Cardiology

Hypertension is a major risk factor for heart disease, stroke, and kidney disease.The prevalence of hypertension increases with age, primarily due to age-related changes in arterial physiology.¹ For older adults, current guidelines regarding blood pressure (BP) treatment goals vary. The American Heart Association/American College of Cardiology 2017 clinical practice guidelines recommend a systolic BP (SBP) treatment goal of < 130 mm Hg for community-dwelling, ambulatory, noninstitutionalized adults aged ≥ 65 years; whereas the American College of Physicians/American Academy of Family Physicians recommend a goal of < 150 mm Hg for those aged ≥ 60 years without comorbidities and < 140 mm Hg for those with increased cardiovascular risk.^1-3 Regardless of the specific threshold, agreement that some degree of BP control even in those with advanced age improves outcomes.²

First-line therapy for uncomplicated hypertension includes thiazide diuretics, long-acting calcium channel blockers, and renin-angiotensin system inhibitors. When choosing between these options, it is recommended to engage in shared decision making and to consider the patient’s comorbidities. Among patients who are likely to require a second agent (eg, if initial BP is > 20/10 mm Hg above goal), it is recommended to begin both drugs at the same time, preferably benazepril plus amlodipine due to the reduction in cardiovascular events reported in the ACCOMPLISH trial.⁴ If BP remains elevated despite 2 agents at moderate to maximum doses, it is important to investigate for secondary hypertension causes and to explore medication adherence as possible etiologies of treatment failure. Older adults are often at higher risk of adverse drug events due to age-related changes in pharmacodynamics. Despite this, there are no guidelines for choosing between different classes of antihypertensives in this population. We present a case of thiazide-induced hyponatremia in an older adult and review the risks of thiazide use in this population.

Case Presentation

A man aged > 90 years was admitted to the hospital after a syncopal episode. His history was significant for hypertension, hyperlipidemia, and vitamin D deficiency. At the time, his home medications were amlodipine 5 mg daily, atorvastatin 40 mg daily, ergocalciferol 50,000 IU weekly, and polyethylene glycol 17 g daily as needed. His syncope workup was unremarkable and included negative orthostatic vital signs, normal serial troponins, an electrocardiogram without ischemic changes, normal serum creatinine, sodium, and glucose, and a head computed tomography without any acute abnormality. Throughout the patient’s hospital stay, he had multiple elevated SBP readings, including many > 200 mm Hg. On discharge, in addition to continuing his home medications, he was started on valsartan 20 mg daily and enrolled in a remote BP monitoring program.

Three weeks later, the patient was seen by their primary care practitioner for follow-up. He reported adherence to his antihypertensive regimen. However, his remote BP monitoring revealed persistently elevated BPs, with an average of 179/79 mm Hg, a high of 205/85 mm Hg, and a low of 150/67 mm Hg over the previous 7 days. Laboratory tests obtained at the visit were notable for serum sodium of 138 mmol/L and potassium of 4.1 mmol/L. His weight was 87 kg. Given persistently elevated BP readings, in addition to continuing his amlodipine 5 mg daily and valsartan 20 mg daily, he was started on hydrochlorothiazide 25 mg daily, with plans to repeat a basic metabolic panel in 2 weeks.

Two weeks later, he fell after getting out of his bed. On examination, he was noted to have dry mucous membranes, and although no formal delirium screening was performed, he was able to repeat the months of the year backward. Vital signs were notable for positive postural hypertension, and his laboratory tests revealed a normal serum creatinine, serum sodium of 117 mmol/L (reference range, 135-145 mmol/L), serum potassium of 3.2 mmol/L (reference range, 3.0-5.0 mmol/L), a low serum osmolality, and urine sodium of 35 mmol/L most consistent with hypovolemic hypoosmotic hyponatremia secondary to thiazide initiation. The patient’s hydrochlorothiazide was discontinued, and he was admitted to the hospital for close monitoring. His sodium levels gradually normalized over the next 2 weeks without any other intervention.

Discussion

Although thiazide diuretics are recommended as first-line therapy for uncomplicated hypertension, they are known to cause electrolyte abnormalities, including hypomagnesemia, hypokalemia, and hyponatremia.⁴ These metabolic derangements are more likely to occur in older adults. One study of adults aged ≥ 65 years found that at 9 months of follow-up, 14.3% of new thiazide users had developed a thiazide-related metabolic adverse event (hyponatremia < 135 mmol/L, hypokalemia < 3.5 mmol/L, and decrease in estimated glomerular filtration rate by > 25%) compared with 6.0% of nonusers (P < .001; number needed to harm [NNH] = 12).⁵ In addition, 3.8% of new thiazide users had an emergency department visit or were hospitalized for complications related to thiazides compared with only 2.0% of nonusers (P = .02; NNH = 56).⁵ Independent risk factors for thiazide-induced hyponatremia include high-comorbidity burden, low body weight, low-normal or unmeasured serum sodium, low potassium, and aged > 70 years.^5-7 Each 10-year increment in age is associated with a 2-fold increase in risk, suggesting that older adults are at a much higher risk for hyponatremia than their younger peers.⁶

Despite their designation as a first-line option for uncomplicated hypertension, thiazide diuretics may cause more harm than good in some older adults, especially those with additional risk factors for thiazide-induced hyponatremia. In this population, these adverse effects should be discussed before starting thiazides for the treatment of hypertension. If thiazides are initiated, they should be started at the lowest possible dose, and plans made to monitor bloodwork within 1 to 2 weeks of initiation or dose change and periodically thereafter while the patient remains on the therapy.

