Bariatric Surgery in Patients With Left Ventricular Systolic Dysfunction

Abstract

Obesity, particularly severe obesity, produces a variety of alterations of cardiac performance and morphology that may lead to the development of heart failure.1–9 Excess adipose accumulation in association with increased lean body mass produces an increase in central blood volume.1–4,8,9 In patients with normotensive obesity, this predisposes to an increase in cardiac output which is facilitated by a decrease in systemic vascular resistance.1–4 Because heart rate changes little if at all with obesity, the increase in cardiac output is predominantly caused by augmentation of left ventricular (LV) stroke volume.1–4 In many obese individuals, the high cardiac output state is associated with LV dilatation, a response that may lead to eccentric LV hypertrophy (LVH).1–5,7,8 However, recent studies have suggested that concentric LVH or remodeling occurs as often or perhaps more often than eccentric LVH in obese subjects.10–12 Factors that may predispose to concentric LVH or remodeling in such individuals include the presence of systemic hypertension, increased sympathetic activity, stimulation of the renin–angiotensin–aldosterone system, insulin resistance with hyperinsulinemia (which may predispose to release of insulin-related growth factors), hyperleptinemia, and possibly, lipotoxicity and lipoapoptosis.1–5,12,13 Because LVH is a key morphological alteration in obesity, the predominant functional change is LV diastolic dysfunction, manifested as elevated LV end-diastolic pressure (particularly during exercise) and impaired LV diastolic filling on noninvasive cardiac imaging.1–5,7,8 LV systolic dysfunction (LVSD) is relatively uncommon in obesity. LV ejection phase indices are usually normal or supranormal, and when abnormal, they are usually mildly reduced.1–5,7,8,14,15 LVSD in uncomplicated obesity may be related in part to inadequate LVH leading to persistently high …