Cardiology

Complications during pregnancy may be a wake-up call pointing to a higher risk for cardiovascular (CVD) and other diseases later in life. Therefore, the postpartum and interpregnancy periods are opportune windows for reducing CVD susceptibility and providing preventive care, especially for mothers with a history of adverse pregnancy outcomes (APOs). To that end, the American Heart Association recently released a scientific statement in Circulation outlining pregnancy-related CVD risks and reviewing evidence for preventive lifestyle strategies based on the AHA’s Life’s Essential 8 recommendations.

The Life’s Essential 8 encompass healthy eating, sleeping, and activity patterns; controlling weight, blood pressure, cholesterol, and blood sugar; and avoiding tobacco use.

“The motivation behind this statement was that complications in pregnancy are becoming more common and we now have more understanding that these serve as important risk factors for heart disease later in life,” said Jennifer Lewey, MD, MPH, director of the Penn Women’s Cardiovascular Health Program and an assistant professor of medicine at the University of Pennsylvania Perelman School of Medicine in Philadelphia.

Perelman School of Medicine

“These risk factors are underrecognized and underappreciated. Clinicians don’t feel comfortable counseling their patients about how to reduce their cardiovascular disease risk,” Dr. Lewey, chair of the AHA writing group, said in an interview.

“So we thought this was the perfect time to highlight what we know and don’t know about how to care for this population,” she said.

APOs predispose mothers to heart disease and other long-term complications, including heart failure, stroke, chronic kidney disease, and vascular dementia. “Pregnancy is a significant stress on the body, and APOs such as preeclampsia can lead to vascular changes in the blood vessels and structural changes to the heart that can persist long term,” Dr. Lewey explained. Reduced maternal physical activity and unshed weight can compound the problem.

Varying by race and ethnicity, the proportion of mothers experiencing pregnancy complications, such as high blood pressure, gestational diabetes, and/or preterm birth is estimated at 10%-20%, the statement authors noted. These complications may serve as a wake-up call to young mothers.

The AHA panel believes that identifying at-risk women at younger ages will enable prevention through lifestyle changes and timely treatment. Little is known, however about what specific care may best reduce long-term CVD risk in women who had pregnancy complications, Dr. Lewey said. While randomized clinical trials have yet to evaluate the effects of postpartum interventions on CVD outcomes, the need for strategies supported by rigorous evidence is clear. “In particular, the fourth trimester, defined as the 12 weeks after delivery, is an optimal time to engage postpartum individuals in care to reduce maternal morbidity and improve care transitions,” the AHA group wrote.

An earlier AHA statement in 2021 recommended frequent cardiac risk factor screening in the first year postpartum at 6 and 12 weeks and again at 6 and 12 months, with appropriate transition from postpartum to longitudinal primary care around the 8- to 12-week mark.

Among the current statement’s findings: High blood pressure is the most prevalent cardiovascular condition during pregnancy, and the last two decades have seen a 25% increase in preeclampsia.

Hypertension during pregnancy carries a two- to fourfold higher risk of chronic hypertension within 2-7 years.

Women with one or more APOs experience heart attack and stroke at younger ages. Commenting on the statement but not involved in it, internist Natalie A. Cameron, MD, a primary and preventive care physician at Northwestern Medicine in Chicago, said, “This statement will be very helpful for physicians from a primary care perspective, especially since in internal medicine we don’t standardly receive education in cardiovascular health in the context of pregnancy and the first year postpartum.”

Northwestern Medicine

Complications during pregnancy may be a wake-up call pointing to a higher risk for cardiovascular (CVD) and other diseases later in life. Therefore, the postpartum and interpregnancy periods are opportune windows for reducing CVD susceptibility and providing preventive care, especially for mothers with a history of adverse pregnancy outcomes (APOs). To that end, the American Heart Association recently released a scientific statement in Circulation outlining pregnancy-related CVD risks and reviewing evidence for preventive lifestyle strategies based on the AHA’s Life’s Essential 8 recommendations.

The Life’s Essential 8 encompass healthy eating, sleeping, and activity patterns; controlling weight, blood pressure, cholesterol, and blood sugar; and avoiding tobacco use.

“The motivation behind this statement was that complications in pregnancy are becoming more common and we now have more understanding that these serve as important risk factors for heart disease later in life,” said Jennifer Lewey, MD, MPH, director of the Penn Women’s Cardiovascular Health Program and an assistant professor of medicine at the University of Pennsylvania Perelman School of Medicine in Philadelphia.

Perelman School of Medicine

“These risk factors are underrecognized and underappreciated. Clinicians don’t feel comfortable counseling their patients about how to reduce their cardiovascular disease risk,” Dr. Lewey, chair of the AHA writing group, said in an interview.

“So we thought this was the perfect time to highlight what we know and don’t know about how to care for this population,” she said.

APOs predispose mothers to heart disease and other long-term complications, including heart failure, stroke, chronic kidney disease, and vascular dementia. “Pregnancy is a significant stress on the body, and APOs such as preeclampsia can lead to vascular changes in the blood vessels and structural changes to the heart that can persist long term,” Dr. Lewey explained. Reduced maternal physical activity and unshed weight can compound the problem.

Varying by race and ethnicity, the proportion of mothers experiencing pregnancy complications, such as high blood pressure, gestational diabetes, and/or preterm birth is estimated at 10%-20%, the statement authors noted. These complications may serve as a wake-up call to young mothers.

The AHA panel believes that identifying at-risk women at younger ages will enable prevention through lifestyle changes and timely treatment. Little is known, however about what specific care may best reduce long-term CVD risk in women who had pregnancy complications, Dr. Lewey said. While randomized clinical trials have yet to evaluate the effects of postpartum interventions on CVD outcomes, the need for strategies supported by rigorous evidence is clear. “In particular, the fourth trimester, defined as the 12 weeks after delivery, is an optimal time to engage postpartum individuals in care to reduce maternal morbidity and improve care transitions,” the AHA group wrote.

An earlier AHA statement in 2021 recommended frequent cardiac risk factor screening in the first year postpartum at 6 and 12 weeks and again at 6 and 12 months, with appropriate transition from postpartum to longitudinal primary care around the 8- to 12-week mark.

Among the current statement’s findings: High blood pressure is the most prevalent cardiovascular condition during pregnancy, and the last two decades have seen a 25% increase in preeclampsia.

Hypertension during pregnancy carries a two- to fourfold higher risk of chronic hypertension within 2-7 years.

Women with one or more APOs experience heart attack and stroke at younger ages. Commenting on the statement but not involved in it, internist Natalie A. Cameron, MD, a primary and preventive care physician at Northwestern Medicine in Chicago, said, “This statement will be very helpful for physicians from a primary care perspective, especially since in internal medicine we don’t standardly receive education in cardiovascular health in the context of pregnancy and the first year postpartum.”

Northwestern Medicine

Complications during pregnancy may be a wake-up call pointing to a higher risk for cardiovascular (CVD) and other diseases later in life. Therefore, the postpartum and interpregnancy periods are opportune windows for reducing CVD susceptibility and providing preventive care, especially for mothers with a history of adverse pregnancy outcomes (APOs). To that end, the American Heart Association recently released a scientific statement in Circulation outlining pregnancy-related CVD risks and reviewing evidence for preventive lifestyle strategies based on the AHA’s Life’s Essential 8 recommendations.

The Life’s Essential 8 encompass healthy eating, sleeping, and activity patterns; controlling weight, blood pressure, cholesterol, and blood sugar; and avoiding tobacco use.

“The motivation behind this statement was that complications in pregnancy are becoming more common and we now have more understanding that these serve as important risk factors for heart disease later in life,” said Jennifer Lewey, MD, MPH, director of the Penn Women’s Cardiovascular Health Program and an assistant professor of medicine at the University of Pennsylvania Perelman School of Medicine in Philadelphia.

Perelman School of Medicine

“These risk factors are underrecognized and underappreciated. Clinicians don’t feel comfortable counseling their patients about how to reduce their cardiovascular disease risk,” Dr. Lewey, chair of the AHA writing group, said in an interview.

“So we thought this was the perfect time to highlight what we know and don’t know about how to care for this population,” she said.

APOs predispose mothers to heart disease and other long-term complications, including heart failure, stroke, chronic kidney disease, and vascular dementia. “Pregnancy is a significant stress on the body, and APOs such as preeclampsia can lead to vascular changes in the blood vessels and structural changes to the heart that can persist long term,” Dr. Lewey explained. Reduced maternal physical activity and unshed weight can compound the problem.

Varying by race and ethnicity, the proportion of mothers experiencing pregnancy complications, such as high blood pressure, gestational diabetes, and/or preterm birth is estimated at 10%-20%, the statement authors noted. These complications may serve as a wake-up call to young mothers.

The AHA panel believes that identifying at-risk women at younger ages will enable prevention through lifestyle changes and timely treatment. Little is known, however about what specific care may best reduce long-term CVD risk in women who had pregnancy complications, Dr. Lewey said. While randomized clinical trials have yet to evaluate the effects of postpartum interventions on CVD outcomes, the need for strategies supported by rigorous evidence is clear. “In particular, the fourth trimester, defined as the 12 weeks after delivery, is an optimal time to engage postpartum individuals in care to reduce maternal morbidity and improve care transitions,” the AHA group wrote.

An earlier AHA statement in 2021 recommended frequent cardiac risk factor screening in the first year postpartum at 6 and 12 weeks and again at 6 and 12 months, with appropriate transition from postpartum to longitudinal primary care around the 8- to 12-week mark.

Among the current statement’s findings: High blood pressure is the most prevalent cardiovascular condition during pregnancy, and the last two decades have seen a 25% increase in preeclampsia.

Hypertension during pregnancy carries a two- to fourfold higher risk of chronic hypertension within 2-7 years.

Women with one or more APOs experience heart attack and stroke at younger ages. Commenting on the statement but not involved in it, internist Natalie A. Cameron, MD, a primary and preventive care physician at Northwestern Medicine in Chicago, said, “This statement will be very helpful for physicians from a primary care perspective, especially since in internal medicine we don’t standardly receive education in cardiovascular health in the context of pregnancy and the first year postpartum.”

Northwestern Medicine

Eugene Yang, MD, often confronts the complexities of weighing various medical interventions for high blood pressure. Among these is when to scale back antihypertensive drugs or stop them completely.

He considers a patient’s comorbidities, severity of symptoms, and risk factors for heart attack and stroke, among other variables. Central to this calculus is the recognition of age as a pivotal determinant of quality of life, according to Dr. Yang, the chair of the Prevention of Cardiovascular Disease Council at the American College of Cardiology.

For older adults, for example, the variance in functional status can be striking. One octogenarian may be bedbound due to severe dementia, while another might be playing pickleball three times a week.

“This happens to me in my practice all the time. I have patients who are restricted in mobility and have severe memory loss: Their functionality is quite poor,” Dr. Yang said. “In a patient where we have a limited life expectancy, where they have limited function or core memory, the goal is not to prolong life: It’s to make them more comfortable.”

Knowing when to deprescribe blood pressure medications is crucial. For some, lifestyle changes can do the trick. For others, particularly older patients, their comorbid conditions and medication regimens need to be considered.

“There’s a recognition that we need to move to a new paradigm where we need to decide when to be aggressive and when to be less aggressive,” Dr. Yang said.

The American Heart Association and the American College of Cardiology most recently released guidelines in 2017, changing the cutoff for diagnosis from 140/90 to 130/80 mm Hg. The groups have issued no updates since then, leaving primary care physicians and their colleagues to navigate this territory with caution, balancing the benefits of reduction with the potential harms of undertreatment.

One example of an area that needs updating is the consideration of the age, currently missing from current guidance on hypertension management from government and medical bodies in the United States. However, European Society of Hypertension guidelines, updated in June 2023, recommend adults over age 80 or those classified as frail should be treated when their systolic blood pressure exceeds 160.

“For the first time, we have a chapter in the guidelines on hypertension and management in older people,” Reinhold Kreutz, MD, PhD, immediate past-president of the European Society of Hypertension, said. “If a patient has low blood pressure and symptoms such as dizziness or frailty, a reduction in medication should be considered.”

High blood pressure does not always present with noticeable symptoms, and patients do not always show up for an office visit in time for early intervention. It can pave the way for severe health complications including heart failure, stroke, kidney disease, heart attack, and, ultimately, death.

Grim statistics reveal its toll: Hypertension was a primary or contributing cause of nearly 700,000 deaths in the United States in 2021, and nearly half of adults have the condition. Only about one in four adults have their high blood pressure under control.
 

New Research Provides Insight

A recent study may provide needed insights for primary care clinicians: Gradually reducing hypertensive medication may not induce the feared fluctuations in blood pressure, contrary to prior concerns.

Researchers in Seoul, South Korea, analyzed the blood pressure of 83 patients diagnosed with hypertension who reduced their use of medication. They found that the use of less medication was associated with an increase in blood pressure readings taken at home but not in the clinic nor did it appear to influence blood pressure variability. The mean age of participants was 66 years.

Research shows systolic blood pressure variability is an important predictor of cardiovascular outcomes, as well as the risk for dementia.

When crafting treatment plans, clinicians should recognize the diverse factors at play for a particular patient, particularly concerning other health conditions.

Obesity, diabetes, and hyperlipidemia are among the common comorbidities often intertwined with hypertension. Because additional conditions come with more symptoms to consider and various medications, these health profiles demand tailored approaches to hypertension treatment.

Clinicians can recommend lifestyle modifications like dietary changes and regular exercise as first steps for patients who are diagnosed with grade 1 hypertension but who do not have cardiovascular disease, chronic kidney disease, diabetes, or organ damage. However, in cases where comorbidities are present or hypertension escalates to grade 2, clinicians should turn to medications for management, according to the International Society of Hypertension.

Patients with heart failure and reduced ejection fraction have unique challenges, according to Keith C. Ferdinand, MD, the Gereld S. Berenson Endowed Chair in Preventative Cardiology at the Tulane School of Medicine in New Orleans, Louisiana.

“Patients who have heart disease, they get a pump so the blood pressure comes down — but medicine is often needed to prevent further heart failure,” Dr. Ferdinand said.

Dr. Ferdinand stressed the importance of continuous medication to stave off further cardiac deterioration. He advocated for a cautious approach, emphasizing the continued use of medications like sacubitril/valsartan, beta-blockers, or sodium-glucose transport protein inhibitors to safeguard against heart failure progression.

Patients should also self-monitor blood pressure at home and be taught how to properly fit a cuff to enable accurate measurements. This approach empowers patients to actively engage in their health management and detect any deviations that warrant further attention, he said.
 

Medications for Hypertension

The use of any of the five major drug classes — angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, beta-blockers, calcium blockers, and thiazide/thiazide-like diuretics — and their combinations are recommended as the basis of antihypertensive treatment strategies.

Dr. Yang said primary care clinicians must be careful to decrease doses slowly. Central-acting medications such as clonidine and beta-blockers ultimately reduce heart rate and dilate blood vessels.

Decreasing the dose too quickly can create a rebound effect, and medication should be means reduced and closely monitored over the course of several weeks, Dr. Yang said.

“You cannot just withdraw abruptly with certain medications — you have to wean off slowly,” because patients may experience high blood pressure again, Dr. Yang said.

A version of this article appeared on Medscape.com.

Eugene Yang, MD, often confronts the complexities of weighing various medical interventions for high blood pressure. Among these is when to scale back antihypertensive drugs or stop them completely.

He considers a patient’s comorbidities, severity of symptoms, and risk factors for heart attack and stroke, among other variables. Central to this calculus is the recognition of age as a pivotal determinant of quality of life, according to Dr. Yang, the chair of the Prevention of Cardiovascular Disease Council at the American College of Cardiology.

For older adults, for example, the variance in functional status can be striking. One octogenarian may be bedbound due to severe dementia, while another might be playing pickleball three times a week.

“This happens to me in my practice all the time. I have patients who are restricted in mobility and have severe memory loss: Their functionality is quite poor,” Dr. Yang said. “In a patient where we have a limited life expectancy, where they have limited function or core memory, the goal is not to prolong life: It’s to make them more comfortable.”

Knowing when to deprescribe blood pressure medications is crucial. For some, lifestyle changes can do the trick. For others, particularly older patients, their comorbid conditions and medication regimens need to be considered.

“There’s a recognition that we need to move to a new paradigm where we need to decide when to be aggressive and when to be less aggressive,” Dr. Yang said.

The American Heart Association and the American College of Cardiology most recently released guidelines in 2017, changing the cutoff for diagnosis from 140/90 to 130/80 mm Hg. The groups have issued no updates since then, leaving primary care physicians and their colleagues to navigate this territory with caution, balancing the benefits of reduction with the potential harms of undertreatment.

One example of an area that needs updating is the consideration of the age, currently missing from current guidance on hypertension management from government and medical bodies in the United States. However, European Society of Hypertension guidelines, updated in June 2023, recommend adults over age 80 or those classified as frail should be treated when their systolic blood pressure exceeds 160.

“For the first time, we have a chapter in the guidelines on hypertension and management in older people,” Reinhold Kreutz, MD, PhD, immediate past-president of the European Society of Hypertension, said. “If a patient has low blood pressure and symptoms such as dizziness or frailty, a reduction in medication should be considered.”

High blood pressure does not always present with noticeable symptoms, and patients do not always show up for an office visit in time for early intervention. It can pave the way for severe health complications including heart failure, stroke, kidney disease, heart attack, and, ultimately, death.

Grim statistics reveal its toll: Hypertension was a primary or contributing cause of nearly 700,000 deaths in the United States in 2021, and nearly half of adults have the condition. Only about one in four adults have their high blood pressure under control.
 