Medication Management in Older Adults

Due to the risks of medication use in older adults, the phrase “start low, go slow” is commonly used in geriatric medicine to describe the optimal method for initiation and up-titration of new medication with the hope of mitigating adverse drug events. In our case, we started valsartan at 20 mg daily—one-fourth the recommended initial dose. Although this strategy is reasonable to “start low,” we were not surprised to find that the patient’s BP did not markedly improve on such a low dose. The team could have increased the valsartan dose to a therapeutically efficacious dose before choosing to add another hypertensive agent. In alignment with geriatric prescribing principles, starting at the lowest possible dose of hydrochlorothiazide is recommended.⁵ However, the clinician started hydrochlorothiazide at 25 mg daily, potentially increasing this patient’s risk of electrolyte abnormalities and eventual fall.

Managing hypertension also invites a discussion of polypharmacy and medication adherence. Older adults are at risk of polypharmacy, defined as the prescription of 5 or more medications.⁸ Polypharmacy is associated with increased hospitalizations, higher costs of care for individuals and health care systems, increased risks of adverse drug events, medication nonadherence, and lower quality of life for patients.⁹ In some situations, the risks of polypharmacy may outweigh the benefits of using multiple antihypertensives with different mechanisms of action if patients can reach their BP goal on the maximum dose of a single agent. For patients taking multiple antihypertensives, it is important to routinely monitor BP and assess whether deprescribing is indicated. Cognitive impairment and decreased social support may affect medication adherence for older adults.⁶ Clinicians should be aware of strategies, such as medication reminders and pillboxes, to increase antihypertensive medication adherence. Polypills that contain 2 antihypertensives can be another tool used to manage older adults to increase adherence and decrease health care costs.¹⁰

A current strategy that encompasses discussing many, if not all, of these noted elements is the Institute for Healthcare Improvement’s Age-Friendly Health System. This framework uses evidence-based tools to provide care for older adults across all clinical settings and highlights the 4Ms: what matters, medication, mentation, and mobility.¹¹ Medication considers whether a medication is necessary, whether its use has benefits that outweigh the risks, and how it interacts with what matters, mentation, and mobility. In particular, what matters plays an important role in hypertension management in older adults given the recommended target BP differs, depending on which specialty organization guideline is followed. By better understanding what matters to patients, including their goals and priorities, clinicians can engage patients in shared decision making and provide individualized recommendations based on geriatric principles (eg, start low, go slow, principles of medication adherence) and patient comorbidities (eg, medical history and risk factors for hyponatremia) to help patients make a more informed choice about their antihypertensive treatment regimen (Figure).

Conclusions

This case illustrates the need for a specialized approach to hypertension management in older adults and the risks of thiazide diuretics in this population. Clinicians should consider BP goals, patient-specific factors, and principles of medication management in older adults. If initiating thiazide therapy, discuss the risks associated with use, start at the lowest possible dose, and monitor bloodwork within 1 to 2 weeks of initiation/dose change and periodically thereafter while the patient remains on the therapy to decrease the risk of adverse events. Finally, the Institute for Healthcare Improvement’s Age-Friendly Health System framework can be a useful when considering the addition of a new medication in an older adult’s treatment plan.

Acknowledgments

This material is the result of work supported with resources and the use of facilities at the New England Geriatrics Research, Education, and Clinical Center, Veterans Affairs Boston Healthcare System, and the Cincinnati VeteransAffairs Medical Center.

