Cardiology

Early treatment with ibuprofen had no significant impact on the risk of death or adverse outcomes in preterm infants with patent ductus arteriosus vs. placebo.

The study population included infants born between 23 weeks 0 days’ and 28 weeks 6 days’ gestation. The researchers randomized 326 extremely preterm infants with patent ductus arteriosus (PDA) at 72 hours or less after birth to ibuprofen at a loading dose of 10 mg/kg followed by two doses of 5 mg/kg at least 24 hours apart, and 327 to placebo.

The PDAs in the infants had a diameter of at least 1.5 mm with pulsatile flow.

Severe dysplasia outcome

The study’s primary outcome was a composite of death or moderate to severe bronchopulmonary dysplasia at 36 weeks’ postmenstrual age. Overall, a primary outcome occurred in 69.2% of infants who received ibuprofen and 63.5% of those who received a placebo.

Risk of death or bronchopulmonary dysplasia at 36 weeks’ postmenstrual age was not reduced by early ibuprofen vs. placebo for preterm infants, the researchers concluded. Moderate or severe bronchopulmonary dysplasia occurred in 64.2% of the infants in the ibuprofen group and 59.3% of the placebo group who survived to 36 weeks’ postmenstrual age.

‘Unforeseeable’ serious adverse events

Forty-four deaths occurred in the ibuprofen group and 33 in the placebo group (adjusted risk ratio 1.09). Two “unforeseeable” serious adverse events occurred during the study that were potentially related to ibuprofen.

The lead author was Samir Gupta, MD, of Sidra Medicine, Doha, Qatar. The study was published online in the New England Journal of Medicine.

Study limitations include incomplete data for some patients.

The study was supported by the National Institute for Health Research Health Technology Assessment Programme. The researchers had no financial conflicts to disclose.

Early treatment with ibuprofen had no significant impact on the risk of death or adverse outcomes in preterm infants with patent ductus arteriosus vs. placebo.

The study population included infants born between 23 weeks 0 days’ and 28 weeks 6 days’ gestation. The researchers randomized 326 extremely preterm infants with patent ductus arteriosus (PDA) at 72 hours or less after birth to ibuprofen at a loading dose of 10 mg/kg followed by two doses of 5 mg/kg at least 24 hours apart, and 327 to placebo.

The PDAs in the infants had a diameter of at least 1.5 mm with pulsatile flow.

Severe dysplasia outcome

The study’s primary outcome was a composite of death or moderate to severe bronchopulmonary dysplasia at 36 weeks’ postmenstrual age. Overall, a primary outcome occurred in 69.2% of infants who received ibuprofen and 63.5% of those who received a placebo.

Risk of death or bronchopulmonary dysplasia at 36 weeks’ postmenstrual age was not reduced by early ibuprofen vs. placebo for preterm infants, the researchers concluded. Moderate or severe bronchopulmonary dysplasia occurred in 64.2% of the infants in the ibuprofen group and 59.3% of the placebo group who survived to 36 weeks’ postmenstrual age.

‘Unforeseeable’ serious adverse events

Forty-four deaths occurred in the ibuprofen group and 33 in the placebo group (adjusted risk ratio 1.09). Two “unforeseeable” serious adverse events occurred during the study that were potentially related to ibuprofen.

The lead author was Samir Gupta, MD, of Sidra Medicine, Doha, Qatar. The study was published online in the New England Journal of Medicine.

Study limitations include incomplete data for some patients.

The study was supported by the National Institute for Health Research Health Technology Assessment Programme. The researchers had no financial conflicts to disclose.

Early treatment with ibuprofen had no significant impact on the risk of death or adverse outcomes in preterm infants with patent ductus arteriosus vs. placebo.

The study population included infants born between 23 weeks 0 days’ and 28 weeks 6 days’ gestation. The researchers randomized 326 extremely preterm infants with patent ductus arteriosus (PDA) at 72 hours or less after birth to ibuprofen at a loading dose of 10 mg/kg followed by two doses of 5 mg/kg at least 24 hours apart, and 327 to placebo.

The PDAs in the infants had a diameter of at least 1.5 mm with pulsatile flow.

Severe dysplasia outcome

The study’s primary outcome was a composite of death or moderate to severe bronchopulmonary dysplasia at 36 weeks’ postmenstrual age. Overall, a primary outcome occurred in 69.2% of infants who received ibuprofen and 63.5% of those who received a placebo.

Risk of death or bronchopulmonary dysplasia at 36 weeks’ postmenstrual age was not reduced by early ibuprofen vs. placebo for preterm infants, the researchers concluded. Moderate or severe bronchopulmonary dysplasia occurred in 64.2% of the infants in the ibuprofen group and 59.3% of the placebo group who survived to 36 weeks’ postmenstrual age.

‘Unforeseeable’ serious adverse events

Forty-four deaths occurred in the ibuprofen group and 33 in the placebo group (adjusted risk ratio 1.09). Two “unforeseeable” serious adverse events occurred during the study that were potentially related to ibuprofen.

The lead author was Samir Gupta, MD, of Sidra Medicine, Doha, Qatar. The study was published online in the New England Journal of Medicine.

Study limitations include incomplete data for some patients.

The study was supported by the National Institute for Health Research Health Technology Assessment Programme. The researchers had no financial conflicts to disclose.

TOPLINE:

A daily low dose of colchicine significantly reduces ischemic cardiovascular events in patients with type 2 diabetes (T2D) and a recent myocardial infarction (MI). 

METHODOLOGY:

• After an MI, patients with vs without T2D have a higher risk for another cardiovascular event.
• The Colchicine Cardiovascular Outcomes Trial (COLCOT), a randomized, double-blinded trial, found a lower risk for ischemic cardiovascular events with 0.5 mg colchicine taken daily vs placebo, initiated within 30 days of an MI.
• Researchers conducted a prespecified subgroup analysis of 959 adult patients with T2D (mean age, 62.4 years; 22.2% women) in COLCOT (462 patients in colchicine and 497 patients in placebo groups).
• The primary efficacy endpoint was a composite of cardiovascular death, resuscitated cardiac arrest, MI, stroke, or urgent hospitalization for angina requiring coronary revascularization within a median 23 months.
• The patients were taking a variety of appropriate medications, including aspirin and another antiplatelet agent and a statin (98%-99%) and metformin (75%-76%).

TAKEAWAY:

• The risk for the primary endpoint was reduced by 35% in patients with T2D who received colchicine than in those who received placebo (hazard ratio, 0.65; P = .03).
• The primary endpoint event rate per 100 patient-months was significantly lower in the colchicine group than in the placebo group (rate ratio, 0.53; P = .01).
• The frequencies of adverse events were similar in both the treatment and placebo groups (14.6% and 12.8%, respectively; P = .41), with gastrointestinal adverse events being the most common.
• In COLCOT, patients with T2D had a 1.86-fold higher risk for a primary endpoint cardiovascular event, but there was no significant difference in the primary endpoint between those with and without T2D on colchicine.

IN PRACTICE:

“Patients with both T2D and a recent MI derive a large benefit from inflammation-reducing therapy with colchicine,” the authors noted.

SOURCE:

This study, led by François Roubille, University Hospital of Montpellier, France, was published online on January 5, 2024, in Diabetes Care. 

LIMITATIONS:

Patients were not stratified at inclusion for the presence of diabetes. Also, the study did not evaluate the role of glycated hemoglobin and low-density lipoprotein cholesterol, as well as the effects of different glucose-lowering medications or possible hypoglycemic episodes.

DISCLOSURES:

The COLCOT study was funded by the Government of Quebec, the Canadian Institutes of Health Research, and philanthropic foundations. Coauthors Jean-Claude Tardif and Wolfgang Koenig declared receiving research grants, honoraria, advisory board fees, and lecture fees from pharmaceutical companies, as well as having other ties with various sources.
 

A version of this article appeared on Medscape.com.

TOPLINE:

A daily low dose of colchicine significantly reduces ischemic cardiovascular events in patients with type 2 diabetes (T2D) and a recent myocardial infarction (MI). 

METHODOLOGY:

• After an MI, patients with vs without T2D have a higher risk for another cardiovascular event.
• The Colchicine Cardiovascular Outcomes Trial (COLCOT), a randomized, double-blinded trial, found a lower risk for ischemic cardiovascular events with 0.5 mg colchicine taken daily vs placebo, initiated within 30 days of an MI.
• Researchers conducted a prespecified subgroup analysis of 959 adult patients with T2D (mean age, 62.4 years; 22.2% women) in COLCOT (462 patients in colchicine and 497 patients in placebo groups).
• The primary efficacy endpoint was a composite of cardiovascular death, resuscitated cardiac arrest, MI, stroke, or urgent hospitalization for angina requiring coronary revascularization within a median 23 months.
• The patients were taking a variety of appropriate medications, including aspirin and another antiplatelet agent and a statin (98%-99%) and metformin (75%-76%).

TAKEAWAY:

• The risk for the primary endpoint was reduced by 35% in patients with T2D who received colchicine than in those who received placebo (hazard ratio, 0.65; P = .03).
• The primary endpoint event rate per 100 patient-months was significantly lower in the colchicine group than in the placebo group (rate ratio, 0.53; P = .01).
• The frequencies of adverse events were similar in both the treatment and placebo groups (14.6% and 12.8%, respectively; P = .41), with gastrointestinal adverse events being the most common.
• In COLCOT, patients with T2D had a 1.86-fold higher risk for a primary endpoint cardiovascular event, but there was no significant difference in the primary endpoint between those with and without T2D on colchicine.

IN PRACTICE:

“Patients with both T2D and a recent MI derive a large benefit from inflammation-reducing therapy with colchicine,” the authors noted.

SOURCE:

This study, led by François Roubille, University Hospital of Montpellier, France, was published online on January 5, 2024, in Diabetes Care. 

LIMITATIONS:

Patients were not stratified at inclusion for the presence of diabetes. Also, the study did not evaluate the role of glycated hemoglobin and low-density lipoprotein cholesterol, as well as the effects of different glucose-lowering medications or possible hypoglycemic episodes.

DISCLOSURES:

The COLCOT study was funded by the Government of Quebec, the Canadian Institutes of Health Research, and philanthropic foundations. Coauthors Jean-Claude Tardif and Wolfgang Koenig declared receiving research grants, honoraria, advisory board fees, and lecture fees from pharmaceutical companies, as well as having other ties with various sources.
 

A version of this article appeared on Medscape.com.

TOPLINE:

A daily low dose of colchicine significantly reduces ischemic cardiovascular events in patients with type 2 diabetes (T2D) and a recent myocardial infarction (MI). 

METHODOLOGY:

• After an MI, patients with vs without T2D have a higher risk for another cardiovascular event.
• The Colchicine Cardiovascular Outcomes Trial (COLCOT), a randomized, double-blinded trial, found a lower risk for ischemic cardiovascular events with 0.5 mg colchicine taken daily vs placebo, initiated within 30 days of an MI.
• Researchers conducted a prespecified subgroup analysis of 959 adult patients with T2D (mean age, 62.4 years; 22.2% women) in COLCOT (462 patients in colchicine and 497 patients in placebo groups).
• The primary efficacy endpoint was a composite of cardiovascular death, resuscitated cardiac arrest, MI, stroke, or urgent hospitalization for angina requiring coronary revascularization within a median 23 months.
• The patients were taking a variety of appropriate medications, including aspirin and another antiplatelet agent and a statin (98%-99%) and metformin (75%-76%).

TAKEAWAY:

• The risk for the primary endpoint was reduced by 35% in patients with T2D who received colchicine than in those who received placebo (hazard ratio, 0.65; P = .03).
• The primary endpoint event rate per 100 patient-months was significantly lower in the colchicine group than in the placebo group (rate ratio, 0.53; P = .01).
• The frequencies of adverse events were similar in both the treatment and placebo groups (14.6% and 12.8%, respectively; P = .41), with gastrointestinal adverse events being the most common.
• In COLCOT, patients with T2D had a 1.86-fold higher risk for a primary endpoint cardiovascular event, but there was no significant difference in the primary endpoint between those with and without T2D on colchicine.

IN PRACTICE:

“Patients with both T2D and a recent MI derive a large benefit from inflammation-reducing therapy with colchicine,” the authors noted.

SOURCE:

This study, led by François Roubille, University Hospital of Montpellier, France, was published online on January 5, 2024, in Diabetes Care. 

LIMITATIONS:

Patients were not stratified at inclusion for the presence of diabetes. Also, the study did not evaluate the role of glycated hemoglobin and low-density lipoprotein cholesterol, as well as the effects of different glucose-lowering medications or possible hypoglycemic episodes.

