Although an abnormal blood pressure has been defined as 140/90 mm Hg, recent recommendations from agencies and associations have suggested levels below 120/80 mm Hg,9 because this lowers the risk of CHD morbidity considerably. Blood pressure is a strong risk factor for CVD (7th report). The risk of CVD increases beginning at 115/75 mm Hg. There is no threshold, rather it is a continuously increasing risk.10 A large study by Stamler11 showed the impressive effects of a small reduction of BP on reduction of mortality. A number of subsequent studies have confirmed the excellent impact of weight loss in lowering blood pressure in overweight individuals.12,13

Matabolic Syndrome (MetS) consists of a cluster of risk factors that are predictive of the progression to type 2 diabetes and CHD. It has five components and is considered to be present if three of five components are present in an individual.3 MetS, as defined in the United States, is shown in Table 35.1.3 Defining the MetS has not been an attempt to declare the existence of a new disease produced by a single pathogenesis but an effort to put together risk factors that as a group have a greater ability to predict disease than is the case if they are considered separately. This cluster of lipid and nonlipid risk factors enhances the risk for CHD at any given level of LDL-C. Patients who present such a cluster are at much greater danger of morbidity and mortality from type 2 diabetes and CHD than are patients who do not.14,15 It is therefore an alert for physicians that they should pay particular attention to these patients and address their risk factors vigorously to prevent progression to serious disease. The MetS has been described as a secondary target of therapy by ATP III.3

Macrovascular disease is the leading cause of death in diabetic persons. Many patients presenting with an AMI have either impaired glucose tolerance, impaired fasting glucose, or type 2 diabetes. Individuals with type 2 diabetes have great risk of developing CHD and eventual AMI.16 Adults with diabetes have heart disease death rates and risks for stroke two- to fourfold higher than adults without diabetes.17 Furthermore, the mortality rate for those diabetic individuals who have already suffered one AMI is higher than for nondiabetic persons who have suffered an AMI.18,19 It is critical to try to improve all risk factors for AMI in these patients.

The improvement in glucose control does not in itself seem to have a great deal of effect in improving morbidity and mortality from coronary artery disease (CAD). It is likely that the pathogenesis for this accelerated CAD in diabetic patients is the dyslipidemia seen with central obesity and diabetes. This is characterized by elevated very-low-density lipoproteins (VLDL) leading to hypertriglyceridemia. There is overproduction of VLDL triglyceride and VLDL apoB, and also a defect in clearance. The composition of LDL particles is altered, with smaller and denser particles being present, which are significantly more atherogenic.20,21 In addition, the elevated prevailing glucose can enhance the glycosylation of the LDL particles adding to their atherogenicity. Moreover, an increased susceptibility of the LDL particles to oxidation makes them more atherogenic. Finally, HDL production is decreased in obesity and diabetes, so that circulating levels are lower. These patients have elevated triglycerides also.22 Each of these lipid abnormalities has been shown to increase the risk for CAD in patients with type 2 diabetes.23,24

In type 2 diabetes, weight loss not only improves glycemic control but also ameliorates coexisting disorders such as dyslipidemia and hypertension. With dieting, the elevated triglyceride levels of obese patients with type 2 diabetes rapidly decline.25,26 Furthermore, with weight loss, significant increases in HDL-C levels have been reported in studies that have been of sufficient duration.27,28

Approximately 65% of U.S. adults are overweight or obese.29 Overweight and obesity are associated with an increased risk for CHD and heart failure. Obesity increases the risk of CVD. This has been well documented in the Framingham trial30 and the Nurses Health Study.31 In a more recent report, Wilson et al.32 have shown increased relative and population-attributable risk for hypertension and cardiovascular sequelae in Framingham Heart Study obese participants. This is thought to be related to the increased prevalence of dyslipidemia in obesity. The dyslipidemia, as in type 2 diabetes, comprises primarily of an elevation in triglycerides and a decrease in the level of HDL-C. Levels of total cholesterol and LDL-C may be elevated but are often normal. Although LDL-C levels are not elevated, the LDL particles are, nevertheless, qualitatively different, showing a shift to smaller, denser particles that are more atherogenic.33 These abnormalities are made worse by increased central or intra-abdominal fat.34,35 and 36

The evidence for the effect of weight loss as secondary prevention on reduction of adverse cardiac events is not large. Not many intervention studies have been carried out focusing on this question. Williamson et al.37 and Gregg et al.38 carried out retrospective analyses in women and men on the effect of intentional weight loss on mortality. They examined the life expectancy of >43,000 white U.S. women in the American Cancer Society Study. Overweight women with obesity-related health conditions had significantly higher mortality rates compared with women with no preexisting illness. Women with obesityrelated conditions who intentionally lost weight showed a significant reduction in all-cause mortality compared with women whose weight remained stable. The risk of cardiovascular mortality was reduced by 14% to 24% in obese women who intentionally lost weight.37 Gregg et al.38 then carried out a similar study in men, using the same American Cancer Society database. They found that men with obesity-related conditions who intentionally lost weight had a reduced all-cause and cardiovascular mortality. A 4-year prospective study of >7,500 middleaged men found an independent decrease in cardiovascular
mortality of almost 50% in those whose weight loss brought them below a body mass index (BMI) of 28 and a reduction of 77% in those who had associated hypertension.39 It has been suggested that CHD mortality could be reduced by 15% if everyone had a BMI between 21 and 25.

Because many obese persons also manifest hypertension and dyslipidemia, it has sometimes been difficult to assign causality for the CHD to obesity independent of these other conditions. Because obesity is associated with a number of CHD risk factors, it is not surprising that it has been related directly to greater cardiovascular risk.40

In both obesity and diabetes, there is an increased inflammatory environment. Obesity and fat cell size correlate with macrophage infiltration into adipose tissue.41 Cytokines released from both adipocytes and macrophages in adipose tissue contribute to a state of chronic systemic and local vascular inflammation and enhanced coagulation.42,43 and 44

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