Hypertension is a major risk factor for heart disease, stroke, and kidney disease.The prevalence of hypertension increases with age, primarily due to age-related changes in arterial physiology.¹ For older adults, current guidelines regarding blood pressure (BP) treatment goals vary. The American Heart Association/American College of Cardiology 2017 clinical practice guidelines recommend a systolic BP (SBP) treatment goal of < 130 mm Hg for community-dwelling, ambulatory, noninstitutionalized adults aged ≥ 65 years; whereas the American College of Physicians/American Academy of Family Physicians recommend a goal of < 150 mm Hg for those aged ≥ 60 years without comorbidities and < 140 mm Hg for those with increased cardiovascular risk.^1-3 Regardless of the specific threshold, agreement that some degree of BP control even in those with advanced age improves outcomes.²

First-line therapy for uncomplicated hypertension includes thiazide diuretics, long-acting calcium channel blockers, and renin-angiotensin system inhibitors. When choosing between these options, it is recommended to engage in shared decision making and to consider the patient’s comorbidities. Among patients who are likely to require a second agent (eg, if initial BP is > 20/10 mm Hg above goal), it is recommended to begin both drugs at the same time, preferably benazepril plus amlodipine due to the reduction in cardiovascular events reported in the ACCOMPLISH trial.⁴ If BP remains elevated despite 2 agents at moderate to maximum doses, it is important to investigate for secondary hypertension causes and to explore medication adherence as possible etiologies of treatment failure. Older adults are often at higher risk of adverse drug events due to age-related changes in pharmacodynamics. Despite this, there are no guidelines for choosing between different classes of antihypertensives in this population. We present a case of thiazide-induced hyponatremia in an older adult and review the risks of thiazide use in this population.

Case Presentation

A man aged > 90 years was admitted to the hospital after a syncopal episode. His history was significant for hypertension, hyperlipidemia, and vitamin D deficiency. At the time, his home medications were amlodipine 5 mg daily, atorvastatin 40 mg daily, ergocalciferol 50,000 IU weekly, and polyethylene glycol 17 g daily as needed. His syncope workup was unremarkable and included negative orthostatic vital signs, normal serial troponins, an electrocardiogram without ischemic changes, normal serum creatinine, sodium, and glucose, and a head computed tomography without any acute abnormality. Throughout the patient’s hospital stay, he had multiple elevated SBP readings, including many > 200 mm Hg. On discharge, in addition to continuing his home medications, he was started on valsartan 20 mg daily and enrolled in a remote BP monitoring program.

Three weeks later, the patient was seen by their primary care practitioner for follow-up. He reported adherence to his antihypertensive regimen. However, his remote BP monitoring revealed persistently elevated BPs, with an average of 179/79 mm Hg, a high of 205/85 mm Hg, and a low of 150/67 mm Hg over the previous 7 days. Laboratory tests obtained at the visit were notable for serum sodium of 138 mmol/L and potassium of 4.1 mmol/L. His weight was 87 kg. Given persistently elevated BP readings, in addition to continuing his amlodipine 5 mg daily and valsartan 20 mg daily, he was started on hydrochlorothiazide 25 mg daily, with plans to repeat a basic metabolic panel in 2 weeks.

Two weeks later, he fell after getting out of his bed. On examination, he was noted to have dry mucous membranes, and although no formal delirium screening was performed, he was able to repeat the months of the year backward. Vital signs were notable for positive postural hypertension, and his laboratory tests revealed a normal serum creatinine, serum sodium of 117 mmol/L (reference range, 135-145 mmol/L), serum potassium of 3.2 mmol/L (reference range, 3.0-5.0 mmol/L), a low serum osmolality, and urine sodium of 35 mmol/L most consistent with hypovolemic hypoosmotic hyponatremia secondary to thiazide initiation. The patient’s hydrochlorothiazide was discontinued, and he was admitted to the hospital for close monitoring. His sodium levels gradually normalized over the next 2 weeks without any other intervention.

Discussion

Although thiazide diuretics are recommended as first-line therapy for uncomplicated hypertension, they are known to cause electrolyte abnormalities, including hypomagnesemia, hypokalemia, and hyponatremia.⁴ These metabolic derangements are more likely to occur in older adults. One study of adults aged ≥ 65 years found that at 9 months of follow-up, 14.3% of new thiazide users had developed a thiazide-related metabolic adverse event (hyponatremia < 135 mmol/L, hypokalemia < 3.5 mmol/L, and decrease in estimated glomerular filtration rate by > 25%) compared with 6.0% of nonusers (P < .001; number needed to harm [NNH] = 12).⁵ In addition, 3.8% of new thiazide users had an emergency department visit or were hospitalized for complications related to thiazides compared with only 2.0% of nonusers (P = .02; NNH = 56).⁵ Independent risk factors for thiazide-induced hyponatremia include high-comorbidity burden, low body weight, low-normal or unmeasured serum sodium, low potassium, and aged > 70 years.^5-7 Each 10-year increment in age is associated with a 2-fold increase in risk, suggesting that older adults are at a much higher risk for hyponatremia than their younger peers.⁶

Despite their designation as a first-line option for uncomplicated hypertension, thiazide diuretics may cause more harm than good in some older adults, especially those with additional risk factors for thiazide-induced hyponatremia. In this population, these adverse effects should be discussed before starting thiazides for the treatment of hypertension. If thiazides are initiated, they should be started at the lowest possible dose, and plans made to monitor bloodwork within 1 to 2 weeks of initiation or dose change and periodically thereafter while the patient remains on the therapy.