DISCLOSURES:

The COLCOT study was funded by the Government of Quebec, the Canadian Institutes of Health Research, and philanthropic foundations. Coauthors Jean-Claude Tardif and Wolfgang Koenig declared receiving research grants, honoraria, advisory board fees, and lecture fees from pharmaceutical companies, as well as having other ties with various sources.
 

A version of this article appeared on Medscape.com.

TOPLINE:

While low-density lipoprotein (LDL) particles are much more abundant than lipoprotein(a) [Lp(a)] particles and carry the greatest overall risk for coronary heart disease (CHD), on a per-particle basis, Lp(a) is associated with about six times the atherogenic risk for LDL, new observational research suggested.

METHODOLOGY:

• To compare the atherogenicity of Lp(a) relative to LDL on a per-particle basis, researchers used a genetic analysis because Lp(a) and LDL both contain one apolipoprotein B (apoB) per particle.
• In a genome-wide association study of 502,413 UK Biobank participants, they identified genetic variants uniquely affecting plasma levels of either Lp(a) or LDL particles.
• For these two genetic clusters, they related the change in apoB to the respective change in CHD risk, which allowed them to directly compare the atherogenicity of LDL and Lp(a), particle to particle.

TAKEAWAY:

• The odds ratio for CHD for a 50 nmol/L higher Lp(a)-apoB was 1.28 (95% CI, 1.24-1.33) compared with 1.04 (95% CI, 1.03-1.05) for the same increment in LDL-apoB.
• Additional supporting evidence was provided by using polygenic scores to rank participants according to the difference in Lp(a)-apoB vs LDL-apoB, which revealed a greater risk for CHD per 50 nmol/L apoB for the Lp(a) cluster (hazard ratio [HR], 1.47; 95% CI, 1.36-1.58) than the LDL cluster (HR, 1.04; 95% CI, 1.02-1.05).
• Based on the data, the researchers estimate that the atherogenicity of Lp(a) is roughly sixfold greater (point estimate of 6.6; 95% CI, 5.1-8.8) than that of LDL on a per-particle basis.

IN PRACTICE:

“There are two clinical implications. First, to completely characterize atherosclerotic cardiovascular disease risk, it is imperative to measure Lp(a) in all adult patients at least once. Second, these studies provide a rationale that targeting Lp(a) with potent and specific drugs may lead to clinically meaningful benefit,” wrote the authors of an accompanying commentary on the study.

SOURCE:

The study, with first author Elias Björnson, PhD, University of Gothenburg, Gothenburg, Sweden, and an editorial by Sotirios Tsimikas, MD, University of California, San Diego, and Vera Bittner, MD, University of Alabama at Birmingham, was published in the Journal of the American College of Cardiology.

LIMITATIONS:

The UK Biobank consists primarily of a Caucasian population, and confirmatory studies in more diverse samples are needed. The working range for the Lp(a) assay used in the study did not cover the full range of Lp(a) values seen in the population. Variations in Lp(a)-apoB and LDL-apoB were estimated from genetic analysis and not measured specifically in biochemical assays.

DISCLOSURES:

The study had no commercial funding. Some authors received honoraria from the pharmaceutical industry. A complete list of author disclosures is available with the original article.

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

TOPLINE:

While low-density lipoprotein (LDL) particles are much more abundant than lipoprotein(a) [Lp(a)] particles and carry the greatest overall risk for coronary heart disease (CHD), on a per-particle basis, Lp(a) is associated with about six times the atherogenic risk for LDL, new observational research suggested.

METHODOLOGY:

• To compare the atherogenicity of Lp(a) relative to LDL on a per-particle basis, researchers used a genetic analysis because Lp(a) and LDL both contain one apolipoprotein B (apoB) per particle.
• In a genome-wide association study of 502,413 UK Biobank participants, they identified genetic variants uniquely affecting plasma levels of either Lp(a) or LDL particles.
• For these two genetic clusters, they related the change in apoB to the respective change in CHD risk, which allowed them to directly compare the atherogenicity of LDL and Lp(a), particle to particle.

TAKEAWAY:

• The odds ratio for CHD for a 50 nmol/L higher Lp(a)-apoB was 1.28 (95% CI, 1.24-1.33) compared with 1.04 (95% CI, 1.03-1.05) for the same increment in LDL-apoB.
• Additional supporting evidence was provided by using polygenic scores to rank participants according to the difference in Lp(a)-apoB vs LDL-apoB, which revealed a greater risk for CHD per 50 nmol/L apoB for the Lp(a) cluster (hazard ratio [HR], 1.47; 95% CI, 1.36-1.58) than the LDL cluster (HR, 1.04; 95% CI, 1.02-1.05).
• Based on the data, the researchers estimate that the atherogenicity of Lp(a) is roughly sixfold greater (point estimate of 6.6; 95% CI, 5.1-8.8) than that of LDL on a per-particle basis.

IN PRACTICE:

“There are two clinical implications. First, to completely characterize atherosclerotic cardiovascular disease risk, it is imperative to measure Lp(a) in all adult patients at least once. Second, these studies provide a rationale that targeting Lp(a) with potent and specific drugs may lead to clinically meaningful benefit,” wrote the authors of an accompanying commentary on the study.

SOURCE:

The study, with first author Elias Björnson, PhD, University of Gothenburg, Gothenburg, Sweden, and an editorial by Sotirios Tsimikas, MD, University of California, San Diego, and Vera Bittner, MD, University of Alabama at Birmingham, was published in the Journal of the American College of Cardiology.

LIMITATIONS:

The UK Biobank consists primarily of a Caucasian population, and confirmatory studies in more diverse samples are needed. The working range for the Lp(a) assay used in the study did not cover the full range of Lp(a) values seen in the population. Variations in Lp(a)-apoB and LDL-apoB were estimated from genetic analysis and not measured specifically in biochemical assays.

DISCLOSURES:

The study had no commercial funding. Some authors received honoraria from the pharmaceutical industry. A complete list of author disclosures is available with the original article.

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

TOPLINE:

While low-density lipoprotein (LDL) particles are much more abundant than lipoprotein(a) [Lp(a)] particles and carry the greatest overall risk for coronary heart disease (CHD), on a per-particle basis, Lp(a) is associated with about six times the atherogenic risk for LDL, new observational research suggested.

METHODOLOGY:

• To compare the atherogenicity of Lp(a) relative to LDL on a per-particle basis, researchers used a genetic analysis because Lp(a) and LDL both contain one apolipoprotein B (apoB) per particle.
• In a genome-wide association study of 502,413 UK Biobank participants, they identified genetic variants uniquely affecting plasma levels of either Lp(a) or LDL particles.
• For these two genetic clusters, they related the change in apoB to the respective change in CHD risk, which allowed them to directly compare the atherogenicity of LDL and Lp(a), particle to particle.

TAKEAWAY:

• The odds ratio for CHD for a 50 nmol/L higher Lp(a)-apoB was 1.28 (95% CI, 1.24-1.33) compared with 1.04 (95% CI, 1.03-1.05) for the same increment in LDL-apoB.
• Additional supporting evidence was provided by using polygenic scores to rank participants according to the difference in Lp(a)-apoB vs LDL-apoB, which revealed a greater risk for CHD per 50 nmol/L apoB for the Lp(a) cluster (hazard ratio [HR], 1.47; 95% CI, 1.36-1.58) than the LDL cluster (HR, 1.04; 95% CI, 1.02-1.05).
• Based on the data, the researchers estimate that the atherogenicity of Lp(a) is roughly sixfold greater (point estimate of 6.6; 95% CI, 5.1-8.8) than that of LDL on a per-particle basis.

IN PRACTICE:

“There are two clinical implications. First, to completely characterize atherosclerotic cardiovascular disease risk, it is imperative to measure Lp(a) in all adult patients at least once. Second, these studies provide a rationale that targeting Lp(a) with potent and specific drugs may lead to clinically meaningful benefit,” wrote the authors of an accompanying commentary on the study.

SOURCE:

The study, with first author Elias Björnson, PhD, University of Gothenburg, Gothenburg, Sweden, and an editorial by Sotirios Tsimikas, MD, University of California, San Diego, and Vera Bittner, MD, University of Alabama at Birmingham, was published in the Journal of the American College of Cardiology.

LIMITATIONS:

The UK Biobank consists primarily of a Caucasian population, and confirmatory studies in more diverse samples are needed. The working range for the Lp(a) assay used in the study did not cover the full range of Lp(a) values seen in the population. Variations in Lp(a)-apoB and LDL-apoB were estimated from genetic analysis and not measured specifically in biochemical assays.

DISCLOSURES:

The study had no commercial funding. Some authors received honoraria from the pharmaceutical industry. A complete list of author disclosures is available with the original article.

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

TOPLINE:

In patients with chronic kidney disease (CKD) and type 2 diabetes, baseline insulin resistance was associated with increased cardiovascular (CV) but not kidney risk and did not affect the efficacy of finerenone. 

METHODOLOGY:

• Insulin resistance is implicated in CV disease in patients with CKD, but its role in CKD progression is less clear.
• This post hoc analysis of FIDELITY, a pooled analysis of the  and  trials, randomly assigned patients with type 2 diabetes and CKD (who received optimized renin-angiotensin system blockade) to receive finerenone (10 mg or 20 mg) once daily or placebo and followed them for a median of 3 years.
• An estimated glucose disposal rate (eGDR), a measure of insulin resistance, was calculated for 12,964 patients (median age, 65 years), using waist circumference, hypertension status, and glycated hemoglobin.
• Outcomes included a CV composite (time to CV death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for heart failure) and a kidney composite (time to renal failure, a sustained decrease ≥ 57% in the initial estimated glomerular filtration rate, or renal death).

TAKEAWAY:

• The median eGDR was 4.1 mg/kg/min. The 50% of patients with a lower eGDR were considered insulin resistant, whereas the remaining half with a higher eGDR were considered insulin sensitive.
• The incidence rate of CV outcomes was higher among patients with insulin resistance in both the finerenone group (incidence rate per 100 patient-years, 5.18 vs 3.47 among insulin-sensitive patients) and the placebo group (6.34 vs 3.76), but eGDR showed no association with kidney outcomes.
• The efficacy of finerenone vs placebo on CV (Wald test P = .063) and kidney outcomes (Wald test P = .51) did not change significantly across the range of baseline eGDR values.
• The incidences of treatment-emergent adverse events and severe adverse events with finerenone were similar between the insulin-resistant and insulin-sensitive subgroups.

IN PRACTICE:

“The efficacy and safety of finerenone were not modified by baseline insulin resistance. A higher risk of CV — but not kidney outcomes was observed in patients with CKD and T2D with greater insulin resistance,” the authors wrote.

SOURCE:

This study was led by Thomas Ebert of the Medical Department III — Endocrinology, Nephrology, Rheumatology, University of Leipzig Medical Center, Leipzig, Germany, and published online in Diabetes Care.

LIMITATIONS:

This study was not adequately powered to evaluate the statistical significance of the association of eGDR with CV and kidney outcomes and was hypothesis-generating. Further studies are needed to examine whether the effects of insulin resistance differ between individuals with diabetes vs those with advanced CKD with or without diabetes.

DISCLOSURES:

The FIDELIO-DKD and FIGARO-DKD trials were conducted and sponsored by Bayer AG. Three authors declared being full-time employees of Bayer. Several authors declared receiving personal fees, consulting fees, grants, or research support from; holding patents with; or having ownership interests in various pharmaceutical companies, including Bayer.

A version of this article appeared on Medscape.com.

TOPLINE:

In patients with chronic kidney disease (CKD) and type 2 diabetes, baseline insulin resistance was associated with increased cardiovascular (CV) but not kidney risk and did not affect the efficacy of finerenone. 

METHODOLOGY:

• Insulin resistance is implicated in CV disease in patients with CKD, but its role in CKD progression is less clear.
• This post hoc analysis of FIDELITY, a pooled analysis of the  and  trials, randomly assigned patients with type 2 diabetes and CKD (who received optimized renin-angiotensin system blockade) to receive finerenone (10 mg or 20 mg) once daily or placebo and followed them for a median of 3 years.
• An estimated glucose disposal rate (eGDR), a measure of insulin resistance, was calculated for 12,964 patients (median age, 65 years), using waist circumference, hypertension status, and glycated hemoglobin.
• Outcomes included a CV composite (time to CV death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for heart failure) and a kidney composite (time to renal failure, a sustained decrease ≥ 57% in the initial estimated glomerular filtration rate, or renal death).

