with other days, based on data from nearly 88,000 deaths over a 5-year period.
Previous research has shown the harmful effect of air pollution on human health in highly polluted areas, but Eastern Poland, a region with so-called “Polish smog” has exceptionally high levels of pollution. However, the specific impact of Polish smog, caused primarily by burning coal, on cardiovascular disease (CVD) mortality has not been well studied, said Michal Swieczkowski, MD, of the Medical University of Bialystok (Poland) in a presentation at the annual congress of the European Association of Preventive Cardiology.
Dr. Swieczkowski and colleagues reviewed all-cause deaths from five main cities in Eastern Poland during 2016-2020 for associations with pollution levels and days when deaths occurred. Mortality data were obtained from the Central Statistical Office. Air pollution concentrations for two types of particulate matter (PM2.5, PM10) and nitrogen oxide were collected from the Voivodeship Inspectorate for Environmental Protection. The main sources of the pollutants were road traffic and household heaters using coal or wood.
The final analysis included nearly 6 million person-years of follow-up. The researchers used a time-stratified case-crossover design. For each participant, the researchers compared levels of each pollutant on the day of the week a death occurred (such as a Wednesday) with pollutant levels on the same day of the week without any deaths in the same month (the remaining Wednesdays of that month). This design eliminated the potential confounding effects of participant characteristics, including other cardiovascular risk factors such as smoking and hyperlipidemia, and time trends. Essentially, participants “served as their own controls,” Dr. Swieczkowski said. The researchers conducted similar analyses for pollution levels 1 day and 2 days before a death occurred.
Overall, 87,990 deaths were identified during the study period; of these, 34,907 were from CVD, 9,688 from acute coronary syndromes, and 3,776 from ischemic stroke.
“Exposure to PM2.5 and PM10 was associated with increased mortality on the day of exposure, the next day, and up to 2 days after exposure,” said Dr. Swieczkowski.
Overall, an increase of 10 mcg/m3 in the three pollutants was significantly associated with increase in CVD mortality on the day of exposure to the increased pollution levels, with odds ratios of 1.034, 1.033, and 1.083 for PM2.5, PM10, and NO2, respectively (all P < .001).
The risks of dying from CVD were similar 1 and 2 days after the polluted day.
An increase in PM levels, but not NO2, was significantly associated with acute coronary syndrome (ACS) on the day of exposure to increased pollutants (ORs, 1.029 for PM2.5 [P = .002] and 1.015 [P = .049] for PM10). Both ischemic stroke and ACS mortality were significantly higher at 1 day after exposure, compared with other days. Ischemic stroke was associated with increases in PM2.5 and PM10, while ACS was associated with increases in PM2.5, PM10, and NO2.
When stratified by gender, the effects were more noticeable in women, Dr. Swieczkowski said. “Exposure to both types of particulate caused increased mortality due to acute coronary syndrome as well as ischemic stroke.” Among men, only death from acute coronary syndrome was significantly associated with exposure to increased particulate matter.
In a head-to-head comparison, women were more vulnerable to air pollution by up to 2.5%, he added.
When stratified by age, the effects of all three pollutants were associated with increased risk of death from ischemic stroke and ACS in participants older than 65 years. For those aged 65 years and younger, the only significant association was between ACS-associated mortality and ischemic stroke.
The results suggest “a special need for developing calculators to estimate the risk of CVD incidence depending on the place of residence that could be used for everyday practice,” said Dr. Swieczkowski. “Systemic changes should become a priority for policy makers, and, simultaneously, we as physicians should educate and protect our patients, especially those with high risk of cardiovascular disease,” he said.
Gender differences rooted in anatomy
When asked for an explanation of the difference in the impact of pollution on mortality between men and women, Dr. Swieczkowski explained that women are likely more vulnerable because of differences in anatomy of the pharynx and larynx, and breathing patterns. Previous studies have shown that air pollution causes more oxidative stress in women. Also, in the current study, the mean age of the women was 8 to 9 years older, he said.
The study design was an “elegant way to take away the impact of other cardiovascular risk factors,” noted session moderator Maryam Kavousi, MD, of Erasmus University Medical Center, Rotterdam, the Netherlands.
The study was supported by the National Science Centre, Poland. The researchers had no financial conflicts to disclose.
FROM ESC CONGRESS 2023
‘Substantial’ variation in responses to BP meds
A new study has shown a substantial variation in the blood pressure response to various antihypertensive medications between individuals, raising the possibility of future personalized therapy.
“We found that using the optimal antihypertensive drug for a particular patient resulted in an average of a 4.4 mm Hg greater reduction of blood pressure compared with a random choice of the other drugs. That is quite a substantial difference, and could be equivalent to adding in another drug,” lead author Johan Sundström, MD, Uppsala (Sweden) University Hospital, told this news organization.
“These preliminary findings suggest that some people may be better treated with one antihypertensive drug rather than another. This is opening up the field of hypertension for personalized medicine,” he added.
The study was published online in the Journal of the American Medical Association.
The authors noted that despite global access to multiple classes of highly effective blood pressure-lowering drugs, only one in four women and one in five men with hypertension reach treatment targets. While most hypertension guidelines advocate combination pharmacotherapy, many patients in routine care continue to be treated with monotherapy, with adverse effects and nonadherence being important clinical problems.
“One drug often does not give enough blood pressure reduction, but patients are often reluctant to up-titrate to two drugs,” Dr. Sundström said. “While we know that the four recommended classes of antihypertensives lower blood pressure equally well on average, we don’t know if their efficacy is the same in individual patients.
“We wondered whether there could be different optimal drugs for different people, and if we could identify the optimal drug for each person then maybe more patients could get to target levels with just one drug,” he said.
The researchers conducted a randomized, double-blind, repeated crossover trial at an outpatient research clinic in Sweden, studying 280 men and women with grade 1 hypertension at low risk for cardiovascular events.
Each participant was scheduled for 2 months’ treatment in random order with each of four different classes of antihypertensive drugs: an ACE inhibitor, lisinopril; an angiotensin II blocker, candesartan; a thiazide diuretic, hydrochlorothiazide; a calcium channel blocker, amlodipine.
There were then repeated treatment periods for two drug classes to try to account for any effect of a particular event that might have affected the blood pressure at one point in time. Ambulatory daytime systolic blood pressure was measured at the end of each treatment period.
Results showed that variation in systolic blood pressure was large between treatments on average, between participants on average, within participants taking the same treatment, and between treatments in the same participant.
Overall, personalized treatment using the optimal single-drug therapy led to a 4.4–mm Hg lower systolic blood pressure in the trial population than a random choice of any of the other drug classes.
Taking into consideration that lisinopril was found to be on average the most efficacious of the drugs at the selected doses, personalized treatment compared with lisinopril still led to a 3.1–mm Hg improvement in systolic blood pressure.
The researchers noted that the mean additional blood pressure reduction achievable by using the optimal agent was of a magnitude twice that achieved by doubling the dose of a first drug, and more than half that of adding a second drug on average.
While there were only small differences between certain drugs (e.g., candesartan vs. lisinopril; amlodipine vs. hydrochlorothiazide), for all other comparisons tested, the choice was important, with particularly large gains to be made by personalizing the choice between candesartan vs. amlodipine and between lisinopril vs. amlodipine.
In addition, some people showed very large differences in response to different drugs, whereas others did not have much difference at all.
How to identify the optimal drug?
“The million-dollar question is how we identify the best drug for each individual patient,” Dr. Sundström said. “This study has opened Pandora’s box. We now need to figure out how to go forward and how we tailor treatment in each patient.”
In the study, the researchers suggest that personalizing therapy could be achieved either by identifying the phenotypic characteristics that are associated with enhanced response to one treatment vs. another or by directly measuring the individual’s responses to a series of treatments to ascertain which is most effective.
Addressing the first scenario, Dr. Sundström explained: “We can analyze the characteristics of patients who did best on each drug. There are many variables we can look at here such as age, diet, baseline blood pressure, exercise levels, smoking status, race, body weight, salt intake, and findings from genetic tests. We are going to try to look into these to see if we can find any predictors of response to various different drugs.”
For the second strategy, he suggested that patients starting pharmacologic therapy could try a few different treatments. “For example, we could give patients two different drugs and ask them to alternate treatment periods with each of them and measure their blood pressure with a home monitoring kit and record adverse effects.”
Nonadherence “is such a big problem with antihypertensives,” he added. “This approach may allow patients to be more empowered when choosing the right treatment, which should help adherence in the longer term.”
‘Proof-of-principle’
Commenting on the study in an accompanying editorial, Robert M. Carey, MD, University of Virginia Health System, Charlottesville, wrote: “At this stage, the findings are more theoretical than immediately practical for the implementation of personalized antihypertensive drug therapy, but the study does provide proof-of-principle and the authors suggest a few scenarios in which a personalized approach could be used in the future.”