Medication Management in Older Adults

Due to the risks of medication use in older adults, the phrase “start low, go slow” is commonly used in geriatric medicine to describe the optimal method for initiation and up-titration of new medication with the hope of mitigating adverse drug events. In our case, we started valsartan at 20 mg daily—one-fourth the recommended initial dose. Although this strategy is reasonable to “start low,” we were not surprised to find that the patient’s BP did not markedly improve on such a low dose. The team could have increased the valsartan dose to a therapeutically efficacious dose before choosing to add another hypertensive agent. In alignment with geriatric prescribing principles, starting at the lowest possible dose of hydrochlorothiazide is recommended.⁵ However, the clinician started hydrochlorothiazide at 25 mg daily, potentially increasing this patient’s risk of electrolyte abnormalities and eventual fall.

Managing hypertension also invites a discussion of polypharmacy and medication adherence. Older adults are at risk of polypharmacy, defined as the prescription of 5 or more medications.⁸ Polypharmacy is associated with increased hospitalizations, higher costs of care for individuals and health care systems, increased risks of adverse drug events, medication nonadherence, and lower quality of life for patients.⁹ In some situations, the risks of polypharmacy may outweigh the benefits of using multiple antihypertensives with different mechanisms of action if patients can reach their BP goal on the maximum dose of a single agent. For patients taking multiple antihypertensives, it is important to routinely monitor BP and assess whether deprescribing is indicated. Cognitive impairment and decreased social support may affect medication adherence for older adults.⁶ Clinicians should be aware of strategies, such as medication reminders and pillboxes, to increase antihypertensive medication adherence. Polypills that contain 2 antihypertensives can be another tool used to manage older adults to increase adherence and decrease health care costs.¹⁰

A current strategy that encompasses discussing many, if not all, of these noted elements is the Institute for Healthcare Improvement’s Age-Friendly Health System. This framework uses evidence-based tools to provide care for older adults across all clinical settings and highlights the 4Ms: what matters, medication, mentation, and mobility.¹¹ Medication considers whether a medication is necessary, whether its use has benefits that outweigh the risks, and how it interacts with what matters, mentation, and mobility. In particular, what matters plays an important role in hypertension management in older adults given the recommended target BP differs, depending on which specialty organization guideline is followed. By better understanding what matters to patients, including their goals and priorities, clinicians can engage patients in shared decision making and provide individualized recommendations based on geriatric principles (eg, start low, go slow, principles of medication adherence) and patient comorbidities (eg, medical history and risk factors for hyponatremia) to help patients make a more informed choice about their antihypertensive treatment regimen (Figure).

Conclusions

This case illustrates the need for a specialized approach to hypertension management in older adults and the risks of thiazide diuretics in this population. Clinicians should consider BP goals, patient-specific factors, and principles of medication management in older adults. If initiating thiazide therapy, discuss the risks associated with use, start at the lowest possible dose, and monitor bloodwork within 1 to 2 weeks of initiation/dose change and periodically thereafter while the patient remains on the therapy to decrease the risk of adverse events. Finally, the Institute for Healthcare Improvement’s Age-Friendly Health System framework can be a useful when considering the addition of a new medication in an older adult’s treatment plan.

Acknowledgments

This material is the result of work supported with resources and the use of facilities at the New England Geriatrics Research, Education, and Clinical Center, Veterans Affairs Boston Healthcare System, and the Cincinnati VeteransAffairs Medical Center.

Hypertension is a major risk factor for heart disease, stroke, and kidney disease.The prevalence of hypertension increases with age, primarily due to age-related changes in arterial physiology.¹ For older adults, current guidelines regarding blood pressure (BP) treatment goals vary. The American Heart Association/American College of Cardiology 2017 clinical practice guidelines recommend a systolic BP (SBP) treatment goal of < 130 mm Hg for community-dwelling, ambulatory, noninstitutionalized adults aged ≥ 65 years; whereas the American College of Physicians/American Academy of Family Physicians recommend a goal of < 150 mm Hg for those aged ≥ 60 years without comorbidities and < 140 mm Hg for those with increased cardiovascular risk.^1-3 Regardless of the specific threshold, agreement that some degree of BP control even in those with advanced age improves outcomes.²

First-line therapy for uncomplicated hypertension includes thiazide diuretics, long-acting calcium channel blockers, and renin-angiotensin system inhibitors. When choosing between these options, it is recommended to engage in shared decision making and to consider the patient’s comorbidities. Among patients who are likely to require a second agent (eg, if initial BP is > 20/10 mm Hg above goal), it is recommended to begin both drugs at the same time, preferably benazepril plus amlodipine due to the reduction in cardiovascular events reported in the ACCOMPLISH trial.⁴ If BP remains elevated despite 2 agents at moderate to maximum doses, it is important to investigate for secondary hypertension causes and to explore medication adherence as possible etiologies of treatment failure. Older adults are often at higher risk of adverse drug events due to age-related changes in pharmacodynamics. Despite this, there are no guidelines for choosing between different classes of antihypertensives in this population. We present a case of thiazide-induced hyponatremia in an older adult and review the risks of thiazide use in this population.