TAKEAWAY:

• The median eGDR was 4.1 mg/kg/min. The 50% of patients with a lower eGDR were considered insulin resistant, whereas the remaining half with a higher eGDR were considered insulin sensitive.
• The incidence rate of CV outcomes was higher among patients with insulin resistance in both the finerenone group (incidence rate per 100 patient-years, 5.18 vs 3.47 among insulin-sensitive patients) and the placebo group (6.34 vs 3.76), but eGDR showed no association with kidney outcomes.
• The efficacy of finerenone vs placebo on CV (Wald test P = .063) and kidney outcomes (Wald test P = .51) did not change significantly across the range of baseline eGDR values.
• The incidences of treatment-emergent adverse events and severe adverse events with finerenone were similar between the insulin-resistant and insulin-sensitive subgroups.

IN PRACTICE:

“The efficacy and safety of finerenone were not modified by baseline insulin resistance. A higher risk of CV — but not kidney outcomes was observed in patients with CKD and T2D with greater insulin resistance,” the authors wrote.

SOURCE:

This study was led by Thomas Ebert of the Medical Department III — Endocrinology, Nephrology, Rheumatology, University of Leipzig Medical Center, Leipzig, Germany, and published online in Diabetes Care.

LIMITATIONS:

This study was not adequately powered to evaluate the statistical significance of the association of eGDR with CV and kidney outcomes and was hypothesis-generating. Further studies are needed to examine whether the effects of insulin resistance differ between individuals with diabetes vs those with advanced CKD with or without diabetes.

DISCLOSURES:

The FIDELIO-DKD and FIGARO-DKD trials were conducted and sponsored by Bayer AG. Three authors declared being full-time employees of Bayer. Several authors declared receiving personal fees, consulting fees, grants, or research support from; holding patents with; or having ownership interests in various pharmaceutical companies, including Bayer.

A version of this article appeared on Medscape.com.

TOPLINE:

In patients with chronic kidney disease (CKD) and type 2 diabetes, baseline insulin resistance was associated with increased cardiovascular (CV) but not kidney risk and did not affect the efficacy of finerenone. 

METHODOLOGY:

• Insulin resistance is implicated in CV disease in patients with CKD, but its role in CKD progression is less clear.
• This post hoc analysis of FIDELITY, a pooled analysis of the  and  trials, randomly assigned patients with type 2 diabetes and CKD (who received optimized renin-angiotensin system blockade) to receive finerenone (10 mg or 20 mg) once daily or placebo and followed them for a median of 3 years.
• An estimated glucose disposal rate (eGDR), a measure of insulin resistance, was calculated for 12,964 patients (median age, 65 years), using waist circumference, hypertension status, and glycated hemoglobin.
• Outcomes included a CV composite (time to CV death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for heart failure) and a kidney composite (time to renal failure, a sustained decrease ≥ 57% in the initial estimated glomerular filtration rate, or renal death).

TAKEAWAY:

• The median eGDR was 4.1 mg/kg/min. The 50% of patients with a lower eGDR were considered insulin resistant, whereas the remaining half with a higher eGDR were considered insulin sensitive.
• The incidence rate of CV outcomes was higher among patients with insulin resistance in both the finerenone group (incidence rate per 100 patient-years, 5.18 vs 3.47 among insulin-sensitive patients) and the placebo group (6.34 vs 3.76), but eGDR showed no association with kidney outcomes.
• The efficacy of finerenone vs placebo on CV (Wald test P = .063) and kidney outcomes (Wald test P = .51) did not change significantly across the range of baseline eGDR values.
• The incidences of treatment-emergent adverse events and severe adverse events with finerenone were similar between the insulin-resistant and insulin-sensitive subgroups.

IN PRACTICE:

“The efficacy and safety of finerenone were not modified by baseline insulin resistance. A higher risk of CV — but not kidney outcomes was observed in patients with CKD and T2D with greater insulin resistance,” the authors wrote.

SOURCE:

This study was led by Thomas Ebert of the Medical Department III — Endocrinology, Nephrology, Rheumatology, University of Leipzig Medical Center, Leipzig, Germany, and published online in Diabetes Care.

LIMITATIONS:

This study was not adequately powered to evaluate the statistical significance of the association of eGDR with CV and kidney outcomes and was hypothesis-generating. Further studies are needed to examine whether the effects of insulin resistance differ between individuals with diabetes vs those with advanced CKD with or without diabetes.

DISCLOSURES:

The FIDELIO-DKD and FIGARO-DKD trials were conducted and sponsored by Bayer AG. Three authors declared being full-time employees of Bayer. Several authors declared receiving personal fees, consulting fees, grants, or research support from; holding patents with; or having ownership interests in various pharmaceutical companies, including Bayer.

A version of this article appeared on Medscape.com.

TOPLINE:

Circulating levels of serum 25-hydroxyvitamin D (25[OH]D) may be a marker of cardiovascular disease (CVD) risk in healthy young adults, small study finds.

METHODOLOGY:

• A secondary analysis of the Activating Brown Adipose Tissue Through Exercise (ACTIBATE) trial assessed the association between serum 25(OH)D levels and CVD risk factors.
• The cross-sectional study used baseline data of in 177 healthy sedentary adults ages 18-25 years (65% women; all White individuals), who were recruited between October 2015 and December 2016 from Granada, a region in the south of Spain.
• Study participants were nonsmokers, led a sedentary lifestyle, and did not have a prior history of CVD or chronic illnesses.
• The CVD risk factors included anthropometrical and body composition profiles, glucose and lipid metabolism, liver, and pro- and anti-inflammatory biomarkers.
• 25(OH)D serum concentrations were measured with a competitive chemiluminescence immunoassay and defined as deficient (< 20 ng/mL), insufficient (21-29 ng/mL), or normal (> 30 ng/mL).

TAKEAWAY:

• The  levels correlated inversely with body mass index (BMI; standardized regression coefficient [beta], −0.177; P = .018), fat mass index (beta, −0.195; P = .011), and systolic blood pressure (beta, −0.137; P = .038), after adjusting for sex.
• Glucose metabolism markers (serum glucose and insulin concentrations, insulin/glucose ratio, and homeostatic model assessment of  index) also correlated inversely with vitamin D levels.
• The trend was similar for liver markers serum γ-glutamyl transferase and alkaline phosphatase) and the anti-inflammatory marker interleukin-4.
• BMI, waist/hip ratio, fat mass index, blood pressure, and levels of glucose, insulin, , and liver markers were higher in the 44 participants with vitamin D deficiency vs 41 participants with normal vitamin D levels.

IN PRACTICE:

“Collectively, these findings support the idea that 25(OH)D concentrations may be used as a useful marker of CVD status, which can be easily monitored in young individuals,” the authors wrote.

SOURCE:

This study was led by first author Francisco J. AmaroGahete, MD, PhD, from the Department of Physiology, Faculty of Medicine, University of Granada, Spain, who also holds positions in other institutions. It was published online in the Journal of Endocrinological Investigation.

LIMITATIONS:

This study could not establish causal relationships due to its cross-sectional design. The results might not apply to younger or older people from different locations and ethnic backgrounds. The gold standard method for analyzing vitamin D levels, liquid chromatography–mass spectrometry, was not used in this study.

DISCLOSURES:

This study was supported by the Spanish Ministry of Economy and Competitiveness, Spanish Ministry of Education, AstraZeneca HealthCare Foundation, and other sources. The authors declared no conflicts of interest.

A version of this article appeared on Medscape.com.

TOPLINE:

Circulating levels of serum 25-hydroxyvitamin D (25[OH]D) may be a marker of cardiovascular disease (CVD) risk in healthy young adults, small study finds.

METHODOLOGY:

• A secondary analysis of the Activating Brown Adipose Tissue Through Exercise (ACTIBATE) trial assessed the association between serum 25(OH)D levels and CVD risk factors.
• The cross-sectional study used baseline data of in 177 healthy sedentary adults ages 18-25 years (65% women; all White individuals), who were recruited between October 2015 and December 2016 from Granada, a region in the south of Spain.
• Study participants were nonsmokers, led a sedentary lifestyle, and did not have a prior history of CVD or chronic illnesses.
• The CVD risk factors included anthropometrical and body composition profiles, glucose and lipid metabolism, liver, and pro- and anti-inflammatory biomarkers.
• 25(OH)D serum concentrations were measured with a competitive chemiluminescence immunoassay and defined as deficient (< 20 ng/mL), insufficient (21-29 ng/mL), or normal (> 30 ng/mL).

TAKEAWAY:

• The  levels correlated inversely with body mass index (BMI; standardized regression coefficient [beta], −0.177; P = .018), fat mass index (beta, −0.195; P = .011), and systolic blood pressure (beta, −0.137; P = .038), after adjusting for sex.
• Glucose metabolism markers (serum glucose and insulin concentrations, insulin/glucose ratio, and homeostatic model assessment of  index) also correlated inversely with vitamin D levels.
• The trend was similar for liver markers serum γ-glutamyl transferase and alkaline phosphatase) and the anti-inflammatory marker interleukin-4.
• BMI, waist/hip ratio, fat mass index, blood pressure, and levels of glucose, insulin, , and liver markers were higher in the 44 participants with vitamin D deficiency vs 41 participants with normal vitamin D levels.

IN PRACTICE:

“Collectively, these findings support the idea that 25(OH)D concentrations may be used as a useful marker of CVD status, which can be easily monitored in young individuals,” the authors wrote.

SOURCE:

This study was led by first author Francisco J. AmaroGahete, MD, PhD, from the Department of Physiology, Faculty of Medicine, University of Granada, Spain, who also holds positions in other institutions. It was published online in the Journal of Endocrinological Investigation.

LIMITATIONS:

This study could not establish causal relationships due to its cross-sectional design. The results might not apply to younger or older people from different locations and ethnic backgrounds. The gold standard method for analyzing vitamin D levels, liquid chromatography–mass spectrometry, was not used in this study.

DISCLOSURES:

This study was supported by the Spanish Ministry of Economy and Competitiveness, Spanish Ministry of Education, AstraZeneca HealthCare Foundation, and other sources. The authors declared no conflicts of interest.

A version of this article appeared on Medscape.com.

TOPLINE:

Circulating levels of serum 25-hydroxyvitamin D (25[OH]D) may be a marker of cardiovascular disease (CVD) risk in healthy young adults, small study finds.

METHODOLOGY:

• A secondary analysis of the Activating Brown Adipose Tissue Through Exercise (ACTIBATE) trial assessed the association between serum 25(OH)D levels and CVD risk factors.
• The cross-sectional study used baseline data of in 177 healthy sedentary adults ages 18-25 years (65% women; all White individuals), who were recruited between October 2015 and December 2016 from Granada, a region in the south of Spain.
• Study participants were nonsmokers, led a sedentary lifestyle, and did not have a prior history of CVD or chronic illnesses.
• The CVD risk factors included anthropometrical and body composition profiles, glucose and lipid metabolism, liver, and pro- and anti-inflammatory biomarkers.
• 25(OH)D serum concentrations were measured with a competitive chemiluminescence immunoassay and defined as deficient (< 20 ng/mL), insufficient (21-29 ng/mL), or normal (> 30 ng/mL).

TAKEAWAY:

• The  levels correlated inversely with body mass index (BMI; standardized regression coefficient [beta], −0.177; P = .018), fat mass index (beta, −0.195; P = .011), and systolic blood pressure (beta, −0.137; P = .038), after adjusting for sex.
• Glucose metabolism markers (serum glucose and insulin concentrations, insulin/glucose ratio, and homeostatic model assessment of  index) also correlated inversely with vitamin D levels.
• The trend was similar for liver markers serum γ-glutamyl transferase and alkaline phosphatase) and the anti-inflammatory marker interleukin-4.
• BMI, waist/hip ratio, fat mass index, blood pressure, and levels of glucose, insulin, , and liver markers were higher in the 44 participants with vitamin D deficiency vs 41 participants with normal vitamin D levels.

IN PRACTICE:

“Collectively, these findings support the idea that 25(OH)D concentrations may be used as a useful marker of CVD status, which can be easily monitored in young individuals,” the authors wrote.

SOURCE:

This study was led by first author Francisco J. AmaroGahete, MD, PhD, from the Department of Physiology, Faculty of Medicine, University of Granada, Spain, who also holds positions in other institutions. It was published online in the Journal of Endocrinological Investigation.

LIMITATIONS:

This study could not establish causal relationships due to its cross-sectional design. The results might not apply to younger or older people from different locations and ethnic backgrounds. The gold standard method for analyzing vitamin D levels, liquid chromatography–mass spectrometry, was not used in this study.

DISCLOSURES:

This study was supported by the Spanish Ministry of Economy and Competitiveness, Spanish Ministry of Education, AstraZeneca HealthCare Foundation, and other sources. The authors declared no conflicts of interest.

A version of this article appeared on Medscape.com.

People who mainly sit while on the job increase their risk of dying of cardiovascular disease (CVD) by more than one third compared with peers who largely don’t sit at work, new research shows. 