He said the practical ramifications of personally targeted therapy remain unclear, given that determination of an individual’s response to a series of short test treatments before selecting long-term therapy may be considered too cumbersome, and currently few phenotypic markers are currently available that would be likely to accurately predict the individual response to a particular therapy.
Dr. Carey concluded that the results of this study “encourage the further pursuit of larger randomized trials using similar repeated crossover designs to validate this concept and eventually in trials with longer follow-up data to determine whether there is improvement in long-term clinical outcomes compared with current strategies.”
He added that the results support the possibility that personalized medical treatment of hypertension “may ultimately supplement or even supplant the current method of antihypertensive drug decision-making in the future.”
This study was supported by the Swedish Research Council; Kjell and Märta Beijer Foundation; and Anders Wiklöf. Dr. Sundström reported owning stock in Symptoms Europe AB and Anagram Kommunikation AB. Coauthor Emil Hagström, MD, PhD, reported receiving grants from Pfizer and Amgen and personal fees from Amgen, Novo Nordisk, Bayer, AstraZeneca, Amarin, and Novartis. Coauthor Ollie Östlund, PhD, reported fees from Uppsala University paid to his institution, Uppsala Clinical Research Center, for its participation in the PHYSIC trial during the conduct of the study. Dr. Carey reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
A new study has shown a substantial variation in the blood pressure response to various antihypertensive medications between individuals, raising the possibility of future personalized therapy.
“We found that using the optimal antihypertensive drug for a particular patient resulted in an average of a 4.4 mm Hg greater reduction of blood pressure compared with a random choice of the other drugs. That is quite a substantial difference, and could be equivalent to adding in another drug,” lead author Johan Sundström, MD, Uppsala (Sweden) University Hospital, told this news organization.
“These preliminary findings suggest that some people may be better treated with one antihypertensive drug rather than another. This is opening up the field of hypertension for personalized medicine,” he added.
The study was published online in the Journal of the American Medical Association.
The authors noted that despite global access to multiple classes of highly effective blood pressure-lowering drugs, only one in four women and one in five men with hypertension reach treatment targets. While most hypertension guidelines advocate combination pharmacotherapy, many patients in routine care continue to be treated with monotherapy, with adverse effects and nonadherence being important clinical problems.
“One drug often does not give enough blood pressure reduction, but patients are often reluctant to up-titrate to two drugs,” Dr. Sundström said. “While we know that the four recommended classes of antihypertensives lower blood pressure equally well on average, we don’t know if their efficacy is the same in individual patients.
“We wondered whether there could be different optimal drugs for different people, and if we could identify the optimal drug for each person then maybe more patients could get to target levels with just one drug,” he said.
The researchers conducted a randomized, double-blind, repeated crossover trial at an outpatient research clinic in Sweden, studying 280 men and women with grade 1 hypertension at low risk for cardiovascular events.
Each participant was scheduled for 2 months’ treatment in random order with each of four different classes of antihypertensive drugs: an ACE inhibitor, lisinopril; an angiotensin II blocker, candesartan; a thiazide diuretic, hydrochlorothiazide; a calcium channel blocker, amlodipine.
There were then repeated treatment periods for two drug classes to try to account for any effect of a particular event that might have affected the blood pressure at one point in time. Ambulatory daytime systolic blood pressure was measured at the end of each treatment period.
Results showed that variation in systolic blood pressure was large between treatments on average, between participants on average, within participants taking the same treatment, and between treatments in the same participant.
Overall, personalized treatment using the optimal single-drug therapy led to a 4.4–mm Hg lower systolic blood pressure in the trial population than a random choice of any of the other drug classes.
Taking into consideration that lisinopril was found to be on average the most efficacious of the drugs at the selected doses, personalized treatment compared with lisinopril still led to a 3.1–mm Hg improvement in systolic blood pressure.
The researchers noted that the mean additional blood pressure reduction achievable by using the optimal agent was of a magnitude twice that achieved by doubling the dose of a first drug, and more than half that of adding a second drug on average.
While there were only small differences between certain drugs (e.g., candesartan vs. lisinopril; amlodipine vs. hydrochlorothiazide), for all other comparisons tested, the choice was important, with particularly large gains to be made by personalizing the choice between candesartan vs. amlodipine and between lisinopril vs. amlodipine.
In addition, some people showed very large differences in response to different drugs, whereas others did not have much difference at all.
How to identify the optimal drug?
“The million-dollar question is how we identify the best drug for each individual patient,” Dr. Sundström said. “This study has opened Pandora’s box. We now need to figure out how to go forward and how we tailor treatment in each patient.”
In the study, the researchers suggest that personalizing therapy could be achieved either by identifying the phenotypic characteristics that are associated with enhanced response to one treatment vs. another or by directly measuring the individual’s responses to a series of treatments to ascertain which is most effective.
Addressing the first scenario, Dr. Sundström explained: “We can analyze the characteristics of patients who did best on each drug. There are many variables we can look at here such as age, diet, baseline blood pressure, exercise levels, smoking status, race, body weight, salt intake, and findings from genetic tests. We are going to try to look into these to see if we can find any predictors of response to various different drugs.”
For the second strategy, he suggested that patients starting pharmacologic therapy could try a few different treatments. “For example, we could give patients two different drugs and ask them to alternate treatment periods with each of them and measure their blood pressure with a home monitoring kit and record adverse effects.”
Nonadherence “is such a big problem with antihypertensives,” he added. “This approach may allow patients to be more empowered when choosing the right treatment, which should help adherence in the longer term.”
‘Proof-of-principle’
Commenting on the study in an accompanying editorial, Robert M. Carey, MD, University of Virginia Health System, Charlottesville, wrote: “At this stage, the findings are more theoretical than immediately practical for the implementation of personalized antihypertensive drug therapy, but the study does provide proof-of-principle and the authors suggest a few scenarios in which a personalized approach could be used in the future.”
He said the practical ramifications of personally targeted therapy remain unclear, given that determination of an individual’s response to a series of short test treatments before selecting long-term therapy may be considered too cumbersome, and currently few phenotypic markers are currently available that would be likely to accurately predict the individual response to a particular therapy.
Dr. Carey concluded that the results of this study “encourage the further pursuit of larger randomized trials using similar repeated crossover designs to validate this concept and eventually in trials with longer follow-up data to determine whether there is improvement in long-term clinical outcomes compared with current strategies.”
He added that the results support the possibility that personalized medical treatment of hypertension “may ultimately supplement or even supplant the current method of antihypertensive drug decision-making in the future.”
This study was supported by the Swedish Research Council; Kjell and Märta Beijer Foundation; and Anders Wiklöf. Dr. Sundström reported owning stock in Symptoms Europe AB and Anagram Kommunikation AB. Coauthor Emil Hagström, MD, PhD, reported receiving grants from Pfizer and Amgen and personal fees from Amgen, Novo Nordisk, Bayer, AstraZeneca, Amarin, and Novartis. Coauthor Ollie Östlund, PhD, reported fees from Uppsala University paid to his institution, Uppsala Clinical Research Center, for its participation in the PHYSIC trial during the conduct of the study. Dr. Carey reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
A new study has shown a substantial variation in the blood pressure response to various antihypertensive medications between individuals, raising the possibility of future personalized therapy.
“We found that using the optimal antihypertensive drug for a particular patient resulted in an average of a 4.4 mm Hg greater reduction of blood pressure compared with a random choice of the other drugs. That is quite a substantial difference, and could be equivalent to adding in another drug,” lead author Johan Sundström, MD, Uppsala (Sweden) University Hospital, told this news organization.
“These preliminary findings suggest that some people may be better treated with one antihypertensive drug rather than another. This is opening up the field of hypertension for personalized medicine,” he added.
The study was published online in the Journal of the American Medical Association.
The authors noted that despite global access to multiple classes of highly effective blood pressure-lowering drugs, only one in four women and one in five men with hypertension reach treatment targets. While most hypertension guidelines advocate combination pharmacotherapy, many patients in routine care continue to be treated with monotherapy, with adverse effects and nonadherence being important clinical problems.
“One drug often does not give enough blood pressure reduction, but patients are often reluctant to up-titrate to two drugs,” Dr. Sundström said. “While we know that the four recommended classes of antihypertensives lower blood pressure equally well on average, we don’t know if their efficacy is the same in individual patients.
“We wondered whether there could be different optimal drugs for different people, and if we could identify the optimal drug for each person then maybe more patients could get to target levels with just one drug,” he said.
The researchers conducted a randomized, double-blind, repeated crossover trial at an outpatient research clinic in Sweden, studying 280 men and women with grade 1 hypertension at low risk for cardiovascular events.
Each participant was scheduled for 2 months’ treatment in random order with each of four different classes of antihypertensive drugs: an ACE inhibitor, lisinopril; an angiotensin II blocker, candesartan; a thiazide diuretic, hydrochlorothiazide; a calcium channel blocker, amlodipine.