Case Presentation

A man aged > 90 years was admitted to the hospital after a syncopal episode. His history was significant for hypertension, hyperlipidemia, and vitamin D deficiency. At the time, his home medications were amlodipine 5 mg daily, atorvastatin 40 mg daily, ergocalciferol 50,000 IU weekly, and polyethylene glycol 17 g daily as needed. His syncope workup was unremarkable and included negative orthostatic vital signs, normal serial troponins, an electrocardiogram without ischemic changes, normal serum creatinine, sodium, and glucose, and a head computed tomography without any acute abnormality. Throughout the patient’s hospital stay, he had multiple elevated SBP readings, including many > 200 mm Hg. On discharge, in addition to continuing his home medications, he was started on valsartan 20 mg daily and enrolled in a remote BP monitoring program.

Three weeks later, the patient was seen by their primary care practitioner for follow-up. He reported adherence to his antihypertensive regimen. However, his remote BP monitoring revealed persistently elevated BPs, with an average of 179/79 mm Hg, a high of 205/85 mm Hg, and a low of 150/67 mm Hg over the previous 7 days. Laboratory tests obtained at the visit were notable for serum sodium of 138 mmol/L and potassium of 4.1 mmol/L. His weight was 87 kg. Given persistently elevated BP readings, in addition to continuing his amlodipine 5 mg daily and valsartan 20 mg daily, he was started on hydrochlorothiazide 25 mg daily, with plans to repeat a basic metabolic panel in 2 weeks.

Two weeks later, he fell after getting out of his bed. On examination, he was noted to have dry mucous membranes, and although no formal delirium screening was performed, he was able to repeat the months of the year backward. Vital signs were notable for positive postural hypertension, and his laboratory tests revealed a normal serum creatinine, serum sodium of 117 mmol/L (reference range, 135-145 mmol/L), serum potassium of 3.2 mmol/L (reference range, 3.0-5.0 mmol/L), a low serum osmolality, and urine sodium of 35 mmol/L most consistent with hypovolemic hypoosmotic hyponatremia secondary to thiazide initiation. The patient’s hydrochlorothiazide was discontinued, and he was admitted to the hospital for close monitoring. His sodium levels gradually normalized over the next 2 weeks without any other intervention.

Discussion

Although thiazide diuretics are recommended as first-line therapy for uncomplicated hypertension, they are known to cause electrolyte abnormalities, including hypomagnesemia, hypokalemia, and hyponatremia.⁴ These metabolic derangements are more likely to occur in older adults. One study of adults aged ≥ 65 years found that at 9 months of follow-up, 14.3% of new thiazide users had developed a thiazide-related metabolic adverse event (hyponatremia < 135 mmol/L, hypokalemia < 3.5 mmol/L, and decrease in estimated glomerular filtration rate by > 25%) compared with 6.0% of nonusers (P < .001; number needed to harm [NNH] = 12).⁵ In addition, 3.8% of new thiazide users had an emergency department visit or were hospitalized for complications related to thiazides compared with only 2.0% of nonusers (P = .02; NNH = 56).⁵ Independent risk factors for thiazide-induced hyponatremia include high-comorbidity burden, low body weight, low-normal or unmeasured serum sodium, low potassium, and aged > 70 years.^5-7 Each 10-year increment in age is associated with a 2-fold increase in risk, suggesting that older adults are at a much higher risk for hyponatremia than their younger peers.⁶

Despite their designation as a first-line option for uncomplicated hypertension, thiazide diuretics may cause more harm than good in some older adults, especially those with additional risk factors for thiazide-induced hyponatremia. In this population, these adverse effects should be discussed before starting thiazides for the treatment of hypertension. If thiazides are initiated, they should be started at the lowest possible dose, and plans made to monitor bloodwork within 1 to 2 weeks of initiation or dose change and periodically thereafter while the patient remains on the therapy.

Medication Management in Older Adults

Due to the risks of medication use in older adults, the phrase “start low, go slow” is commonly used in geriatric medicine to describe the optimal method for initiation and up-titration of new medication with the hope of mitigating adverse drug events. In our case, we started valsartan at 20 mg daily—one-fourth the recommended initial dose. Although this strategy is reasonable to “start low,” we were not surprised to find that the patient’s BP did not markedly improve on such a low dose. The team could have increased the valsartan dose to a therapeutically efficacious dose before choosing to add another hypertensive agent. In alignment with geriatric prescribing principles, starting at the lowest possible dose of hydrochlorothiazide is recommended.⁵ However, the clinician started hydrochlorothiazide at 25 mg daily, potentially increasing this patient’s risk of electrolyte abnormalities and eventual fall.

