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Does Excess Body Weight Equal Adverse Heart Health Outcomes?

Maggie L. Shaw
Hypertrophic cardiomyopathy is an abnormal thickening of the heart muscle, with causes that include genetic mutations and myofiber disarray (an abnormal heart muscle cell arrangement). Individuals who have this condition are prone to obesity (body mass index, 25 to <30 kg/m2).
Hypertrophic cardiomyopathy is an abnormal thickening of the heart muscle, with causes that include genetic mutations and myofiber disarray, or an abnormal heart muscle cell arrangement. Individuals who have this condition are prone to obesity (body mass index [BMI], 25 to <30 kg/m2). Whether this also predisposes them to long-term adverse outcomes remains in question, and it served as the basis for a recent retrospective cohort study in JAMA Cardiology.

The investigators mined the Sarcomeric Human Cardiomyopathy Registry for data on 3282 patients, with a mean (SD) age of 47 (15) years, who they followed for a median 6.8 years. The 2 primary outcomes were all-cause and cardiovascular (CV) mortality, and there were 3 composite end points: overall, heart failure (HF), and ventricular arrhythmic.

They study subjects were divided into 3 groups:
  1. Normal weight (n = 962): BMI below 25 kg/m2
  2. Preobesity (n = 1280): BMI 25 to 30 kg/m2
  3. Obesity (n = 1040): BMI above 30 kg/m2
 Compared with the normal weight group (9%), the preobesity and obesity groups (10.8% and 20.7%, respectively) were more often symptomatic (New York Heart Association class III/IV), with hypertension and diabetes being more common, as well. Hypertension occurred almost twice as often, and diabetes 4 times more, in the obesity group than among the normal weight cohort: 51.5% and 16.1%, respectively, compared with 27.0% and 4.6%.

Patients in the obesity group also had the highest rates of left-ventricular outflow tract (LVOT) obstruction at rest or via the Valsalva maneuver: 32.4% compared with 20.9% in the normal weight group and 25.5% in the preobesity group. Surgery (septal myectomy, alcohol septal ablation, or both) was also most often recommended to correct LVOT in obese and preobese patients (31.7% and 21.7%) than in the normal-weight group (16.3%). Left ventricular ejection fraction, however, was comparable across the 3 groups.

“When assessing the individual causes of death, no difference was found in all-cause mortality, cardiovascular mortality, or the ventricular arrhythmic composite end point based on BMI class,” the authors stated. “[However], obesity was independently associated with overall disease progression, irrespective of other well-known factors, such as age, sex, left atrial size, LVOT obstruction, and genotype.”

Going forward, they propose longitudinal studies with longer follow-up. For example, the phase 3 EXPLORER-HCM trial, from MyoKardia, is investigating the use of mavacamten versus placebo in patients with hypertrophic cardiomyopathy for improvements in symptoms and function.

They also stress the importance of an individualized approach to prevent obesity in the long term that covers the following areas:
  1. Low- to moderate-intensity exercise programs to enhance physical functioning and weight control
  2. Comorbidity (hypertension, diabetes, coronary artery disease) treatment and prevention
  3. Nutritional counseling
  4. Modifiable CV risk factors
  5. Psychosocial adjustment
  6. The possibility of bariatric surgery for patients classified as morbidly obese
Reference

Fumagalli C, Maurizi N, Day SM, et al. Association of obesity with adverse long-term outcomes in hypertrophic cardiomyopathy. JAMA Cardiol. 2020;5(1):65-72. doi: 10.1001/jamacardio.2019.4268.

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