New Research Provides Insight

A recent study may provide needed insights for primary care clinicians: Gradually reducing hypertensive medication may not induce the feared fluctuations in blood pressure, contrary to prior concerns.

Researchers in Seoul, South Korea, analyzed the blood pressure of 83 patients diagnosed with hypertension who reduced their use of medication. They found that the use of less medication was associated with an increase in blood pressure readings taken at home but not in the clinic nor did it appear to influence blood pressure variability. The mean age of participants was 66 years.

Research shows systolic blood pressure variability is an important predictor of cardiovascular outcomes, as well as the risk for dementia.

When crafting treatment plans, clinicians should recognize the diverse factors at play for a particular patient, particularly concerning other health conditions.

Obesity, diabetes, and hyperlipidemia are among the common comorbidities often intertwined with hypertension. Because additional conditions come with more symptoms to consider and various medications, these health profiles demand tailored approaches to hypertension treatment.

Clinicians can recommend lifestyle modifications like dietary changes and regular exercise as first steps for patients who are diagnosed with grade 1 hypertension but who do not have cardiovascular disease, chronic kidney disease, diabetes, or organ damage. However, in cases where comorbidities are present or hypertension escalates to grade 2, clinicians should turn to medications for management, according to the International Society of Hypertension.

Patients with heart failure and reduced ejection fraction have unique challenges, according to Keith C. Ferdinand, MD, the Gereld S. Berenson Endowed Chair in Preventative Cardiology at the Tulane School of Medicine in New Orleans, Louisiana.

“Patients who have heart disease, they get a pump so the blood pressure comes down — but medicine is often needed to prevent further heart failure,” Dr. Ferdinand said.

Dr. Ferdinand stressed the importance of continuous medication to stave off further cardiac deterioration. He advocated for a cautious approach, emphasizing the continued use of medications like sacubitril/valsartan, beta-blockers, or sodium-glucose transport protein inhibitors to safeguard against heart failure progression.

Patients should also self-monitor blood pressure at home and be taught how to properly fit a cuff to enable accurate measurements. This approach empowers patients to actively engage in their health management and detect any deviations that warrant further attention, he said.
 

Medications for Hypertension

The use of any of the five major drug classes — angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, beta-blockers, calcium blockers, and thiazide/thiazide-like diuretics — and their combinations are recommended as the basis of antihypertensive treatment strategies.

Dr. Yang said primary care clinicians must be careful to decrease doses slowly. Central-acting medications such as clonidine and beta-blockers ultimately reduce heart rate and dilate blood vessels.

Decreasing the dose too quickly can create a rebound effect, and medication should be means reduced and closely monitored over the course of several weeks, Dr. Yang said.

“You cannot just withdraw abruptly with certain medications — you have to wean off slowly,” because patients may experience high blood pressure again, Dr. Yang said.

A version of this article appeared on Medscape.com.

Eugene Yang, MD, often confronts the complexities of weighing various medical interventions for high blood pressure. Among these is when to scale back antihypertensive drugs or stop them completely.

He considers a patient’s comorbidities, severity of symptoms, and risk factors for heart attack and stroke, among other variables. Central to this calculus is the recognition of age as a pivotal determinant of quality of life, according to Dr. Yang, the chair of the Prevention of Cardiovascular Disease Council at the American College of Cardiology.

For older adults, for example, the variance in functional status can be striking. One octogenarian may be bedbound due to severe dementia, while another might be playing pickleball three times a week.

“This happens to me in my practice all the time. I have patients who are restricted in mobility and have severe memory loss: Their functionality is quite poor,” Dr. Yang said. “In a patient where we have a limited life expectancy, where they have limited function or core memory, the goal is not to prolong life: It’s to make them more comfortable.”

Knowing when to deprescribe blood pressure medications is crucial. For some, lifestyle changes can do the trick. For others, particularly older patients, their comorbid conditions and medication regimens need to be considered.

“There’s a recognition that we need to move to a new paradigm where we need to decide when to be aggressive and when to be less aggressive,” Dr. Yang said.

The American Heart Association and the American College of Cardiology most recently released guidelines in 2017, changing the cutoff for diagnosis from 140/90 to 130/80 mm Hg. The groups have issued no updates since then, leaving primary care physicians and their colleagues to navigate this territory with caution, balancing the benefits of reduction with the potential harms of undertreatment.

One example of an area that needs updating is the consideration of the age, currently missing from current guidance on hypertension management from government and medical bodies in the United States. However, European Society of Hypertension guidelines, updated in June 2023, recommend adults over age 80 or those classified as frail should be treated when their systolic blood pressure exceeds 160.

“For the first time, we have a chapter in the guidelines on hypertension and management in older people,” Reinhold Kreutz, MD, PhD, immediate past-president of the European Society of Hypertension, said. “If a patient has low blood pressure and symptoms such as dizziness or frailty, a reduction in medication should be considered.”

High blood pressure does not always present with noticeable symptoms, and patients do not always show up for an office visit in time for early intervention. It can pave the way for severe health complications including heart failure, stroke, kidney disease, heart attack, and, ultimately, death.

Grim statistics reveal its toll: Hypertension was a primary or contributing cause of nearly 700,000 deaths in the United States in 2021, and nearly half of adults have the condition. Only about one in four adults have their high blood pressure under control.
 

New Research Provides Insight

A recent study may provide needed insights for primary care clinicians: Gradually reducing hypertensive medication may not induce the feared fluctuations in blood pressure, contrary to prior concerns.

Researchers in Seoul, South Korea, analyzed the blood pressure of 83 patients diagnosed with hypertension who reduced their use of medication. They found that the use of less medication was associated with an increase in blood pressure readings taken at home but not in the clinic nor did it appear to influence blood pressure variability. The mean age of participants was 66 years.

Research shows systolic blood pressure variability is an important predictor of cardiovascular outcomes, as well as the risk for dementia.

When crafting treatment plans, clinicians should recognize the diverse factors at play for a particular patient, particularly concerning other health conditions.

Obesity, diabetes, and hyperlipidemia are among the common comorbidities often intertwined with hypertension. Because additional conditions come with more symptoms to consider and various medications, these health profiles demand tailored approaches to hypertension treatment.

Clinicians can recommend lifestyle modifications like dietary changes and regular exercise as first steps for patients who are diagnosed with grade 1 hypertension but who do not have cardiovascular disease, chronic kidney disease, diabetes, or organ damage. However, in cases where comorbidities are present or hypertension escalates to grade 2, clinicians should turn to medications for management, according to the International Society of Hypertension.

Patients with heart failure and reduced ejection fraction have unique challenges, according to Keith C. Ferdinand, MD, the Gereld S. Berenson Endowed Chair in Preventative Cardiology at the Tulane School of Medicine in New Orleans, Louisiana.

“Patients who have heart disease, they get a pump so the blood pressure comes down — but medicine is often needed to prevent further heart failure,” Dr. Ferdinand said.

Dr. Ferdinand stressed the importance of continuous medication to stave off further cardiac deterioration. He advocated for a cautious approach, emphasizing the continued use of medications like sacubitril/valsartan, beta-blockers, or sodium-glucose transport protein inhibitors to safeguard against heart failure progression.

Patients should also self-monitor blood pressure at home and be taught how to properly fit a cuff to enable accurate measurements. This approach empowers patients to actively engage in their health management and detect any deviations that warrant further attention, he said.
 

Medications for Hypertension

The use of any of the five major drug classes — angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, beta-blockers, calcium blockers, and thiazide/thiazide-like diuretics — and their combinations are recommended as the basis of antihypertensive treatment strategies.

Dr. Yang said primary care clinicians must be careful to decrease doses slowly. Central-acting medications such as clonidine and beta-blockers ultimately reduce heart rate and dilate blood vessels.

Decreasing the dose too quickly can create a rebound effect, and medication should be means reduced and closely monitored over the course of several weeks, Dr. Yang said.

“You cannot just withdraw abruptly with certain medications — you have to wean off slowly,” because patients may experience high blood pressure again, Dr. Yang said.

A version of this article appeared on Medscape.com.

TOPLINE:

A universal cardiovascular disease (CVD) prediction tool performs well in patients with and without atherosclerotic CVD (ASCVD), a new study showed, suggesting this model could facilitate transition from primary to secondary prevention by streamlining risk classification.

METHODOLOGY:

• Researchers used different models to evaluate whether established CVD predictors, including age, sex, race, diabetes, systolic blood pressure, or smoking, are associated with major adverse cardiovascular events (MACEs), including myocardial infarction (MI), stroke, and heart failure (HF), among 9138 patients, mean age 63.8 years, in the Atherosclerosis Risk in Communities (ARIC) study.
• Of these, 609 had ASCVD (history of MI, ischemic stroke, or symptomatic peripheral artery disease) and 8529 did not.
• They extended their exploration to other predictors available in clinical practice, including family history of premature ASCVD, high-sensitivity C-reactive protein, lipoprotein(a), triglycerides, and apolipoprotein B, as well as predictors of HF such as body mass index and heart rate and blood-based cardiac biomarkers.
• An external validation analysis included 5322 participants in the Multi-Ethnic Study of Atherosclerosis (MESA).
• Over a median follow-up of 18.9 years, 3209 ARIC participants (35%) developed MACE for an incidence rate per 1000 person-years of 21.3 for MACE, 12.6 for MI/stroke, and 13.8 for HF.

TAKEAWAY:

• Of all candidate predictors, 10 variables (including established predictors and cardiac biomarkers) were included in the universal prediction model, which demonstrated good calibration in both those with ASCVD (hazard ratio [HR] C-statistic, 0.692; 95% CI, 0.650-0.735) and without ASCVD (HR C-statistic, 0.748; 95% CI, 0.726-0.770).
• As anticipated, the risk for MACE was generally lower in those with no prior ASCVD, but the 5-year risk in the highest quintile of predicted risk in those without ASCVD was higher than that in the lowest two quintiles of the ASCVD group.
• The universal risk prediction model was validated in the MESA community–based cohort; over a median follow-up of 13.7 years, 12% of participants with and without prior ASCVD developed MACE for an incidence rate per 1000 person-years of 10.2 for MACE, 7.4 for MI/stroke, and 4.3 for HF.
• The results were generally similar when examining individual outcomes (MI/stroke and HF) and for both no ASCVD and ASCVD groups across demographic subgroups by age, sex, and race.

IN PRACTICE:

The findings “support the importance of established predictors for classifying long-term CVD risk in both primary and secondary prevention settings,” the authors wrote, adding an advantage to this risk prediction approach could be to help providers and patients “further personalize secondary prevention.”

In an accompanying editorial, Pier Sergio Saba, MD, PhD, Clinical and Interventional Cardiology, Sassari University Hospital, Sassari, Italy, and others said the universal risk assessment approach “is conceptually promising” but noted patients with ASCVD represented only 7% of the study population, and this population was relatively young, potentially limiting the applicability of this risk model in older individuals. Before the risk model can be used in clinical settings, results need to be validated and given incorporation of cardiac biomarkers, “careful cost-benefit analyses may also be needed,” the editorial writers added.

SOURCE:

The study was conducted by Yejin Mok, PHD, MPH, Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, and colleagues. It was published online on January 29, 2024, in the Journal of the American College of Cardiology (JACC).

LIMITATIONS:

The somewhat limited number of study participants with prior ASCVD precluded researchers from quantifying the prognostic impact of ASCVD subtypes (eg, history of MI vs stroke vs peripheral artery disease). The study didn’t have data on some predictors recognized in guidelines (eg, coronary artery calcium and left ventricular ejection fraction). The ARIC analysis included only Black and White participants, and although models were validated in MESA, which included Chinese and Hispanic adults, extrapolation of results to more racially/ethnically diverse populations should be done with care.

DISCLOSURES:

The ARIC study received funding from the National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health, and Department of Health and Human Services. The MESA study was supported by the NHLBI and National Center for Advancing Translational Sciences. The study authors and editorial writers had no relevant conflicts of interest.

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

TOPLINE:

A universal cardiovascular disease (CVD) prediction tool performs well in patients with and without atherosclerotic CVD (ASCVD), a new study showed, suggesting this model could facilitate transition from primary to secondary prevention by streamlining risk classification.

METHODOLOGY:

• Researchers used different models to evaluate whether established CVD predictors, including age, sex, race, diabetes, systolic blood pressure, or smoking, are associated with major adverse cardiovascular events (MACEs), including myocardial infarction (MI), stroke, and heart failure (HF), among 9138 patients, mean age 63.8 years, in the Atherosclerosis Risk in Communities (ARIC) study.
• Of these, 609 had ASCVD (history of MI, ischemic stroke, or symptomatic peripheral artery disease) and 8529 did not.
• They extended their exploration to other predictors available in clinical practice, including family history of premature ASCVD, high-sensitivity C-reactive protein, lipoprotein(a), triglycerides, and apolipoprotein B, as well as predictors of HF such as body mass index and heart rate and blood-based cardiac biomarkers.
• An external validation analysis included 5322 participants in the Multi-Ethnic Study of Atherosclerosis (MESA).
• Over a median follow-up of 18.9 years, 3209 ARIC participants (35%) developed MACE for an incidence rate per 1000 person-years of 21.3 for MACE, 12.6 for MI/stroke, and 13.8 for HF.

TAKEAWAY:

• Of all candidate predictors, 10 variables (including established predictors and cardiac biomarkers) were included in the universal prediction model, which demonstrated good calibration in both those with ASCVD (hazard ratio [HR] C-statistic, 0.692; 95% CI, 0.650-0.735) and without ASCVD (HR C-statistic, 0.748; 95% CI, 0.726-0.770).
• As anticipated, the risk for MACE was generally lower in those with no prior ASCVD, but the 5-year risk in the highest quintile of predicted risk in those without ASCVD was higher than that in the lowest two quintiles of the ASCVD group.
• The universal risk prediction model was validated in the MESA community–based cohort; over a median follow-up of 13.7 years, 12% of participants with and without prior ASCVD developed MACE for an incidence rate per 1000 person-years of 10.2 for MACE, 7.4 for MI/stroke, and 4.3 for HF.
• The results were generally similar when examining individual outcomes (MI/stroke and HF) and for both no ASCVD and ASCVD groups across demographic subgroups by age, sex, and race.

IN PRACTICE:

The findings “support the importance of established predictors for classifying long-term CVD risk in both primary and secondary prevention settings,” the authors wrote, adding an advantage to this risk prediction approach could be to help providers and patients “further personalize secondary prevention.”

In an accompanying editorial, Pier Sergio Saba, MD, PhD, Clinical and Interventional Cardiology, Sassari University Hospital, Sassari, Italy, and others said the universal risk assessment approach “is conceptually promising” but noted patients with ASCVD represented only 7% of the study population, and this population was relatively young, potentially limiting the applicability of this risk model in older individuals. Before the risk model can be used in clinical settings, results need to be validated and given incorporation of cardiac biomarkers, “careful cost-benefit analyses may also be needed,” the editorial writers added.

SOURCE:

The study was conducted by Yejin Mok, PHD, MPH, Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, and colleagues. It was published online on January 29, 2024, in the Journal of the American College of Cardiology (JACC).

LIMITATIONS:

The somewhat limited number of study participants with prior ASCVD precluded researchers from quantifying the prognostic impact of ASCVD subtypes (eg, history of MI vs stroke vs peripheral artery disease). The study didn’t have data on some predictors recognized in guidelines (eg, coronary artery calcium and left ventricular ejection fraction). The ARIC analysis included only Black and White participants, and although models were validated in MESA, which included Chinese and Hispanic adults, extrapolation of results to more racially/ethnically diverse populations should be done with care.

DISCLOSURES:

The ARIC study received funding from the National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health, and Department of Health and Human Services. The MESA study was supported by the NHLBI and National Center for Advancing Translational Sciences. The study authors and editorial writers had no relevant conflicts of interest.

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

TOPLINE:

A universal cardiovascular disease (CVD) prediction tool performs well in patients with and without atherosclerotic CVD (ASCVD), a new study showed, suggesting this model could facilitate transition from primary to secondary prevention by streamlining risk classification.

METHODOLOGY:

• Researchers used different models to evaluate whether established CVD predictors, including age, sex, race, diabetes, systolic blood pressure, or smoking, are associated with major adverse cardiovascular events (MACEs), including myocardial infarction (MI), stroke, and heart failure (HF), among 9138 patients, mean age 63.8 years, in the Atherosclerosis Risk in Communities (ARIC) study.
• Of these, 609 had ASCVD (history of MI, ischemic stroke, or symptomatic peripheral artery disease) and 8529 did not.
• They extended their exploration to other predictors available in clinical practice, including family history of premature ASCVD, high-sensitivity C-reactive protein, lipoprotein(a), triglycerides, and apolipoprotein B, as well as predictors of HF such as body mass index and heart rate and blood-based cardiac biomarkers.
• An external validation analysis included 5322 participants in the Multi-Ethnic Study of Atherosclerosis (MESA).
• Over a median follow-up of 18.9 years, 3209 ARIC participants (35%) developed MACE for an incidence rate per 1000 person-years of 21.3 for MACE, 12.6 for MI/stroke, and 13.8 for HF.

