Obesity and cardiovascular disease

Obesity is a major contributor to the risk of cardiovascular disease. In the Fram-ingham Heart Study, the 26-year incidence of coronary heart disease (CHD) was increased by a factor of 2.4 in obese women and 2 in obese men under age of 50 years (Hubert et al., 1983). Excess weight was an independent predictor of coronary artery disease, coronary death and congestive heart failure after adjusting for other known recognized risk factors.

In the Nurses' Health Study from the United States, the risk of developing CHD increased 3.3-fold with BMI > 29 kg/m2 and 1.8-fold between 25 and 29 kg/m2, compared to those women with BMI < 21 kg/m2 (Manson et al., 1990, 1995). Each kg of weight gained from the age of 18 years was associated with 3.1% higher risk of cardiovascular disease (Willett et al., 1995).

This increased risk extends to overweight children and adolescents, who are at risk of premature cardiovascular morbidity and death. Excess weight in adolescence was a better predictor of these risks than excessive weight in adulthood (Gunnell et al., 1998).

Along with an increased risk of CHD, obese populations experience a higher recurrence of cardiac event rates after acute myocardial infarction. The relative risk of recurrent infarction or death was 1.5 with BMI 30-34.5 kg/m2 and 1.8 with BMI > 35 kg/m2 compared to BMI 16-24 kg/m2 as seen in a population based study of 2541 patients (Rea et al., 2001).

The increased CHD risk is better correlated with abdominal or central obesity than simple BMI (Rich-Edwards et al., 1995). In the Nurses' Health Study, a waist-hip ratio (WHR) of >0.88 versus WHR < 0.72 was associated with an increased relative risk of CHD of 3.25 (Rexrode et al., 1998).

The increased CHD morbidity and mortality could be related to traditional risk factors like hypertension and dyslipidaemia or due to the effect of obesity per se on the cardiovasculature. Obesity is associated with disturbances in cardiac function and structural changes in the absence of hypertension and underlying organic heart disease. There is an increase in total blood volume in proportion to body weight resulting in higher cardiac output. Volume overload of the left ventricle results in increased left ventricular stress which stimulates eccentric hypertrophy of the ventricle with resultant diastolic dysfunction. Over time, excessive wall stress causes ventricular dilatation resulting in systolic dysfunction, termed obesity cardiomyopathy. The presence of hypertension in obesity exacerbates left ventricular wall changes, which can increase progression towards heart failure (Albert and Hashini, 1993).

Left ventricular wall abnormality is implicated in the propensity for sudden death seen in obesity. The reason for sudden death from cardiomyopathy may be due to complex ventricular arrhythmias. Prolonged Q-T interval which predisposes to cardiac arrhythmias, occurs in up to one third of obese subjects (Frank et al., 1986). Other ECG changes observed in a study of 100 obese subjects compared with 100 normal subjects, without any evidence of cardiac disease included more leftward shift of P, QRS and T axes, evidence of left ventricular hypertrophy and left atrial abnormality and T-wave flattening seen in the inferior and lateral leads (Alpert et al., 2000). Autonomic dysfunction due to alteration in parasympathetic and sympathetic cardiac innervation may also contribute towards arrhythmias.

The structural and functional changes are also seen in the right side of the heart in obesity. Right ventricular dysfunction could be secondary to left ventricular dysfunction or due to obstructive sleep apnoea and/or obesity hyperventilation syndrome which occurs in 5 per cent of morbidly obese individuals (Alpert and Hashini, 1993).

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