Managing hypertension also invites a discussion of polypharmacy and medication adherence. Older adults are at risk of polypharmacy, defined as the prescription of 5 or more medications.⁸ Polypharmacy is associated with increased hospitalizations, higher costs of care for individuals and health care systems, increased risks of adverse drug events, medication nonadherence, and lower quality of life for patients.⁹ In some situations, the risks of polypharmacy may outweigh the benefits of using multiple antihypertensives with different mechanisms of action if patients can reach their BP goal on the maximum dose of a single agent. For patients taking multiple antihypertensives, it is important to routinely monitor BP and assess whether deprescribing is indicated. Cognitive impairment and decreased social support may affect medication adherence for older adults.⁶ Clinicians should be aware of strategies, such as medication reminders and pillboxes, to increase antihypertensive medication adherence. Polypills that contain 2 antihypertensives can be another tool used to manage older adults to increase adherence and decrease health care costs.¹⁰

A current strategy that encompasses discussing many, if not all, of these noted elements is the Institute for Healthcare Improvement’s Age-Friendly Health System. This framework uses evidence-based tools to provide care for older adults across all clinical settings and highlights the 4Ms: what matters, medication, mentation, and mobility.¹¹ Medication considers whether a medication is necessary, whether its use has benefits that outweigh the risks, and how it interacts with what matters, mentation, and mobility. In particular, what matters plays an important role in hypertension management in older adults given the recommended target BP differs, depending on which specialty organization guideline is followed. By better understanding what matters to patients, including their goals and priorities, clinicians can engage patients in shared decision making and provide individualized recommendations based on geriatric principles (eg, start low, go slow, principles of medication adherence) and patient comorbidities (eg, medical history and risk factors for hyponatremia) to help patients make a more informed choice about their antihypertensive treatment regimen (Figure).

Conclusions

This case illustrates the need for a specialized approach to hypertension management in older adults and the risks of thiazide diuretics in this population. Clinicians should consider BP goals, patient-specific factors, and principles of medication management in older adults. If initiating thiazide therapy, discuss the risks associated with use, start at the lowest possible dose, and monitor bloodwork within 1 to 2 weeks of initiation/dose change and periodically thereafter while the patient remains on the therapy to decrease the risk of adverse events. Finally, the Institute for Healthcare Improvement’s Age-Friendly Health System framework can be a useful when considering the addition of a new medication in an older adult’s treatment plan.

Acknowledgments

This material is the result of work supported with resources and the use of facilities at the New England Geriatrics Research, Education, and Clinical Center, Veterans Affairs Boston Healthcare System, and the Cincinnati VeteransAffairs Medical Center.

TOPLINE:

Patients with heart failure (HF) and depression who receive psychotherapy have the same (almost 50% reduction) in depressive symptoms as those treated with pharmacotherapy, show more improvement in physical-related quality of life, and are less likely to visit emergency departments (EDs), a comparative trial of these interventions found.

METHODOLOGY:

• The study included 416 patients with HF and a confirmed depressive disorder from the Cedars-Sinai Health System, with a mean age of 60.71 years, including nearly 42% women and 30% Black individuals, who were randomized to receive one of two evidence-based treatments for depression in HF: Antidepressant medication management (MEDS) or behavioral activation (BA) psychotherapy. BA therapy promotes engaging in pleasurable and rewarding activities without delving into complex cognitive domains explored in cognitive behavioral therapy, another psychotherapy type.
• All patients received 12 weekly sessions delivered via video or telephone, followed by monthly sessions for 3 months, and were then contacted as needed for an additional 6 months.
• The primary outcome was depressive symptom severity at 6 months, measured by the Patient Health Questionnaire 9-Item (PHQ-9), and secondary outcomes included three measures of health-related quality of life (HRQOL) — caregiver burden, morbidity, and mortality — collected at 3, 6, and 12 months.
• Physical and mental HRQOL were measured with the 12-Item Short-Form Medical Outcomes Study (SF-12), HF-specific HRQOL with the 23-item patient-reported Kansas City Cardiomyopathy Questionnaire, caregiver burden with the 26-item Caregiver Burden Questionnaire for HF, morbidity by ED visits, hospital readmissions, and days hospitalized, and mortality data came from medical records and family or caregiver reports, with survival assessed using Kaplan-Meier plots at 3, 6, and 12 months.
• Covariates included age, sex, race, ethnicity, marital status, employment, education, insurance type, recruitment site (inpatient or outpatient), ejection fraction (preserved or reduced), New York Heart Association class, medical history, and medications.