TAKEAWAY:

• Of all candidate predictors, 10 variables (including established predictors and cardiac biomarkers) were included in the universal prediction model, which demonstrated good calibration in both those with ASCVD (hazard ratio [HR] C-statistic, 0.692; 95% CI, 0.650-0.735) and without ASCVD (HR C-statistic, 0.748; 95% CI, 0.726-0.770).
• As anticipated, the risk for MACE was generally lower in those with no prior ASCVD, but the 5-year risk in the highest quintile of predicted risk in those without ASCVD was higher than that in the lowest two quintiles of the ASCVD group.
• The universal risk prediction model was validated in the MESA community–based cohort; over a median follow-up of 13.7 years, 12% of participants with and without prior ASCVD developed MACE for an incidence rate per 1000 person-years of 10.2 for MACE, 7.4 for MI/stroke, and 4.3 for HF.
• The results were generally similar when examining individual outcomes (MI/stroke and HF) and for both no ASCVD and ASCVD groups across demographic subgroups by age, sex, and race.

IN PRACTICE:

The findings “support the importance of established predictors for classifying long-term CVD risk in both primary and secondary prevention settings,” the authors wrote, adding an advantage to this risk prediction approach could be to help providers and patients “further personalize secondary prevention.”

In an accompanying editorial, Pier Sergio Saba, MD, PhD, Clinical and Interventional Cardiology, Sassari University Hospital, Sassari, Italy, and others said the universal risk assessment approach “is conceptually promising” but noted patients with ASCVD represented only 7% of the study population, and this population was relatively young, potentially limiting the applicability of this risk model in older individuals. Before the risk model can be used in clinical settings, results need to be validated and given incorporation of cardiac biomarkers, “careful cost-benefit analyses may also be needed,” the editorial writers added.

SOURCE:

The study was conducted by Yejin Mok, PHD, MPH, Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, and colleagues. It was published online on January 29, 2024, in the Journal of the American College of Cardiology (JACC).

LIMITATIONS:

The somewhat limited number of study participants with prior ASCVD precluded researchers from quantifying the prognostic impact of ASCVD subtypes (eg, history of MI vs stroke vs peripheral artery disease). The study didn’t have data on some predictors recognized in guidelines (eg, coronary artery calcium and left ventricular ejection fraction). The ARIC analysis included only Black and White participants, and although models were validated in MESA, which included Chinese and Hispanic adults, extrapolation of results to more racially/ethnically diverse populations should be done with care.

DISCLOSURES:

The ARIC study received funding from the National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health, and Department of Health and Human Services. The MESA study was supported by the NHLBI and National Center for Advancing Translational Sciences. The study authors and editorial writers had no relevant conflicts of interest.

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

Replacing regular salt with a salt substitute reduced the incidence of new hypertension compared with a usual salt group, without provoking hypotension, new data showed.

Among a group of older adults with normal blood pressure (BP), those who swapped table salt for a salt substitute — consisting of 62.5% sodium chloride, 25% potassium chloride, and 12.5% flavorings — were 40% less apt to develop hypertension over 2 years than were peers who continued with regular salt.

“From a public health perspective, our study results indicate that everyone in the whole population, either hypertensive or normotensive, can benefit from replacing regular salt with potassium-enriched salt substitute,” lead author Yangfeng Wu, MD, PhD, professor and executive associate director, Peking University Clinical Research Institute, Beijing, China, told this news organization.

“Thus, salt substitution should be considered and promoted as a whole-population strategy for prevention and control of hypertension and cardiovascular disease,” Dr. Wu said.

The study was published online on February 12 in the Journal of the American College of Cardiology.

“Considering the failing strategy to reduce the intake of salt worldwide, salt substitution is an attractive alternative. The food industry and authorities should prepare strategies for wide-scale implementation of salt substitutes,” Rik Olde Engberink, MD, PhD, with Amsterdam University Medical Center, wrote in a linked editorial.

Population Strategy for Hypertension Prevention

The DECIDE-Salt clinical trial was a cluster-randomized trial conducted in 48 residential elderly care facilities in China with 1612 participants (1230 men and 382 women) aged 55 years or older. The trial assessed the effect of two sodium reduction strategies in lowering BP — replacing salt with a salt substitute and progressive restriction of the salt supply.

In the original study, the salt substitute intervention lowered systolic/diastolic BP significantly by 7.1/1.9 mm Hg vs the usual salt group. The progressive restriction of salt had no impact on BP vs usual salt or salt substitute groups.

This post hoc analysis of DECIDE-Salt focused on 609 participants (mean age, 71 years; 74% men) who were normotensive at baseline (mean BP, 122/74 mm Hg), with 298 in the usual salt group and 313 in the salt substitute group.

Compared with the usual salt group, the salt substitute group had a lower incidence of hypertension over 2 years (adjusted hazard ratio [HR], 0.60; 95% CI, 0.39-0.92; P = .02), with no increase in episodes of hypotension (P = .76).

From baseline to 2 years, there was no change in mean systolic/diastolic BP in the salt substitution group, whereas the usual salt group experienced a significant increase in systolic/diastolic BP (mean, 7.0/2.1 mm Hg).

The post hoc results from DECIDE-Salt are in line with a previous study from Peru, which also investigated mostly normotensive participants and reported a 51% lower risk of developing hypertension in the salt substitute group, as reported previously by this news organization.

“Although the study involved only participants aged 55 years and above, the epidemic of hypertension and its relations with sodium and potassium intake are not limited to older adults. Thus, we believe the salt substitution should also be beneficial to younger adults,” Dr. Wu said.

Notable Analysis

Reached for comment, Ankur Shah, MD, Division of Kidney Disease and Hypertension, Warren Alpert Medical School of Brown University, Providence, Rhode Island, said the study is “notable due to the limited and conflicting reports on the effects of salt substitution in individuals with normal blood pressure.”

“There is a growing body of literature on the impact of salt substitution in controlling hypertension, but less is known about prevention,” Dr. Shah, who was not involved in the study, told this news organization.

“The study certainly has population-level implications, as the design of a cluster-randomized trial at the facility level makes for a clear path to implementation — sodium substitution in elderly care facilities. That said, this is also the greatest limitation — extrapolating to the general population may not be accurate,” Dr. Shah noted.

There is also a potential concern with salt substitutes in patients with kidney disease, who typically are advised to lower potassium intake.

“Supplementing potassium could result in hyperkalemia, which can be life-threatening if severe, and patients taking medications that interfere with the kidney’s ability to excrete potassium should be cautious as well,” Dr. Shah said.

This research was supported by a grant from the National Key Research and Development Program, Ministry of Science and Technology of China. China Salt General Company at Yulin provided the usual salt and salt substitute used in the study free of charge. Dr. Wu, Dr. Engberink, and Dr. Shah had no relevant conflicts of interest.

A version of this article appeared on Medscape.com.

Replacing regular salt with a salt substitute reduced the incidence of new hypertension compared with a usual salt group, without provoking hypotension, new data showed.

Among a group of older adults with normal blood pressure (BP), those who swapped table salt for a salt substitute — consisting of 62.5% sodium chloride, 25% potassium chloride, and 12.5% flavorings — were 40% less apt to develop hypertension over 2 years than were peers who continued with regular salt.

“From a public health perspective, our study results indicate that everyone in the whole population, either hypertensive or normotensive, can benefit from replacing regular salt with potassium-enriched salt substitute,” lead author Yangfeng Wu, MD, PhD, professor and executive associate director, Peking University Clinical Research Institute, Beijing, China, told this news organization.

“Thus, salt substitution should be considered and promoted as a whole-population strategy for prevention and control of hypertension and cardiovascular disease,” Dr. Wu said.

The study was published online on February 12 in the Journal of the American College of Cardiology.

“Considering the failing strategy to reduce the intake of salt worldwide, salt substitution is an attractive alternative. The food industry and authorities should prepare strategies for wide-scale implementation of salt substitutes,” Rik Olde Engberink, MD, PhD, with Amsterdam University Medical Center, wrote in a linked editorial.

Population Strategy for Hypertension Prevention

The DECIDE-Salt clinical trial was a cluster-randomized trial conducted in 48 residential elderly care facilities in China with 1612 participants (1230 men and 382 women) aged 55 years or older. The trial assessed the effect of two sodium reduction strategies in lowering BP — replacing salt with a salt substitute and progressive restriction of the salt supply.

In the original study, the salt substitute intervention lowered systolic/diastolic BP significantly by 7.1/1.9 mm Hg vs the usual salt group. The progressive restriction of salt had no impact on BP vs usual salt or salt substitute groups.

This post hoc analysis of DECIDE-Salt focused on 609 participants (mean age, 71 years; 74% men) who were normotensive at baseline (mean BP, 122/74 mm Hg), with 298 in the usual salt group and 313 in the salt substitute group.

Compared with the usual salt group, the salt substitute group had a lower incidence of hypertension over 2 years (adjusted hazard ratio [HR], 0.60; 95% CI, 0.39-0.92; P = .02), with no increase in episodes of hypotension (P = .76).

From baseline to 2 years, there was no change in mean systolic/diastolic BP in the salt substitution group, whereas the usual salt group experienced a significant increase in systolic/diastolic BP (mean, 7.0/2.1 mm Hg).

The post hoc results from DECIDE-Salt are in line with a previous study from Peru, which also investigated mostly normotensive participants and reported a 51% lower risk of developing hypertension in the salt substitute group, as reported previously by this news organization.

“Although the study involved only participants aged 55 years and above, the epidemic of hypertension and its relations with sodium and potassium intake are not limited to older adults. Thus, we believe the salt substitution should also be beneficial to younger adults,” Dr. Wu said.

Notable Analysis

Reached for comment, Ankur Shah, MD, Division of Kidney Disease and Hypertension, Warren Alpert Medical School of Brown University, Providence, Rhode Island, said the study is “notable due to the limited and conflicting reports on the effects of salt substitution in individuals with normal blood pressure.”

“There is a growing body of literature on the impact of salt substitution in controlling hypertension, but less is known about prevention,” Dr. Shah, who was not involved in the study, told this news organization.

“The study certainly has population-level implications, as the design of a cluster-randomized trial at the facility level makes for a clear path to implementation — sodium substitution in elderly care facilities. That said, this is also the greatest limitation — extrapolating to the general population may not be accurate,” Dr. Shah noted.

There is also a potential concern with salt substitutes in patients with kidney disease, who typically are advised to lower potassium intake.

“Supplementing potassium could result in hyperkalemia, which can be life-threatening if severe, and patients taking medications that interfere with the kidney’s ability to excrete potassium should be cautious as well,” Dr. Shah said.

This research was supported by a grant from the National Key Research and Development Program, Ministry of Science and Technology of China. China Salt General Company at Yulin provided the usual salt and salt substitute used in the study free of charge. Dr. Wu, Dr. Engberink, and Dr. Shah had no relevant conflicts of interest.

A version of this article appeared on Medscape.com.

Replacing regular salt with a salt substitute reduced the incidence of new hypertension compared with a usual salt group, without provoking hypotension, new data showed.

Among a group of older adults with normal blood pressure (BP), those who swapped table salt for a salt substitute — consisting of 62.5% sodium chloride, 25% potassium chloride, and 12.5% flavorings — were 40% less apt to develop hypertension over 2 years than were peers who continued with regular salt.

“From a public health perspective, our study results indicate that everyone in the whole population, either hypertensive or normotensive, can benefit from replacing regular salt with potassium-enriched salt substitute,” lead author Yangfeng Wu, MD, PhD, professor and executive associate director, Peking University Clinical Research Institute, Beijing, China, told this news organization.

“Thus, salt substitution should be considered and promoted as a whole-population strategy for prevention and control of hypertension and cardiovascular disease,” Dr. Wu said.

The study was published online on February 12 in the Journal of the American College of Cardiology.

“Considering the failing strategy to reduce the intake of salt worldwide, salt substitution is an attractive alternative. The food industry and authorities should prepare strategies for wide-scale implementation of salt substitutes,” Rik Olde Engberink, MD, PhD, with Amsterdam University Medical Center, wrote in a linked editorial.

Population Strategy for Hypertension Prevention

The DECIDE-Salt clinical trial was a cluster-randomized trial conducted in 48 residential elderly care facilities in China with 1612 participants (1230 men and 382 women) aged 55 years or older. The trial assessed the effect of two sodium reduction strategies in lowering BP — replacing salt with a salt substitute and progressive restriction of the salt supply.

In the original study, the salt substitute intervention lowered systolic/diastolic BP significantly by 7.1/1.9 mm Hg vs the usual salt group. The progressive restriction of salt had no impact on BP vs usual salt or salt substitute groups.

This post hoc analysis of DECIDE-Salt focused on 609 participants (mean age, 71 years; 74% men) who were normotensive at baseline (mean BP, 122/74 mm Hg), with 298 in the usual salt group and 313 in the salt substitute group.

Compared with the usual salt group, the salt substitute group had a lower incidence of hypertension over 2 years (adjusted hazard ratio [HR], 0.60; 95% CI, 0.39-0.92; P = .02), with no increase in episodes of hypotension (P = .76).

From baseline to 2 years, there was no change in mean systolic/diastolic BP in the salt substitution group, whereas the usual salt group experienced a significant increase in systolic/diastolic BP (mean, 7.0/2.1 mm Hg).

The post hoc results from DECIDE-Salt are in line with a previous study from Peru, which also investigated mostly normotensive participants and reported a 51% lower risk of developing hypertension in the salt substitute group, as reported previously by this news organization.

“Although the study involved only participants aged 55 years and above, the epidemic of hypertension and its relations with sodium and potassium intake are not limited to older adults. Thus, we believe the salt substitution should also be beneficial to younger adults,” Dr. Wu said.

Notable Analysis

Reached for comment, Ankur Shah, MD, Division of Kidney Disease and Hypertension, Warren Alpert Medical School of Brown University, Providence, Rhode Island, said the study is “notable due to the limited and conflicting reports on the effects of salt substitution in individuals with normal blood pressure.”

“There is a growing body of literature on the impact of salt substitution in controlling hypertension, but less is known about prevention,” Dr. Shah, who was not involved in the study, told this news organization.

“The study certainly has population-level implications, as the design of a cluster-randomized trial at the facility level makes for a clear path to implementation — sodium substitution in elderly care facilities. That said, this is also the greatest limitation — extrapolating to the general population may not be accurate,” Dr. Shah noted.

There is also a potential concern with salt substitutes in patients with kidney disease, who typically are advised to lower potassium intake.

“Supplementing potassium could result in hyperkalemia, which can be life-threatening if severe, and patients taking medications that interfere with the kidney’s ability to excrete potassium should be cautious as well,” Dr. Shah said.

This research was supported by a grant from the National Key Research and Development Program, Ministry of Science and Technology of China. China Salt General Company at Yulin provided the usual salt and salt substitute used in the study free of charge. Dr. Wu, Dr. Engberink, and Dr. Shah had no relevant conflicts of interest.

A version of this article appeared on Medscape.com.

TOPLINE:

Spinal cord injury (SCI) is associated with a significantly greater risk for heart disease than that of the general non-SCI population, especially among those with severe disability, new observational data suggest.

METHODOLOGY:

• Researchers analyzed data from Korea’s National Health Insurance Service on 5083 patients with cervical, thoracic, or lumbar SCI (mean age, 58; 75% men) and 1:3 age- and sex-matched non-SCI controls.
• The study endpoint was new-onset myocardial infarction (MI), heart failure (HF), or atrial fibrillation (AF) during a mean follow-up of 4.3 years.
• Covariates included low income, living in an urban or rural area, alcohol consumption, smoking status, physical activity engagement, body mass index, and blood pressure; comorbidities included hypertension, type 2 diabetes, and dyslipidemia.

TAKEAWAY:

• A total of 169 MI events (7.3 per 1000 person-years), 426 HF events (18.8 per 1000 person-years), and 158 AF events (6.8 per 1000 person-years) occurred among SCI survivors.
• After adjustment, SCI survivors had a higher risk for MI (adjusted hazard ratio [aHR], 2.41), HF (aHR, 2.24), and AF (aHR, 1.84) than that of controls.
• Among SCI survivors with a disability, the risks increased with disability severity, and those with severe disability had the highest risks for MI (aHR, 3.74), HF (aHR, 3.96), and AF (aHR, 3.32).
• Cervical and lumbar SCI survivors had an increased risk for heart disease compared with controls regardless of disability, and the risk was slightly higher for those with a disability; for cervical SCI survivors with a disability, aHRs for MI, HF, and AF, respectively, were 2.30, 2.05, and 1.73; for lumbar SCI survivors with a disability, aHRs were 2.79, 2.35, and 2.47.
• Thoracic SCI survivors with disability had a higher risk for MI (aHR, 5.62) and HF (aHR, 3.31) than controls.

IN PRACTICE:

“[T]he recognition and treatment of modifiable cardiovascular risk factors must be reinforced in the SCI population, [and] proper rehabilitation and education should be considered to prevent autonomic dysreflexia or orthostatic hypotension,” the authors wrote.

In an accompanying editorial, Christopher R. West, PhD, and Jacquelyn J. Cragg, PhD, both of the University of British Columbia, Vancouver, Canada, noted that clinical guidelines for cardiovascular and cardiometabolic disease after SCI don’t include approaches to help mitigate the risk for cardiac events such as those reported in the study; therefore, they wrote, the findings “should act as ‘call-to-arms’ to researchers and clinicians to shift gears from tradition and begin studying the clinical efficacy of neuraxial therapies that could help restore autonomic balance [in SCI], such as targeted neuromodulation.”

SOURCE:

The study was led by Jung Eun Yoo, MD, PhD of Seoul National University College of Medicine, Seoul, South Korea, and published online on February 12 in the Journal of the American College of Cardiology.