There were then repeated treatment periods for two drug classes to try to account for any effect of a particular event that might have affected the blood pressure at one point in time. Ambulatory daytime systolic blood pressure was measured at the end of each treatment period.
Results showed that variation in systolic blood pressure was large between treatments on average, between participants on average, within participants taking the same treatment, and between treatments in the same participant.
Overall, personalized treatment using the optimal single-drug therapy led to a 4.4–mm Hg lower systolic blood pressure in the trial population than a random choice of any of the other drug classes.
Taking into consideration that lisinopril was found to be on average the most efficacious of the drugs at the selected doses, personalized treatment compared with lisinopril still led to a 3.1–mm Hg improvement in systolic blood pressure.
The researchers noted that the mean additional blood pressure reduction achievable by using the optimal agent was of a magnitude twice that achieved by doubling the dose of a first drug, and more than half that of adding a second drug on average.
While there were only small differences between certain drugs (e.g., candesartan vs. lisinopril; amlodipine vs. hydrochlorothiazide), for all other comparisons tested, the choice was important, with particularly large gains to be made by personalizing the choice between candesartan vs. amlodipine and between lisinopril vs. amlodipine.
In addition, some people showed very large differences in response to different drugs, whereas others did not have much difference at all.
How to identify the optimal drug?
“The million-dollar question is how we identify the best drug for each individual patient,” Dr. Sundström said. “This study has opened Pandora’s box. We now need to figure out how to go forward and how we tailor treatment in each patient.”
In the study, the researchers suggest that personalizing therapy could be achieved either by identifying the phenotypic characteristics that are associated with enhanced response to one treatment vs. another or by directly measuring the individual’s responses to a series of treatments to ascertain which is most effective.
Addressing the first scenario, Dr. Sundström explained: “We can analyze the characteristics of patients who did best on each drug. There are many variables we can look at here such as age, diet, baseline blood pressure, exercise levels, smoking status, race, body weight, salt intake, and findings from genetic tests. We are going to try to look into these to see if we can find any predictors of response to various different drugs.”
For the second strategy, he suggested that patients starting pharmacologic therapy could try a few different treatments. “For example, we could give patients two different drugs and ask them to alternate treatment periods with each of them and measure their blood pressure with a home monitoring kit and record adverse effects.”
Nonadherence “is such a big problem with antihypertensives,” he added. “This approach may allow patients to be more empowered when choosing the right treatment, which should help adherence in the longer term.”
‘Proof-of-principle’
Commenting on the study in an accompanying editorial, Robert M. Carey, MD, University of Virginia Health System, Charlottesville, wrote: “At this stage, the findings are more theoretical than immediately practical for the implementation of personalized antihypertensive drug therapy, but the study does provide proof-of-principle and the authors suggest a few scenarios in which a personalized approach could be used in the future.”
He said the practical ramifications of personally targeted therapy remain unclear, given that determination of an individual’s response to a series of short test treatments before selecting long-term therapy may be considered too cumbersome, and currently few phenotypic markers are currently available that would be likely to accurately predict the individual response to a particular therapy.
Dr. Carey concluded that the results of this study “encourage the further pursuit of larger randomized trials using similar repeated crossover designs to validate this concept and eventually in trials with longer follow-up data to determine whether there is improvement in long-term clinical outcomes compared with current strategies.”
He added that the results support the possibility that personalized medical treatment of hypertension “may ultimately supplement or even supplant the current method of antihypertensive drug decision-making in the future.”
This study was supported by the Swedish Research Council; Kjell and Märta Beijer Foundation; and Anders Wiklöf. Dr. Sundström reported owning stock in Symptoms Europe AB and Anagram Kommunikation AB. Coauthor Emil Hagström, MD, PhD, reported receiving grants from Pfizer and Amgen and personal fees from Amgen, Novo Nordisk, Bayer, AstraZeneca, Amarin, and Novartis. Coauthor Ollie Östlund, PhD, reported fees from Uppsala University paid to his institution, Uppsala Clinical Research Center, for its participation in the PHYSIC trial during the conduct of the study. Dr. Carey reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Cancer, heart disease vaccines may be ready by 2030, Moderna says
The announcement is yet another sign of what many are calling “the golden age” of vaccine development, which is largely credited to the pandemic’s use of mRNA technology to create COVID-19 vaccines.
“I think what we have learned in recent months is that if you ever thought that mRNA was just for infectious diseases, or just for COVID, the evidence now is that that’s absolutely not the case,” Moderna Chief Medical Officer Paul Burton, MD, PhD, told The Guardian. “It can be applied to all sorts of disease areas; we are in cancer, infectious disease, cardiovascular disease, autoimmune diseases, rare disease. We have studies in all of those areas, and they have all shown tremendous promise.”
The U.S. Food and Drug Administration recently designated two new Moderna vaccines as breakthrough therapies: a shot that prevents respiratory syncytial virus (RSV) in older people and a shot that helps prevent the recurrence of melanoma. The FDA’s breakthrough designation is given when a new treatment’s early trial results are substantially better than an existing therapy.
The mRNA vaccine technology that made headlines for its role in COVID-19 vaccines works by teaching the body how to make a specific protein to help the immune system prevent or target a certain disease.
Dr. Burton anticipates that mRNA technology will result in breakthroughs such as a cancer vaccine that can be personalized based on the features of a specific tumor.
“I think we will have mRNA-based therapies for rare diseases that were previously undruggable, and I think that 10 years from now, we will be approaching a world where you truly can identify the genetic cause of a disease and, with relative simplicity, go and edit that out and repair it using mRNA-based technology,” he said.
The Moderna executive made the statements before its annual update on its vaccine pipeline projects, which the company calls “Vaccines Day.” The Massachusetts-based drugmaker said it has given someone the first dose of a “next-generation” COVID-19 vaccine in a phase III trial, has made progress on a Lyme disease shot, and is developing a vaccine for the highly contagious norovirus.
In all, Moderna expects “six major vaccine product launches in the next few years,” the company said in a statement, adding that it expects the COVID-19 booster market alone to be valued at $15 billion.
A version of this article first appeared on WebMD.com.
The announcement is yet another sign of what many are calling “the golden age” of vaccine development, which is largely credited to the pandemic’s use of mRNA technology to create COVID-19 vaccines.
“I think what we have learned in recent months is that if you ever thought that mRNA was just for infectious diseases, or just for COVID, the evidence now is that that’s absolutely not the case,” Moderna Chief Medical Officer Paul Burton, MD, PhD, told The Guardian. “It can be applied to all sorts of disease areas; we are in cancer, infectious disease, cardiovascular disease, autoimmune diseases, rare disease. We have studies in all of those areas, and they have all shown tremendous promise.”
The U.S. Food and Drug Administration recently designated two new Moderna vaccines as breakthrough therapies: a shot that prevents respiratory syncytial virus (RSV) in older people and a shot that helps prevent the recurrence of melanoma. The FDA’s breakthrough designation is given when a new treatment’s early trial results are substantially better than an existing therapy.
The mRNA vaccine technology that made headlines for its role in COVID-19 vaccines works by teaching the body how to make a specific protein to help the immune system prevent or target a certain disease.
Dr. Burton anticipates that mRNA technology will result in breakthroughs such as a cancer vaccine that can be personalized based on the features of a specific tumor.
“I think we will have mRNA-based therapies for rare diseases that were previously undruggable, and I think that 10 years from now, we will be approaching a world where you truly can identify the genetic cause of a disease and, with relative simplicity, go and edit that out and repair it using mRNA-based technology,” he said.
The Moderna executive made the statements before its annual update on its vaccine pipeline projects, which the company calls “Vaccines Day.” The Massachusetts-based drugmaker said it has given someone the first dose of a “next-generation” COVID-19 vaccine in a phase III trial, has made progress on a Lyme disease shot, and is developing a vaccine for the highly contagious norovirus.
In all, Moderna expects “six major vaccine product launches in the next few years,” the company said in a statement, adding that it expects the COVID-19 booster market alone to be valued at $15 billion.
A version of this article first appeared on WebMD.com.
The announcement is yet another sign of what many are calling “the golden age” of vaccine development, which is largely credited to the pandemic’s use of mRNA technology to create COVID-19 vaccines.
“I think what we have learned in recent months is that if you ever thought that mRNA was just for infectious diseases, or just for COVID, the evidence now is that that’s absolutely not the case,” Moderna Chief Medical Officer Paul Burton, MD, PhD, told The Guardian. “It can be applied to all sorts of disease areas; we are in cancer, infectious disease, cardiovascular disease, autoimmune diseases, rare disease. We have studies in all of those areas, and they have all shown tremendous promise.”
The U.S. Food and Drug Administration recently designated two new Moderna vaccines as breakthrough therapies: a shot that prevents respiratory syncytial virus (RSV) in older people and a shot that helps prevent the recurrence of melanoma. The FDA’s breakthrough designation is given when a new treatment’s early trial results are substantially better than an existing therapy.