TAKEAWAY:

• Depressive symptom severity was reduced at 6 months by nearly 50% for both BA (mean PHQ-9 score, 7.53; P vs baseline < .001) and MEDS (mean PHQ-9 score, 8.09; P vs baseline < .001) participants, with reductions persisting at 12 months and no significant difference between groups.
• Compared with MEDS recipients, those who received BA had slightly higher improvement in physical HRQOL at 6 months (multivariable mean difference without imputation, 2.13; 95% CI, 0.06-4.20; P = .04), but there were no statistically significant differences between groups in mental HRQOL, HF-specific HRQOL, or caregiver burden at 3, 6, or 12 months.
• Patients who received BA were significantly less likely than those in the MEDS group to have ED visits and spent fewer days in hospital at 3, 6, and 12 months, but there was no significant difference in number of hospital readmissions or in mortality at 3, 6, or 12 months.

IN PRACTICE:

“Our findings of comparable primary effects between BA and MEDS suggest both options are effective and that personal preferences, patient values, and availability of services could inform decisions,” the authors wrote. They noted BA has no pharmacological adverse effects but requires more engagement than drug therapy and might be less accessible.

SOURCE:

The study was conducted by Waguih William IsHak, MD, Department of Psychiatry and Behavioral Neurosciences, Cedars-Sinai Medical Center, Los Angeles, and others. It was published online on January 17, 2024, in JAMA Network Open.

LIMITATIONS:

As the study had no control group, such as a waiting list, it was impossible to draw conclusions about the natural course of depressive symptoms in HF. However, the authors noted improvements were sustained at 12 months despite substantially diminished contact with intervention teams after 6 months. Researchers were unable to collect data for ED visits, readmissions, and hospital stays outside of California and didn’t assess treatment preference at enrollment, which could have helped inform the association with outcomes and adherence.

DISCLOSURES:

The study was funded by the Patient-Centered Outcome Research Institute, paid to Cedars-Sinai Medical Center. Dr. IsHak reported receiving royalties from Springer Nature and Cambridge University Press. No other disclosures were reported.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Patients with heart failure (HF) and depression who receive psychotherapy have the same (almost 50% reduction) in depressive symptoms as those treated with pharmacotherapy, show more improvement in physical-related quality of life, and are less likely to visit emergency departments (EDs), a comparative trial of these interventions found.

METHODOLOGY:

• The study included 416 patients with HF and a confirmed depressive disorder from the Cedars-Sinai Health System, with a mean age of 60.71 years, including nearly 42% women and 30% Black individuals, who were randomized to receive one of two evidence-based treatments for depression in HF: Antidepressant medication management (MEDS) or behavioral activation (BA) psychotherapy. BA therapy promotes engaging in pleasurable and rewarding activities without delving into complex cognitive domains explored in cognitive behavioral therapy, another psychotherapy type.
• All patients received 12 weekly sessions delivered via video or telephone, followed by monthly sessions for 3 months, and were then contacted as needed for an additional 6 months.
• The primary outcome was depressive symptom severity at 6 months, measured by the Patient Health Questionnaire 9-Item (PHQ-9), and secondary outcomes included three measures of health-related quality of life (HRQOL) — caregiver burden, morbidity, and mortality — collected at 3, 6, and 12 months.
• Physical and mental HRQOL were measured with the 12-Item Short-Form Medical Outcomes Study (SF-12), HF-specific HRQOL with the 23-item patient-reported Kansas City Cardiomyopathy Questionnaire, caregiver burden with the 26-item Caregiver Burden Questionnaire for HF, morbidity by ED visits, hospital readmissions, and days hospitalized, and mortality data came from medical records and family or caregiver reports, with survival assessed using Kaplan-Meier plots at 3, 6, and 12 months.
• Covariates included age, sex, race, ethnicity, marital status, employment, education, insurance type, recruitment site (inpatient or outpatient), ejection fraction (preserved or reduced), New York Heart Association class, medical history, and medications.

TAKEAWAY:

• Depressive symptom severity was reduced at 6 months by nearly 50% for both BA (mean PHQ-9 score, 7.53; P vs baseline < .001) and MEDS (mean PHQ-9 score, 8.09; P vs baseline < .001) participants, with reductions persisting at 12 months and no significant difference between groups.
• Compared with MEDS recipients, those who received BA had slightly higher improvement in physical HRQOL at 6 months (multivariable mean difference without imputation, 2.13; 95% CI, 0.06-4.20; P = .04), but there were no statistically significant differences between groups in mental HRQOL, HF-specific HRQOL, or caregiver burden at 3, 6, or 12 months.
• Patients who received BA were significantly less likely than those in the MEDS group to have ED visits and spent fewer days in hospital at 3, 6, and 12 months, but there was no significant difference in number of hospital readmissions or in mortality at 3, 6, or 12 months.

IN PRACTICE:

“Our findings of comparable primary effects between BA and MEDS suggest both options are effective and that personal preferences, patient values, and availability of services could inform decisions,” the authors wrote. They noted BA has no pharmacological adverse effects but requires more engagement than drug therapy and might be less accessible.

