الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Large parts of the world today are at moderate or high levels of risk for CVD, and cumulative behavioral, biological, and social risks will increase the global impact of chronic diseases in the future. CVDs are, and will remain for decades, the major causes of death in the world.
Obesity is defined as an excess of body fat, it should be noted that the obesity-related CVD risk factors themselves are based on arbitrary cut-offs and do not necessarily indicate a clinical condition; everything could change if they were redefined.
An increasing prevalence of obesity, especially abdominal obesity, is driving the global pandemic of diabetes with its associated burden of insulin resistance and CV complications.
The breadth of determinants that contribute to CVDs points to the need for lifelong and multisectoral approaches. Because unhealthful diet, tobacco use, and decreased physical activity levels are among the major drivers of the CVD epidemic, prevention through promoting healthful diet and lifestyle should remain one of the cornerstones of global CVD reduction efforts. This does not exclude the importance of the potential to reduce CVD burden through better health care delivery, including better integration and development of chronic disease care models. Together, these approaches have the potential to address the burden of disease and overlapping determinants that are common in most emerging economies.
Prevention efforts need to start early in life and continue through the life course. A new and far greater emphasis on early childhood development is warranted, including greater attention to chronic disease risk in maternal and child health programs. However, trends in major risks will continue to influence incidence for many decades even if childhood prevention is rapidly implemented. Therefore, concerted and combined primary and secondary prevention efforts are also needed to reduce death rates in middle age and beyond.
Finally, Obesity is particularly important, as excess intra-abdominal adiposity increases cardio-metabolic risk directly, via altered secretion of adipokines and indirectly via promotion of insulin resistance and the metabolic syndrome. Risk stratification should include measurement of waist circumference as an index of intra-abdominal adiposity, and therapeutic interventions should focus on the management of intra-abdominal adiposity, insulin resistance, and inflammation.
The complex, interrelated determinants of CVD and the associated risk for obesity means that prevention efforts will only be effective if they are adapted to account for the specific needs of the settings in which they will be applied. To achieve this, additional surveillance and implementation research in all global regions, but especially in low and middle income countries, is required.
Conclusion
Obesity is a chronic metabolic disorder associated with CVD and increased morbidity and mortality. It is apparent that a variety of adaptations/alterations in cardiac structure and function occur as excessive adipose tissue accumulates, even in the absence of systemic hypertension or underlying organic heart disease. To meet increased metabolic needs, circulating blood volume, plasma volume, and cardiac output all increase. The increase in blood volume in turn increases venous return to the right and the left ventricles, eventually producing dilatation of these cardiac cavities, increasing wall tension. This leads to LVH, which is accompanied by a decrease in diastolic chamber compliance, eventually resulting in an increase in left ventricular filling pressure and left ventricular enlargement. As long as LVH adapts to left ventricular chamber enlargement, systolic function is preserved. When LVH fails to keep pace with progressive left ventricular dilatation, wall tension increases even more and systolic dysfunction may ensue. Systemic hypertension, pulmonary hypertension (left ventricular failure, chronic hypoxia), and CHD all occur with disproportionately high frequency in obese individuals and may cause or contribute to alterations in cardiac structure and function. There is also an increased risk of sudden cardiac death in obesity. Hopefully, within the next decade, new information may be provided that weight reduction is beneficial for hard CVD outcomes, ie, CHD events, CHD death, CHF, stroke, and total mortality. Until then, the clinical approach must hope that such a favorable result will ensue. The problem of overweight/ obesity has been identified as one of the major CVD risk factors since 1998, and although we understand to some extent the pathophysiological link between overweight/obesity and many forms of CVD, a number of remaining scientific questions need to be addressed for us to have a more complete understanding of the relationship between overweight/ obesity and CVD.