Lost in Translation

Abstract

In the United States, the prevalence of diabetes mellitus has increased dramatically over the past 30 years with most cases being attributed to type-2 diabetes (T2DM).1, 2 Cardiovascular disease is the leading cause of death in these patients, with atherosclerosis accounting for approximately 80% of the cases.3, 4 The cluster of insulin resistance, hyperglycemia, dyslipidemia, hypercoagubility, obesity and hypertension typically that track with T2DM is largely responsible for the increase in coronary atherosclerosis. 1 However, the presence of T2DM also increases the manifestations of coronary atherosclerosis with larger infarct size and greater post-infarction remodeling in T2DM patients compared with their non-diabetic counterparts being prime examples. Even in the absence of coronary atherosclerosis, the presence of T2DM potentiates the manifestations of a variety of cardiovascular disease processes such as left ventricular (LV) hypertrophy and heart failure secondary to dilated cardiomyopathy.5-7 Indeed, there is increasing evidence for a true diabetic cardiomyopathy -- the presence of LV systolic and diastolic dysfunction that occurs in the absence of concomitant coronary artery disease and hypertension.8 The mechanisms by which these cardiovascular complications become manifest in T2DM are multifactorial and include an increased prevalence of hyperlipidemia and hypertension, impaired fibrinolysis, abnormal myocardial endothelial function and reduced sympathetic neuronal function.