The mRNA vaccine technology that made headlines for its role in COVID-19 vaccines works by teaching the body how to make a specific protein to help the immune system prevent or target a certain disease.
Dr. Burton anticipates that mRNA technology will result in breakthroughs such as a cancer vaccine that can be personalized based on the features of a specific tumor.
“I think we will have mRNA-based therapies for rare diseases that were previously undruggable, and I think that 10 years from now, we will be approaching a world where you truly can identify the genetic cause of a disease and, with relative simplicity, go and edit that out and repair it using mRNA-based technology,” he said.
The Moderna executive made the statements before its annual update on its vaccine pipeline projects, which the company calls “Vaccines Day.” The Massachusetts-based drugmaker said it has given someone the first dose of a “next-generation” COVID-19 vaccine in a phase III trial, has made progress on a Lyme disease shot, and is developing a vaccine for the highly contagious norovirus.
In all, Moderna expects “six major vaccine product launches in the next few years,” the company said in a statement, adding that it expects the COVID-19 booster market alone to be valued at $15 billion.
A version of this article first appeared on WebMD.com.
AHA statement targets nuance in CVD risk assessment of women
In a new scientific statement, the American Heart Association highlighted the importance of incorporating nonbiological risk factors and social determinants of health in cardiovascular disease (CVD) risk assessment for women, particularly women from different racial and ethnic backgrounds.
CVD risk assessment in women is multifaceted and goes well beyond traditional risk factors to include sex-specific biological risk factors, as well as social, behavioral, and environmental factors, the writing group noted.
They said a greater focus on addressing all CVD risk factors among women from underrepresented races and ethnicities is warranted to avert future CVD.
The scientific statement was published online in Circulation.
Look beyond traditional risk factors
“Risk assessment is the first step in preventing heart disease, yet there are many limitations to traditional risk factors and their ability to comprehensively estimate a woman’s risk for cardiovascular disease,” Jennifer H. Mieres, MD, vice chair of the writing group and professor of cardiology at Hofstra University, Hempstead, N.Y., said in a news release.
“The delivery of equitable cardiovascular health care for women depends on improving the knowledge and awareness of all members of the healthcare team about the full spectrum of cardiovascular risk factors for women, including female-specific and female-predominant risk factors,” Dr. Mieres added.
Female-specific factors that should be included in CVD risk assessment include pregnancy-related conditions such as preeclampsia, preterm delivery, and gestational diabetes, the writing group said.
Other factors include menstrual cycle history; types of birth control and/or hormone replacement therapy used; polycystic ovarian syndrome (PCOS), which affects 10% of women of reproductive age and is associated with increased CVD risk; and autoimmune disorders, depression, and PTSD, all of which are more common in women and are also associated with higher risk for CVD.
The statement also highlights the key role that social determinants of health (SDOH) play in the development of CVD in women, particularly women from diverse racial and ethnic backgrounds. SDOH include education level, economic stability, neighborhood safety, working conditions, environmental hazards, and access to quality health care.
“It is critical that risk assessment be expanded to include [SDOH] as risk factors if we are to improve health outcomes in all women,” Laxmi Mehta, MD, chair of the writing group and director of preventative cardiology and women’s cardiovascular health at Ohio State University Wexner Medical Center, Columbus, said in the news release.
“It is also important for the health care team to consider [SDOH] when working with women on shared decisions about cardiovascular disease prevention and treatment,” Dr. Mehta noted.
No one-size-fits-all approach
The statement highlighted significant differences in CVD risk among women of different racial and ethnic backgrounds and provides detailed CV risk factor profiles for non-Hispanic Black, Hispanic/Latinx, Asian and American Indian/Alaska Native women.
It noted that language barriers, discrimination, acculturation, and health care access disproportionately affect women of underrepresented racial and ethnic groups. These factors result in a higher prevalence of CVD and significant challenges in CVD diagnosis and treatment.
“When customizing CVD prevention and treatment strategies to improve cardiovascular health for women, a one-size-fits-all approach is unlikely to be successful,” Dr. Mieres said.
“We must be cognizant of the complex interplay of sex, race and ethnicity, as well as social determinants of health, and how they impact the risk of cardiovascular disease and adverse outcomes in order to avert future CVD morbidity and mortality,” Dr. Mieres added.
Looking ahead, the writing group said future CVD prevention guidelines could be strengthened by including culturally-specific lifestyle recommendations.
They also said community-based approaches, faith-based community partnerships, and peer support to encourage a healthy lifestyle could play a key role in preventing CVD among all women.
This scientific statement was prepared by the volunteer writing group on behalf of the AHA’s Cardiovascular Disease and Stroke in Women and Underrepresented Populations Committee of the Council on Clinical Cardiology, the Council on Cardiovascular and Stroke Nursing, the Council on Hypertension, the Council on Lifelong Congenital Heart Disease and Heart Health in the Young, the Council on Lifestyle and Cardiometabolic Health, the Council on Peripheral Vascular Disease, and the Stroke Council.
A version of this article first appeared on Medscape.com.
In a new scientific statement, the American Heart Association highlighted the importance of incorporating nonbiological risk factors and social determinants of health in cardiovascular disease (CVD) risk assessment for women, particularly women from different racial and ethnic backgrounds.
CVD risk assessment in women is multifaceted and goes well beyond traditional risk factors to include sex-specific biological risk factors, as well as social, behavioral, and environmental factors, the writing group noted.
They said a greater focus on addressing all CVD risk factors among women from underrepresented races and ethnicities is warranted to avert future CVD.
The scientific statement was published online in Circulation.
Look beyond traditional risk factors
“Risk assessment is the first step in preventing heart disease, yet there are many limitations to traditional risk factors and their ability to comprehensively estimate a woman’s risk for cardiovascular disease,” Jennifer H. Mieres, MD, vice chair of the writing group and professor of cardiology at Hofstra University, Hempstead, N.Y., said in a news release.
“The delivery of equitable cardiovascular health care for women depends on improving the knowledge and awareness of all members of the healthcare team about the full spectrum of cardiovascular risk factors for women, including female-specific and female-predominant risk factors,” Dr. Mieres added.
Female-specific factors that should be included in CVD risk assessment include pregnancy-related conditions such as preeclampsia, preterm delivery, and gestational diabetes, the writing group said.
Other factors include menstrual cycle history; types of birth control and/or hormone replacement therapy used; polycystic ovarian syndrome (PCOS), which affects 10% of women of reproductive age and is associated with increased CVD risk; and autoimmune disorders, depression, and PTSD, all of which are more common in women and are also associated with higher risk for CVD.
The statement also highlights the key role that social determinants of health (SDOH) play in the development of CVD in women, particularly women from diverse racial and ethnic backgrounds. SDOH include education level, economic stability, neighborhood safety, working conditions, environmental hazards, and access to quality health care.
“It is critical that risk assessment be expanded to include [SDOH] as risk factors if we are to improve health outcomes in all women,” Laxmi Mehta, MD, chair of the writing group and director of preventative cardiology and women’s cardiovascular health at Ohio State University Wexner Medical Center, Columbus, said in the news release.
“It is also important for the health care team to consider [SDOH] when working with women on shared decisions about cardiovascular disease prevention and treatment,” Dr. Mehta noted.
No one-size-fits-all approach
The statement highlighted significant differences in CVD risk among women of different racial and ethnic backgrounds and provides detailed CV risk factor profiles for non-Hispanic Black, Hispanic/Latinx, Asian and American Indian/Alaska Native women.
It noted that language barriers, discrimination, acculturation, and health care access disproportionately affect women of underrepresented racial and ethnic groups. These factors result in a higher prevalence of CVD and significant challenges in CVD diagnosis and treatment.
“When customizing CVD prevention and treatment strategies to improve cardiovascular health for women, a one-size-fits-all approach is unlikely to be successful,” Dr. Mieres said.
“We must be cognizant of the complex interplay of sex, race and ethnicity, as well as social determinants of health, and how they impact the risk of cardiovascular disease and adverse outcomes in order to avert future CVD morbidity and mortality,” Dr. Mieres added.
Looking ahead, the writing group said future CVD prevention guidelines could be strengthened by including culturally-specific lifestyle recommendations.
They also said community-based approaches, faith-based community partnerships, and peer support to encourage a healthy lifestyle could play a key role in preventing CVD among all women.
This scientific statement was prepared by the volunteer writing group on behalf of the AHA’s Cardiovascular Disease and Stroke in Women and Underrepresented Populations Committee of the Council on Clinical Cardiology, the Council on Cardiovascular and Stroke Nursing, the Council on Hypertension, the Council on Lifelong Congenital Heart Disease and Heart Health in the Young, the Council on Lifestyle and Cardiometabolic Health, the Council on Peripheral Vascular Disease, and the Stroke Council.
A version of this article first appeared on Medscape.com.
