Cardiovascular Pathophysiology of Obesity

The INTERHEART study has recently led to the consideration of visceral obesity as an independent risk factor for cardiovascular diseases. The high rate of morbidity and mortality in obese patients recognises metabolic, haemodynamic, endothelial and endocrine mechanisms as influencing factors. Insulin resistance and the resulting hyperinsulinaemia represents one of the most relevant elements for developing visceral obesity, which is involved in volume overload, sympathetic hyperactivity, increased vascular sensitivity and tone, stable hypertension, left ventricular hypertrophy and atherogenic dyslipidaemia. On the other hand, hypertension, hyperinsulinaemia, and sympathetic and renin-angiotensin hyperactivity may promote the structural changes in cardiac geometry, defined as remodelling, concentric and eccentric hypertrophy, and diastolic and systolic dysfunction and failure. In this view, the adipose tissue has to be considered not only as a deposit tissue, but also as an endocrine organ. Several molecules produced by adipocytes act by an endocrine, paracrine and autocrine function on different tissues. Leptin, adiponectin, tumour necrosis factor-alpha and interleukin-6 are some of these molecules, which are involved in glucose and lipid metabolism in the atherosclerosis process and in thrombosis and haemodynamic homeostasis. In summary, visceral obesity, as an independent risk factor, may result in insulin resistance, hypertension, cardiovascular remodelling, endothelial dysfunction, dyslipidaemia and consequent atherosclerosis.