**1. Introduction**

Obesity has traditionally been defined as a body mass index (BMI) value >30 kg/m2 , and its prevalence in the Western world, according to recent epidemiological data, could be as high as 36.5% [1]. Evidence of the growing prevalence of obesity can be inferred from the USA, where almost 70% of the population has been classified as obese; a significant increase from the 25% reported forty years ago [2]. The clinical relevance of obesity and its cluster of associated disorders, like arterial hypertension, dyslipidemia, diabetes mellitus, and sleep apnea syndrome, are demonstrated by its persistent link to an increased morbidity as well as

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© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, © 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

 mortality [3, 4]. It is for this reason that initiatives detailing the primary and secondary prevention of cardiovascular disease in overweight and obese patients have laid specific emphasis on the significance of weight loss so as to modify cardiovascular risk [5–7]. Obese patients have an increased preponderance to develop atherosclerotic disease, especially coronary artery disease, which is characterized by a reduced sensitivity to insulin, enhanced free fatty acid turnover, increased basal sympathetic tone, a hyper‐coagulable state, and finally with promotion of systemic inflammation [8, 9]. Population‐based data suggest that 43 and 24% of all coronary revascularization in recent years were carried out in overweight and obese patients, respectively [10]. It has been speculated that the obese patient cohort is somehow associated with a clinical outcome far worse than that of a normal weight patient, and this theory is further substantiated by the existence of evidence describing the causative association of morbid obesity in cardiovascular disease. Interestingly, contemporary studies have recently elucidated the role of an "obesity paradoxon," describing the protective effect of obesity (when considering postoperative morbidity and mortality) in patients receiving either surgical or minimally invasive coronary revascularization [11]. This observation suggesting a better clinical outcome for obese patients is not only restricted to the clinical setting of coronary revascularization, as similar data have also been reported in cases of an acute myocardial infarction and heart failure [12, 13].

In this review article, we attempt to present an overview and summarize the evidence documented on "obesity paradoxon" in coronary artery disease.