In a new scientific statement, the American Heart Association highlighted the importance of incorporating nonbiological risk factors and social determinants of health in cardiovascular disease (CVD) risk assessment for women, particularly women from different racial and ethnic backgrounds.
CVD risk assessment in women is multifaceted and goes well beyond traditional risk factors to include sex-specific biological risk factors, as well as social, behavioral, and environmental factors, the writing group noted.
They said a greater focus on addressing all CVD risk factors among women from underrepresented races and ethnicities is warranted to avert future CVD.
The scientific statement was published online in Circulation.
Look beyond traditional risk factors
“Risk assessment is the first step in preventing heart disease, yet there are many limitations to traditional risk factors and their ability to comprehensively estimate a woman’s risk for cardiovascular disease,” Jennifer H. Mieres, MD, vice chair of the writing group and professor of cardiology at Hofstra University, Hempstead, N.Y., said in a news release.
“The delivery of equitable cardiovascular health care for women depends on improving the knowledge and awareness of all members of the healthcare team about the full spectrum of cardiovascular risk factors for women, including female-specific and female-predominant risk factors,” Dr. Mieres added.
Female-specific factors that should be included in CVD risk assessment include pregnancy-related conditions such as preeclampsia, preterm delivery, and gestational diabetes, the writing group said.
Other factors include menstrual cycle history; types of birth control and/or hormone replacement therapy used; polycystic ovarian syndrome (PCOS), which affects 10% of women of reproductive age and is associated with increased CVD risk; and autoimmune disorders, depression, and PTSD, all of which are more common in women and are also associated with higher risk for CVD.
The statement also highlights the key role that social determinants of health (SDOH) play in the development of CVD in women, particularly women from diverse racial and ethnic backgrounds. SDOH include education level, economic stability, neighborhood safety, working conditions, environmental hazards, and access to quality health care.
“It is critical that risk assessment be expanded to include [SDOH] as risk factors if we are to improve health outcomes in all women,” Laxmi Mehta, MD, chair of the writing group and director of preventative cardiology and women’s cardiovascular health at Ohio State University Wexner Medical Center, Columbus, said in the news release.
“It is also important for the health care team to consider [SDOH] when working with women on shared decisions about cardiovascular disease prevention and treatment,” Dr. Mehta noted.
No one-size-fits-all approach
The statement highlighted significant differences in CVD risk among women of different racial and ethnic backgrounds and provides detailed CV risk factor profiles for non-Hispanic Black, Hispanic/Latinx, Asian and American Indian/Alaska Native women.
It noted that language barriers, discrimination, acculturation, and health care access disproportionately affect women of underrepresented racial and ethnic groups. These factors result in a higher prevalence of CVD and significant challenges in CVD diagnosis and treatment.
“When customizing CVD prevention and treatment strategies to improve cardiovascular health for women, a one-size-fits-all approach is unlikely to be successful,” Dr. Mieres said.
“We must be cognizant of the complex interplay of sex, race and ethnicity, as well as social determinants of health, and how they impact the risk of cardiovascular disease and adverse outcomes in order to avert future CVD morbidity and mortality,” Dr. Mieres added.
Looking ahead, the writing group said future CVD prevention guidelines could be strengthened by including culturally-specific lifestyle recommendations.
They also said community-based approaches, faith-based community partnerships, and peer support to encourage a healthy lifestyle could play a key role in preventing CVD among all women.
This scientific statement was prepared by the volunteer writing group on behalf of the AHA’s Cardiovascular Disease and Stroke in Women and Underrepresented Populations Committee of the Council on Clinical Cardiology, the Council on Cardiovascular and Stroke Nursing, the Council on Hypertension, the Council on Lifelong Congenital Heart Disease and Heart Health in the Young, the Council on Lifestyle and Cardiometabolic Health, the Council on Peripheral Vascular Disease, and the Stroke Council.
A version of this article first appeared on Medscape.com.
FROM CIRCULATION
NSAID use in diabetes may worsen risk for first HF hospitalization
suggests a prospective, controlled study.
Certain subgroups may account for much of the excess risk, the results suggest, including the very elderly, patients with uncontrolled diabetes, those prescribed an NSAID for the first time, and patients already taking both a renin-angiotensin system inhibitor (RASi) and a diuretic.
Such patients with a firm indication for NSAIDs potentially could “be the ones benefiting most from closer follow-up, reduced dosage, or other mitigation strategies,” Anders Holt, MD, said in an interview.
Dr. Holt, of Copenhagen University Hospital and Herlev-Gentofte Hospital in Hellerup, Denmark, is lead author on the analysis of Danish registry data published in the Journal of the American College of Cardiology. He presented essentially the same results in preliminary form at the 2022 annual congress of the European Society of Cardiology.
HF hospitalizations linked to NSAIDs, the published report notes, are often attributed to symptoms from temporary fluid overload, often without worsening cardiac function, that stem from the drugs’ renal effects.
“One could speculate,” Dr. Holt said, that such HF events might be less severe and even associated with better outcomes, compared with other forms of heart failure.
But the current analysis provides a hint to the contrary, he observed. The 5-year mortality was similar for patients with HF linked to NSAIDs and those with other forms of HF, “which could suggest that NSAID-associated heart failure is more than transient fluid overload.”
The drugs may promote HF through direct effects on the heart by any of several proposed mechanisms, including “induction of arrhythmias and heart fibrosis, vasoconstriction, subclinical inflammation, and blood pressure elevation,” Dr. Holt said.
The current study doesn’t determine whether NSAID-associated HF stems from transient fluid overload or direct cardiac effects, but it’s “most likely both.”
In other limitations, the analysis is unable to “reliably explore” whether promotion of HF is an NSAID class effect, a “clinically relevant” point given the drugs’ varying effects on cardiovascular risk, states an accompanying editorial. Nor was it able to determine whether the drugs exert a dose-response effect on HF risk, noted Hassan Khan, MD, PhD, Norton Healthcare, Louisville, Ky., and Setor K. Kunutsor, MD, PhD, University of Leicester (England).
Still, “given the well-established relationship between the use of NSAIDs and increased HF, these findings are not unexpected because type 2 diabetes is also a major risk factor for HF.”
But it may be “premature to issue guideline recommendations based on a single observational study,” the editorialists wrote. “Further robust clinical trial evidence is needed to replicate these results and investigate the relationship of the type and dose of NSAIDs with HF risk. However, it should be realized that short-term or long-term use of NSAIDs may be detrimental to cardiovascular health.”
The analysis covered 23,308 patients from throughout Denmark with a type 2 diabetes diagnosis and no HF history who experienced a first HF hospitalization; their age averaged 76 years and 39% were women.
They served as their own controls; their NSAID exposures at two 28-day periods preceding the HF event, the one immediately before and the other preceding it by 56 days, were compared as the index and control periods, respectively.
Exposure to NSAIDs was defined as obtaining a prescription for celecoxib, diclofenac, ibuprofen, or naproxen, “as these are NSAIDs used primarily in Denmark,” the report states.
The odds ratios for HF hospitalization associated with NSAID exposure within 28 days preceding the event were 1.43 (95% confidence interval, 1.27-1.63) overall, 1.41 (95% CI, 1.16-1.71) for an NSAID given on top of both RASi and diuretics, 1.68 (95% CI, 1.00-2.88) for patients with elevated hemoglobin A1c, 1.78 (95% CI, 1.39-2.28) for those 80 or older, and 2.71 (95% CI, 1.78-4.23) for those with prior NSAID use.
That NSAID use and diabetes are each associated with increased risk for HF is well established, Dr. Holt observed. Yet the drugs had been prescribed to 16% of patients in the study.
“One of the more surprising findings, to me, was the quite substantial use of prescribed NSAIDs in a population of patients with diabetes, a patient group with a well-established cardiovascular risk,” he said.
“This patient group is only growing, so emphasis on the possible associations between even short-term NSAID use and incident heart failure is probably timely and perhaps needed.”
Dr. Holt and the study were supported by grants from Ib Mogens Kristiansens Almene Fond, Helsefonden, Snedkermester Sophus Jacobsen og hustru Astrid Jacobsen Fond, Marie og M.B. Richters Fond, and the Dagmar Marshalls Fond. Dr. Khan and Dr. Kunutsor reported no relevant relationships.
A version of this article first appeared on Medscape.com.
suggests a prospective, controlled study.
Certain subgroups may account for much of the excess risk, the results suggest, including the very elderly, patients with uncontrolled diabetes, those prescribed an NSAID for the first time, and patients already taking both a renin-angiotensin system inhibitor (RASi) and a diuretic.
Such patients with a firm indication for NSAIDs potentially could “be the ones benefiting most from closer follow-up, reduced dosage, or other mitigation strategies,” Anders Holt, MD, said in an interview.
Dr. Holt, of Copenhagen University Hospital and Herlev-Gentofte Hospital in Hellerup, Denmark, is lead author on the analysis of Danish registry data published in the Journal of the American College of Cardiology. He presented essentially the same results in preliminary form at the 2022 annual congress of the European Society of Cardiology.