However, daily breaks from sitting and leisure-time activity can help mitigate the “serious” risks associated with prolonged occupational sitting, the researchers say. 

“As part of modern lifestyles, prolonged occupational sitting is considered normal and has not received due attention, even though its deleterious effect on health outcomes has been demonstrated,” wrote the authors, led by Wayne Gao, PhD, with Taipei Medical University College of Public Health, Taipei City, Taiwan. 

“The importance of physical activity and moving around can never be overstated,” Michelle Bloom, MD, director of the cardio-oncology program at NYU Langone Health in New York, who wasn’t involved in the study, told this news organization. 

“As a cardiologist, I bring this up at almost every visit with every patient regardless of why they’re seeing me, because I think that patients respond better when their doctor says it than when they just kind of know it in the back of their mind,” said Dr. Bloom, who is also a professor in the Division of Cardiology, NYU Grossman Long Island School of Medicine, New York. 

The study was published online in JAMA Network Open.

Prolonged Sitting Hard on the Heart 

2020 marked the first time that guidelines on physical activity from the World Health Organization recommended reducing sedentary behaviors owing to their health consequences. Less is known on the specific association of prolonged occupational sitting with health outcomes, especially in the context of low physical activity. 

For their study, Dr. Gao and colleagues quantified health risks associated with prolonged sitting on the job and determined whether a certain threshold of physical activity may attenuate this risk. 

Participants included 481,688 adults (mean age, 39 years; 53% women) in a health surveillance program in Taiwan. Data on occupational sitting, leisure-time physical activity, lifestyle, and metabolic parameters were collected. 

During an average follow up of nearly 13 years, 26,257 participants died; more than half (57%) of the deaths occurred in individuals who mostly sat at work. There were 5371 CVD-related deaths, with 60% occurring in the mostly sitting group. 

In multivariate analysis that adjusted for sex, age, education, smoking, drinking, and body mass index, adults who mostly sat at work had a 16% higher risk of dying of any cause (hazard ratio [HR], 1.16; 95% CI, 1.11-1.20) and a 34% increased risk of dying of CVD (HR, 1.34; 95% CI, 1.22-1.46) compared with those who mostly did not sit at work. 

Adults who mostly alternated between sitting and not sitting at work were not at increased risk of all-cause mortality compared with individuals who mostly did not at work (HR, 1.01; 95% CI, 0.97-1.05). 

Among adults who mostly sat at work and engaged in low (15-29 minutes) or no (< 15 minutes) daily leisure-time activity, increasing activity by 15 and 30 minutes per day, respectively, lowered the risk for mortality to a level similar to that of inactive individuals who mostly do not sit at work. 

“Overall, our findings from a large prospective cohort help to strengthen the increasingly accumulating evidence linking a sedentary lifestyle and health risks,” the authors wrote. 

“Systemic changes, such as more frequent breaks, standing desks, designated workplace areas for physical activity, and gym membership benefits, can help reduce risk,” they added. 

Simple Yet Profound Message 

Reached for comment, Anu Lala, MD, with Icahn School of Medicine at Mount Sinai and Mount Sinai Fuster Heart Hospital in New York, said this study provides a “simple yet profound message” about the dangers of prolonged sitting. 

The finding of a 16% higher all-cause mortality in those who mostly sat at work after adjustment for major risk factors is “pretty remarkable. And for CVD mortality, it’s double that,” Dr. Lala told this news organization.

“I think we undervalue the importance of movement, however simple it is. Even simple actions, like squatting and standing up have benefits for the heart,” Dr. Lala added. 

Dr. Bloom said she tells her patients, “You don’t have to go out tomorrow and run a marathon. Just get up a few times a day, walk a few laps in your office, walk back and forth from the mailbox, walk up and down your steps a couple of times — just do something more than you’re doing already.”

The study had no commercial funding. Dr. Gao and Dr. Bloom have no relevant disclosures. Dr. Lala has serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for Novartis, AstraZeneca, Merck, Bayer, Novo Nordisk, Cordio, Zoll, and Sequana Medical.

A version of this article appeared on Medscape.com.

People who mainly sit while on the job increase their risk of dying of cardiovascular disease (CVD) by more than one third compared with peers who largely don’t sit at work, new research shows. 

However, daily breaks from sitting and leisure-time activity can help mitigate the “serious” risks associated with prolonged occupational sitting, the researchers say. 

“As part of modern lifestyles, prolonged occupational sitting is considered normal and has not received due attention, even though its deleterious effect on health outcomes has been demonstrated,” wrote the authors, led by Wayne Gao, PhD, with Taipei Medical University College of Public Health, Taipei City, Taiwan. 

“The importance of physical activity and moving around can never be overstated,” Michelle Bloom, MD, director of the cardio-oncology program at NYU Langone Health in New York, who wasn’t involved in the study, told this news organization. 

“As a cardiologist, I bring this up at almost every visit with every patient regardless of why they’re seeing me, because I think that patients respond better when their doctor says it than when they just kind of know it in the back of their mind,” said Dr. Bloom, who is also a professor in the Division of Cardiology, NYU Grossman Long Island School of Medicine, New York. 

The study was published online in JAMA Network Open.

Prolonged Sitting Hard on the Heart 

2020 marked the first time that guidelines on physical activity from the World Health Organization recommended reducing sedentary behaviors owing to their health consequences. Less is known on the specific association of prolonged occupational sitting with health outcomes, especially in the context of low physical activity. 

For their study, Dr. Gao and colleagues quantified health risks associated with prolonged sitting on the job and determined whether a certain threshold of physical activity may attenuate this risk. 

Participants included 481,688 adults (mean age, 39 years; 53% women) in a health surveillance program in Taiwan. Data on occupational sitting, leisure-time physical activity, lifestyle, and metabolic parameters were collected. 

During an average follow up of nearly 13 years, 26,257 participants died; more than half (57%) of the deaths occurred in individuals who mostly sat at work. There were 5371 CVD-related deaths, with 60% occurring in the mostly sitting group. 

In multivariate analysis that adjusted for sex, age, education, smoking, drinking, and body mass index, adults who mostly sat at work had a 16% higher risk of dying of any cause (hazard ratio [HR], 1.16; 95% CI, 1.11-1.20) and a 34% increased risk of dying of CVD (HR, 1.34; 95% CI, 1.22-1.46) compared with those who mostly did not sit at work. 

Adults who mostly alternated between sitting and not sitting at work were not at increased risk of all-cause mortality compared with individuals who mostly did not at work (HR, 1.01; 95% CI, 0.97-1.05). 

Among adults who mostly sat at work and engaged in low (15-29 minutes) or no (< 15 minutes) daily leisure-time activity, increasing activity by 15 and 30 minutes per day, respectively, lowered the risk for mortality to a level similar to that of inactive individuals who mostly do not sit at work. 

“Overall, our findings from a large prospective cohort help to strengthen the increasingly accumulating evidence linking a sedentary lifestyle and health risks,” the authors wrote. 

“Systemic changes, such as more frequent breaks, standing desks, designated workplace areas for physical activity, and gym membership benefits, can help reduce risk,” they added. 

Simple Yet Profound Message 

Reached for comment, Anu Lala, MD, with Icahn School of Medicine at Mount Sinai and Mount Sinai Fuster Heart Hospital in New York, said this study provides a “simple yet profound message” about the dangers of prolonged sitting. 

The finding of a 16% higher all-cause mortality in those who mostly sat at work after adjustment for major risk factors is “pretty remarkable. And for CVD mortality, it’s double that,” Dr. Lala told this news organization.

“I think we undervalue the importance of movement, however simple it is. Even simple actions, like squatting and standing up have benefits for the heart,” Dr. Lala added. 

Dr. Bloom said she tells her patients, “You don’t have to go out tomorrow and run a marathon. Just get up a few times a day, walk a few laps in your office, walk back and forth from the mailbox, walk up and down your steps a couple of times — just do something more than you’re doing already.”

The study had no commercial funding. Dr. Gao and Dr. Bloom have no relevant disclosures. Dr. Lala has serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for Novartis, AstraZeneca, Merck, Bayer, Novo Nordisk, Cordio, Zoll, and Sequana Medical.

A version of this article appeared on Medscape.com.

People who mainly sit while on the job increase their risk of dying of cardiovascular disease (CVD) by more than one third compared with peers who largely don’t sit at work, new research shows. 

However, daily breaks from sitting and leisure-time activity can help mitigate the “serious” risks associated with prolonged occupational sitting, the researchers say. 

“As part of modern lifestyles, prolonged occupational sitting is considered normal and has not received due attention, even though its deleterious effect on health outcomes has been demonstrated,” wrote the authors, led by Wayne Gao, PhD, with Taipei Medical University College of Public Health, Taipei City, Taiwan. 

“The importance of physical activity and moving around can never be overstated,” Michelle Bloom, MD, director of the cardio-oncology program at NYU Langone Health in New York, who wasn’t involved in the study, told this news organization. 

“As a cardiologist, I bring this up at almost every visit with every patient regardless of why they’re seeing me, because I think that patients respond better when their doctor says it than when they just kind of know it in the back of their mind,” said Dr. Bloom, who is also a professor in the Division of Cardiology, NYU Grossman Long Island School of Medicine, New York. 

The study was published online in JAMA Network Open.

Prolonged Sitting Hard on the Heart 

2020 marked the first time that guidelines on physical activity from the World Health Organization recommended reducing sedentary behaviors owing to their health consequences. Less is known on the specific association of prolonged occupational sitting with health outcomes, especially in the context of low physical activity. 

For their study, Dr. Gao and colleagues quantified health risks associated with prolonged sitting on the job and determined whether a certain threshold of physical activity may attenuate this risk. 

Participants included 481,688 adults (mean age, 39 years; 53% women) in a health surveillance program in Taiwan. Data on occupational sitting, leisure-time physical activity, lifestyle, and metabolic parameters were collected. 

During an average follow up of nearly 13 years, 26,257 participants died; more than half (57%) of the deaths occurred in individuals who mostly sat at work. There were 5371 CVD-related deaths, with 60% occurring in the mostly sitting group. 

In multivariate analysis that adjusted for sex, age, education, smoking, drinking, and body mass index, adults who mostly sat at work had a 16% higher risk of dying of any cause (hazard ratio [HR], 1.16; 95% CI, 1.11-1.20) and a 34% increased risk of dying of CVD (HR, 1.34; 95% CI, 1.22-1.46) compared with those who mostly did not sit at work. 

Adults who mostly alternated between sitting and not sitting at work were not at increased risk of all-cause mortality compared with individuals who mostly did not at work (HR, 1.01; 95% CI, 0.97-1.05). 

Among adults who mostly sat at work and engaged in low (15-29 minutes) or no (< 15 minutes) daily leisure-time activity, increasing activity by 15 and 30 minutes per day, respectively, lowered the risk for mortality to a level similar to that of inactive individuals who mostly do not sit at work. 

“Overall, our findings from a large prospective cohort help to strengthen the increasingly accumulating evidence linking a sedentary lifestyle and health risks,” the authors wrote. 

“Systemic changes, such as more frequent breaks, standing desks, designated workplace areas for physical activity, and gym membership benefits, can help reduce risk,” they added. 

Simple Yet Profound Message 

Reached for comment, Anu Lala, MD, with Icahn School of Medicine at Mount Sinai and Mount Sinai Fuster Heart Hospital in New York, said this study provides a “simple yet profound message” about the dangers of prolonged sitting. 

The finding of a 16% higher all-cause mortality in those who mostly sat at work after adjustment for major risk factors is “pretty remarkable. And for CVD mortality, it’s double that,” Dr. Lala told this news organization.

“I think we undervalue the importance of movement, however simple it is. Even simple actions, like squatting and standing up have benefits for the heart,” Dr. Lala added. 

Dr. Bloom said she tells her patients, “You don’t have to go out tomorrow and run a marathon. Just get up a few times a day, walk a few laps in your office, walk back and forth from the mailbox, walk up and down your steps a couple of times — just do something more than you’re doing already.”

The study had no commercial funding. Dr. Gao and Dr. Bloom have no relevant disclosures. Dr. Lala has serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for Novartis, AstraZeneca, Merck, Bayer, Novo Nordisk, Cordio, Zoll, and Sequana Medical.

A version of this article appeared on Medscape.com.

TOPLINE:

Deaths caused by both substance use (SU) and cardiovascular disease (CVD) increased substantially in the United States between 1999 and 2019, with the most pronounced rise among women, American Indians, younger people, rural residents, and users of cannabis and psychostimulants, results of new research suggest.