LIMITATIONS:

The database was not designed for the SCI population, so data are incomplete. The incidence of thoracic SCI was particularly low. Because SCI survivors may have impaired perception of chest pain in ischemic heart disease, those with asymptomatic or silent heart disease may not have been captured during follow-up. All study participants were Korean, so the findings may not be generalizable to other ethnicities.

DISCLOSURES:

This research was partially supported by a grant from the Korea Health Technology R&D Project through the Korea Health Industry Development Institute, funded by the Ministry of Health and Welfare, South Korea. The study authors and the editorialists had no relevant relationships to disclose.

A version of this article appeared on Medscape.com.

TOPLINE:

Spinal cord injury (SCI) is associated with a significantly greater risk for heart disease than that of the general non-SCI population, especially among those with severe disability, new observational data suggest.

METHODOLOGY:

• Researchers analyzed data from Korea’s National Health Insurance Service on 5083 patients with cervical, thoracic, or lumbar SCI (mean age, 58; 75% men) and 1:3 age- and sex-matched non-SCI controls.
• The study endpoint was new-onset myocardial infarction (MI), heart failure (HF), or atrial fibrillation (AF) during a mean follow-up of 4.3 years.
• Covariates included low income, living in an urban or rural area, alcohol consumption, smoking status, physical activity engagement, body mass index, and blood pressure; comorbidities included hypertension, type 2 diabetes, and dyslipidemia.

TAKEAWAY:

• A total of 169 MI events (7.3 per 1000 person-years), 426 HF events (18.8 per 1000 person-years), and 158 AF events (6.8 per 1000 person-years) occurred among SCI survivors.
• After adjustment, SCI survivors had a higher risk for MI (adjusted hazard ratio [aHR], 2.41), HF (aHR, 2.24), and AF (aHR, 1.84) than that of controls.
• Among SCI survivors with a disability, the risks increased with disability severity, and those with severe disability had the highest risks for MI (aHR, 3.74), HF (aHR, 3.96), and AF (aHR, 3.32).
• Cervical and lumbar SCI survivors had an increased risk for heart disease compared with controls regardless of disability, and the risk was slightly higher for those with a disability; for cervical SCI survivors with a disability, aHRs for MI, HF, and AF, respectively, were 2.30, 2.05, and 1.73; for lumbar SCI survivors with a disability, aHRs were 2.79, 2.35, and 2.47.
• Thoracic SCI survivors with disability had a higher risk for MI (aHR, 5.62) and HF (aHR, 3.31) than controls.

IN PRACTICE:

“[T]he recognition and treatment of modifiable cardiovascular risk factors must be reinforced in the SCI population, [and] proper rehabilitation and education should be considered to prevent autonomic dysreflexia or orthostatic hypotension,” the authors wrote.

In an accompanying editorial, Christopher R. West, PhD, and Jacquelyn J. Cragg, PhD, both of the University of British Columbia, Vancouver, Canada, noted that clinical guidelines for cardiovascular and cardiometabolic disease after SCI don’t include approaches to help mitigate the risk for cardiac events such as those reported in the study; therefore, they wrote, the findings “should act as ‘call-to-arms’ to researchers and clinicians to shift gears from tradition and begin studying the clinical efficacy of neuraxial therapies that could help restore autonomic balance [in SCI], such as targeted neuromodulation.”

SOURCE:

The study was led by Jung Eun Yoo, MD, PhD of Seoul National University College of Medicine, Seoul, South Korea, and published online on February 12 in the Journal of the American College of Cardiology.

LIMITATIONS:

The database was not designed for the SCI population, so data are incomplete. The incidence of thoracic SCI was particularly low. Because SCI survivors may have impaired perception of chest pain in ischemic heart disease, those with asymptomatic or silent heart disease may not have been captured during follow-up. All study participants were Korean, so the findings may not be generalizable to other ethnicities.

DISCLOSURES:

This research was partially supported by a grant from the Korea Health Technology R&D Project through the Korea Health Industry Development Institute, funded by the Ministry of Health and Welfare, South Korea. The study authors and the editorialists had no relevant relationships to disclose.

A version of this article appeared on Medscape.com.

TOPLINE:

Spinal cord injury (SCI) is associated with a significantly greater risk for heart disease than that of the general non-SCI population, especially among those with severe disability, new observational data suggest.

METHODOLOGY:

• Researchers analyzed data from Korea’s National Health Insurance Service on 5083 patients with cervical, thoracic, or lumbar SCI (mean age, 58; 75% men) and 1:3 age- and sex-matched non-SCI controls.
• The study endpoint was new-onset myocardial infarction (MI), heart failure (HF), or atrial fibrillation (AF) during a mean follow-up of 4.3 years.
• Covariates included low income, living in an urban or rural area, alcohol consumption, smoking status, physical activity engagement, body mass index, and blood pressure; comorbidities included hypertension, type 2 diabetes, and dyslipidemia.

TAKEAWAY:

• A total of 169 MI events (7.3 per 1000 person-years), 426 HF events (18.8 per 1000 person-years), and 158 AF events (6.8 per 1000 person-years) occurred among SCI survivors.
• After adjustment, SCI survivors had a higher risk for MI (adjusted hazard ratio [aHR], 2.41), HF (aHR, 2.24), and AF (aHR, 1.84) than that of controls.
• Among SCI survivors with a disability, the risks increased with disability severity, and those with severe disability had the highest risks for MI (aHR, 3.74), HF (aHR, 3.96), and AF (aHR, 3.32).
• Cervical and lumbar SCI survivors had an increased risk for heart disease compared with controls regardless of disability, and the risk was slightly higher for those with a disability; for cervical SCI survivors with a disability, aHRs for MI, HF, and AF, respectively, were 2.30, 2.05, and 1.73; for lumbar SCI survivors with a disability, aHRs were 2.79, 2.35, and 2.47.
• Thoracic SCI survivors with disability had a higher risk for MI (aHR, 5.62) and HF (aHR, 3.31) than controls.

IN PRACTICE:

“[T]he recognition and treatment of modifiable cardiovascular risk factors must be reinforced in the SCI population, [and] proper rehabilitation and education should be considered to prevent autonomic dysreflexia or orthostatic hypotension,” the authors wrote.

In an accompanying editorial, Christopher R. West, PhD, and Jacquelyn J. Cragg, PhD, both of the University of British Columbia, Vancouver, Canada, noted that clinical guidelines for cardiovascular and cardiometabolic disease after SCI don’t include approaches to help mitigate the risk for cardiac events such as those reported in the study; therefore, they wrote, the findings “should act as ‘call-to-arms’ to researchers and clinicians to shift gears from tradition and begin studying the clinical efficacy of neuraxial therapies that could help restore autonomic balance [in SCI], such as targeted neuromodulation.”

SOURCE:

The study was led by Jung Eun Yoo, MD, PhD of Seoul National University College of Medicine, Seoul, South Korea, and published online on February 12 in the Journal of the American College of Cardiology.

LIMITATIONS:

The database was not designed for the SCI population, so data are incomplete. The incidence of thoracic SCI was particularly low. Because SCI survivors may have impaired perception of chest pain in ischemic heart disease, those with asymptomatic or silent heart disease may not have been captured during follow-up. All study participants were Korean, so the findings may not be generalizable to other ethnicities.

DISCLOSURES:

This research was partially supported by a grant from the Korea Health Technology R&D Project through the Korea Health Industry Development Institute, funded by the Ministry of Health and Welfare, South Korea. The study authors and the editorialists had no relevant relationships to disclose.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

Hi. I’m Art Caplan. I’m at the Division of Medical Ethics at the New York University Grossman School of Medicine in New York City.

I think we had a breakthrough on a very controversial subject over the past month. Over and over again, debates have been breaking out, cases have been going to court, and fights have been coming to ethics committees about brain death. How do we know what brain death is, how do we diagnose it, and what rights do families have with respect to the diagnosis?

The American Academy of Neurology decided to form a task force, and they just issued guidelines on the definition, tests to use it, and the rights of families. Whether you›re a neurologist, someone involved in actually diagnosing brain death, or you›re dealing with very ill people whose families are trying to direct the kinds of things that you or the nurses can do, these guidelines, I think, are excellent. They did a wonderful job, in my view. They›ve achieved clarity.

First, they tried to handle both adults and children. Children are, if you will, more difficult — and that’s been known — to test for brain death. Their brains are smaller. You get more interference and false signals coming from muscle or nerve activity that might be going on elsewhere in their bodies.

The guidelines say we’re going to try to see whether a person can breathe without support. If it’s an adult, one test over a 24-hour period would be sufficient. If you had them off the ventilator and they can’t breathe and show no signs of being able to do that, that’s a very fundamental test for brain death. For children, you’re going to have to do it twice. The guidelines are saying to be cautious.

Second, they say it’s very important to know the cause of the suspected brain death condition. If someone has a massive head injury, that’s different from a situation in which someone overdoses from drugs or drowns. Those conditions can be a little deceptive. In the case of drowning, sometimes the brain has protective mechanisms to protect circulation to the brain naturally for a little bit of time. I’m talking about minutes, not hours.

You want to be careful to make sure that you know the cause of the massive brain injury or insult that makes someone believe that the patient is brain-dead, whether it’s a stroke, an embolism, a bleed, a gunshot wound, or trauma to the head. Those factors really drive the certainty with which brain death should be pronounced. I think that’s very, very important.

They also said that brain death means the permanent loss of brain function. You may get a few cells still firing or you may be in a situation, because the life support is still there, where the body looks pink and perhaps might appear to still be alive to someone. When you know that the damage to the brain is so severe that there’s nothing that can be done to bring back the support of heart function, breathing, and most likely any ability to sense or feel anything, that is death.

I believe it’s very important, when talking to families, to say there are two ways that we pronounce people dead, and they’re equal: One is to say their heart has stopped, their breathing has stopped, and there’s nothing we can do to resuscitate them, which is cardiac death. The other is to say their brain has permanently ceased to function in any kind of integrated way. That means no heartbeat, no breathing, and no mental sensations. That is death.

In approaching families, it is critical that doctors and nurses don’t say, “Your relative is brain-dead.” That gives the family a sense that maybe they’re only “partially dead” or maybe there’s one key organ that has stopped working but maybe you can bring it back. Death is death. The law recognizes both cardiac death and brain death as death.

When you approach a family, if you believe that death has occurred, you say, “I’m very sorry. With regret, I have to tell you, your loved one is dead.” If they ask how you know, you can say, “We’ve determined it through brain death or through cardiac death.” You don’t give them a sense that people could be kind of dead, sort of dead, or nearly dead. Those states are comas or permanent vegetative states; they’re not the same as death.

What if the family says, “I don’t want you to do any testing. I don’t want to find out whether my relative is dead”? The American Academy of Neurology looked at this carefully and said that any test for death can be done without the permission or consent of the family. They said that because doctors need to know what steps to take to treat someone.

If a person is dead, then treatment is going to stop. It may not stop immediately. There may be issues about organ donation. There may be issues about gathering the family to come to the bedside to say goodbye, because many people think that’s more humane than saying goodbye at the morgue or in another setting.

This is all well and good, but patients cannot protect against bad news when it comes to death. We don’t want to be doing things to the dead that cost money or are futile because of death and using resources that might go to others.

We’ve got much more clarity than we have ever had with respect to the issue of brain death and how it works in any hospital. We have certain tests, including being off the ventilator and some other tests, that the guidelines supply. We know we have to be more careful with children. We want to know the etiology of the cause of the brain trauma, the devastating brain injury, to be sure that this is something that really is permanent cessation of integrated brain function.

We know that if you believe the person has died, you don’t need the consent of the family in order to do a brain-death test. You have to do it because there is no point in continuing treatment in expensive ICU settings and denying resources to others who might want to use those resources. The family can’t hold the medical team hostage.

We do know that when we approach someone with the determination, whatever it is, we should lead by saying that the person has died and then explain how that was determined, whether it be by cardiac death pronouncement — where you tried to resuscitate and the heart’s not beating — or brain-death analysis.

I’m Art Caplan at the Division of Medical Ethics at the NYU Grossman School of Medicine. Thanks for watching.

Dr. Caplan has disclosed the following relevant financial relationships: Served as a director, officer, partner, employee, advisor, consultant, or trustee for: Johnson & Johnson’s Panel for Compassionate Drug Use (unpaid position); serves as a contributing author and adviser for this news organization.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

Hi. I’m Art Caplan. I’m at the Division of Medical Ethics at the New York University Grossman School of Medicine in New York City.

I think we had a breakthrough on a very controversial subject over the past month. Over and over again, debates have been breaking out, cases have been going to court, and fights have been coming to ethics committees about brain death. How do we know what brain death is, how do we diagnose it, and what rights do families have with respect to the diagnosis?

The American Academy of Neurology decided to form a task force, and they just issued guidelines on the definition, tests to use it, and the rights of families. Whether you›re a neurologist, someone involved in actually diagnosing brain death, or you›re dealing with very ill people whose families are trying to direct the kinds of things that you or the nurses can do, these guidelines, I think, are excellent. They did a wonderful job, in my view. They›ve achieved clarity.

First, they tried to handle both adults and children. Children are, if you will, more difficult — and that’s been known — to test for brain death. Their brains are smaller. You get more interference and false signals coming from muscle or nerve activity that might be going on elsewhere in their bodies.

The guidelines say we’re going to try to see whether a person can breathe without support. If it’s an adult, one test over a 24-hour period would be sufficient. If you had them off the ventilator and they can’t breathe and show no signs of being able to do that, that’s a very fundamental test for brain death. For children, you’re going to have to do it twice. The guidelines are saying to be cautious.

Second, they say it’s very important to know the cause of the suspected brain death condition. If someone has a massive head injury, that’s different from a situation in which someone overdoses from drugs or drowns. Those conditions can be a little deceptive. In the case of drowning, sometimes the brain has protective mechanisms to protect circulation to the brain naturally for a little bit of time. I’m talking about minutes, not hours.

You want to be careful to make sure that you know the cause of the massive brain injury or insult that makes someone believe that the patient is brain-dead, whether it’s a stroke, an embolism, a bleed, a gunshot wound, or trauma to the head. Those factors really drive the certainty with which brain death should be pronounced. I think that’s very, very important.

They also said that brain death means the permanent loss of brain function. You may get a few cells still firing or you may be in a situation, because the life support is still there, where the body looks pink and perhaps might appear to still be alive to someone. When you know that the damage to the brain is so severe that there’s nothing that can be done to bring back the support of heart function, breathing, and most likely any ability to sense or feel anything, that is death.

I believe it’s very important, when talking to families, to say there are two ways that we pronounce people dead, and they’re equal: One is to say their heart has stopped, their breathing has stopped, and there’s nothing we can do to resuscitate them, which is cardiac death. The other is to say their brain has permanently ceased to function in any kind of integrated way. That means no heartbeat, no breathing, and no mental sensations. That is death.

In approaching families, it is critical that doctors and nurses don’t say, “Your relative is brain-dead.” That gives the family a sense that maybe they’re only “partially dead” or maybe there’s one key organ that has stopped working but maybe you can bring it back. Death is death. The law recognizes both cardiac death and brain death as death.

When you approach a family, if you believe that death has occurred, you say, “I’m very sorry. With regret, I have to tell you, your loved one is dead.” If they ask how you know, you can say, “We’ve determined it through brain death or through cardiac death.” You don’t give them a sense that people could be kind of dead, sort of dead, or nearly dead. Those states are comas or permanent vegetative states; they’re not the same as death.

What if the family says, “I don’t want you to do any testing. I don’t want to find out whether my relative is dead”? The American Academy of Neurology looked at this carefully and said that any test for death can be done without the permission or consent of the family. They said that because doctors need to know what steps to take to treat someone.

If a person is dead, then treatment is going to stop. It may not stop immediately. There may be issues about organ donation. There may be issues about gathering the family to come to the bedside to say goodbye, because many people think that’s more humane than saying goodbye at the morgue or in another setting.

This is all well and good, but patients cannot protect against bad news when it comes to death. We don’t want to be doing things to the dead that cost money or are futile because of death and using resources that might go to others.

We’ve got much more clarity than we have ever had with respect to the issue of brain death and how it works in any hospital. We have certain tests, including being off the ventilator and some other tests, that the guidelines supply. We know we have to be more careful with children. We want to know the etiology of the cause of the brain trauma, the devastating brain injury, to be sure that this is something that really is permanent cessation of integrated brain function.

We know that if you believe the person has died, you don’t need the consent of the family in order to do a brain-death test. You have to do it because there is no point in continuing treatment in expensive ICU settings and denying resources to others who might want to use those resources. The family can’t hold the medical team hostage.

We do know that when we approach someone with the determination, whatever it is, we should lead by saying that the person has died and then explain how that was determined, whether it be by cardiac death pronouncement — where you tried to resuscitate and the heart’s not beating — or brain-death analysis.

I’m Art Caplan at the Division of Medical Ethics at the NYU Grossman School of Medicine. Thanks for watching.

Dr. Caplan has disclosed the following relevant financial relationships: Served as a director, officer, partner, employee, advisor, consultant, or trustee for: Johnson & Johnson’s Panel for Compassionate Drug Use (unpaid position); serves as a contributing author and adviser for this news organization.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

Hi. I’m Art Caplan. I’m at the Division of Medical Ethics at the New York University Grossman School of Medicine in New York City.

I think we had a breakthrough on a very controversial subject over the past month. Over and over again, debates have been breaking out, cases have been going to court, and fights have been coming to ethics committees about brain death. How do we know what brain death is, how do we diagnose it, and what rights do families have with respect to the diagnosis?