HF hospitalizations linked to NSAIDs, the published report notes, are often attributed to symptoms from temporary fluid overload, often without worsening cardiac function, that stem from the drugs’ renal effects.
“One could speculate,” Dr. Holt said, that such HF events might be less severe and even associated with better outcomes, compared with other forms of heart failure.
But the current analysis provides a hint to the contrary, he observed. The 5-year mortality was similar for patients with HF linked to NSAIDs and those with other forms of HF, “which could suggest that NSAID-associated heart failure is more than transient fluid overload.”
The drugs may promote HF through direct effects on the heart by any of several proposed mechanisms, including “induction of arrhythmias and heart fibrosis, vasoconstriction, subclinical inflammation, and blood pressure elevation,” Dr. Holt said.
The current study doesn’t determine whether NSAID-associated HF stems from transient fluid overload or direct cardiac effects, but it’s “most likely both.”
In other limitations, the analysis is unable to “reliably explore” whether promotion of HF is an NSAID class effect, a “clinically relevant” point given the drugs’ varying effects on cardiovascular risk, states an accompanying editorial. Nor was it able to determine whether the drugs exert a dose-response effect on HF risk, noted Hassan Khan, MD, PhD, Norton Healthcare, Louisville, Ky., and Setor K. Kunutsor, MD, PhD, University of Leicester (England).
Still, “given the well-established relationship between the use of NSAIDs and increased HF, these findings are not unexpected because type 2 diabetes is also a major risk factor for HF.”
But it may be “premature to issue guideline recommendations based on a single observational study,” the editorialists wrote. “Further robust clinical trial evidence is needed to replicate these results and investigate the relationship of the type and dose of NSAIDs with HF risk. However, it should be realized that short-term or long-term use of NSAIDs may be detrimental to cardiovascular health.”
The analysis covered 23,308 patients from throughout Denmark with a type 2 diabetes diagnosis and no HF history who experienced a first HF hospitalization; their age averaged 76 years and 39% were women.
They served as their own controls; their NSAID exposures at two 28-day periods preceding the HF event, the one immediately before and the other preceding it by 56 days, were compared as the index and control periods, respectively.
Exposure to NSAIDs was defined as obtaining a prescription for celecoxib, diclofenac, ibuprofen, or naproxen, “as these are NSAIDs used primarily in Denmark,” the report states.
The odds ratios for HF hospitalization associated with NSAID exposure within 28 days preceding the event were 1.43 (95% confidence interval, 1.27-1.63) overall, 1.41 (95% CI, 1.16-1.71) for an NSAID given on top of both RASi and diuretics, 1.68 (95% CI, 1.00-2.88) for patients with elevated hemoglobin A1c, 1.78 (95% CI, 1.39-2.28) for those 80 or older, and 2.71 (95% CI, 1.78-4.23) for those with prior NSAID use.
That NSAID use and diabetes are each associated with increased risk for HF is well established, Dr. Holt observed. Yet the drugs had been prescribed to 16% of patients in the study.
“One of the more surprising findings, to me, was the quite substantial use of prescribed NSAIDs in a population of patients with diabetes, a patient group with a well-established cardiovascular risk,” he said.
“This patient group is only growing, so emphasis on the possible associations between even short-term NSAID use and incident heart failure is probably timely and perhaps needed.”
Dr. Holt and the study were supported by grants from Ib Mogens Kristiansens Almene Fond, Helsefonden, Snedkermester Sophus Jacobsen og hustru Astrid Jacobsen Fond, Marie og M.B. Richters Fond, and the Dagmar Marshalls Fond. Dr. Khan and Dr. Kunutsor reported no relevant relationships.
A version of this article first appeared on Medscape.com.
suggests a prospective, controlled study.
Certain subgroups may account for much of the excess risk, the results suggest, including the very elderly, patients with uncontrolled diabetes, those prescribed an NSAID for the first time, and patients already taking both a renin-angiotensin system inhibitor (RASi) and a diuretic.
Such patients with a firm indication for NSAIDs potentially could “be the ones benefiting most from closer follow-up, reduced dosage, or other mitigation strategies,” Anders Holt, MD, said in an interview.
Dr. Holt, of Copenhagen University Hospital and Herlev-Gentofte Hospital in Hellerup, Denmark, is lead author on the analysis of Danish registry data published in the Journal of the American College of Cardiology. He presented essentially the same results in preliminary form at the 2022 annual congress of the European Society of Cardiology.
HF hospitalizations linked to NSAIDs, the published report notes, are often attributed to symptoms from temporary fluid overload, often without worsening cardiac function, that stem from the drugs’ renal effects.
“One could speculate,” Dr. Holt said, that such HF events might be less severe and even associated with better outcomes, compared with other forms of heart failure.
But the current analysis provides a hint to the contrary, he observed. The 5-year mortality was similar for patients with HF linked to NSAIDs and those with other forms of HF, “which could suggest that NSAID-associated heart failure is more than transient fluid overload.”
The drugs may promote HF through direct effects on the heart by any of several proposed mechanisms, including “induction of arrhythmias and heart fibrosis, vasoconstriction, subclinical inflammation, and blood pressure elevation,” Dr. Holt said.
The current study doesn’t determine whether NSAID-associated HF stems from transient fluid overload or direct cardiac effects, but it’s “most likely both.”
In other limitations, the analysis is unable to “reliably explore” whether promotion of HF is an NSAID class effect, a “clinically relevant” point given the drugs’ varying effects on cardiovascular risk, states an accompanying editorial. Nor was it able to determine whether the drugs exert a dose-response effect on HF risk, noted Hassan Khan, MD, PhD, Norton Healthcare, Louisville, Ky., and Setor K. Kunutsor, MD, PhD, University of Leicester (England).
Still, “given the well-established relationship between the use of NSAIDs and increased HF, these findings are not unexpected because type 2 diabetes is also a major risk factor for HF.”
But it may be “premature to issue guideline recommendations based on a single observational study,” the editorialists wrote. “Further robust clinical trial evidence is needed to replicate these results and investigate the relationship of the type and dose of NSAIDs with HF risk. However, it should be realized that short-term or long-term use of NSAIDs may be detrimental to cardiovascular health.”
The analysis covered 23,308 patients from throughout Denmark with a type 2 diabetes diagnosis and no HF history who experienced a first HF hospitalization; their age averaged 76 years and 39% were women.
They served as their own controls; their NSAID exposures at two 28-day periods preceding the HF event, the one immediately before and the other preceding it by 56 days, were compared as the index and control periods, respectively.
Exposure to NSAIDs was defined as obtaining a prescription for celecoxib, diclofenac, ibuprofen, or naproxen, “as these are NSAIDs used primarily in Denmark,” the report states.
The odds ratios for HF hospitalization associated with NSAID exposure within 28 days preceding the event were 1.43 (95% confidence interval, 1.27-1.63) overall, 1.41 (95% CI, 1.16-1.71) for an NSAID given on top of both RASi and diuretics, 1.68 (95% CI, 1.00-2.88) for patients with elevated hemoglobin A1c, 1.78 (95% CI, 1.39-2.28) for those 80 or older, and 2.71 (95% CI, 1.78-4.23) for those with prior NSAID use.
That NSAID use and diabetes are each associated with increased risk for HF is well established, Dr. Holt observed. Yet the drugs had been prescribed to 16% of patients in the study.
“One of the more surprising findings, to me, was the quite substantial use of prescribed NSAIDs in a population of patients with diabetes, a patient group with a well-established cardiovascular risk,” he said.
“This patient group is only growing, so emphasis on the possible associations between even short-term NSAID use and incident heart failure is probably timely and perhaps needed.”
Dr. Holt and the study were supported by grants from Ib Mogens Kristiansens Almene Fond, Helsefonden, Snedkermester Sophus Jacobsen og hustru Astrid Jacobsen Fond, Marie og M.B. Richters Fond, and the Dagmar Marshalls Fond. Dr. Khan and Dr. Kunutsor reported no relevant relationships.
A version of this article first appeared on Medscape.com.
FROM THE JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
Study offers dozens of reasons to cut sugar
A new compilation of nearly all research to date on the health impacts of sugar offers dozens of reasons to cut back.
The studies accounted for decades of research on the topic, stretching back to the beginning of the largest electronic databases for scientific papers.
The result is a list that cites the world’s most common health problems like heart disease, diabetes, obesity, high blood pressure, heart attack, high cholesterol, cancer, and depression. The findings were published in the BMJ. Researchers looked at studies that evaluated the impacts of consuming free sugars, which means any food that contains processed or naturally occurring sugars like table sugar, honey, or maple syrup. Sugar found in whole fruits and vegetables and in milk is not free sugar.
