The Heavy Heart
Metabolic Mechanisms and Myocardial Mechanics
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Obesity is an independent risk factor for the development of left ventricular hypertrophy (LVH) and heart failure (HF) and, in particular, HF with preserved ejection fraction.1,2 The pathways from excess adiposity to abnormal myocardial structure and function, and then onwards to clinically overt HF, remain incompletely defined. Obesity is associated with a range of hemodynamic adaptations, including increased stroke volume, heart rate, sympathetic activity, and cardiac output, and an increase in left ventricular mass to accommodate the increased wall stress. Consequently, most obese individuals have normal or hyperdynamic left ventricular systolic function.3 Diastolic dysfunction may be detectable in as many as 57% of obese individuals (body mass index [BMI] ≥30 kg/m2) aged >50 years4; the proportion of obese individuals with systolic dysfunction is less clear, and the proposition of an obesity cardiomyopathy has been controversial. In this issue of Circulation: Heart Failure, Ho et al5 sought to examine the link between obesity-related metabolic traits and subclinical alterations in systolic myocardial mechanics detected by strain echocardiography.
See Article by Ho et al
Whether it is the obesity per se, the associated metabolic syndrome, or dysfunctional adipokine signaling that lead to myocardial dysfunction and HF has been a source of much investigation. It seems that abnormalities of myocardial structure and function start early in life. Obese children without additional cardiovascular risk factors show an association between excess adiposity and LVH, diastolic dysfunction, and abnormal circumferential strain, which may be independent of hypertension and insulin resistance.6,7 Among adults, obese individuals with greater insulin resistance and metabolic dysfunction show the greatest risk of HF development—for example, there is a greater risk of HF in normal-weight individuals with metabolic syndrome …