Obesity is associated with abnormalities in cardiac structure and function (37-39), which can often be alleviated by weight loss (see Table 1). As there is an increased energy requirement to move excess body weight at any given level of activity, the cardiac workload is greater for obese subjects than for nonobese individuals (39). Thus, obese subjects are known to have higher cardiac output (CO) and a lower total peripheral resistance in the absence of hypertension (23). The high CO is attributable to increased stroke volume, whereas heart rate (HR) is usually unchanged (24). The increase in blood volume and CO in obesity is in proportion to the amount of excess body weight (40). Recent evidence from the HyperGen study shows that both increased total fat mass and fat-free mass are able to cause these physiological changes although centrally located adipose tissue is particularly strongly associated with increased CO (41). In moderate to severe cases of obesity, an increased CO may lead to left ventricular
Prevalence of Cardiovascular Complications Associated With Obesity and Changes With Weight Loss
Weight loss with increased
Obesity physical activity
Cardiac output ^ ^
Endothelial function ^ ^
Stroke volume ^ ^
Resting heart rate Unchanged ^
Blood pressure ^ ^
Left ventricular mass ^ ^
Extent of Weight Loss Needed to See a Benefit in CVD Risk Factors
Extent of weight loss (%)a
Left ventricular function 5
aThese effects are not certain and may depend on the length and severity of disease. OSA, obstructive sleep apnea.
dilation, increased left ventricular wall stress, compensatory (eccentric) left ventricular hypertrophy (42-44), and left ventricular diastolic dysfunction (45). It is important to emphasize that left ventricular hypertrophy is an important risk factor for CHF.
These complications from obesity occur irrespective of age. It has been reported that in children as young as 12 yr, obesity impairs the ability to exercise, elevates blood pressure (BP), and increases left ventricular mass (LVM), indicating the development of early cardiovascular adaptation/damage in young individuals (46). In fact, the P-DAY Study in young men aged 15 to 34 yr demonstrated an accelerated progression of atherosclerosis at autopsy in obese individuals (47). Higher LVM and left ventricular dysfunction have been documented with longer durations of obesity (45). As previously mentioned, weight loss is able to diminish some of these anatomical and pathophysiological adaptations, including increased LVM (48) and abnormal ventricular filling (49,50) (Table 2).
The overproduction of adipocytokines in obesity also contributes to physiological changes to cardiac function. Changes in adipose tissue production of TGF-^1 may be a potential pathophysiological mechanism for the development of left ventricular filling abnormalities in obesity-associated hypertension (51). A relative deficiency of adiponectin may promote inflammation and vascular dysfunction by a reduced ability to inhibit local proinflammatory signals and prevent plaque formation (52). Proatherogenic chemokines, such as monocyte chemoattractant protein (MCP)-1, are also elevated in obesity. Such molecules may modulate the migration of granulocytes and monocytes into the arterial wall (53). Increased MCP-1 is associated with a number of alterations in the cardiac system, including increased LVM and altered diastolic filling (54).
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