U.S. dietary guidelines recommend getting no more than 10% of daily calories from added sugars. For a typical 2,000-calorie-per-day diet, that equals no more than 200 calories, or about 12 teaspoons. The CDC reports that the average person consumes 17 teaspoons per day, with the largest sources being sugar-sweetened beverages, desserts, and snacks. (For context: one 12-ounce can of soda contains the equivalent of 9 teaspoons of sugar, according to beverage maker Coca-Cola.)
The new analysis also found links between sugary beverage consumption and other diet and lifestyle characteristics that may contribute to health problems.
“People who consumed sugar-sweetened beverages more frequently were likely to ingest more total and saturated fat, carbohydrate, and sodium, and less fruit, fiber, dairy products, and whole grain foods,” the authors wrote. “This dietary pattern was also associated with more frequent smoking and drinking, lower physical activity levels, and more time spent watching television. Therefore, the role of these confounding factors should be taken into consideration when explaining the association between sugar consumption and burden of disease.”
Recommendations for limiting sugar consumption are in place worldwide, the authors noted. They concluded that more needs to be done given the known health dangers of sugar.
“To change sugar consumption patterns, especially for children and adolescents, a combination of widespread public health education and policies worldwide is urgently needed,” they said.
A version of this article first appeared on WebMD.com.
A new compilation of nearly all research to date on the health impacts of sugar offers dozens of reasons to cut back.
The studies accounted for decades of research on the topic, stretching back to the beginning of the largest electronic databases for scientific papers.
The result is a list that cites the world’s most common health problems like heart disease, diabetes, obesity, high blood pressure, heart attack, high cholesterol, cancer, and depression. The findings were published in the BMJ. Researchers looked at studies that evaluated the impacts of consuming free sugars, which means any food that contains processed or naturally occurring sugars like table sugar, honey, or maple syrup. Sugar found in whole fruits and vegetables and in milk is not free sugar.
U.S. dietary guidelines recommend getting no more than 10% of daily calories from added sugars. For a typical 2,000-calorie-per-day diet, that equals no more than 200 calories, or about 12 teaspoons. The CDC reports that the average person consumes 17 teaspoons per day, with the largest sources being sugar-sweetened beverages, desserts, and snacks. (For context: one 12-ounce can of soda contains the equivalent of 9 teaspoons of sugar, according to beverage maker Coca-Cola.)
The new analysis also found links between sugary beverage consumption and other diet and lifestyle characteristics that may contribute to health problems.
“People who consumed sugar-sweetened beverages more frequently were likely to ingest more total and saturated fat, carbohydrate, and sodium, and less fruit, fiber, dairy products, and whole grain foods,” the authors wrote. “This dietary pattern was also associated with more frequent smoking and drinking, lower physical activity levels, and more time spent watching television. Therefore, the role of these confounding factors should be taken into consideration when explaining the association between sugar consumption and burden of disease.”
Recommendations for limiting sugar consumption are in place worldwide, the authors noted. They concluded that more needs to be done given the known health dangers of sugar.
“To change sugar consumption patterns, especially for children and adolescents, a combination of widespread public health education and policies worldwide is urgently needed,” they said.
A version of this article first appeared on WebMD.com.
A new compilation of nearly all research to date on the health impacts of sugar offers dozens of reasons to cut back.
The studies accounted for decades of research on the topic, stretching back to the beginning of the largest electronic databases for scientific papers.
The result is a list that cites the world’s most common health problems like heart disease, diabetes, obesity, high blood pressure, heart attack, high cholesterol, cancer, and depression. The findings were published in the BMJ. Researchers looked at studies that evaluated the impacts of consuming free sugars, which means any food that contains processed or naturally occurring sugars like table sugar, honey, or maple syrup. Sugar found in whole fruits and vegetables and in milk is not free sugar.
U.S. dietary guidelines recommend getting no more than 10% of daily calories from added sugars. For a typical 2,000-calorie-per-day diet, that equals no more than 200 calories, or about 12 teaspoons. The CDC reports that the average person consumes 17 teaspoons per day, with the largest sources being sugar-sweetened beverages, desserts, and snacks. (For context: one 12-ounce can of soda contains the equivalent of 9 teaspoons of sugar, according to beverage maker Coca-Cola.)
The new analysis also found links between sugary beverage consumption and other diet and lifestyle characteristics that may contribute to health problems.
“People who consumed sugar-sweetened beverages more frequently were likely to ingest more total and saturated fat, carbohydrate, and sodium, and less fruit, fiber, dairy products, and whole grain foods,” the authors wrote. “This dietary pattern was also associated with more frequent smoking and drinking, lower physical activity levels, and more time spent watching television. Therefore, the role of these confounding factors should be taken into consideration when explaining the association between sugar consumption and burden of disease.”
Recommendations for limiting sugar consumption are in place worldwide, the authors noted. They concluded that more needs to be done given the known health dangers of sugar.
“To change sugar consumption patterns, especially for children and adolescents, a combination of widespread public health education and policies worldwide is urgently needed,” they said.
A version of this article first appeared on WebMD.com.
FROM THE BMJ
Antiphospholipid antibodies linked to future CV events
The presence of antiphospholipid antibodies is associated with an increased risk for future cardiovascular events, according to a new study.
The findings point to possible new approaches to risk stratification and the potential for new therapeutic targets in heart disease.
“In this study of the general population, we found that two antiphospholipid antibodies were associated with an increased risk of having a serious cardiovascular event over a follow-up of 8 years,” coauthor Jason Knight, MD, University of Michigan, Ann Arbor, said in an interview.
“If confirmed in further studies, these findings could be used to identify a subgroup of patients who need more careful monitoring and more aggressive risk-factor modification, and if the increased risk linked to these antibodies is high enough, it may also justify preemptive treatments such as the anticoagulants that are routinely used in antiphospholipid syndrome,” Dr. Knight said.
“The long-term vision is that we may identify some people in the general population who would benefit from treating the immune system for the prevention and treatment of cardiovascular disease instead of, or in addition to, using typical cardiovascular medications,” he added.
The study was published online in JAMA Network Open.
Individuals with autoimmune and inflammatory diseases have a greater risk for cardiovascular events than expected based on traditional cardiovascular risk factors, with mechanisms proposed to explain this risk including inflammation-mediated disruption of vascular integrity and activation of platelets and coagulation pathways, the authors explained. However, the role of autoantibodies remains unclear.
They noted that antiphospholipid antibodies can activate endothelial cells, platelets, and neutrophils, and some patients with persistently circulating antiphospholipid antibodies can develop antiphospholipid syndrome – an acquired thromboinflammatory disease characterized by arterial, venous, and microvascular thrombotic events and obstetric complications.
Cross-sectional studies have shown that antiphospholipid antibodies are acutely present in up to 17.4% of patients with stroke or transient ischemic attack, and small cohort studies have suggested that such antibodies may be present in 1%-12% of seemingly healthy individuals. However, the impact of sex, race, and ethnicity on the prevalence of antiphospholipid antibodies and their association with atherosclerotic cardiovascular disease is not known.
The researchers conducted the current study to look at the association between antiphospholipid antibodies and future risk for atherosclerotic cardiovascular events.
They analyzed data from 2,427 participants in the population-based Dallas Heart Study who had no history of atherosclerotic cardiovascular disease or autoimmune diseases requiring immunosuppressive medications at the time of blood sampling at study entry in 2007-2009.
Eight different types of antiphospholipid antibodies were measured, and data on cardiovascular events over the next 8 years was recorded.
Results showed that 14.5% of the cohort tested positive for one of these antiphospholipid antibodies at the start of the study, with approximately one-third of those detected at a moderate or high titer.
The researchers also found that the IgA isotypes of two antiphospholipid antibodies – anticardiolipin and anti-beta-2 glycoprotein – were associated with future atherosclerotic cardiovascular events.
After adjustment for other known risk factors, individuals testing positive for the IgA isotype of anticardiolipin had an almost five times increased risk (hazard ratio, 4.92) of the primary endpoint (myocardial infarction, stroke, coronary revascularization, or cardiovascular death); while those testing positive for anti–beta2-glycoprotein had an almost three times increased risk (HR, 2.91).
Furthermore, there was what appeared to be a dose effect. People with the highest levels of these antibodies also had the highest risk for cardiovascular events, with up to an almost 10-fold increased risk with the higher level of anticardiolipin.
Dr. Knight said that more research into the IgA isotypes of these antiphospholipid antibodies is needed.
“Most of the mechanistic work in the antiphospholipid syndrome field has focused on IgG antiphospholipid antibodies. While we commonly find these IgA antibodies in patients with APS, the extent to which they contribute to disease has not been firmly established,” he said. “The fact that IgA was the primary hit in our unbiased screen suggests that there is more to the story and we need to better understand the implications of having these antibodies in circulation, and what specific problems they may be causing.”
Noting that antiphospholipid antibodies can form transiently after certain situations, such as infections, Dr. Knight said that further studies were needed with repeat blood testing to detect the chronic presence of the antibodies.