SOURCE:

The study was conducted by Waguih William IsHak, MD, Department of Psychiatry and Behavioral Neurosciences, Cedars-Sinai Medical Center, Los Angeles, and others. It was published online on January 17, 2024, in JAMA Network Open.

LIMITATIONS:

As the study had no control group, such as a waiting list, it was impossible to draw conclusions about the natural course of depressive symptoms in HF. However, the authors noted improvements were sustained at 12 months despite substantially diminished contact with intervention teams after 6 months. Researchers were unable to collect data for ED visits, readmissions, and hospital stays outside of California and didn’t assess treatment preference at enrollment, which could have helped inform the association with outcomes and adherence.

DISCLOSURES:

The study was funded by the Patient-Centered Outcome Research Institute, paid to Cedars-Sinai Medical Center. Dr. IsHak reported receiving royalties from Springer Nature and Cambridge University Press. No other disclosures were reported.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Patients with heart failure (HF) and depression who receive psychotherapy have the same (almost 50% reduction) in depressive symptoms as those treated with pharmacotherapy, show more improvement in physical-related quality of life, and are less likely to visit emergency departments (EDs), a comparative trial of these interventions found.

METHODOLOGY:

• The study included 416 patients with HF and a confirmed depressive disorder from the Cedars-Sinai Health System, with a mean age of 60.71 years, including nearly 42% women and 30% Black individuals, who were randomized to receive one of two evidence-based treatments for depression in HF: Antidepressant medication management (MEDS) or behavioral activation (BA) psychotherapy. BA therapy promotes engaging in pleasurable and rewarding activities without delving into complex cognitive domains explored in cognitive behavioral therapy, another psychotherapy type.
• All patients received 12 weekly sessions delivered via video or telephone, followed by monthly sessions for 3 months, and were then contacted as needed for an additional 6 months.
• The primary outcome was depressive symptom severity at 6 months, measured by the Patient Health Questionnaire 9-Item (PHQ-9), and secondary outcomes included three measures of health-related quality of life (HRQOL) — caregiver burden, morbidity, and mortality — collected at 3, 6, and 12 months.
• Physical and mental HRQOL were measured with the 12-Item Short-Form Medical Outcomes Study (SF-12), HF-specific HRQOL with the 23-item patient-reported Kansas City Cardiomyopathy Questionnaire, caregiver burden with the 26-item Caregiver Burden Questionnaire for HF, morbidity by ED visits, hospital readmissions, and days hospitalized, and mortality data came from medical records and family or caregiver reports, with survival assessed using Kaplan-Meier plots at 3, 6, and 12 months.
• Covariates included age, sex, race, ethnicity, marital status, employment, education, insurance type, recruitment site (inpatient or outpatient), ejection fraction (preserved or reduced), New York Heart Association class, medical history, and medications.

TAKEAWAY:

• Depressive symptom severity was reduced at 6 months by nearly 50% for both BA (mean PHQ-9 score, 7.53; P vs baseline < .001) and MEDS (mean PHQ-9 score, 8.09; P vs baseline < .001) participants, with reductions persisting at 12 months and no significant difference between groups.
• Compared with MEDS recipients, those who received BA had slightly higher improvement in physical HRQOL at 6 months (multivariable mean difference without imputation, 2.13; 95% CI, 0.06-4.20; P = .04), but there were no statistically significant differences between groups in mental HRQOL, HF-specific HRQOL, or caregiver burden at 3, 6, or 12 months.
• Patients who received BA were significantly less likely than those in the MEDS group to have ED visits and spent fewer days in hospital at 3, 6, and 12 months, but there was no significant difference in number of hospital readmissions or in mortality at 3, 6, or 12 months.

IN PRACTICE:

“Our findings of comparable primary effects between BA and MEDS suggest both options are effective and that personal preferences, patient values, and availability of services could inform decisions,” the authors wrote. They noted BA has no pharmacological adverse effects but requires more engagement than drug therapy and might be less accessible.

SOURCE:

The study was conducted by Waguih William IsHak, MD, Department of Psychiatry and Behavioral Neurosciences, Cedars-Sinai Medical Center, Los Angeles, and others. It was published online on January 17, 2024, in JAMA Network Open.

LIMITATIONS:

As the study had no control group, such as a waiting list, it was impossible to draw conclusions about the natural course of depressive symptoms in HF. However, the authors noted improvements were sustained at 12 months despite substantially diminished contact with intervention teams after 6 months. Researchers were unable to collect data for ED visits, readmissions, and hospital stays outside of California and didn’t assess treatment preference at enrollment, which could have helped inform the association with outcomes and adherence.

DISCLOSURES:

The study was funded by the Patient-Centered Outcome Research Institute, paid to Cedars-Sinai Medical Center. Dr. IsHak reported receiving royalties from Springer Nature and Cambridge University Press. No other disclosures were reported.
 

A version of this article appeared on Medscape.com.

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.