The American Academy of Neurology decided to form a task force, and they just issued guidelines on the definition, tests to use it, and the rights of families. Whether you›re a neurologist, someone involved in actually diagnosing brain death, or you›re dealing with very ill people whose families are trying to direct the kinds of things that you or the nurses can do, these guidelines, I think, are excellent. They did a wonderful job, in my view. They›ve achieved clarity.

First, they tried to handle both adults and children. Children are, if you will, more difficult — and that’s been known — to test for brain death. Their brains are smaller. You get more interference and false signals coming from muscle or nerve activity that might be going on elsewhere in their bodies.

The guidelines say we’re going to try to see whether a person can breathe without support. If it’s an adult, one test over a 24-hour period would be sufficient. If you had them off the ventilator and they can’t breathe and show no signs of being able to do that, that’s a very fundamental test for brain death. For children, you’re going to have to do it twice. The guidelines are saying to be cautious.

Second, they say it’s very important to know the cause of the suspected brain death condition. If someone has a massive head injury, that’s different from a situation in which someone overdoses from drugs or drowns. Those conditions can be a little deceptive. In the case of drowning, sometimes the brain has protective mechanisms to protect circulation to the brain naturally for a little bit of time. I’m talking about minutes, not hours.

You want to be careful to make sure that you know the cause of the massive brain injury or insult that makes someone believe that the patient is brain-dead, whether it’s a stroke, an embolism, a bleed, a gunshot wound, or trauma to the head. Those factors really drive the certainty with which brain death should be pronounced. I think that’s very, very important.

They also said that brain death means the permanent loss of brain function. You may get a few cells still firing or you may be in a situation, because the life support is still there, where the body looks pink and perhaps might appear to still be alive to someone. When you know that the damage to the brain is so severe that there’s nothing that can be done to bring back the support of heart function, breathing, and most likely any ability to sense or feel anything, that is death.

I believe it’s very important, when talking to families, to say there are two ways that we pronounce people dead, and they’re equal: One is to say their heart has stopped, their breathing has stopped, and there’s nothing we can do to resuscitate them, which is cardiac death. The other is to say their brain has permanently ceased to function in any kind of integrated way. That means no heartbeat, no breathing, and no mental sensations. That is death.

In approaching families, it is critical that doctors and nurses don’t say, “Your relative is brain-dead.” That gives the family a sense that maybe they’re only “partially dead” or maybe there’s one key organ that has stopped working but maybe you can bring it back. Death is death. The law recognizes both cardiac death and brain death as death.

When you approach a family, if you believe that death has occurred, you say, “I’m very sorry. With regret, I have to tell you, your loved one is dead.” If they ask how you know, you can say, “We’ve determined it through brain death or through cardiac death.” You don’t give them a sense that people could be kind of dead, sort of dead, or nearly dead. Those states are comas or permanent vegetative states; they’re not the same as death.

What if the family says, “I don’t want you to do any testing. I don’t want to find out whether my relative is dead”? The American Academy of Neurology looked at this carefully and said that any test for death can be done without the permission or consent of the family. They said that because doctors need to know what steps to take to treat someone.

If a person is dead, then treatment is going to stop. It may not stop immediately. There may be issues about organ donation. There may be issues about gathering the family to come to the bedside to say goodbye, because many people think that’s more humane than saying goodbye at the morgue or in another setting.

This is all well and good, but patients cannot protect against bad news when it comes to death. We don’t want to be doing things to the dead that cost money or are futile because of death and using resources that might go to others.

We’ve got much more clarity than we have ever had with respect to the issue of brain death and how it works in any hospital. We have certain tests, including being off the ventilator and some other tests, that the guidelines supply. We know we have to be more careful with children. We want to know the etiology of the cause of the brain trauma, the devastating brain injury, to be sure that this is something that really is permanent cessation of integrated brain function.

We know that if you believe the person has died, you don’t need the consent of the family in order to do a brain-death test. You have to do it because there is no point in continuing treatment in expensive ICU settings and denying resources to others who might want to use those resources. The family can’t hold the medical team hostage.

We do know that when we approach someone with the determination, whatever it is, we should lead by saying that the person has died and then explain how that was determined, whether it be by cardiac death pronouncement — where you tried to resuscitate and the heart’s not beating — or brain-death analysis.

I’m Art Caplan at the Division of Medical Ethics at the NYU Grossman School of Medicine. Thanks for watching.

Dr. Caplan has disclosed the following relevant financial relationships: Served as a director, officer, partner, employee, advisor, consultant, or trustee for: Johnson & Johnson’s Panel for Compassionate Drug Use (unpaid position); serves as a contributing author and adviser for this news organization.

A version of this article appeared on Medscape.com.

Exposure to even moderate concentrations of radon is associated with a significant increase in stroke risk, new research suggests.

An analysis of radon exposures in more than 150,000 postmenopausal women in the Women’s Health Initiative revealed a 14% higher stroke risk in those exposed to the highest concentrations compared with those exposed to the lowest concentrations. Even moderate concentrations of radon were associated with a 6% higher stroke risk.

Radon is the second leading cause of lung cancer, but little was known about how exposure to the gas might affect stroke risk in women. 

“Our research found an increased risk of stroke among participants exposed to radon above — and as many as 2 picocuries per liter (pCi/L) below — concentrations that usually trigger Environmental Protection Agency recommendations to install a home radon mitigation system,” senior author Eric A. Whitsel, MD, MPH, professor of epidemiology and medicine, University of North Carolina, Chapel Hill, said in a news release.

The study was published online on January 31, 2024, in Neurology.

Women Particularly Affected

Radon is a naturally occurring odorless radioactive gas produced when uranium or radium break down in rocks and soil. Its presence is increasing as a result of climate change, and it is increasingly being found in people’s homes. When inhaled, this air pollutant releases ionizing radiation in the lungs and is seen as second only to smoking as an established cause of lung cancer.

The National Radon Action Plan of the US Environmental Protection Agency (EPA) lays out testing and mitigation guidelines based on the known role of radon in lung carcinogenesis. But radon testing and mitigation are less common than recommended, and the EPA’s action plan doesn’t cover diseases other than lung cancer.

Compared with men, women have a higher rate of stroke and, in the US, typically spend about 11% more hours per day indoors at home, which investigators note highlights a “potential role of the residential environment among other risk factors specific to women.”

Researchers examined longitudinal associations between home radon exposure and incident stroke in 158,910 women at baseline (mean age 63.2 years; 83% White) over a mean follow-up of 13.4 years. During this time, participants experienced a total of 6979 strokes.

Participants’ home addresses were linked to radon concentration data drawn from the US Geological Survey and the EPA, which recommends that average indoor radon concentrations not exceed 4 pCi/L. 

The highest radon exposure group resided in areas where average radon concentrations were < 4 pCi/L; the middle exposure group lived in regions with average concentrations of 2-4 pCi/L; and the lowest exposure group lived in areas with average concentrations < 2 pCi/L. 

The researchers adjusted for demographic, social, behavioral, and clinical characteristics.

Public Health Implications

The incidence rates of stroke per 100,000 women in the lowest, middle, and highest radon concentration areas were 333, 343, and 349, respectively.

Stroke risk was 6% higher among those in the middle exposure group (adjusted hazard ratio [aHR], 1.06; 95% CI, 0.99-1.13) and 14% higher in the highest exposure group (aHR, 1.14; 95% CI, 1.05-1.22) compared with the lowest exposure group.

Notably, stroke risk was significant even at concentrations ranging from 2 to 4 pCi/L (P = .0004) vs < 2 pCi/L, which is below the EPA›s Radon Action Level for mitigation. 

The findings remained robust in sensitivity analyses, although the associations were slightly stronger for ischemic stroke (especially cardioembolic, small-vessel occlusive, and very large artery atherosclerotic) compared with hemorrhagic stroke.

“Radon is an indoor air pollutant that can only be detected through testing that measures concentrations of the gas in homes,” Dr. Whitsel said in the release. “More studies are needed to confirm our findings. Confirmation would present an opportunity to improve public health by addressing an emerging risk factor for stroke.”

The study lacked gender and racial/ethnic diversity, so the findings may not be generalizable to other populations. 

“Replication studies of individual-level radon exposures are needed to confirm this positive radon-stroke association,” the authors write. “Confirmation would present a potential opportunity to affect public health by addressing a pervasive environmental risk factor for stroke and thereby merit reconsideration of extant radon policy.”

The study was funded by the National Institute of Environmental Health Sciences and National Heart, Lung, and Blood Institute. Dr. Whitsel and coauthors report no relevant financial relationships.

A version of this article appeared on Medscape.com.

Exposure to even moderate concentrations of radon is associated with a significant increase in stroke risk, new research suggests.

An analysis of radon exposures in more than 150,000 postmenopausal women in the Women’s Health Initiative revealed a 14% higher stroke risk in those exposed to the highest concentrations compared with those exposed to the lowest concentrations. Even moderate concentrations of radon were associated with a 6% higher stroke risk.

Radon is the second leading cause of lung cancer, but little was known about how exposure to the gas might affect stroke risk in women. 

“Our research found an increased risk of stroke among participants exposed to radon above — and as many as 2 picocuries per liter (pCi/L) below — concentrations that usually trigger Environmental Protection Agency recommendations to install a home radon mitigation system,” senior author Eric A. Whitsel, MD, MPH, professor of epidemiology and medicine, University of North Carolina, Chapel Hill, said in a news release.

The study was published online on January 31, 2024, in Neurology.

Women Particularly Affected

Radon is a naturally occurring odorless radioactive gas produced when uranium or radium break down in rocks and soil. Its presence is increasing as a result of climate change, and it is increasingly being found in people’s homes. When inhaled, this air pollutant releases ionizing radiation in the lungs and is seen as second only to smoking as an established cause of lung cancer.

The National Radon Action Plan of the US Environmental Protection Agency (EPA) lays out testing and mitigation guidelines based on the known role of radon in lung carcinogenesis. But radon testing and mitigation are less common than recommended, and the EPA’s action plan doesn’t cover diseases other than lung cancer.

Compared with men, women have a higher rate of stroke and, in the US, typically spend about 11% more hours per day indoors at home, which investigators note highlights a “potential role of the residential environment among other risk factors specific to women.”

Researchers examined longitudinal associations between home radon exposure and incident stroke in 158,910 women at baseline (mean age 63.2 years; 83% White) over a mean follow-up of 13.4 years. During this time, participants experienced a total of 6979 strokes.

Participants’ home addresses were linked to radon concentration data drawn from the US Geological Survey and the EPA, which recommends that average indoor radon concentrations not exceed 4 pCi/L. 

The highest radon exposure group resided in areas where average radon concentrations were < 4 pCi/L; the middle exposure group lived in regions with average concentrations of 2-4 pCi/L; and the lowest exposure group lived in areas with average concentrations < 2 pCi/L. 

The researchers adjusted for demographic, social, behavioral, and clinical characteristics.

Public Health Implications

The incidence rates of stroke per 100,000 women in the lowest, middle, and highest radon concentration areas were 333, 343, and 349, respectively.

Stroke risk was 6% higher among those in the middle exposure group (adjusted hazard ratio [aHR], 1.06; 95% CI, 0.99-1.13) and 14% higher in the highest exposure group (aHR, 1.14; 95% CI, 1.05-1.22) compared with the lowest exposure group.

Notably, stroke risk was significant even at concentrations ranging from 2 to 4 pCi/L (P = .0004) vs < 2 pCi/L, which is below the EPA›s Radon Action Level for mitigation. 

The findings remained robust in sensitivity analyses, although the associations were slightly stronger for ischemic stroke (especially cardioembolic, small-vessel occlusive, and very large artery atherosclerotic) compared with hemorrhagic stroke.

“Radon is an indoor air pollutant that can only be detected through testing that measures concentrations of the gas in homes,” Dr. Whitsel said in the release. “More studies are needed to confirm our findings. Confirmation would present an opportunity to improve public health by addressing an emerging risk factor for stroke.”

The study lacked gender and racial/ethnic diversity, so the findings may not be generalizable to other populations. 

“Replication studies of individual-level radon exposures are needed to confirm this positive radon-stroke association,” the authors write. “Confirmation would present a potential opportunity to affect public health by addressing a pervasive environmental risk factor for stroke and thereby merit reconsideration of extant radon policy.”

The study was funded by the National Institute of Environmental Health Sciences and National Heart, Lung, and Blood Institute. Dr. Whitsel and coauthors report no relevant financial relationships.

A version of this article appeared on Medscape.com.

Exposure to even moderate concentrations of radon is associated with a significant increase in stroke risk, new research suggests.

An analysis of radon exposures in more than 150,000 postmenopausal women in the Women’s Health Initiative revealed a 14% higher stroke risk in those exposed to the highest concentrations compared with those exposed to the lowest concentrations. Even moderate concentrations of radon were associated with a 6% higher stroke risk.

Radon is the second leading cause of lung cancer, but little was known about how exposure to the gas might affect stroke risk in women. 

“Our research found an increased risk of stroke among participants exposed to radon above — and as many as 2 picocuries per liter (pCi/L) below — concentrations that usually trigger Environmental Protection Agency recommendations to install a home radon mitigation system,” senior author Eric A. Whitsel, MD, MPH, professor of epidemiology and medicine, University of North Carolina, Chapel Hill, said in a news release.

The study was published online on January 31, 2024, in Neurology.

Women Particularly Affected

Radon is a naturally occurring odorless radioactive gas produced when uranium or radium break down in rocks and soil. Its presence is increasing as a result of climate change, and it is increasingly being found in people’s homes. When inhaled, this air pollutant releases ionizing radiation in the lungs and is seen as second only to smoking as an established cause of lung cancer.

The National Radon Action Plan of the US Environmental Protection Agency (EPA) lays out testing and mitigation guidelines based on the known role of radon in lung carcinogenesis. But radon testing and mitigation are less common than recommended, and the EPA’s action plan doesn’t cover diseases other than lung cancer.

Compared with men, women have a higher rate of stroke and, in the US, typically spend about 11% more hours per day indoors at home, which investigators note highlights a “potential role of the residential environment among other risk factors specific to women.”

Researchers examined longitudinal associations between home radon exposure and incident stroke in 158,910 women at baseline (mean age 63.2 years; 83% White) over a mean follow-up of 13.4 years. During this time, participants experienced a total of 6979 strokes.

Participants’ home addresses were linked to radon concentration data drawn from the US Geological Survey and the EPA, which recommends that average indoor radon concentrations not exceed 4 pCi/L. 

The highest radon exposure group resided in areas where average radon concentrations were < 4 pCi/L; the middle exposure group lived in regions with average concentrations of 2-4 pCi/L; and the lowest exposure group lived in areas with average concentrations < 2 pCi/L. 

The researchers adjusted for demographic, social, behavioral, and clinical characteristics.

Public Health Implications

The incidence rates of stroke per 100,000 women in the lowest, middle, and highest radon concentration areas were 333, 343, and 349, respectively.

Stroke risk was 6% higher among those in the middle exposure group (adjusted hazard ratio [aHR], 1.06; 95% CI, 0.99-1.13) and 14% higher in the highest exposure group (aHR, 1.14; 95% CI, 1.05-1.22) compared with the lowest exposure group.

Notably, stroke risk was significant even at concentrations ranging from 2 to 4 pCi/L (P = .0004) vs < 2 pCi/L, which is below the EPA›s Radon Action Level for mitigation. 

The findings remained robust in sensitivity analyses, although the associations were slightly stronger for ischemic stroke (especially cardioembolic, small-vessel occlusive, and very large artery atherosclerotic) compared with hemorrhagic stroke.

“Radon is an indoor air pollutant that can only be detected through testing that measures concentrations of the gas in homes,” Dr. Whitsel said in the release. “More studies are needed to confirm our findings. Confirmation would present an opportunity to improve public health by addressing an emerging risk factor for stroke.”

The study lacked gender and racial/ethnic diversity, so the findings may not be generalizable to other populations. 

“Replication studies of individual-level radon exposures are needed to confirm this positive radon-stroke association,” the authors write. “Confirmation would present a potential opportunity to affect public health by addressing a pervasive environmental risk factor for stroke and thereby merit reconsideration of extant radon policy.”

The study was funded by the National Institute of Environmental Health Sciences and National Heart, Lung, and Blood Institute. Dr. Whitsel and coauthors report no relevant financial relationships.

A version of this article appeared on Medscape.com.

If someone has been in cardiac arrest for 10 minutes, the brain is permanently damaged and there’s nothing to do, right?

Not so according to emerging evidence that suggests that the brain shows signs of electrical recovery for as long as an hour into ongoing cardiopulmonary resuscitation (CPR). This time between cardiac arrest and awakening can be a period of vivid experiences for the dying patient before they return to life — a phenomenon known as “recalled death.”

This should be an impetus to increase the use of devices that measure the quality of CPR and to find new treatments to restart the heart or prevent brain injury, experts advised. Cardiologists and critical care clinicians are among those who will need to manage patients in the aftermath.

“If people who go into cardiac arrest receive good quality chest compressions that restore blood flow to the brain, then consciousness is restored, as well, said Jasmeet Soar, MD, consultant in Anesthetics & Intensive Care Medicine, North Bristol NHS Trust, Bristol, England, and an editor of the journal Resuscitation.

“We know that because if chest compressions are stopped, the person becomes unconscious again,” he said. “This CPR-induced consciousness has become more common when professionals do the CPR because resuscitation guidelines now place a much bigger focus on high-quality CPR — ‘push hard, push fast.’ ” 

“People are giving up too soon on trying to revive individuals, and they should be trying more modern strategies, such as extracorporeal membrane oxygenation,” said Sam Parnia, MD, PhD, associate professor in the Department of Medicine at NYU Langone Health and director of critical care and resuscitation research at NYU Langone, New York City.

