Abdominal obesity and the metabolic syndrome: a surgeon's perspective

Abstract

Over the past decade, a major shift in the clinical risk factors in the population undergoing a cardiac surgery has been observed. In the general population, an increasing prevalence of obesity has largely contributed to the development of cardiovascular disorders. Obesity is a heterogeneous condition in which body fat distribution largely determines metabolic perturbations. Consequently, individuals characterized by increased abdominal fat deposition and the so-called metabolic syndrome (MetS) have a higher risk of developing coronary artery disease. Recent studies have also emphasized that visceral obesity is a strong risk factor for the development of heart valve diseases. In fact, individuals characterized by visceral obesity and its metabolic consequences, such as the small dense low-density lipoprotein phenotype, have a faster progression rate of aortic stenosis, which is related to increased valvular inflammation. Furthermore, the degenerative process of implanted bioprostheses is increased in subjects with the MetS and/or diabetes, suggesting that a process akin to atherosclerosis could be involved in the failure of bioprostheses. In addition to being an important risk factor for the development of cardiovascular disorders, the MetS is increasing the operative mortality risk following coronary artery bypass graft surgery. Thus, recent evidence supports visceral obesity as a global risk factor that is affecting the development of many heart disorders, and that is also impacting negatively on the results of patients undergoing surgical treatment for cardiovascular diseases. In the present paper, recent concepts surrounding the MetS and its implications in various cardiovascular disorders are reviewed along with the clinical implications.

Figure 1)

In 102 patients, mean progression of aortic stenosis evaluated with the annualized peak gradient in relation to the proportion of circulating small size low-density lipoprotein (LDL) (percentage of LDL particles less than 255 Å).

Figure 2)

Macroscopic view (A) and x-ray analysis (B) of an explanted bioprosthesis showing that calcifications and tears (arrows) are two interconnected mechanisms actively participating in structural valve degeneration

Figure 3)

In 217 patients with an aortic bioprosthesis, the annualized mean transprosthetic gradient was significantly increased in patients having diabetes and the metabolic syndrome. Reproduced from reference with permission of the American Heart Association

Figure 4)

Patients in chronic positive energy balance and deficient lipid partitioning, which may be at least in part dependent on leptin resistance, will develop ectopic fat accumulation. Abdominal fat promotes the formation of small, dense low-density lipoprotein (LDL) particles as well as lower level of high-density lipoproteins (HDLs), which in turn have detrimental roles in the development of atherosclerotic plaque. Accumulation of ectopic epicardial fat could influence atherosclerosis development through the production of cytokines diffusing to the plaque by the vasa vasorum and neo-vascularization process