He added that information of venous thromboses was not available in this study and “perhaps some of the other antibodies might have stood out if we were able to analyze for different outcomes.”
This study was supported by a Pfizer Aspire Award. Dr. Knight reported receiving research funding and consulting fees from Jazz Pharmaceuticals outside the submitted work.
A version of this article first appeared on Medscape.com.
The presence of antiphospholipid antibodies is associated with an increased risk for future cardiovascular events, according to a new study.
The findings point to possible new approaches to risk stratification and the potential for new therapeutic targets in heart disease.
“In this study of the general population, we found that two antiphospholipid antibodies were associated with an increased risk of having a serious cardiovascular event over a follow-up of 8 years,” coauthor Jason Knight, MD, University of Michigan, Ann Arbor, said in an interview.
“If confirmed in further studies, these findings could be used to identify a subgroup of patients who need more careful monitoring and more aggressive risk-factor modification, and if the increased risk linked to these antibodies is high enough, it may also justify preemptive treatments such as the anticoagulants that are routinely used in antiphospholipid syndrome,” Dr. Knight said.
“The long-term vision is that we may identify some people in the general population who would benefit from treating the immune system for the prevention and treatment of cardiovascular disease instead of, or in addition to, using typical cardiovascular medications,” he added.
The study was published online in JAMA Network Open.
Individuals with autoimmune and inflammatory diseases have a greater risk for cardiovascular events than expected based on traditional cardiovascular risk factors, with mechanisms proposed to explain this risk including inflammation-mediated disruption of vascular integrity and activation of platelets and coagulation pathways, the authors explained. However, the role of autoantibodies remains unclear.
They noted that antiphospholipid antibodies can activate endothelial cells, platelets, and neutrophils, and some patients with persistently circulating antiphospholipid antibodies can develop antiphospholipid syndrome – an acquired thromboinflammatory disease characterized by arterial, venous, and microvascular thrombotic events and obstetric complications.
Cross-sectional studies have shown that antiphospholipid antibodies are acutely present in up to 17.4% of patients with stroke or transient ischemic attack, and small cohort studies have suggested that such antibodies may be present in 1%-12% of seemingly healthy individuals. However, the impact of sex, race, and ethnicity on the prevalence of antiphospholipid antibodies and their association with atherosclerotic cardiovascular disease is not known.
The researchers conducted the current study to look at the association between antiphospholipid antibodies and future risk for atherosclerotic cardiovascular events.
They analyzed data from 2,427 participants in the population-based Dallas Heart Study who had no history of atherosclerotic cardiovascular disease or autoimmune diseases requiring immunosuppressive medications at the time of blood sampling at study entry in 2007-2009.
Eight different types of antiphospholipid antibodies were measured, and data on cardiovascular events over the next 8 years was recorded.
Results showed that 14.5% of the cohort tested positive for one of these antiphospholipid antibodies at the start of the study, with approximately one-third of those detected at a moderate or high titer.
The researchers also found that the IgA isotypes of two antiphospholipid antibodies – anticardiolipin and anti-beta-2 glycoprotein – were associated with future atherosclerotic cardiovascular events.
After adjustment for other known risk factors, individuals testing positive for the IgA isotype of anticardiolipin had an almost five times increased risk (hazard ratio, 4.92) of the primary endpoint (myocardial infarction, stroke, coronary revascularization, or cardiovascular death); while those testing positive for anti–beta2-glycoprotein had an almost three times increased risk (HR, 2.91).
Furthermore, there was what appeared to be a dose effect. People with the highest levels of these antibodies also had the highest risk for cardiovascular events, with up to an almost 10-fold increased risk with the higher level of anticardiolipin.
Dr. Knight said that more research into the IgA isotypes of these antiphospholipid antibodies is needed.
“Most of the mechanistic work in the antiphospholipid syndrome field has focused on IgG antiphospholipid antibodies. While we commonly find these IgA antibodies in patients with APS, the extent to which they contribute to disease has not been firmly established,” he said. “The fact that IgA was the primary hit in our unbiased screen suggests that there is more to the story and we need to better understand the implications of having these antibodies in circulation, and what specific problems they may be causing.”
Noting that antiphospholipid antibodies can form transiently after certain situations, such as infections, Dr. Knight said that further studies were needed with repeat blood testing to detect the chronic presence of the antibodies.
He added that information of venous thromboses was not available in this study and “perhaps some of the other antibodies might have stood out if we were able to analyze for different outcomes.”
This study was supported by a Pfizer Aspire Award. Dr. Knight reported receiving research funding and consulting fees from Jazz Pharmaceuticals outside the submitted work.
A version of this article first appeared on Medscape.com.
The presence of antiphospholipid antibodies is associated with an increased risk for future cardiovascular events, according to a new study.
The findings point to possible new approaches to risk stratification and the potential for new therapeutic targets in heart disease.
“In this study of the general population, we found that two antiphospholipid antibodies were associated with an increased risk of having a serious cardiovascular event over a follow-up of 8 years,” coauthor Jason Knight, MD, University of Michigan, Ann Arbor, said in an interview.
“If confirmed in further studies, these findings could be used to identify a subgroup of patients who need more careful monitoring and more aggressive risk-factor modification, and if the increased risk linked to these antibodies is high enough, it may also justify preemptive treatments such as the anticoagulants that are routinely used in antiphospholipid syndrome,” Dr. Knight said.
“The long-term vision is that we may identify some people in the general population who would benefit from treating the immune system for the prevention and treatment of cardiovascular disease instead of, or in addition to, using typical cardiovascular medications,” he added.
The study was published online in JAMA Network Open.
Individuals with autoimmune and inflammatory diseases have a greater risk for cardiovascular events than expected based on traditional cardiovascular risk factors, with mechanisms proposed to explain this risk including inflammation-mediated disruption of vascular integrity and activation of platelets and coagulation pathways, the authors explained. However, the role of autoantibodies remains unclear.
They noted that antiphospholipid antibodies can activate endothelial cells, platelets, and neutrophils, and some patients with persistently circulating antiphospholipid antibodies can develop antiphospholipid syndrome – an acquired thromboinflammatory disease characterized by arterial, venous, and microvascular thrombotic events and obstetric complications.
Cross-sectional studies have shown that antiphospholipid antibodies are acutely present in up to 17.4% of patients with stroke or transient ischemic attack, and small cohort studies have suggested that such antibodies may be present in 1%-12% of seemingly healthy individuals. However, the impact of sex, race, and ethnicity on the prevalence of antiphospholipid antibodies and their association with atherosclerotic cardiovascular disease is not known.
The researchers conducted the current study to look at the association between antiphospholipid antibodies and future risk for atherosclerotic cardiovascular events.
They analyzed data from 2,427 participants in the population-based Dallas Heart Study who had no history of atherosclerotic cardiovascular disease or autoimmune diseases requiring immunosuppressive medications at the time of blood sampling at study entry in 2007-2009.
Eight different types of antiphospholipid antibodies were measured, and data on cardiovascular events over the next 8 years was recorded.
Results showed that 14.5% of the cohort tested positive for one of these antiphospholipid antibodies at the start of the study, with approximately one-third of those detected at a moderate or high titer.
The researchers also found that the IgA isotypes of two antiphospholipid antibodies – anticardiolipin and anti-beta-2 glycoprotein – were associated with future atherosclerotic cardiovascular events.
After adjustment for other known risk factors, individuals testing positive for the IgA isotype of anticardiolipin had an almost five times increased risk (hazard ratio, 4.92) of the primary endpoint (myocardial infarction, stroke, coronary revascularization, or cardiovascular death); while those testing positive for anti–beta2-glycoprotein had an almost three times increased risk (HR, 2.91).
Furthermore, there was what appeared to be a dose effect. People with the highest levels of these antibodies also had the highest risk for cardiovascular events, with up to an almost 10-fold increased risk with the higher level of anticardiolipin.
Dr. Knight said that more research into the IgA isotypes of these antiphospholipid antibodies is needed.
“Most of the mechanistic work in the antiphospholipid syndrome field has focused on IgG antiphospholipid antibodies. While we commonly find these IgA antibodies in patients with APS, the extent to which they contribute to disease has not been firmly established,” he said. “The fact that IgA was the primary hit in our unbiased screen suggests that there is more to the story and we need to better understand the implications of having these antibodies in circulation, and what specific problems they may be causing.”
Noting that antiphospholipid antibodies can form transiently after certain situations, such as infections, Dr. Knight said that further studies were needed with repeat blood testing to detect the chronic presence of the antibodies.
He added that information of venous thromboses was not available in this study and “perhaps some of the other antibodies might have stood out if we were able to analyze for different outcomes.”
This study was supported by a Pfizer Aspire Award. Dr. Knight reported receiving research funding and consulting fees from Jazz Pharmaceuticals outside the submitted work.
A version of this article first appeared on Medscape.com.
FROM JAMA NETWORK OPEN