Brain Activity, Heightened Experiences

Two types of brain activity may occur when CPR works. The first, called CPR-induced consciousness, is when an individual recovers consciousness while in cardiac arrest. Signs of consciousness include combativeness, groaning, and eye-opening, Soar explained.

The second type is a perception of lucidity with recall of events, he said. “Patients who experience this may form memories that they can recall. We’re not sure whether that happens during CPR or while the patient is waking up during intensive care, or how the brain creates these memories, or if they’re real memories or coincidental, but it’s clear the brain does form them during the dying and recovery process.”

This latter phenomenon was explored in detail in a recent study led by Dr. Parnia.

In that study of 567 in-hospital patients with cardiac arrest from 25 centers in the United States and United Kingdom, 53 survived, 28 of those survivors were interviewed, and 11 reported memories or perceptions suggestive of consciousness.

Four types of experiences occurred:

• Recalled experiences of death: “I thought I heard my grandma [who had passed] saying ‘you need to go back.’”
• Emergence from coma during CPR/CPR-induced consciousness: “I remember when I came back and they were putting those two electrodes to my chest, and I remember the shock.”
• Emergence from coma in the post-resuscitation period: “I heard my partner saying [patient’s name] and my son saying ‘mom.’”
• Dreams and dream-like experiences: “[I] felt as though someone was holding my hand. It was very black; I couldn’t see anything.”

In a complementary cross-sectional study, 126 community cardiac arrest survivors reported similar experiences plus a fifth type, “delusions,” or “misattribution of medical events,” for example, “I heard my name, over and over again. All around me were things like demons and monsters. It felt like they were trying to tear off my body parts.”

“Many people label recalled experiences of death as ‘near-death’ experiences, but they’re not,” Dr. Parnia said. “Medically speaking, being near to death means your heart is about to stop. But the whole point is that these people are not near death. They actually died and came back from it.”

One of the big implications of the study, he said, is that “a lot of physicians are taught that somehow after, say, 3-5 minutes of oxygen deprivation, the brain dies. Our study showed this is not true. It showed that the brain may not be functioning, which is why they flatline. But if you’re able to resuscitate them appropriately, you can restore activity up to an hour later.”

Because some clinicians questioned or dismissed previous work in this area by Dr. Parnia and others, the latest study used EEG monitoring in a subset of 53 patients. Among those with evaluable EEG data, brain activity returned to normal or near-normal after flatlining in about 40% of images; spikes were seen in the delta (22%), theta (12%), alpha (6%), and beta (1%) waves associated with higher mental function.

“The team recorded what was happening in the brain during real-time CPR using various tests of consciousness, including EEG measurements and tests of visual and auditory awareness using a tablet with a special app and a Bluetooth headphone.”

“Incredibly, we found that even though the brain flatlines, which is what we expect when the heart stops, with professionally given CPR even up to about an hour after this, the brainwaves changed into normal to near-normal patterns,” Dr. Parnia said. “We were able to identify these brain waves in patients while they were being resuscitated, which confirms the fact that people can have lucid consciousness even though they appear to be unconscious.”

Asked what implications, if any, his work has for current definitions of brain death and cardiac death, Dr. Parnia said that the problem is that these are based on the concept of “a permanent irreversible loss of function,” but “that’s only relative to what medical treatments are developed at a given time.”

Potential Mechanism

Dr. Parnia and his team proposed a potential mechanism for recalled experiences of death. Essentially, when the brain flatlines, the dying brain removes natural inhibitory (braking) systems that are needed to support daily functioning. This disinhibition may open access to “new dimensions of reality, including lucid recall of stored memories from early childhood to death,” he said.

From a clinical perspective, he noted, “although the brain stops working when it flatlines, it does not die within 5 or 10 minutes of oxygen deprivation.”

This is contrary to what many doctors believe, and because of that, he said, “nobody has tried to find treatments or new ways to restart the heart or prevent brain injury. They think it’s futile. So, with this work, we’ve opened up the window to developing cocktails of drugs that could be given to patients who have technically gone through death to bring them back to life again.”

Probe Patients or Leave Well Enough Alone?

The findings have ramifications for clinicians who may be caring for patients who survive cardiac arrest, said Lance B. Becker, MD, professor and chair, Department of Emergency Medicine, Donald & Barbara Zucker School of Medicine at Hofstra/Northwell, Manhasset, New York, and chair, Department of Emergency Medicine at North Shore University Hospital, Manhasset, and Long Island Jewish Medical Center, Queens, New York.

“I’ve talked with a lot of patients who have had some kind of recalled experience around cardiac arrest and some who have had zero recall, as well, like in the paper,” he told this news organization. “The ones who do have an experience are sometimes mystified by it and have questions. And very often, clinicians don’t want to listen, don’t think it’s important, and downplay it.”

“I think it is important, and when people have important things happen to them, it’s really imperative that doctors listen, learn, and respond,” he said. “When I started in this field a long time ago, there were so few survivors that there wasn’t even a concept of survivorship,” he said.

Dr. Becker noted that it’s not uncommon for cardiac arrest survivors to have depression, problems with executive function, or a small brain injury they need to recover from. “Now survivorship organizations are springing up that these people can turn to, but clinicians still need to become more aware and sensitive to this.”

Not all are. “I had a number of patients who said I was the only doctor who ever asked them about what they experienced,” he recalled. “I was a young doctor at the time and didn’t exactly know what to say to them, but they were just happy to have a doctor who would listen to them and not be afraid to hear what they had to say.”

Recognizing that support is an issue, the American Heart Association released a scientific statement in 2020 on sudden cardiac arrest survivorship, which “expands the cardiac arrest resuscitation system of care to include patients, caregivers, and rehabilitative healthcare partnerships, which are central to cardiac survivorship.”

Soar has a more nuanced view of survivorship support, however. “I suspect some people are very glad to be alive, and that trying to dig deep and bring things out may actually be harmful,” he said. “It’s not as clear cut as everybody thinks.”

He noted that follow-up and rehabilitation should be an option for people who specifically need it who would need to be identified. “But human beings are resilient, and while some people will require help, not everybody will,” he said.

Better CPR, New Treatments

Experts in emergency and intensive care medicine studying survival after cardiac arrest hope to find ways to save patients before too much damage is done to the brain and other organs from loss of oxygen, Dr. Parnia said. He is the lead author in a recent multidisciplinary consensus statement on guidelines and standards for the study of death and recalled experiences of death.

“One of my bugbears is that our survival outcomes from cardiac arrest resuscitation have not changed very much for 60 years because we haven’t developed new treatments and innovative methods,” he said. “Unlike the rest of medicine, we’re living in the past.”

Currently, his team is developing cocktails of treatments. These include hypothermic circulatory arrest — cooling the body to stop blood circulation and brain function for up to 40 minutes — and giving magnesium, a brain-protective treatment, to people whose hearts stop.

Dr. Becker would like to see optimal care of patients with cardiac arrest. “The first step is to increase blood flow with good CPR and then measure whether CPR is working,” he said. Adding that despite the availability of devices that provide feedback on the quality of CPR, they’re rarely used. He cited ultrasound devices that measure the blood flow generated during CPR, compression meter devices that go between the patient’s chest and the rescuer’s hands that gauge the rate and depth of compression, and invasive devices that measure blood pressure during CPR.

His group is trying to design even better devices, he said. “An example would be a little probe that you could pop on the neck that would study blood flow to the brain with ultrasound, so that while you were pumping on the person, you could see if you’re making them better or not.”

“We also have some preliminary data showing that the American Heart Association recommended position on the chest for doing CPR is not the perfect place for everybody,” he said. The 2020 AHA guidelines recommended the center of the lower half of the sternum. At the 2023 American College of Emergency Physicians meeting, Dr. Becker›s team at Hofstra/Northwell presented data on 175 video-recorded adult cardiac arrests in their emergency department over more than 2 years, 22 of which involved at least one change of compression location (for a total of 29 location changes). They found that 41% of compression location changes were associated with return of spontaneous circulation.

For about a third of people, the hands need to be repositioned slightly. “This is not anything that is taught to the public because you can only figure it out if you have some kind of sensor that will let you know how you’re doing. That’s very achievable. We could have that in the future on every ambulance and even in people’s homes.”

When the person arrives at the hospital, he said, “we can make it easier and more likely that they can be put on extracorporeal membrane oxygenation (ECMO). We do that on selected patients in our hospital, even though it’s very difficult to do, because we know that when it’s done properly, it can change survival rates dramatically, from maybe 10%-50%.”

Dr. Dr. Becker, like Dr. Parnia, also favors the development of drug cocktails, and his team has been experimenting with various combinations in animal models. “We think those two things together — ECMO and a drug cocktail — would be a very powerful one to two knock out for cardiac arrest,” he said. “We have a long way to go — 10 or 20 years. But most people around the world working in this area believe that will be the future.”

Dr. Parnia’s study on recalled death was supported by The John Templeton Foundation, Resuscitation Council (UK), and New York University Grossman School of Medicine, with research support staff provided by the UK’s National Institutes for Health Research. Soar is the editor of the journal Resuscitation and receives payment from the publisher Elsevier. Dr. Becker’s institute has received grants from Philips Medical Systems, NIH, Zoll Medical Corp, Nihon Kohden, PCORI, BrainCool, and United Therapeutics. He has received advisory/consultancy honoraria from NIH, Nihon Kohden, HP, and Philips, and he holds several patents in hypothermia induction and reperfusion therapies and several pending patents involving the use of medical slurries as human coolant devices to create reperfusion cocktails and measurement of respiratory quotient.

A version of this article appeared on Medscape.com.

If someone has been in cardiac arrest for 10 minutes, the brain is permanently damaged and there’s nothing to do, right?

Not so according to emerging evidence that suggests that the brain shows signs of electrical recovery for as long as an hour into ongoing cardiopulmonary resuscitation (CPR). This time between cardiac arrest and awakening can be a period of vivid experiences for the dying patient before they return to life — a phenomenon known as “recalled death.”

This should be an impetus to increase the use of devices that measure the quality of CPR and to find new treatments to restart the heart or prevent brain injury, experts advised. Cardiologists and critical care clinicians are among those who will need to manage patients in the aftermath.

“If people who go into cardiac arrest receive good quality chest compressions that restore blood flow to the brain, then consciousness is restored, as well, said Jasmeet Soar, MD, consultant in Anesthetics & Intensive Care Medicine, North Bristol NHS Trust, Bristol, England, and an editor of the journal Resuscitation.

“We know that because if chest compressions are stopped, the person becomes unconscious again,” he said. “This CPR-induced consciousness has become more common when professionals do the CPR because resuscitation guidelines now place a much bigger focus on high-quality CPR — ‘push hard, push fast.’ ” 

“People are giving up too soon on trying to revive individuals, and they should be trying more modern strategies, such as extracorporeal membrane oxygenation,” said Sam Parnia, MD, PhD, associate professor in the Department of Medicine at NYU Langone Health and director of critical care and resuscitation research at NYU Langone, New York City.

Brain Activity, Heightened Experiences

Two types of brain activity may occur when CPR works. The first, called CPR-induced consciousness, is when an individual recovers consciousness while in cardiac arrest. Signs of consciousness include combativeness, groaning, and eye-opening, Soar explained.

The second type is a perception of lucidity with recall of events, he said. “Patients who experience this may form memories that they can recall. We’re not sure whether that happens during CPR or while the patient is waking up during intensive care, or how the brain creates these memories, or if they’re real memories or coincidental, but it’s clear the brain does form them during the dying and recovery process.”

This latter phenomenon was explored in detail in a recent study led by Dr. Parnia.

In that study of 567 in-hospital patients with cardiac arrest from 25 centers in the United States and United Kingdom, 53 survived, 28 of those survivors were interviewed, and 11 reported memories or perceptions suggestive of consciousness.

Four types of experiences occurred:

• Recalled experiences of death: “I thought I heard my grandma [who had passed] saying ‘you need to go back.’”
• Emergence from coma during CPR/CPR-induced consciousness: “I remember when I came back and they were putting those two electrodes to my chest, and I remember the shock.”
• Emergence from coma in the post-resuscitation period: “I heard my partner saying [patient’s name] and my son saying ‘mom.’”
• Dreams and dream-like experiences: “[I] felt as though someone was holding my hand. It was very black; I couldn’t see anything.”

In a complementary cross-sectional study, 126 community cardiac arrest survivors reported similar experiences plus a fifth type, “delusions,” or “misattribution of medical events,” for example, “I heard my name, over and over again. All around me were things like demons and monsters. It felt like they were trying to tear off my body parts.”

“Many people label recalled experiences of death as ‘near-death’ experiences, but they’re not,” Dr. Parnia said. “Medically speaking, being near to death means your heart is about to stop. But the whole point is that these people are not near death. They actually died and came back from it.”

One of the big implications of the study, he said, is that “a lot of physicians are taught that somehow after, say, 3-5 minutes of oxygen deprivation, the brain dies. Our study showed this is not true. It showed that the brain may not be functioning, which is why they flatline. But if you’re able to resuscitate them appropriately, you can restore activity up to an hour later.”

Because some clinicians questioned or dismissed previous work in this area by Dr. Parnia and others, the latest study used EEG monitoring in a subset of 53 patients. Among those with evaluable EEG data, brain activity returned to normal or near-normal after flatlining in about 40% of images; spikes were seen in the delta (22%), theta (12%), alpha (6%), and beta (1%) waves associated with higher mental function.

“The team recorded what was happening in the brain during real-time CPR using various tests of consciousness, including EEG measurements and tests of visual and auditory awareness using a tablet with a special app and a Bluetooth headphone.”

“Incredibly, we found that even though the brain flatlines, which is what we expect when the heart stops, with professionally given CPR even up to about an hour after this, the brainwaves changed into normal to near-normal patterns,” Dr. Parnia said. “We were able to identify these brain waves in patients while they were being resuscitated, which confirms the fact that people can have lucid consciousness even though they appear to be unconscious.”

Asked what implications, if any, his work has for current definitions of brain death and cardiac death, Dr. Parnia said that the problem is that these are based on the concept of “a permanent irreversible loss of function,” but “that’s only relative to what medical treatments are developed at a given time.”

Potential Mechanism

Dr. Parnia and his team proposed a potential mechanism for recalled experiences of death. Essentially, when the brain flatlines, the dying brain removes natural inhibitory (braking) systems that are needed to support daily functioning. This disinhibition may open access to “new dimensions of reality, including lucid recall of stored memories from early childhood to death,” he said.

From a clinical perspective, he noted, “although the brain stops working when it flatlines, it does not die within 5 or 10 minutes of oxygen deprivation.”

This is contrary to what many doctors believe, and because of that, he said, “nobody has tried to find treatments or new ways to restart the heart or prevent brain injury. They think it’s futile. So, with this work, we’ve opened up the window to developing cocktails of drugs that could be given to patients who have technically gone through death to bring them back to life again.”

Probe Patients or Leave Well Enough Alone?

The findings have ramifications for clinicians who may be caring for patients who survive cardiac arrest, said Lance B. Becker, MD, professor and chair, Department of Emergency Medicine, Donald & Barbara Zucker School of Medicine at Hofstra/Northwell, Manhasset, New York, and chair, Department of Emergency Medicine at North Shore University Hospital, Manhasset, and Long Island Jewish Medical Center, Queens, New York.

“I’ve talked with a lot of patients who have had some kind of recalled experience around cardiac arrest and some who have had zero recall, as well, like in the paper,” he told this news organization. “The ones who do have an experience are sometimes mystified by it and have questions. And very often, clinicians don’t want to listen, don’t think it’s important, and downplay it.”

“I think it is important, and when people have important things happen to them, it’s really imperative that doctors listen, learn, and respond,” he said. “When I started in this field a long time ago, there were so few survivors that there wasn’t even a concept of survivorship,” he said.

Dr. Becker noted that it’s not uncommon for cardiac arrest survivors to have depression, problems with executive function, or a small brain injury they need to recover from. “Now survivorship organizations are springing up that these people can turn to, but clinicians still need to become more aware and sensitive to this.”

Not all are. “I had a number of patients who said I was the only doctor who ever asked them about what they experienced,” he recalled. “I was a young doctor at the time and didn’t exactly know what to say to them, but they were just happy to have a doctor who would listen to them and not be afraid to hear what they had to say.”

Recognizing that support is an issue, the American Heart Association released a scientific statement in 2020 on sudden cardiac arrest survivorship, which “expands the cardiac arrest resuscitation system of care to include patients, caregivers, and rehabilitative healthcare partnerships, which are central to cardiac survivorship.”

Soar has a more nuanced view of survivorship support, however. “I suspect some people are very glad to be alive, and that trying to dig deep and bring things out may actually be harmful,” he said. “It’s not as clear cut as everybody thinks.”

He noted that follow-up and rehabilitation should be an option for people who specifically need it who would need to be identified. “But human beings are resilient, and while some people will require help, not everybody will,” he said.

Better CPR, New Treatments

Experts in emergency and intensive care medicine studying survival after cardiac arrest hope to find ways to save patients before too much damage is done to the brain and other organs from loss of oxygen, Dr. Parnia said. He is the lead author in a recent multidisciplinary consensus statement on guidelines and standards for the study of death and recalled experiences of death.

“One of my bugbears is that our survival outcomes from cardiac arrest resuscitation have not changed very much for 60 years because we haven’t developed new treatments and innovative methods,” he said. “Unlike the rest of medicine, we’re living in the past.”

