The Concept of CMR

Fat distribution and pro-thrombotic state

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Figure: Adipose tissue and some of the adipokines/factors involved in the pro-thrombotic state of intra-abdominal obesity

Figure: Adipose tissue and some of the adipokines/factors involved in the pro-thrombotic state of intra-abdominal obesity

Obesity and overweight pose a major risk for serious chronic diseases, including type 2 diabetes, cardiovascular disease, hypertension, and stroke (1, 2). However, it remains to be determined whether obesity is truly an independent risk factor or whether it acts in conjunction with other well-known cardiovascular risk factors such as insulin resistance, dyslipidemia, and a pro-inflammatory and pro-thrombotic state. This cluster of atherogenic metabolic abnormalities is now often referred to as the metabolic syndrome. In addition, obesity is a heterogeneous condition (3). Numerous studies have revealed that the amount of body fat does not necessarily determine morbidity and that body fat distribution is most closely linked to metabolic and vascular diseases (3). Several reports have demonstrated that intra-abdominal or visceral fat is associated with significant, and largely preventable, morbidity and mortality, including an increased incidence and prevalence of arterial and venous thrombotic events (4). Moreover, atherothrombotic complications in the metabolic syndrome are partly due to a dysregulation of hemostasis, inducing a pro-thrombotic state that encompasses endothelial activation, platelet hyperactivity, hypercoagulability, and hypofibrinolysis (Figure). All of these changes can be found in abdominally obese, insulin-resistant subjects. However, increased plasminogen activator inhibitor-1 (PAI-1) expression with attendant hypofibrinolysis is the main hemostasis disorder linked to insulin resistance and is now considered part of the cluster of abnormalities of the metabolic syndrome (5).

Reference

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1. Wilson PW, D'Agostino RB, Sullivan L, et al. Overweight and obesity as determinants of cardiovascular risk: the Framingham experience. Arch Intern Med 2002; 162: 1867-72.

2. Chan JM, Rimm EB, Colditz GA, et al. Obesity, fat distribution, and weight gain as risk factors for clinical diabetes in men. Diabetes Care 1994; 17: 961-9.

3. Abate N and Garg A. Heterogeneity in adipose tissue metabolism: causes, implications and management of regional adiposity. Prog Lipid Res 1995; 34: 53-70.

4. Darvall KA, Sam RC, Silverman SH, et al. Obesity and thrombosis. Eur J Vasc Endovasc Surg 2007; 33: 223-33.

5. Juhan-Vague I, Alessi MC and Vague P. Increased plasma plasminogen activator inhibitor 1 levels. A possible link between insulin resistance and atherothrombosis. Diabetologia 1991; 34: 457-62.

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