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Diabetes mellitus affects a significant portion of the population; 1 in 10 adults in the United States has diabetes, with 90% to 95% of patients having type 2 diabetes.1 In 2012, nearly 20.1 million Americans ≥20 years of age were diagnosed with diabetes mellitus, 8.1 million Americans had undiagnosed diabetes mellitus, and an estimated 80.8 million (35.3%) had prediabetes (ie, fasting blood glucose of 100 to <126 mg/dL).1 The prevalence of diabetes mellitus is rapidly increasing and is attributed to the increased frequency of obesity, suboptimal nutritional habits, and aging of the population (Fig. 40-1).2 The total prevalence of diabetes mellitus in the United States is expected to more than double from 2005 to 2050 (from 5.6% to 12.0%) in all age, sex, and race/ethnicity groups, with minorities disproportionately affected.1 This increase, however, is not limited to the United States. The global prevalence of diabetes mellitus for all age groups is also increasing. In 2010, the prevalence of diabetes mellitus worldwide was estimated to be 6.4% and is projected to increase to 7.7% in 2030; the total number of people with diabetes mellitus is projected to increase from 285 million in 2010 to 439 million in 2030.1,3

Figure 40-1

Numbers of people with diabetes (in millions) for 2000 and 2010 (top and middle values, respectively), and the percentage increase. (Reprinted by permission from Macmillan Publishers Ltd: Nature, Zimmet P, Alberti KG, Shaw J. Global and societal implications of the diabetes epidemic. Nature. 2001;414:782-787, Copyright © 2001.)


The interventional cardiologist often encounters patients with diabetes mellitus in more advanced stages, when vascular complications have already occurred. The pathophysiology of vascular disease involves derangements in endothelial, vascular smooth muscle cell, and platelet function.4 The hyperglycemia, increased availability of free fatty acids, and insulin resistance in the diabetic patient collectively decrease nitric oxide availability, increase oxidative stress, disrupt intracellular signal transduction, and activate receptors for free radical–producing advanced glycation end products.4 In addition, several deregulatory factors play a part in the derangements of coagulation and platelet activity seen in patients with diabetes, mostly mediated by enhancement of the prothrombotic state due to insulin resistance and hyperglycemia.5 Subsequently, atherosclerosis ensues, and as such, the risk for adverse cardiovascular events increases.

The concept of diabetes as a coronary artery disease (CAD) risk equivalent has its roots in a landmark Finnish-based study that demonstrated that the presence of diabetes alone increased the 7-year risk of fatal and nonfatal myocardial infarction (MI).6 These results laid the foundation for the recommendation that patients with diabetes receive secondary level prevention per the Adult Treatment Panel III of the National Cholesterol Education Program.7

Indeed, CAD is prevalent in the patient ...

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