METHODOLOGY:

• From the Centers for Disease Control and Prevention Wide-Ranging Online Data for Epidemiologic Research (CDC WONDER) database and using International Classification of Diseases (ICD) codes, researchers collected data on deaths within the United States where both SU and CVD (SU+CVD) were a contributing or an underlying cause and gathered information on location of death (medical facility, home, hospice, nursing home/long-term care facility), demographics (sex, race/ethnicity, age), and region (urban-rural, state).
• Researchers determined crude and age-adjusted mortality rates (AAMRs) per 100,000 population, identified trends in AAMR using annual percent change (APC) and calculated the weighted average of APCs (AAPCs).
• Between 1999 and 2019, there were 636,572 deaths related to CVD+SU, 75.6% of which were among men and 70.6% among non-Hispanic White individuals, with 65% related to alcohol, and where location of death was available, 47.7% occurred in medical facilities.

TAKEAWAY:

• The overall SU+CVD-related AAMR from 1999 to 2019 was 14.3 (95% CI, 14.3-14.3) per 100,000 individuals, with the rate being higher in men (22.5) than in women (6.8) and highest in American Indians or Alaska Natives (37.7) compared with other races/ethnicities.
• Rural areas had higher SU+CVD-related AAMR (15.2; 95% CI, 15.1-15.3) than urban areas, with the District of Columbia having the highest AAMR geographically (25.4), individuals aged 55-69 years having the highest rate agewise (25.1), and alcohol accounting for the highest rate (9.09) among substance types.
• Temporal trends show that the overall SU+CVD-related AAMR increased from 9.9 in 1999 to 21.4 in 2019, a rate that started accelerating in 2012, with an AAPC of 4.0% (95% CI, 3.7-4.3); increases were across all ethnicities and age groups and were particularly pronounced among women (4.8%; 95% CI, 4.5-5.1).
• Cannabis had the highest AAPC of all substances (12.7%), but stimulants had an APC of 21.4 (95% CI, 20.0-22.8) from 2009 to 2019, a period during which stimulants were the fastest-growing substance abuse category.

IN PRACTICE:

These new results identify high-risk groups, which “is crucial for prioritizing preventive measures aiming to reduce substance use and cardiovascular disease-related mortality in these populations,” the researchers wrote.

SOURCE:

Abdul Mannan Khan Minhas, MD, Department of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, and Jakrin Kewcharoen, MD, Division of Cardiology, Loma Linda University Medical Center, Loma Linda, California, were co-first authors of the study, which was published online in the Journal of the American Heart Association.

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

TOPLINE:

Deaths caused by both substance use (SU) and cardiovascular disease (CVD) increased substantially in the United States between 1999 and 2019, with the most pronounced rise among women, American Indians, younger people, rural residents, and users of cannabis and psychostimulants, results of new research suggest.

METHODOLOGY:

• From the Centers for Disease Control and Prevention Wide-Ranging Online Data for Epidemiologic Research (CDC WONDER) database and using International Classification of Diseases (ICD) codes, researchers collected data on deaths within the United States where both SU and CVD (SU+CVD) were a contributing or an underlying cause and gathered information on location of death (medical facility, home, hospice, nursing home/long-term care facility), demographics (sex, race/ethnicity, age), and region (urban-rural, state).
• Researchers determined crude and age-adjusted mortality rates (AAMRs) per 100,000 population, identified trends in AAMR using annual percent change (APC) and calculated the weighted average of APCs (AAPCs).
• Between 1999 and 2019, there were 636,572 deaths related to CVD+SU, 75.6% of which were among men and 70.6% among non-Hispanic White individuals, with 65% related to alcohol, and where location of death was available, 47.7% occurred in medical facilities.

TAKEAWAY:

• The overall SU+CVD-related AAMR from 1999 to 2019 was 14.3 (95% CI, 14.3-14.3) per 100,000 individuals, with the rate being higher in men (22.5) than in women (6.8) and highest in American Indians or Alaska Natives (37.7) compared with other races/ethnicities.
• Rural areas had higher SU+CVD-related AAMR (15.2; 95% CI, 15.1-15.3) than urban areas, with the District of Columbia having the highest AAMR geographically (25.4), individuals aged 55-69 years having the highest rate agewise (25.1), and alcohol accounting for the highest rate (9.09) among substance types.
• Temporal trends show that the overall SU+CVD-related AAMR increased from 9.9 in 1999 to 21.4 in 2019, a rate that started accelerating in 2012, with an AAPC of 4.0% (95% CI, 3.7-4.3); increases were across all ethnicities and age groups and were particularly pronounced among women (4.8%; 95% CI, 4.5-5.1).
• Cannabis had the highest AAPC of all substances (12.7%), but stimulants had an APC of 21.4 (95% CI, 20.0-22.8) from 2009 to 2019, a period during which stimulants were the fastest-growing substance abuse category.

IN PRACTICE:

These new results identify high-risk groups, which “is crucial for prioritizing preventive measures aiming to reduce substance use and cardiovascular disease-related mortality in these populations,” the researchers wrote.

SOURCE:

Abdul Mannan Khan Minhas, MD, Department of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, and Jakrin Kewcharoen, MD, Division of Cardiology, Loma Linda University Medical Center, Loma Linda, California, were co-first authors of the study, which was published online in the Journal of the American Heart Association.

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

TOPLINE:

Deaths caused by both substance use (SU) and cardiovascular disease (CVD) increased substantially in the United States between 1999 and 2019, with the most pronounced rise among women, American Indians, younger people, rural residents, and users of cannabis and psychostimulants, results of new research suggest.

METHODOLOGY:

• From the Centers for Disease Control and Prevention Wide-Ranging Online Data for Epidemiologic Research (CDC WONDER) database and using International Classification of Diseases (ICD) codes, researchers collected data on deaths within the United States where both SU and CVD (SU+CVD) were a contributing or an underlying cause and gathered information on location of death (medical facility, home, hospice, nursing home/long-term care facility), demographics (sex, race/ethnicity, age), and region (urban-rural, state).
• Researchers determined crude and age-adjusted mortality rates (AAMRs) per 100,000 population, identified trends in AAMR using annual percent change (APC) and calculated the weighted average of APCs (AAPCs).
• Between 1999 and 2019, there were 636,572 deaths related to CVD+SU, 75.6% of which were among men and 70.6% among non-Hispanic White individuals, with 65% related to alcohol, and where location of death was available, 47.7% occurred in medical facilities.

TAKEAWAY:

• The overall SU+CVD-related AAMR from 1999 to 2019 was 14.3 (95% CI, 14.3-14.3) per 100,000 individuals, with the rate being higher in men (22.5) than in women (6.8) and highest in American Indians or Alaska Natives (37.7) compared with other races/ethnicities.
• Rural areas had higher SU+CVD-related AAMR (15.2; 95% CI, 15.1-15.3) than urban areas, with the District of Columbia having the highest AAMR geographically (25.4), individuals aged 55-69 years having the highest rate agewise (25.1), and alcohol accounting for the highest rate (9.09) among substance types.
• Temporal trends show that the overall SU+CVD-related AAMR increased from 9.9 in 1999 to 21.4 in 2019, a rate that started accelerating in 2012, with an AAPC of 4.0% (95% CI, 3.7-4.3); increases were across all ethnicities and age groups and were particularly pronounced among women (4.8%; 95% CI, 4.5-5.1).
• Cannabis had the highest AAPC of all substances (12.7%), but stimulants had an APC of 21.4 (95% CI, 20.0-22.8) from 2009 to 2019, a period during which stimulants were the fastest-growing substance abuse category.

IN PRACTICE:

These new results identify high-risk groups, which “is crucial for prioritizing preventive measures aiming to reduce substance use and cardiovascular disease-related mortality in these populations,” the researchers wrote.

SOURCE:

Abdul Mannan Khan Minhas, MD, Department of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, and Jakrin Kewcharoen, MD, Division of Cardiology, Loma Linda University Medical Center, Loma Linda, California, were co-first authors of the study, which was published online in the Journal of the American Heart Association.

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

TOPLINE: 

Among patients hospitalized with a first ischemic stroke, 80% were rehospitalized, primarily because of subsequent primary cardiovascular and cerebrovascular diagnoses.

METHODOLOGY:

• To gather information on post-stroke hospital admission, investigators followed 1412 participants (mean age, 72.4 years; 52.1% women, 35.3% Black individuals) from the Atherosclerosis Risk in Communities (ARIC) study who were living in Maryland, Minnesota, North Carolina, and Mississippi.
• Participants were recruited between 1987 and 1989 when they were 45-64 years old and were followed on an annual and then semiannual basis from the index discharge until discharge after their second hospitalization, death, or end of the study in December 2019.
• Specific diagnoses for each hospitalization were based on hospital records, discharge diagnoses, and annual and semiannual phone interviews.

TAKEAWAY: 

• During the study period, 1143 hospitalizations occurred over 41,849 person-months.
• 81% of participants were hospitalized over a maximum of 26.6 years of follow-up. Primary cardiovascular and cerebrovascular diagnoses were reported for half of readmissions.
• Over the follow-up period, compared with cardioembolic stroke, readmission risk was lower for thrombotic/lacunar stroke (adjusted hazard ratio [aHR], 0.82; 95% CI, 0.71-0.95) and hemorrhagic stroke (aHR, 0.74; 95% CI, 0.58-0.93). However, when adjusting for atrial fibrillation and competing risk for death, there were no significant differences between stroke subtypes.
• Compared with cardioembolic stroke, thrombotic/lacunar stroke was associated with lower readmission risk within 1 month (aHR, 0.66; 95% CI, 0.46-0.93) and from 1 month to 1 year (aHR, 0.78; 95% CI, 0.62-0.97), and hemorrhagic stroke was associated with lower risk from 1 month to 1 year (aHR, 0.60; 95% CI, 0.41-0.87).

IN PRACTICE:

“These results suggest that prevention strategies focused on cardiovascular and cerebrovascular health warrant further investigation, especially within the first year after incident stroke and perhaps particularly among individuals with an incident cardioembolic stroke,” the authors wrote.

SOURCE:

Kelly Sloane, MD, of the University of Pennsylvania Perelman School of Medicine in Philadelphia, led the study along with colleagues at the National Institute of Neurological Disorders and Stroke, Johns Hopkins University in Baltimore, and the University of North Carolina, Chapel Hill. The article was published online on January 5 in Neurology.

LIMITATIONS:

The ARIC study classification of stroke subtype grouped embolic strokes of undetermined source as thrombotic strokes, and investigators were unable to distinguish between the groups. In addition, there was no way to measure stroke severity, which could have played a role in readmission risk.

DISCLOSURES:

The study was funded by the National Heart, Lung, and Blood Institute, the National Institute of Neurological Disorders and Stroke, and the National Institutes of Health.

A version of this article appeared on Medscape.com.

TOPLINE: 

Among patients hospitalized with a first ischemic stroke, 80% were rehospitalized, primarily because of subsequent primary cardiovascular and cerebrovascular diagnoses.

METHODOLOGY:

• To gather information on post-stroke hospital admission, investigators followed 1412 participants (mean age, 72.4 years; 52.1% women, 35.3% Black individuals) from the Atherosclerosis Risk in Communities (ARIC) study who were living in Maryland, Minnesota, North Carolina, and Mississippi.
• Participants were recruited between 1987 and 1989 when they were 45-64 years old and were followed on an annual and then semiannual basis from the index discharge until discharge after their second hospitalization, death, or end of the study in December 2019.
• Specific diagnoses for each hospitalization were based on hospital records, discharge diagnoses, and annual and semiannual phone interviews.

TAKEAWAY: 

• During the study period, 1143 hospitalizations occurred over 41,849 person-months.
• 81% of participants were hospitalized over a maximum of 26.6 years of follow-up. Primary cardiovascular and cerebrovascular diagnoses were reported for half of readmissions.
• Over the follow-up period, compared with cardioembolic stroke, readmission risk was lower for thrombotic/lacunar stroke (adjusted hazard ratio [aHR], 0.82; 95% CI, 0.71-0.95) and hemorrhagic stroke (aHR, 0.74; 95% CI, 0.58-0.93). However, when adjusting for atrial fibrillation and competing risk for death, there were no significant differences between stroke subtypes.
• Compared with cardioembolic stroke, thrombotic/lacunar stroke was associated with lower readmission risk within 1 month (aHR, 0.66; 95% CI, 0.46-0.93) and from 1 month to 1 year (aHR, 0.78; 95% CI, 0.62-0.97), and hemorrhagic stroke was associated with lower risk from 1 month to 1 year (aHR, 0.60; 95% CI, 0.41-0.87).

IN PRACTICE:

“These results suggest that prevention strategies focused on cardiovascular and cerebrovascular health warrant further investigation, especially within the first year after incident stroke and perhaps particularly among individuals with an incident cardioembolic stroke,” the authors wrote.