Currently, his team is developing cocktails of treatments. These include hypothermic circulatory arrest — cooling the body to stop blood circulation and brain function for up to 40 minutes — and giving magnesium, a brain-protective treatment, to people whose hearts stop.

Dr. Becker would like to see optimal care of patients with cardiac arrest. “The first step is to increase blood flow with good CPR and then measure whether CPR is working,” he said. Adding that despite the availability of devices that provide feedback on the quality of CPR, they’re rarely used. He cited ultrasound devices that measure the blood flow generated during CPR, compression meter devices that go between the patient’s chest and the rescuer’s hands that gauge the rate and depth of compression, and invasive devices that measure blood pressure during CPR.

His group is trying to design even better devices, he said. “An example would be a little probe that you could pop on the neck that would study blood flow to the brain with ultrasound, so that while you were pumping on the person, you could see if you’re making them better or not.”

“We also have some preliminary data showing that the American Heart Association recommended position on the chest for doing CPR is not the perfect place for everybody,” he said. The 2020 AHA guidelines recommended the center of the lower half of the sternum. At the 2023 American College of Emergency Physicians meeting, Dr. Becker›s team at Hofstra/Northwell presented data on 175 video-recorded adult cardiac arrests in their emergency department over more than 2 years, 22 of which involved at least one change of compression location (for a total of 29 location changes). They found that 41% of compression location changes were associated with return of spontaneous circulation.

For about a third of people, the hands need to be repositioned slightly. “This is not anything that is taught to the public because you can only figure it out if you have some kind of sensor that will let you know how you’re doing. That’s very achievable. We could have that in the future on every ambulance and even in people’s homes.”

When the person arrives at the hospital, he said, “we can make it easier and more likely that they can be put on extracorporeal membrane oxygenation (ECMO). We do that on selected patients in our hospital, even though it’s very difficult to do, because we know that when it’s done properly, it can change survival rates dramatically, from maybe 10%-50%.”

Dr. Dr. Becker, like Dr. Parnia, also favors the development of drug cocktails, and his team has been experimenting with various combinations in animal models. “We think those two things together — ECMO and a drug cocktail — would be a very powerful one to two knock out for cardiac arrest,” he said. “We have a long way to go — 10 or 20 years. But most people around the world working in this area believe that will be the future.”

Dr. Parnia’s study on recalled death was supported by The John Templeton Foundation, Resuscitation Council (UK), and New York University Grossman School of Medicine, with research support staff provided by the UK’s National Institutes for Health Research. Soar is the editor of the journal Resuscitation and receives payment from the publisher Elsevier. Dr. Becker’s institute has received grants from Philips Medical Systems, NIH, Zoll Medical Corp, Nihon Kohden, PCORI, BrainCool, and United Therapeutics. He has received advisory/consultancy honoraria from NIH, Nihon Kohden, HP, and Philips, and he holds several patents in hypothermia induction and reperfusion therapies and several pending patents involving the use of medical slurries as human coolant devices to create reperfusion cocktails and measurement of respiratory quotient.

A version of this article appeared on Medscape.com.

If someone has been in cardiac arrest for 10 minutes, the brain is permanently damaged and there’s nothing to do, right?

Not so according to emerging evidence that suggests that the brain shows signs of electrical recovery for as long as an hour into ongoing cardiopulmonary resuscitation (CPR). This time between cardiac arrest and awakening can be a period of vivid experiences for the dying patient before they return to life — a phenomenon known as “recalled death.”

This should be an impetus to increase the use of devices that measure the quality of CPR and to find new treatments to restart the heart or prevent brain injury, experts advised. Cardiologists and critical care clinicians are among those who will need to manage patients in the aftermath.

“If people who go into cardiac arrest receive good quality chest compressions that restore blood flow to the brain, then consciousness is restored, as well, said Jasmeet Soar, MD, consultant in Anesthetics & Intensive Care Medicine, North Bristol NHS Trust, Bristol, England, and an editor of the journal Resuscitation.

“We know that because if chest compressions are stopped, the person becomes unconscious again,” he said. “This CPR-induced consciousness has become more common when professionals do the CPR because resuscitation guidelines now place a much bigger focus on high-quality CPR — ‘push hard, push fast.’ ” 

“People are giving up too soon on trying to revive individuals, and they should be trying more modern strategies, such as extracorporeal membrane oxygenation,” said Sam Parnia, MD, PhD, associate professor in the Department of Medicine at NYU Langone Health and director of critical care and resuscitation research at NYU Langone, New York City.

Brain Activity, Heightened Experiences

Two types of brain activity may occur when CPR works. The first, called CPR-induced consciousness, is when an individual recovers consciousness while in cardiac arrest. Signs of consciousness include combativeness, groaning, and eye-opening, Soar explained.

The second type is a perception of lucidity with recall of events, he said. “Patients who experience this may form memories that they can recall. We’re not sure whether that happens during CPR or while the patient is waking up during intensive care, or how the brain creates these memories, or if they’re real memories or coincidental, but it’s clear the brain does form them during the dying and recovery process.”

This latter phenomenon was explored in detail in a recent study led by Dr. Parnia.

In that study of 567 in-hospital patients with cardiac arrest from 25 centers in the United States and United Kingdom, 53 survived, 28 of those survivors were interviewed, and 11 reported memories or perceptions suggestive of consciousness.

Four types of experiences occurred:

• Recalled experiences of death: “I thought I heard my grandma [who had passed] saying ‘you need to go back.’”
• Emergence from coma during CPR/CPR-induced consciousness: “I remember when I came back and they were putting those two electrodes to my chest, and I remember the shock.”
• Emergence from coma in the post-resuscitation period: “I heard my partner saying [patient’s name] and my son saying ‘mom.’”
• Dreams and dream-like experiences: “[I] felt as though someone was holding my hand. It was very black; I couldn’t see anything.”

In a complementary cross-sectional study, 126 community cardiac arrest survivors reported similar experiences plus a fifth type, “delusions,” or “misattribution of medical events,” for example, “I heard my name, over and over again. All around me were things like demons and monsters. It felt like they were trying to tear off my body parts.”

“Many people label recalled experiences of death as ‘near-death’ experiences, but they’re not,” Dr. Parnia said. “Medically speaking, being near to death means your heart is about to stop. But the whole point is that these people are not near death. They actually died and came back from it.”

One of the big implications of the study, he said, is that “a lot of physicians are taught that somehow after, say, 3-5 minutes of oxygen deprivation, the brain dies. Our study showed this is not true. It showed that the brain may not be functioning, which is why they flatline. But if you’re able to resuscitate them appropriately, you can restore activity up to an hour later.”

Because some clinicians questioned or dismissed previous work in this area by Dr. Parnia and others, the latest study used EEG monitoring in a subset of 53 patients. Among those with evaluable EEG data, brain activity returned to normal or near-normal after flatlining in about 40% of images; spikes were seen in the delta (22%), theta (12%), alpha (6%), and beta (1%) waves associated with higher mental function.

“The team recorded what was happening in the brain during real-time CPR using various tests of consciousness, including EEG measurements and tests of visual and auditory awareness using a tablet with a special app and a Bluetooth headphone.”

“Incredibly, we found that even though the brain flatlines, which is what we expect when the heart stops, with professionally given CPR even up to about an hour after this, the brainwaves changed into normal to near-normal patterns,” Dr. Parnia said. “We were able to identify these brain waves in patients while they were being resuscitated, which confirms the fact that people can have lucid consciousness even though they appear to be unconscious.”

Asked what implications, if any, his work has for current definitions of brain death and cardiac death, Dr. Parnia said that the problem is that these are based on the concept of “a permanent irreversible loss of function,” but “that’s only relative to what medical treatments are developed at a given time.”

Potential Mechanism

Dr. Parnia and his team proposed a potential mechanism for recalled experiences of death. Essentially, when the brain flatlines, the dying brain removes natural inhibitory (braking) systems that are needed to support daily functioning. This disinhibition may open access to “new dimensions of reality, including lucid recall of stored memories from early childhood to death,” he said.

From a clinical perspective, he noted, “although the brain stops working when it flatlines, it does not die within 5 or 10 minutes of oxygen deprivation.”

This is contrary to what many doctors believe, and because of that, he said, “nobody has tried to find treatments or new ways to restart the heart or prevent brain injury. They think it’s futile. So, with this work, we’ve opened up the window to developing cocktails of drugs that could be given to patients who have technically gone through death to bring them back to life again.”

Probe Patients or Leave Well Enough Alone?

The findings have ramifications for clinicians who may be caring for patients who survive cardiac arrest, said Lance B. Becker, MD, professor and chair, Department of Emergency Medicine, Donald & Barbara Zucker School of Medicine at Hofstra/Northwell, Manhasset, New York, and chair, Department of Emergency Medicine at North Shore University Hospital, Manhasset, and Long Island Jewish Medical Center, Queens, New York.

“I’ve talked with a lot of patients who have had some kind of recalled experience around cardiac arrest and some who have had zero recall, as well, like in the paper,” he told this news organization. “The ones who do have an experience are sometimes mystified by it and have questions. And very often, clinicians don’t want to listen, don’t think it’s important, and downplay it.”

“I think it is important, and when people have important things happen to them, it’s really imperative that doctors listen, learn, and respond,” he said. “When I started in this field a long time ago, there were so few survivors that there wasn’t even a concept of survivorship,” he said.

Dr. Becker noted that it’s not uncommon for cardiac arrest survivors to have depression, problems with executive function, or a small brain injury they need to recover from. “Now survivorship organizations are springing up that these people can turn to, but clinicians still need to become more aware and sensitive to this.”

Not all are. “I had a number of patients who said I was the only doctor who ever asked them about what they experienced,” he recalled. “I was a young doctor at the time and didn’t exactly know what to say to them, but they were just happy to have a doctor who would listen to them and not be afraid to hear what they had to say.”

Recognizing that support is an issue, the American Heart Association released a scientific statement in 2020 on sudden cardiac arrest survivorship, which “expands the cardiac arrest resuscitation system of care to include patients, caregivers, and rehabilitative healthcare partnerships, which are central to cardiac survivorship.”

Soar has a more nuanced view of survivorship support, however. “I suspect some people are very glad to be alive, and that trying to dig deep and bring things out may actually be harmful,” he said. “It’s not as clear cut as everybody thinks.”

He noted that follow-up and rehabilitation should be an option for people who specifically need it who would need to be identified. “But human beings are resilient, and while some people will require help, not everybody will,” he said.

Better CPR, New Treatments

Experts in emergency and intensive care medicine studying survival after cardiac arrest hope to find ways to save patients before too much damage is done to the brain and other organs from loss of oxygen, Dr. Parnia said. He is the lead author in a recent multidisciplinary consensus statement on guidelines and standards for the study of death and recalled experiences of death.

“One of my bugbears is that our survival outcomes from cardiac arrest resuscitation have not changed very much for 60 years because we haven’t developed new treatments and innovative methods,” he said. “Unlike the rest of medicine, we’re living in the past.”

Currently, his team is developing cocktails of treatments. These include hypothermic circulatory arrest — cooling the body to stop blood circulation and brain function for up to 40 minutes — and giving magnesium, a brain-protective treatment, to people whose hearts stop.

Dr. Becker would like to see optimal care of patients with cardiac arrest. “The first step is to increase blood flow with good CPR and then measure whether CPR is working,” he said. Adding that despite the availability of devices that provide feedback on the quality of CPR, they’re rarely used. He cited ultrasound devices that measure the blood flow generated during CPR, compression meter devices that go between the patient’s chest and the rescuer’s hands that gauge the rate and depth of compression, and invasive devices that measure blood pressure during CPR.

His group is trying to design even better devices, he said. “An example would be a little probe that you could pop on the neck that would study blood flow to the brain with ultrasound, so that while you were pumping on the person, you could see if you’re making them better or not.”

“We also have some preliminary data showing that the American Heart Association recommended position on the chest for doing CPR is not the perfect place for everybody,” he said. The 2020 AHA guidelines recommended the center of the lower half of the sternum. At the 2023 American College of Emergency Physicians meeting, Dr. Becker›s team at Hofstra/Northwell presented data on 175 video-recorded adult cardiac arrests in their emergency department over more than 2 years, 22 of which involved at least one change of compression location (for a total of 29 location changes). They found that 41% of compression location changes were associated with return of spontaneous circulation.

For about a third of people, the hands need to be repositioned slightly. “This is not anything that is taught to the public because you can only figure it out if you have some kind of sensor that will let you know how you’re doing. That’s very achievable. We could have that in the future on every ambulance and even in people’s homes.”

When the person arrives at the hospital, he said, “we can make it easier and more likely that they can be put on extracorporeal membrane oxygenation (ECMO). We do that on selected patients in our hospital, even though it’s very difficult to do, because we know that when it’s done properly, it can change survival rates dramatically, from maybe 10%-50%.”

Dr. Dr. Becker, like Dr. Parnia, also favors the development of drug cocktails, and his team has been experimenting with various combinations in animal models. “We think those two things together — ECMO and a drug cocktail — would be a very powerful one to two knock out for cardiac arrest,” he said. “We have a long way to go — 10 or 20 years. But most people around the world working in this area believe that will be the future.”

Dr. Parnia’s study on recalled death was supported by The John Templeton Foundation, Resuscitation Council (UK), and New York University Grossman School of Medicine, with research support staff provided by the UK’s National Institutes for Health Research. Soar is the editor of the journal Resuscitation and receives payment from the publisher Elsevier. Dr. Becker’s institute has received grants from Philips Medical Systems, NIH, Zoll Medical Corp, Nihon Kohden, PCORI, BrainCool, and United Therapeutics. He has received advisory/consultancy honoraria from NIH, Nihon Kohden, HP, and Philips, and he holds several patents in hypothermia induction and reperfusion therapies and several pending patents involving the use of medical slurries as human coolant devices to create reperfusion cocktails and measurement of respiratory quotient.

A version of this article appeared on Medscape.com.

For adults with obesity and uncontrolled hypertension, bariatric surgery is an effective and durable strategy to control high blood pressure (BP), final, 5-year follow-up data from the GATEWAY trial suggested.

In the trial, those who underwent bariatric surgery had lower body mass index (BMI) and were on fewer antihypertensive medications after 5 years while maintaining normal BP than those who only used antihypertensive medications.

The results show that “bariatric and metabolic surgery can be very effective in the treatment of patients with obesity and hypertension in the long term,” chief investigator Carlos Aurelio Schiavon, MD, with the Research Institute, Heart Hospital, São Paulo, Brazil, told this news organization. 

“The most important clinical implication of this trial is that we must treat obesity to accomplish success when treating patients with cardiovascular diseases, such as hypertension and obesity,” Dr. Schiavon said.

The study was published online on February 5, 2024, in the Journal of the American College of Cardiology. 
 

A Gateway to Lasting BP Control

GATEWAY enrolled 100 adults (76% women) with grade 1/2 obesity (BMI, 30 to < 40 kg/m²; mean, 37 kg/m²) who were on at least two antihypertensive medications at maximum doses at baseline.

Half were randomly allocated to laparoscopic Roux-en-Y gastric-bypass surgery (RYGB) plus medications and half to medication alone. The primary outcome was at least a 30% reduction of antihypertensive medications while maintaining BP < 140/90 mm Hg. Five-year results were based on 37 patients in the surgery group and 32 in the medication only group. 

After 5 years, BMI was 28.01 kg/m² for those who had surgery vs 36.40 kg/m² for those on medication alone (P < .001).

Patients who underwent RYGB had an 80.7% reduction in the number of antihypertensive medications they were taking while maintaining BP < 140/90 mm Hg compared with a 13.7% reduction in those on medication alone.

After 5 years, surgery patients were taking a mean of 0.80 antihypertensive medications vs 2.97 in the medication only group to control BP at or below the target. 

Despite using less antihypertensive medications in the RYGB, ambulatory BP monitoring data revealed similar 24-hour, daytime, and nighttime BP profiles compared with medication alone. 

The rate of hypertension remission (controlled BP without medication) was nearly 20-fold higher in the surgery group than in the medication only group (46.9% vs 2.4%; P < .001).

In addition, the rate of apparent resistant hypertension was lower with than without surgery (0% vs 15.2%). The surgery group also showed evidence of less atrial remodeling. 

The 5-year results were consistent with the 1-year GATEWAY results Dr. Schiavon presented at the American Heart Association 2017 scientific sessions, as reported by this news organization. They also mirrored the results reported at 3 years. 

Limitations of the study include its single-center, open-label design with a small sample size and loss of follow-up in some patients.

“Taken together, these results support the long-term effective role of bariatric surgery in reducing the burden of hypertension and related polypharmacy, which is frequently observed in patients with obesity and is a cause of concern for them,” the authors wrote. 

“In clinical practice, obesity is an overlooked condition. As a consequence, there is a frequent failure in approaching obesity as a crucial step for mitigating the risk of important cardiovascular risk factors including hypertension. Our results underscore the importance of approaching obesity in reducing hypertension rates,” they added. 
 

Important Data, Lingering Questions 

The coauthors of an accompanying editorial said this study provides “important long-term data on the benefits of gastric bypass on weight loss and blood pressure control, but questions remain.”

Yet, Michael Hall, MD, MSc, with University of Mississippi Medical Center in Jackson, and coauthors noted that the study only included patients undergoing RYGB; it remains unclear if other bariatric surgery procedures would have the same long-term results.

“Sleeve gastrectomy has become more common than RYGB because it is less complex and has earlier recovery and similar effectiveness for treating obesity and type 2 diabetes,” they pointed out. “Further comparative randomized controlled trials are needed to determine whether sleeve gastrectomy is as effective as RYGB for long-term BP control.”

