Atherosclerotic and Arteriosclerotic Vascular Diseases

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Diseases of the vascular system provide the greatest contribution to the increased mortality associated with obesity. In both sexes, the excess mortality due to vascular disease increases linearly with BMI greater than 25kg/m2. The vascular complications of obesity can be categorized into five major groups: coronary heart disease, hypertension, congestive heart failure, cerebrovascular disease, and thrombo-embolic disease.

Coronary heart disease Longitudinal studies show a positive correlation of BMI with coronary heart disease (CHD), and obesity is an independent predictor of CHD. However, in the presence of other risk factors, such as hypertension, high serum cholesterol and triglycerides levels, low serum HDL cholesterol levels, and insulin resistance, all of which are increased by obesity, the risk of atherosclerotic CHD increases dramatically. Weight loss reduces all of these risk factors associated with cardiovascular disease, but because long-term reductions in body weight have been difficult to achieve, there are few long-term studies of changes in cardiovascular mortality due to weight loss. A very low-fat diet (10% of total calories as fat) has been shown to reduce the size of atherosclerotic plaques in coronary arteries. Such low-fat diets almost invariably produce weight loss.

Hypertension The prevalence of hypertension among overweight adults in the United States is 2.9 times higher than that of nonoverweight individuals.

Every 10-kg increase in body weight is associated with an increase of 3 and 2mmHg in systolic and diastolic blood pressures, respectively. Persistent hypertension can contribute to the development of left ventricular hypertrophy, coronary ischemia, and stroke.

The etiology of the association between hypertension and obesity is unclear. The following are some of the mechanisms offered to explain the association between obesity and hypertension:

Hyperinsulinemia due to insulin resistance leading to increased renal reabsorption of sodium Sodium retention due to a decreased renal filtration rate, increased intraabdominal pressure, and/or increased plasma renin activity Increased sympathetic nervous system activity

Except in long-standing cases, weight reduction is usually accompanied by a decrease in blood pressure. The reductions in blood pressure with weight loss are not dependent on decreases in salt intake. Many studies have shown that even modest weight losses, in the range of 5-10% of initial body weight, may produce reductions or even normalization of blood pressure in obese individuals.

Congestive heart failure Total blood volume increases with excess body weight. Higher oxygen consumption in obesity and increased blood flow to the splanchnic bed and adipose tissue increase cardiac output. Also, the transverse diameter of heart, thickness of the posterior wall, and thickness of the interventricular septum increase with body weight. Left ventricular mass is a stronger predictor of morbidity and mortality than blood pressure. A combination of these factors may result in the congestive heart failure seen in severely obese people. The heart rate, stroke volume, blood volume, cardiac output, and left ventricular work return to normal with weight reduction. One study that compared weight loss by dieting to treatment with antihypertensive drugs demonstrated a greater improvement in cardiac hypertrophy with weight loss, despite similar reductions in blood pressure.

Cerebrovascular disease Obesity-related atherosclerosis and arteriosclerosis increase the risk of cerebrovascular disease and strokes. Obesity is an independent risk factor for strokes, even in the absence of other comorbidities.

Thromboembolic disease The risks of venous stasis, deep vein thrombosis, and pulmonary embolism are increased in obesity, particularly in people with abdominal obesity. Lower extremity venous disease may result from increased intraabdominal pressure, impaired fibrinolysis, and the increase in inflammatory mediators described previously.

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