SOURCE:

Kelly Sloane, MD, of the University of Pennsylvania Perelman School of Medicine in Philadelphia, led the study along with colleagues at the National Institute of Neurological Disorders and Stroke, Johns Hopkins University in Baltimore, and the University of North Carolina, Chapel Hill. The article was published online on January 5 in Neurology.

LIMITATIONS:

The ARIC study classification of stroke subtype grouped embolic strokes of undetermined source as thrombotic strokes, and investigators were unable to distinguish between the groups. In addition, there was no way to measure stroke severity, which could have played a role in readmission risk.

DISCLOSURES:

The study was funded by the National Heart, Lung, and Blood Institute, the National Institute of Neurological Disorders and Stroke, and the National Institutes of Health.

A version of this article appeared on Medscape.com.

TOPLINE: 

Among patients hospitalized with a first ischemic stroke, 80% were rehospitalized, primarily because of subsequent primary cardiovascular and cerebrovascular diagnoses.

METHODOLOGY:

• To gather information on post-stroke hospital admission, investigators followed 1412 participants (mean age, 72.4 years; 52.1% women, 35.3% Black individuals) from the Atherosclerosis Risk in Communities (ARIC) study who were living in Maryland, Minnesota, North Carolina, and Mississippi.
• Participants were recruited between 1987 and 1989 when they were 45-64 years old and were followed on an annual and then semiannual basis from the index discharge until discharge after their second hospitalization, death, or end of the study in December 2019.
• Specific diagnoses for each hospitalization were based on hospital records, discharge diagnoses, and annual and semiannual phone interviews.

TAKEAWAY: 

• During the study period, 1143 hospitalizations occurred over 41,849 person-months.
• 81% of participants were hospitalized over a maximum of 26.6 years of follow-up. Primary cardiovascular and cerebrovascular diagnoses were reported for half of readmissions.
• Over the follow-up period, compared with cardioembolic stroke, readmission risk was lower for thrombotic/lacunar stroke (adjusted hazard ratio [aHR], 0.82; 95% CI, 0.71-0.95) and hemorrhagic stroke (aHR, 0.74; 95% CI, 0.58-0.93). However, when adjusting for atrial fibrillation and competing risk for death, there were no significant differences between stroke subtypes.
• Compared with cardioembolic stroke, thrombotic/lacunar stroke was associated with lower readmission risk within 1 month (aHR, 0.66; 95% CI, 0.46-0.93) and from 1 month to 1 year (aHR, 0.78; 95% CI, 0.62-0.97), and hemorrhagic stroke was associated with lower risk from 1 month to 1 year (aHR, 0.60; 95% CI, 0.41-0.87).

IN PRACTICE:

“These results suggest that prevention strategies focused on cardiovascular and cerebrovascular health warrant further investigation, especially within the first year after incident stroke and perhaps particularly among individuals with an incident cardioembolic stroke,” the authors wrote.

SOURCE:

Kelly Sloane, MD, of the University of Pennsylvania Perelman School of Medicine in Philadelphia, led the study along with colleagues at the National Institute of Neurological Disorders and Stroke, Johns Hopkins University in Baltimore, and the University of North Carolina, Chapel Hill. The article was published online on January 5 in Neurology.

LIMITATIONS:

The ARIC study classification of stroke subtype grouped embolic strokes of undetermined source as thrombotic strokes, and investigators were unable to distinguish between the groups. In addition, there was no way to measure stroke severity, which could have played a role in readmission risk.

DISCLOSURES:

The study was funded by the National Heart, Lung, and Blood Institute, the National Institute of Neurological Disorders and Stroke, and the National Institutes of Health.

A version of this article appeared on Medscape.com.

The long-term impact of traumatic brain injury (TBI) on neurologic and psychiatric function is well-established, but a growing body of research is pointing to unexpected medical sequalae, including cardiovascular disease (CVD).

A recent review looked at the investigation to date into this surprising connection, not only summarizing study findings but also suggesting potential mechanisms that might account for the association.

“This work offers further evidence that individuals with TBI are at an elevated risk of unfavorable cardiovascular outcomes for an extended period following the initial incident; consequently, they should undergo regular monitoring,” senior author Ross Zafonte, DO, president of Spaulding Rehabilitation Network, Boston, and lead author Saef Izzy, MD, MBChB, a neurologist at the Stroke and Cerebrovascular Center of Brigham and Women’s Hospital, Boston, Massachusetts, told this news organization.

“This holds significant importance for healthcare practitioners, as there exist several strategies to mitigate cardiovascular disease risk — including weight management, adopting a healthy diet, engaging in regular physical activity, and quitting smoking,” they stated.

Leslie Croll, MD, American Heart Association volunteer and assistant professor of clinical neurology at the Temple University Lewis Katz School of Medicine, Philadelphia, Pennsylvania, told this news organization that it’s “extremely important to learn more about the interplay between TBI, neurologic disease, psychiatric complications, and the cardiovascular system.”

Hopefully, she added, “future research will help us understand what kind of cardiovascular disease monitoring and prevention measures stand to give TBI patients the most benefit.”
 

Chronic Condition

TBI is “a major cause of long-term disability and premature death,” and is “highly prevalent among contact sports players, military personnel (eg, due to injuries sustained during conflict), and the general population (eg, due to falls and road traffic incidents),” the authors wrote.

Most studies pertaining to TBI have “primarily focused on establishing connections between single TBI, repetitive TBI, and their acute and chronic neurological and psychiatric consequences, such as Parkinson’s disease, Alzheimer’s disease, and chronic traumatic encephalopathy (CTE),” Drs. Zafonte and Izzy noted. By contrast, there has been a “notable lack of research attention given to non-neurological conditions associated with TBI.”

They pointed out that recent insights into TBI — particularly the acknowledgment of TBI as an “emerging chronic condition rather than merely an acute aftermath of brain injury” — have come to light through epidemiologic and pathologic investigations involving military veterans, professional American-style football players, and the civilian population. “This recognition opens up an opportunity to broaden our perspective and delve into the medical aspects of health that may be influenced by TBI.”

To broaden the investigation, the researchers reviewed literature published between January 1, 2001, and June 18, 2023. Of 26,335 articles, they narrowed their review down to 15 studies that investigated CVD, CVD risk factors, and cerebrovascular disease in the chronic phase of TBI, including community, military, or sport-related brain trauma, regardless of the timing of disease occurrence with respect to brain injury via TBI or repetitive head impact.
 

New Cardiovascular Risk

Studies that used national or local registries tended to be retrospective and predominantly conducted in people with preexisting cardiovascular conditions. In these studies, TBI was found to be an independent risk factor for myocardial dysfunction. However, although these studies do provide evidence of elevated cardiovascular risk subsequent to a single TBI, including individuals with preexisting medical comorbidities “makes it difficult to determine the timing of incident cardiovascular disease and cardiovascular risk factors subsequent to brain injury,” they wrote.

However, some studies showed that even individuals with TBI but without preexisting myocardial dysfunction at baseline had a significantly higher risk for CVD than those without a history of TBI.

In fact, several studies included populations without preexisting medical and cardiovascular comorbidities to “better refine the order and timing of CVD and other risk factors in individuals with TBI.”

For example, one study of concussion survivors without preexisting diagnoses showed that cardiovascular, endocrinological, and neuropsychiatric comorbidities occurred at a “significantly higher incidence within 5 years after concussive TBI compared with healthy individuals who were matched in terms of age, race, and sex and didn’t have a TBI exposure.” Other studies yielded similar findings.

Because cardiovascular risk factors and events become more common with age, it’s important to account for age in evaluating the effects of TBI. Although many studies of TBI and subsequent CVD didn’t stratify individuals by age, one 10-year study of people without any known cardiovascular or neuropsychiatric conditions who sustained TBI found that people as young as 18-40 years were more likely to develop hypertension, hyperlipidemia, obesity, and diabetes within 3-5 years following brain injury than matched individuals in the control group.

“Individuals who have encountered TBI, surprisingly even those who are young and in good health with no prior comorbid conditions, face an increased risk of adverse cardiovascular outcomes for an extended duration after the initial event,” Drs. Zafonte and Izzy summarized. “Therefore, it’s imperative that they receive regular and long-term screenings for CVD and associated risk factors.”
 

Bidirectional Relationship

Brain injury has been associated with acute cardiovascular dysfunction, including autonomic heart-brain axis dysregulation, imbalances between the sympathetic and parasympathetic nervous systems, and excessive catecholamine release, the authors noted.

Drs. Zafonte and Izzy suggested several plausible links between TBI and cardiovascular dysfunction, noting that they are “likely multifaceted, potentially encompassing risk factors that span the pre-injury, injury, and post-injury phases of the condition.”

TBI may induce alterations in neurobiological processes, which have been reported to be associated with an increased risk for CVD (eg, chronic dysfunction of the autonomic system, systemic inflammation, and modifications in the brain-gut connection).

Patients with TBI might develop additional risk factors following the injury, including conditions like posttraumatic stress disorder, depression, and other psychiatric illnesses, which are “known to augment the risk of CVD.”

TBI can lead to subsequent behavioral and lifestyle changes that place patients at an elevated risk for both cardiovascular and cognitive dysfunction when compared to the general population of TBI survivors.

There may be additional as yet undefined risks.

They believe there’s a bidirectional relationship between TBI and CVD. “On one hand, TBI has been associated with an elevated risk of CVD,” they said. “Conversely, cardiovascular risk factors such as diabetes, hypertension, hyperlipidemia, and sleep disturbances that have been demonstrated to negatively influence cognitive function and heighten the risk of dementia. Consequently, this interplay can further compound the long-term consequences of the injury.”

Their work aims to try and disentangle this “complex series of relationships.”

They recommend screening to identify diseases in their earliest and “most manageable phases” because TBI has been “unveiled as an underappreciated risk factor for CVD within contact sports, military, and community setting.”

An effective screening program “should rely on quantifiable and dependable biomarkers such as blood pressure, BMI, waist circumference, blood lipid levels, and glucose. Additionally, it should take into account other factors like smoking habits, physical activity, and dietary choices,” they recommended.
 

Heart-Brain Connection

Dr. Croll noted that TBI is “associated with many poorly understood physiologic changes and complications, so it’s exciting to see research aimed at clarifying this chronic disease process.”

In recent years, “we have seen a greater appreciation and understanding of the heart-brain connection,” she said. “Moving forward, more research, including TBI research, will target that connection.”

She added that there are probably “multiple mechanisms” at play underlying the connection between TBI and CVD.

Most importantly, “we are increasingly learning that TBI is not only a discrete event that requires immediate treatment but also a chronic disease process,” and when we “think about the substantial long-term morbidity associated with TBI, we should keep increased risk for CVD on top of mind,” said Dr. Croll.

The review received no funding. Izzy reported receiving grants from the US National Institutes of Health (NIH) and 2023 Stepping Strong Innovator Award. Dr. Zafonte reported receiving grants from the NIH and royalties from Springer and Demos publishing for serving as a coeditor of Brain Injury Medicine. Dr. Zafonte has also served as an adviser to Myomo, Oncare.ai, Nanodiagnostics, and Kisbee. He reported evaluating patients in the Massachusetts General Hospital Brain and Body–TRUST Program, which is funded by the NFL Players Association. The other authors’ disclosures are listed on the original paper. Dr. Croll declared no relevant financial relationships.

A version of this article appeared on Medscape.com.

The long-term impact of traumatic brain injury (TBI) on neurologic and psychiatric function is well-established, but a growing body of research is pointing to unexpected medical sequalae, including cardiovascular disease (CVD).

A recent review looked at the investigation to date into this surprising connection, not only summarizing study findings but also suggesting potential mechanisms that might account for the association.

“This work offers further evidence that individuals with TBI are at an elevated risk of unfavorable cardiovascular outcomes for an extended period following the initial incident; consequently, they should undergo regular monitoring,” senior author Ross Zafonte, DO, president of Spaulding Rehabilitation Network, Boston, and lead author Saef Izzy, MD, MBChB, a neurologist at the Stroke and Cerebrovascular Center of Brigham and Women’s Hospital, Boston, Massachusetts, told this news organization.

“This holds significant importance for healthcare practitioners, as there exist several strategies to mitigate cardiovascular disease risk — including weight management, adopting a healthy diet, engaging in regular physical activity, and quitting smoking,” they stated.

Leslie Croll, MD, American Heart Association volunteer and assistant professor of clinical neurology at the Temple University Lewis Katz School of Medicine, Philadelphia, Pennsylvania, told this news organization that it’s “extremely important to learn more about the interplay between TBI, neurologic disease, psychiatric complications, and the cardiovascular system.”

Hopefully, she added, “future research will help us understand what kind of cardiovascular disease monitoring and prevention measures stand to give TBI patients the most benefit.”
 

