Abstract

Atherosclerosis is a foreign body that is associated with an inflammatory response. The inflammatory response is clearly important both in terms of the progression of the atherosclerosis and subsequent changes in the plaque morphology that leads to thrombogenesis and clinical disease. However, the ability to identify these markers in the serum when their effects are primarily local may be very limited. We probably do not need another plethora of adhe sion molecules, cytokines and growth factors, each with a modest relative risk and then further debate about which of the numerous variables is more important. Unfortunately, the absence of measures of subclinical disease in most of these populations pre cludes the ability of separating the effects on ath erosclerosis and vessel wall from thrombogenesis and fibrinolysis. Obesity and total body fat, visceral fat and muscle fat, are important determinants of the levels of adipokines, hormone metabolism, liver enzymes, proteins and insulin resistance, which has now been labeled the "metabolic syndrome" [5]. There is, however, little evidence that these adipokines or other markers of body fat distribution play an independent role in atherosclerosis and CVD beyond the collin earity with lipoprotein metabolism, salt retention, elevated blood pressure (BP), insulin resistance and

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