As reported previously by this news organization, in SLEEVEPASS, there was greater weight loss and higher likelihood of hypertension remission with RYGB than with sleeve gastrectomy (24% vs 8%; P = .04), although BP control was not the primary outcome. 

The GATEWAY study was supported by a grant from Ethicon. Dr. Schiavon received a research grant from Ethicon and has received lecture fees from Ethicon and Medtronic. The editorial writers had no relevant disclosures. 
 

A version of this article appeared on Medscape.com.

For adults with obesity and uncontrolled hypertension, bariatric surgery is an effective and durable strategy to control high blood pressure (BP), final, 5-year follow-up data from the GATEWAY trial suggested.

In the trial, those who underwent bariatric surgery had lower body mass index (BMI) and were on fewer antihypertensive medications after 5 years while maintaining normal BP than those who only used antihypertensive medications.

The results show that “bariatric and metabolic surgery can be very effective in the treatment of patients with obesity and hypertension in the long term,” chief investigator Carlos Aurelio Schiavon, MD, with the Research Institute, Heart Hospital, São Paulo, Brazil, told this news organization. 

“The most important clinical implication of this trial is that we must treat obesity to accomplish success when treating patients with cardiovascular diseases, such as hypertension and obesity,” Dr. Schiavon said.

The study was published online on February 5, 2024, in the Journal of the American College of Cardiology. 
 

A Gateway to Lasting BP Control

GATEWAY enrolled 100 adults (76% women) with grade 1/2 obesity (BMI, 30 to < 40 kg/m²; mean, 37 kg/m²) who were on at least two antihypertensive medications at maximum doses at baseline.

Half were randomly allocated to laparoscopic Roux-en-Y gastric-bypass surgery (RYGB) plus medications and half to medication alone. The primary outcome was at least a 30% reduction of antihypertensive medications while maintaining BP < 140/90 mm Hg. Five-year results were based on 37 patients in the surgery group and 32 in the medication only group. 

After 5 years, BMI was 28.01 kg/m² for those who had surgery vs 36.40 kg/m² for those on medication alone (P < .001).

Patients who underwent RYGB had an 80.7% reduction in the number of antihypertensive medications they were taking while maintaining BP < 140/90 mm Hg compared with a 13.7% reduction in those on medication alone.

After 5 years, surgery patients were taking a mean of 0.80 antihypertensive medications vs 2.97 in the medication only group to control BP at or below the target. 

Despite using less antihypertensive medications in the RYGB, ambulatory BP monitoring data revealed similar 24-hour, daytime, and nighttime BP profiles compared with medication alone. 

The rate of hypertension remission (controlled BP without medication) was nearly 20-fold higher in the surgery group than in the medication only group (46.9% vs 2.4%; P < .001).

In addition, the rate of apparent resistant hypertension was lower with than without surgery (0% vs 15.2%). The surgery group also showed evidence of less atrial remodeling. 

The 5-year results were consistent with the 1-year GATEWAY results Dr. Schiavon presented at the American Heart Association 2017 scientific sessions, as reported by this news organization. They also mirrored the results reported at 3 years. 

Limitations of the study include its single-center, open-label design with a small sample size and loss of follow-up in some patients.

“Taken together, these results support the long-term effective role of bariatric surgery in reducing the burden of hypertension and related polypharmacy, which is frequently observed in patients with obesity and is a cause of concern for them,” the authors wrote. 

“In clinical practice, obesity is an overlooked condition. As a consequence, there is a frequent failure in approaching obesity as a crucial step for mitigating the risk of important cardiovascular risk factors including hypertension. Our results underscore the importance of approaching obesity in reducing hypertension rates,” they added. 
 

Important Data, Lingering Questions 

The coauthors of an accompanying editorial said this study provides “important long-term data on the benefits of gastric bypass on weight loss and blood pressure control, but questions remain.”

Yet, Michael Hall, MD, MSc, with University of Mississippi Medical Center in Jackson, and coauthors noted that the study only included patients undergoing RYGB; it remains unclear if other bariatric surgery procedures would have the same long-term results.

“Sleeve gastrectomy has become more common than RYGB because it is less complex and has earlier recovery and similar effectiveness for treating obesity and type 2 diabetes,” they pointed out. “Further comparative randomized controlled trials are needed to determine whether sleeve gastrectomy is as effective as RYGB for long-term BP control.”

As reported previously by this news organization, in SLEEVEPASS, there was greater weight loss and higher likelihood of hypertension remission with RYGB than with sleeve gastrectomy (24% vs 8%; P = .04), although BP control was not the primary outcome. 

The GATEWAY study was supported by a grant from Ethicon. Dr. Schiavon received a research grant from Ethicon and has received lecture fees from Ethicon and Medtronic. The editorial writers had no relevant disclosures. 
 

A version of this article appeared on Medscape.com.

For adults with obesity and uncontrolled hypertension, bariatric surgery is an effective and durable strategy to control high blood pressure (BP), final, 5-year follow-up data from the GATEWAY trial suggested.

In the trial, those who underwent bariatric surgery had lower body mass index (BMI) and were on fewer antihypertensive medications after 5 years while maintaining normal BP than those who only used antihypertensive medications.

The results show that “bariatric and metabolic surgery can be very effective in the treatment of patients with obesity and hypertension in the long term,” chief investigator Carlos Aurelio Schiavon, MD, with the Research Institute, Heart Hospital, São Paulo, Brazil, told this news organization. 

“The most important clinical implication of this trial is that we must treat obesity to accomplish success when treating patients with cardiovascular diseases, such as hypertension and obesity,” Dr. Schiavon said.

The study was published online on February 5, 2024, in the Journal of the American College of Cardiology. 
 

A Gateway to Lasting BP Control

GATEWAY enrolled 100 adults (76% women) with grade 1/2 obesity (BMI, 30 to < 40 kg/m²; mean, 37 kg/m²) who were on at least two antihypertensive medications at maximum doses at baseline.

Half were randomly allocated to laparoscopic Roux-en-Y gastric-bypass surgery (RYGB) plus medications and half to medication alone. The primary outcome was at least a 30% reduction of antihypertensive medications while maintaining BP < 140/90 mm Hg. Five-year results were based on 37 patients in the surgery group and 32 in the medication only group. 

After 5 years, BMI was 28.01 kg/m² for those who had surgery vs 36.40 kg/m² for those on medication alone (P < .001).

Patients who underwent RYGB had an 80.7% reduction in the number of antihypertensive medications they were taking while maintaining BP < 140/90 mm Hg compared with a 13.7% reduction in those on medication alone.

After 5 years, surgery patients were taking a mean of 0.80 antihypertensive medications vs 2.97 in the medication only group to control BP at or below the target. 

Despite using less antihypertensive medications in the RYGB, ambulatory BP monitoring data revealed similar 24-hour, daytime, and nighttime BP profiles compared with medication alone. 

The rate of hypertension remission (controlled BP without medication) was nearly 20-fold higher in the surgery group than in the medication only group (46.9% vs 2.4%; P < .001).

In addition, the rate of apparent resistant hypertension was lower with than without surgery (0% vs 15.2%). The surgery group also showed evidence of less atrial remodeling. 

The 5-year results were consistent with the 1-year GATEWAY results Dr. Schiavon presented at the American Heart Association 2017 scientific sessions, as reported by this news organization. They also mirrored the results reported at 3 years. 

Limitations of the study include its single-center, open-label design with a small sample size and loss of follow-up in some patients.

“Taken together, these results support the long-term effective role of bariatric surgery in reducing the burden of hypertension and related polypharmacy, which is frequently observed in patients with obesity and is a cause of concern for them,” the authors wrote. 

“In clinical practice, obesity is an overlooked condition. As a consequence, there is a frequent failure in approaching obesity as a crucial step for mitigating the risk of important cardiovascular risk factors including hypertension. Our results underscore the importance of approaching obesity in reducing hypertension rates,” they added. 
 

Important Data, Lingering Questions 

The coauthors of an accompanying editorial said this study provides “important long-term data on the benefits of gastric bypass on weight loss and blood pressure control, but questions remain.”

Yet, Michael Hall, MD, MSc, with University of Mississippi Medical Center in Jackson, and coauthors noted that the study only included patients undergoing RYGB; it remains unclear if other bariatric surgery procedures would have the same long-term results.

“Sleeve gastrectomy has become more common than RYGB because it is less complex and has earlier recovery and similar effectiveness for treating obesity and type 2 diabetes,” they pointed out. “Further comparative randomized controlled trials are needed to determine whether sleeve gastrectomy is as effective as RYGB for long-term BP control.”

As reported previously by this news organization, in SLEEVEPASS, there was greater weight loss and higher likelihood of hypertension remission with RYGB than with sleeve gastrectomy (24% vs 8%; P = .04), although BP control was not the primary outcome. 

The GATEWAY study was supported by a grant from Ethicon. Dr. Schiavon received a research grant from Ethicon and has received lecture fees from Ethicon and Medtronic. The editorial writers had no relevant disclosures. 
 

A version of this article appeared on Medscape.com.

TOPLINE:

A two-step screening, using a risk score and biomarkers, can identify patients with diabetes at a higher risk for heart failure who will most likely benefit from preventive drugs.

METHODOLOGY:

• Researchers compared screening methods and downstream risk for heart failure in 5 years, particularly those without atherosclerotic cardiovascular disease (ASCVD).
• They pooled data from 4889 patients (age ≥ 40 years, about half women) with diabetes, no heart failure at baseline, and no signs of ASCVD. All patients had undergone screening to determine their heart failure risk level.
• Researchers assessed the heart failure risk for patients without ASCVD with one-step screening strategies:
• —Clinical risk score (WATCH-DM risk score)
• —Biomarker tests (N-terminal pro-B-type natriuretic peptide [NT-proBNP]) or high-sensitivity cardiac troponin [hs-cTn)
• —Echocardiography
• They next assessed a sequential two-step strategy, using the second test only for those deemed low risk by the first, with a combination of two tests (WATCH-DM/NT-proBNP, NT-proBNP/hs-cTn, or NT-proBNP/echocardiography), the second used for those deemed low-risk by the first test.
• The primary outcome was incident heart failure during the 5-year follow-up. The researchers also assessed the cost-effectiveness of screening and subsequent treatment of high-risk patients with a sodium-glucose cotransporter 2 inhibitor.

TAKEAWAY:

• Overall, 301 (6.2%) heart failure events occurred among participants without ASCVD.
• Of the heart failure events, 53%-71% occurred among participants deemed high risk by a one-step screening strategy, but 75%-89% occurred among patients assessed as high risk in two steps.
• The risk for incident heart failure was 3.0- to 3.6-fold higher in the high- vs low-risk group identified using a two-step screening approach.
• Among the two-step strategies, the WATCH-DM score first, followed by selective NT-proBNP testing for patients deemed low risk by the first test, was the most efficient, with the fewest tests and lowest screening cost.

IN PRACTICE:

“Matching effective but expensive preventive therapies to the highest-risk individuals who are most likely to benefit would be an efficient and cost-effective strategy for heart failure prevention,” the authors wrote.

SOURCE:

The study, led by Kershaw Patel of the Houston Methodist Academic Institute, was published online in Circulation.

LIMITATIONS:

The study findings may not be generalized, as the study included older adults with a high burden of comorbidities. This study may have missed some individuals with diabetes by defining it with fasting plasma glucose, which was consistently available across cohort studies, instead of with the limited A1c data. Moreover, the screening strategies used did not consider other important prognostic factors, such as diabetes duration and socioeconomic status.

DISCLOSURES:

Two authors declared receiving research support from the National Heart, Lung, and Blood Institute. Several authors disclosed financial relationships with multiple pharmaceutical device and medical publishing companies in the form of receiving personal fees; serving in various capacities such as consultants, members of advisory boards, steering committees, or executive committees; and other ties.

A version of this article appeared on Medscape.com.

TOPLINE:

A two-step screening, using a risk score and biomarkers, can identify patients with diabetes at a higher risk for heart failure who will most likely benefit from preventive drugs.

METHODOLOGY:

• Researchers compared screening methods and downstream risk for heart failure in 5 years, particularly those without atherosclerotic cardiovascular disease (ASCVD).
• They pooled data from 4889 patients (age ≥ 40 years, about half women) with diabetes, no heart failure at baseline, and no signs of ASCVD. All patients had undergone screening to determine their heart failure risk level.
• Researchers assessed the heart failure risk for patients without ASCVD with one-step screening strategies:
• —Clinical risk score (WATCH-DM risk score)
• —Biomarker tests (N-terminal pro-B-type natriuretic peptide [NT-proBNP]) or high-sensitivity cardiac troponin [hs-cTn)
• —Echocardiography
• They next assessed a sequential two-step strategy, using the second test only for those deemed low risk by the first, with a combination of two tests (WATCH-DM/NT-proBNP, NT-proBNP/hs-cTn, or NT-proBNP/echocardiography), the second used for those deemed low-risk by the first test.
• The primary outcome was incident heart failure during the 5-year follow-up. The researchers also assessed the cost-effectiveness of screening and subsequent treatment of high-risk patients with a sodium-glucose cotransporter 2 inhibitor.

TAKEAWAY:

• Overall, 301 (6.2%) heart failure events occurred among participants without ASCVD.
• Of the heart failure events, 53%-71% occurred among participants deemed high risk by a one-step screening strategy, but 75%-89% occurred among patients assessed as high risk in two steps.
• The risk for incident heart failure was 3.0- to 3.6-fold higher in the high- vs low-risk group identified using a two-step screening approach.
• Among the two-step strategies, the WATCH-DM score first, followed by selective NT-proBNP testing for patients deemed low risk by the first test, was the most efficient, with the fewest tests and lowest screening cost.

IN PRACTICE:

“Matching effective but expensive preventive therapies to the highest-risk individuals who are most likely to benefit would be an efficient and cost-effective strategy for heart failure prevention,” the authors wrote.

SOURCE:

The study, led by Kershaw Patel of the Houston Methodist Academic Institute, was published online in Circulation.

LIMITATIONS:

The study findings may not be generalized, as the study included older adults with a high burden of comorbidities. This study may have missed some individuals with diabetes by defining it with fasting plasma glucose, which was consistently available across cohort studies, instead of with the limited A1c data. Moreover, the screening strategies used did not consider other important prognostic factors, such as diabetes duration and socioeconomic status.

DISCLOSURES:

Two authors declared receiving research support from the National Heart, Lung, and Blood Institute. Several authors disclosed financial relationships with multiple pharmaceutical device and medical publishing companies in the form of receiving personal fees; serving in various capacities such as consultants, members of advisory boards, steering committees, or executive committees; and other ties.

A version of this article appeared on Medscape.com.

TOPLINE:

A two-step screening, using a risk score and biomarkers, can identify patients with diabetes at a higher risk for heart failure who will most likely benefit from preventive drugs.

METHODOLOGY:

• Researchers compared screening methods and downstream risk for heart failure in 5 years, particularly those without atherosclerotic cardiovascular disease (ASCVD).
• They pooled data from 4889 patients (age ≥ 40 years, about half women) with diabetes, no heart failure at baseline, and no signs of ASCVD. All patients had undergone screening to determine their heart failure risk level.
• Researchers assessed the heart failure risk for patients without ASCVD with one-step screening strategies:
• —Clinical risk score (WATCH-DM risk score)
• —Biomarker tests (N-terminal pro-B-type natriuretic peptide [NT-proBNP]) or high-sensitivity cardiac troponin [hs-cTn)
• —Echocardiography
• They next assessed a sequential two-step strategy, using the second test only for those deemed low risk by the first, with a combination of two tests (WATCH-DM/NT-proBNP, NT-proBNP/hs-cTn, or NT-proBNP/echocardiography), the second used for those deemed low-risk by the first test.
• The primary outcome was incident heart failure during the 5-year follow-up. The researchers also assessed the cost-effectiveness of screening and subsequent treatment of high-risk patients with a sodium-glucose cotransporter 2 inhibitor.

TAKEAWAY:

• Overall, 301 (6.2%) heart failure events occurred among participants without ASCVD.
• Of the heart failure events, 53%-71% occurred among participants deemed high risk by a one-step screening strategy, but 75%-89% occurred among patients assessed as high risk in two steps.
• The risk for incident heart failure was 3.0- to 3.6-fold higher in the high- vs low-risk group identified using a two-step screening approach.
• Among the two-step strategies, the WATCH-DM score first, followed by selective NT-proBNP testing for patients deemed low risk by the first test, was the most efficient, with the fewest tests and lowest screening cost.

IN PRACTICE:

“Matching effective but expensive preventive therapies to the highest-risk individuals who are most likely to benefit would be an efficient and cost-effective strategy for heart failure prevention,” the authors wrote.

SOURCE:

The study, led by Kershaw Patel of the Houston Methodist Academic Institute, was published online in Circulation.

LIMITATIONS:

The study findings may not be generalized, as the study included older adults with a high burden of comorbidities. This study may have missed some individuals with diabetes by defining it with fasting plasma glucose, which was consistently available across cohort studies, instead of with the limited A1c data. Moreover, the screening strategies used did not consider other important prognostic factors, such as diabetes duration and socioeconomic status.

DISCLOSURES:

Two authors declared receiving research support from the National Heart, Lung, and Blood Institute. Several authors disclosed financial relationships with multiple pharmaceutical device and medical publishing companies in the form of receiving personal fees; serving in various capacities such as consultants, members of advisory boards, steering committees, or executive committees; and other ties.

A version of this article appeared on Medscape.com.