Chronic Condition

TBI is “a major cause of long-term disability and premature death,” and is “highly prevalent among contact sports players, military personnel (eg, due to injuries sustained during conflict), and the general population (eg, due to falls and road traffic incidents),” the authors wrote.

Most studies pertaining to TBI have “primarily focused on establishing connections between single TBI, repetitive TBI, and their acute and chronic neurological and psychiatric consequences, such as Parkinson’s disease, Alzheimer’s disease, and chronic traumatic encephalopathy (CTE),” Drs. Zafonte and Izzy noted. By contrast, there has been a “notable lack of research attention given to non-neurological conditions associated with TBI.”

They pointed out that recent insights into TBI — particularly the acknowledgment of TBI as an “emerging chronic condition rather than merely an acute aftermath of brain injury” — have come to light through epidemiologic and pathologic investigations involving military veterans, professional American-style football players, and the civilian population. “This recognition opens up an opportunity to broaden our perspective and delve into the medical aspects of health that may be influenced by TBI.”

To broaden the investigation, the researchers reviewed literature published between January 1, 2001, and June 18, 2023. Of 26,335 articles, they narrowed their review down to 15 studies that investigated CVD, CVD risk factors, and cerebrovascular disease in the chronic phase of TBI, including community, military, or sport-related brain trauma, regardless of the timing of disease occurrence with respect to brain injury via TBI or repetitive head impact.
 

New Cardiovascular Risk

Studies that used national or local registries tended to be retrospective and predominantly conducted in people with preexisting cardiovascular conditions. In these studies, TBI was found to be an independent risk factor for myocardial dysfunction. However, although these studies do provide evidence of elevated cardiovascular risk subsequent to a single TBI, including individuals with preexisting medical comorbidities “makes it difficult to determine the timing of incident cardiovascular disease and cardiovascular risk factors subsequent to brain injury,” they wrote.

However, some studies showed that even individuals with TBI but without preexisting myocardial dysfunction at baseline had a significantly higher risk for CVD than those without a history of TBI.

In fact, several studies included populations without preexisting medical and cardiovascular comorbidities to “better refine the order and timing of CVD and other risk factors in individuals with TBI.”

For example, one study of concussion survivors without preexisting diagnoses showed that cardiovascular, endocrinological, and neuropsychiatric comorbidities occurred at a “significantly higher incidence within 5 years after concussive TBI compared with healthy individuals who were matched in terms of age, race, and sex and didn’t have a TBI exposure.” Other studies yielded similar findings.

Because cardiovascular risk factors and events become more common with age, it’s important to account for age in evaluating the effects of TBI. Although many studies of TBI and subsequent CVD didn’t stratify individuals by age, one 10-year study of people without any known cardiovascular or neuropsychiatric conditions who sustained TBI found that people as young as 18-40 years were more likely to develop hypertension, hyperlipidemia, obesity, and diabetes within 3-5 years following brain injury than matched individuals in the control group.

“Individuals who have encountered TBI, surprisingly even those who are young and in good health with no prior comorbid conditions, face an increased risk of adverse cardiovascular outcomes for an extended duration after the initial event,” Drs. Zafonte and Izzy summarized. “Therefore, it’s imperative that they receive regular and long-term screenings for CVD and associated risk factors.”
 

Bidirectional Relationship

Brain injury has been associated with acute cardiovascular dysfunction, including autonomic heart-brain axis dysregulation, imbalances between the sympathetic and parasympathetic nervous systems, and excessive catecholamine release, the authors noted.

Drs. Zafonte and Izzy suggested several plausible links between TBI and cardiovascular dysfunction, noting that they are “likely multifaceted, potentially encompassing risk factors that span the pre-injury, injury, and post-injury phases of the condition.”

TBI may induce alterations in neurobiological processes, which have been reported to be associated with an increased risk for CVD (eg, chronic dysfunction of the autonomic system, systemic inflammation, and modifications in the brain-gut connection).

Patients with TBI might develop additional risk factors following the injury, including conditions like posttraumatic stress disorder, depression, and other psychiatric illnesses, which are “known to augment the risk of CVD.”

TBI can lead to subsequent behavioral and lifestyle changes that place patients at an elevated risk for both cardiovascular and cognitive dysfunction when compared to the general population of TBI survivors.

There may be additional as yet undefined risks.

They believe there’s a bidirectional relationship between TBI and CVD. “On one hand, TBI has been associated with an elevated risk of CVD,” they said. “Conversely, cardiovascular risk factors such as diabetes, hypertension, hyperlipidemia, and sleep disturbances that have been demonstrated to negatively influence cognitive function and heighten the risk of dementia. Consequently, this interplay can further compound the long-term consequences of the injury.”

Their work aims to try and disentangle this “complex series of relationships.”

They recommend screening to identify diseases in their earliest and “most manageable phases” because TBI has been “unveiled as an underappreciated risk factor for CVD within contact sports, military, and community setting.”

An effective screening program “should rely on quantifiable and dependable biomarkers such as blood pressure, BMI, waist circumference, blood lipid levels, and glucose. Additionally, it should take into account other factors like smoking habits, physical activity, and dietary choices,” they recommended.
 

Heart-Brain Connection

Dr. Croll noted that TBI is “associated with many poorly understood physiologic changes and complications, so it’s exciting to see research aimed at clarifying this chronic disease process.”

In recent years, “we have seen a greater appreciation and understanding of the heart-brain connection,” she said. “Moving forward, more research, including TBI research, will target that connection.”

She added that there are probably “multiple mechanisms” at play underlying the connection between TBI and CVD.

Most importantly, “we are increasingly learning that TBI is not only a discrete event that requires immediate treatment but also a chronic disease process,” and when we “think about the substantial long-term morbidity associated with TBI, we should keep increased risk for CVD on top of mind,” said Dr. Croll.

The review received no funding. Izzy reported receiving grants from the US National Institutes of Health (NIH) and 2023 Stepping Strong Innovator Award. Dr. Zafonte reported receiving grants from the NIH and royalties from Springer and Demos publishing for serving as a coeditor of Brain Injury Medicine. Dr. Zafonte has also served as an adviser to Myomo, Oncare.ai, Nanodiagnostics, and Kisbee. He reported evaluating patients in the Massachusetts General Hospital Brain and Body–TRUST Program, which is funded by the NFL Players Association. The other authors’ disclosures are listed on the original paper. Dr. Croll declared no relevant financial relationships.

A version of this article appeared on Medscape.com.

The long-term impact of traumatic brain injury (TBI) on neurologic and psychiatric function is well-established, but a growing body of research is pointing to unexpected medical sequalae, including cardiovascular disease (CVD).

A recent review looked at the investigation to date into this surprising connection, not only summarizing study findings but also suggesting potential mechanisms that might account for the association.

“This work offers further evidence that individuals with TBI are at an elevated risk of unfavorable cardiovascular outcomes for an extended period following the initial incident; consequently, they should undergo regular monitoring,” senior author Ross Zafonte, DO, president of Spaulding Rehabilitation Network, Boston, and lead author Saef Izzy, MD, MBChB, a neurologist at the Stroke and Cerebrovascular Center of Brigham and Women’s Hospital, Boston, Massachusetts, told this news organization.

“This holds significant importance for healthcare practitioners, as there exist several strategies to mitigate cardiovascular disease risk — including weight management, adopting a healthy diet, engaging in regular physical activity, and quitting smoking,” they stated.

Leslie Croll, MD, American Heart Association volunteer and assistant professor of clinical neurology at the Temple University Lewis Katz School of Medicine, Philadelphia, Pennsylvania, told this news organization that it’s “extremely important to learn more about the interplay between TBI, neurologic disease, psychiatric complications, and the cardiovascular system.”

Hopefully, she added, “future research will help us understand what kind of cardiovascular disease monitoring and prevention measures stand to give TBI patients the most benefit.”
 

Chronic Condition

TBI is “a major cause of long-term disability and premature death,” and is “highly prevalent among contact sports players, military personnel (eg, due to injuries sustained during conflict), and the general population (eg, due to falls and road traffic incidents),” the authors wrote.

Most studies pertaining to TBI have “primarily focused on establishing connections between single TBI, repetitive TBI, and their acute and chronic neurological and psychiatric consequences, such as Parkinson’s disease, Alzheimer’s disease, and chronic traumatic encephalopathy (CTE),” Drs. Zafonte and Izzy noted. By contrast, there has been a “notable lack of research attention given to non-neurological conditions associated with TBI.”

They pointed out that recent insights into TBI — particularly the acknowledgment of TBI as an “emerging chronic condition rather than merely an acute aftermath of brain injury” — have come to light through epidemiologic and pathologic investigations involving military veterans, professional American-style football players, and the civilian population. “This recognition opens up an opportunity to broaden our perspective and delve into the medical aspects of health that may be influenced by TBI.”

To broaden the investigation, the researchers reviewed literature published between January 1, 2001, and June 18, 2023. Of 26,335 articles, they narrowed their review down to 15 studies that investigated CVD, CVD risk factors, and cerebrovascular disease in the chronic phase of TBI, including community, military, or sport-related brain trauma, regardless of the timing of disease occurrence with respect to brain injury via TBI or repetitive head impact.
 

New Cardiovascular Risk

Studies that used national or local registries tended to be retrospective and predominantly conducted in people with preexisting cardiovascular conditions. In these studies, TBI was found to be an independent risk factor for myocardial dysfunction. However, although these studies do provide evidence of elevated cardiovascular risk subsequent to a single TBI, including individuals with preexisting medical comorbidities “makes it difficult to determine the timing of incident cardiovascular disease and cardiovascular risk factors subsequent to brain injury,” they wrote.

However, some studies showed that even individuals with TBI but without preexisting myocardial dysfunction at baseline had a significantly higher risk for CVD than those without a history of TBI.

In fact, several studies included populations without preexisting medical and cardiovascular comorbidities to “better refine the order and timing of CVD and other risk factors in individuals with TBI.”

For example, one study of concussion survivors without preexisting diagnoses showed that cardiovascular, endocrinological, and neuropsychiatric comorbidities occurred at a “significantly higher incidence within 5 years after concussive TBI compared with healthy individuals who were matched in terms of age, race, and sex and didn’t have a TBI exposure.” Other studies yielded similar findings.

Because cardiovascular risk factors and events become more common with age, it’s important to account for age in evaluating the effects of TBI. Although many studies of TBI and subsequent CVD didn’t stratify individuals by age, one 10-year study of people without any known cardiovascular or neuropsychiatric conditions who sustained TBI found that people as young as 18-40 years were more likely to develop hypertension, hyperlipidemia, obesity, and diabetes within 3-5 years following brain injury than matched individuals in the control group.

“Individuals who have encountered TBI, surprisingly even those who are young and in good health with no prior comorbid conditions, face an increased risk of adverse cardiovascular outcomes for an extended duration after the initial event,” Drs. Zafonte and Izzy summarized. “Therefore, it’s imperative that they receive regular and long-term screenings for CVD and associated risk factors.”
 

Bidirectional Relationship

Brain injury has been associated with acute cardiovascular dysfunction, including autonomic heart-brain axis dysregulation, imbalances between the sympathetic and parasympathetic nervous systems, and excessive catecholamine release, the authors noted.

Drs. Zafonte and Izzy suggested several plausible links between TBI and cardiovascular dysfunction, noting that they are “likely multifaceted, potentially encompassing risk factors that span the pre-injury, injury, and post-injury phases of the condition.”

TBI may induce alterations in neurobiological processes, which have been reported to be associated with an increased risk for CVD (eg, chronic dysfunction of the autonomic system, systemic inflammation, and modifications in the brain-gut connection).

Patients with TBI might develop additional risk factors following the injury, including conditions like posttraumatic stress disorder, depression, and other psychiatric illnesses, which are “known to augment the risk of CVD.”

TBI can lead to subsequent behavioral and lifestyle changes that place patients at an elevated risk for both cardiovascular and cognitive dysfunction when compared to the general population of TBI survivors.

There may be additional as yet undefined risks.

They believe there’s a bidirectional relationship between TBI and CVD. “On one hand, TBI has been associated with an elevated risk of CVD,” they said. “Conversely, cardiovascular risk factors such as diabetes, hypertension, hyperlipidemia, and sleep disturbances that have been demonstrated to negatively influence cognitive function and heighten the risk of dementia. Consequently, this interplay can further compound the long-term consequences of the injury.”

Their work aims to try and disentangle this “complex series of relationships.”

They recommend screening to identify diseases in their earliest and “most manageable phases” because TBI has been “unveiled as an underappreciated risk factor for CVD within contact sports, military, and community setting.”

An effective screening program “should rely on quantifiable and dependable biomarkers such as blood pressure, BMI, waist circumference, blood lipid levels, and glucose. Additionally, it should take into account other factors like smoking habits, physical activity, and dietary choices,” they recommended.
 

Heart-Brain Connection

Dr. Croll noted that TBI is “associated with many poorly understood physiologic changes and complications, so it’s exciting to see research aimed at clarifying this chronic disease process.”

In recent years, “we have seen a greater appreciation and understanding of the heart-brain connection,” she said. “Moving forward, more research, including TBI research, will target that connection.”

She added that there are probably “multiple mechanisms” at play underlying the connection between TBI and CVD.

Most importantly, “we are increasingly learning that TBI is not only a discrete event that requires immediate treatment but also a chronic disease process,” and when we “think about the substantial long-term morbidity associated with TBI, we should keep increased risk for CVD on top of mind,” said Dr. Croll.

The review received no funding. Izzy reported receiving grants from the US National Institutes of Health (NIH) and 2023 Stepping Strong Innovator Award. Dr. Zafonte reported receiving grants from the NIH and royalties from Springer and Demos publishing for serving as a coeditor of Brain Injury Medicine. Dr. Zafonte has also served as an adviser to Myomo, Oncare.ai, Nanodiagnostics, and Kisbee. He reported evaluating patients in the Massachusetts General Hospital Brain and Body–TRUST Program, which is funded by the NFL Players Association. The other authors’ disclosures are listed on the original paper. Dr. Croll declared no relevant financial relationships.

A version of this article appeared on Medscape.com.

Primary aldosteronism (PA) is a frequently overlooked yet common cause of secondary hypertension, presenting significant risk for cardiovascular morbidity and mortality.

But fewer than 4% of at-risk patients receive the recommended screening for PA, leaving a substantial gap in early detection and management, according to Adina F. Turcu, MD, MS, associate professor in endocrinology and internal medicine at University of Michigan Health in Ann Arbor. 

In response to this clinical challenge, Dr. Turcu and her colleagues developed a best-practice advisory (BPA) to identify patients who were at risk for PA and embedded it into electronic health record at University of Michigan ambulatory clinics. Her team found that use of the tool led to increased rates of screening for PA, particularly among primary care physicians.

Over a 15-month period, Dr. Turcu and her colleagues tested the BPA through a quality improvement study, identifying 14,603 unique candidates for PA screening, with a mean age of 65.5 years and a diverse representation of ethnic backgrounds. 

Notably, 48.1% of these candidates had treatment-resistant hypertension, 43.5% exhibited hypokalemia, 10.5% were younger than 35 years, and 3.1% had adrenal nodules. Of these candidates, 14.0% received orders for PA screening, with 70.5% completing the recommended screening within the system, and 17.4% receiving positive screening results. 

The study, conducted over 6 months in 2023, targeted adults with hypertension and at least one of the following: Those who took four or more antihypertensive medications, exhibited hypokalemia, were younger than age 35 years, or had adrenal nodules. Patients previously tested for PA were excluded from the analysis. 

The noninterruptive BPA was triggered during outpatient visits with clinicians who specialized in hypertension. The advisory would then offer an order set for PA screening and provide a link to interpretation guidance for results. Clinicians had the option to use, ignore, or decline the BPA.

“Although we were hoping for broader uptake of this EHR-embedded BPA, we were delighted to see an increase in PA screening rates to 14% of identified candidates as compared to an average of less than 3% in retrospective studies of similar populations, including in our own institution prior to implementing this BPA,” Dr. Turcu told this news organization.

Physician specialty played a crucial role in the utilization of the BPA. Internists and family medicine physicians accounted for the majority of screening orders, placing 40.0% and 28.1% of these, respectively. Family practitioners and internists predominantly used the embedded order set (80.3% and 68.9%, respectively).

“Hypertension often gets treated rather than screening for [causes of] secondary hypertension prior to treatment,” said Kaniksha Desai, MD, clinical associate professor and endocrinology quality director at Stanford University School of Medicine, Stanford, California, who was not involved in the research. But “primary hyperaldosteronism is a condition that can be treated surgically and has increased long term cardiovascular consequences if not identified. While guidelines recommend screening at-risk patients, this often can get lost in translation in clinical practice due to many factors, including time constraints and volume of patients.” 

Patients who did vs did not undergo screening were more likely to be women, Black, and younger than age 35 years. Additionally, the likelihood of screening was higher among patients with obesity and dyslipidemia, whereas it was lower in those with chronic kidney disease and established cardiovascular complications.

According to Dr. Turcu, the findings from this study suggest that noninterruptive BPAs, especially when integrated into primary care workflows, hold promise as effective tools for PA screening.

When coupled with artificial intelligence to optimize detection yield, these refined BPAs could significantly contribute to personalized care for hypertension, the investigators said. 

“Considering that in the United States almost one in two adults has hypertension, such automatized tools become instrumental to busy clinicians, particularly those in primary care,” Dr. Turcu said. “Our results indicate a promising opportunity to meaningfully improve PA awareness and enhance its diagnosis.” 

Dr. Turcu reported receiving grants from the National Heart, Lung, and Blood Institute and Doris Duke Foundation, served as an investigator in a CinCor Pharma clinical trial, and received financial support to her institution during the conduct of the study. Dr. Desai reported no relevant financial disclosures. 
 

A version of this article appeared on Medscape.com.

Primary aldosteronism (PA) is a frequently overlooked yet common cause of secondary hypertension, presenting significant risk for cardiovascular morbidity and mortality.

But fewer than 4% of at-risk patients receive the recommended screening for PA, leaving a substantial gap in early detection and management, according to Adina F. Turcu, MD, MS, associate professor in endocrinology and internal medicine at University of Michigan Health in Ann Arbor. 

In response to this clinical challenge, Dr. Turcu and her colleagues developed a best-practice advisory (BPA) to identify patients who were at risk for PA and embedded it into electronic health record at University of Michigan ambulatory clinics. Her team found that use of the tool led to increased rates of screening for PA, particularly among primary care physicians.

Over a 15-month period, Dr. Turcu and her colleagues tested the BPA through a quality improvement study, identifying 14,603 unique candidates for PA screening, with a mean age of 65.5 years and a diverse representation of ethnic backgrounds. 

Notably, 48.1% of these candidates had treatment-resistant hypertension, 43.5% exhibited hypokalemia, 10.5% were younger than 35 years, and 3.1% had adrenal nodules. Of these candidates, 14.0% received orders for PA screening, with 70.5% completing the recommended screening within the system, and 17.4% receiving positive screening results. 

The study, conducted over 6 months in 2023, targeted adults with hypertension and at least one of the following: Those who took four or more antihypertensive medications, exhibited hypokalemia, were younger than age 35 years, or had adrenal nodules. Patients previously tested for PA were excluded from the analysis. 

The noninterruptive BPA was triggered during outpatient visits with clinicians who specialized in hypertension. The advisory would then offer an order set for PA screening and provide a link to interpretation guidance for results. Clinicians had the option to use, ignore, or decline the BPA.

“Although we were hoping for broader uptake of this EHR-embedded BPA, we were delighted to see an increase in PA screening rates to 14% of identified candidates as compared to an average of less than 3% in retrospective studies of similar populations, including in our own institution prior to implementing this BPA,” Dr. Turcu told this news organization.

Physician specialty played a crucial role in the utilization of the BPA. Internists and family medicine physicians accounted for the majority of screening orders, placing 40.0% and 28.1% of these, respectively. Family practitioners and internists predominantly used the embedded order set (80.3% and 68.9%, respectively).

“Hypertension often gets treated rather than screening for [causes of] secondary hypertension prior to treatment,” said Kaniksha Desai, MD, clinical associate professor and endocrinology quality director at Stanford University School of Medicine, Stanford, California, who was not involved in the research. But “primary hyperaldosteronism is a condition that can be treated surgically and has increased long term cardiovascular consequences if not identified. While guidelines recommend screening at-risk patients, this often can get lost in translation in clinical practice due to many factors, including time constraints and volume of patients.” 

Patients who did vs did not undergo screening were more likely to be women, Black, and younger than age 35 years. Additionally, the likelihood of screening was higher among patients with obesity and dyslipidemia, whereas it was lower in those with chronic kidney disease and established cardiovascular complications.

According to Dr. Turcu, the findings from this study suggest that noninterruptive BPAs, especially when integrated into primary care workflows, hold promise as effective tools for PA screening.

When coupled with artificial intelligence to optimize detection yield, these refined BPAs could significantly contribute to personalized care for hypertension, the investigators said. 

“Considering that in the United States almost one in two adults has hypertension, such automatized tools become instrumental to busy clinicians, particularly those in primary care,” Dr. Turcu said. “Our results indicate a promising opportunity to meaningfully improve PA awareness and enhance its diagnosis.” 

Dr. Turcu reported receiving grants from the National Heart, Lung, and Blood Institute and Doris Duke Foundation, served as an investigator in a CinCor Pharma clinical trial, and received financial support to her institution during the conduct of the study. Dr. Desai reported no relevant financial disclosures. 
 

A version of this article appeared on Medscape.com.

Primary aldosteronism (PA) is a frequently overlooked yet common cause of secondary hypertension, presenting significant risk for cardiovascular morbidity and mortality.

But fewer than 4% of at-risk patients receive the recommended screening for PA, leaving a substantial gap in early detection and management, according to Adina F. Turcu, MD, MS, associate professor in endocrinology and internal medicine at University of Michigan Health in Ann Arbor. 

In response to this clinical challenge, Dr. Turcu and her colleagues developed a best-practice advisory (BPA) to identify patients who were at risk for PA and embedded it into electronic health record at University of Michigan ambulatory clinics. Her team found that use of the tool led to increased rates of screening for PA, particularly among primary care physicians.

Over a 15-month period, Dr. Turcu and her colleagues tested the BPA through a quality improvement study, identifying 14,603 unique candidates for PA screening, with a mean age of 65.5 years and a diverse representation of ethnic backgrounds. 

Notably, 48.1% of these candidates had treatment-resistant hypertension, 43.5% exhibited hypokalemia, 10.5% were younger than 35 years, and 3.1% had adrenal nodules. Of these candidates, 14.0% received orders for PA screening, with 70.5% completing the recommended screening within the system, and 17.4% receiving positive screening results. 

The study, conducted over 6 months in 2023, targeted adults with hypertension and at least one of the following: Those who took four or more antihypertensive medications, exhibited hypokalemia, were younger than age 35 years, or had adrenal nodules. Patients previously tested for PA were excluded from the analysis. 

The noninterruptive BPA was triggered during outpatient visits with clinicians who specialized in hypertension. The advisory would then offer an order set for PA screening and provide a link to interpretation guidance for results. Clinicians had the option to use, ignore, or decline the BPA.

“Although we were hoping for broader uptake of this EHR-embedded BPA, we were delighted to see an increase in PA screening rates to 14% of identified candidates as compared to an average of less than 3% in retrospective studies of similar populations, including in our own institution prior to implementing this BPA,” Dr. Turcu told this news organization.

Physician specialty played a crucial role in the utilization of the BPA. Internists and family medicine physicians accounted for the majority of screening orders, placing 40.0% and 28.1% of these, respectively. Family practitioners and internists predominantly used the embedded order set (80.3% and 68.9%, respectively).

“Hypertension often gets treated rather than screening for [causes of] secondary hypertension prior to treatment,” said Kaniksha Desai, MD, clinical associate professor and endocrinology quality director at Stanford University School of Medicine, Stanford, California, who was not involved in the research. But “primary hyperaldosteronism is a condition that can be treated surgically and has increased long term cardiovascular consequences if not identified. While guidelines recommend screening at-risk patients, this often can get lost in translation in clinical practice due to many factors, including time constraints and volume of patients.” 

Patients who did vs did not undergo screening were more likely to be women, Black, and younger than age 35 years. Additionally, the likelihood of screening was higher among patients with obesity and dyslipidemia, whereas it was lower in those with chronic kidney disease and established cardiovascular complications.

According to Dr. Turcu, the findings from this study suggest that noninterruptive BPAs, especially when integrated into primary care workflows, hold promise as effective tools for PA screening.

When coupled with artificial intelligence to optimize detection yield, these refined BPAs could significantly contribute to personalized care for hypertension, the investigators said. 

“Considering that in the United States almost one in two adults has hypertension, such automatized tools become instrumental to busy clinicians, particularly those in primary care,” Dr. Turcu said. “Our results indicate a promising opportunity to meaningfully improve PA awareness and enhance its diagnosis.” 

Dr. Turcu reported receiving grants from the National Heart, Lung, and Blood Institute and Doris Duke Foundation, served as an investigator in a CinCor Pharma clinical trial, and received financial support to her institution during the conduct of the study. Dr. Desai reported no relevant financial disclosures. 
 

A version of this article appeared on Medscape.com.