Pathophysiological mechanism behind diabetic cardiovascular disorders

Fatal and non-fatal Coronary Artery Diseases (CAD) are increased 2-4 fold in patients with diabetes and autopsy as compared to non-diabetic patients with Coronary Heart Disease (CHD). Immediate and long-term post- Myocardial Infarction (MI) mortality is increased 1.5-2 fold among diabetic patients. Despite a comparably small infarct size, diabetic patients have a far greater risk of developing highly fatal post-MI complications when compared to non diabetic patients. Following MI, the surviving myocardium of non-diabetic patients becomes hyperkinetic to compensate for non-viable infarcted myocardium in an attempt to maintain cardiac output. However, in diabetic patients, these areas of myocardium cannot achieve this compensatory enhancement in function due to a complex set of intra- and extra-myocardial factors superimposed on an already reduced coronary artery flow reserve. Endomyocardial samples from diabetic patients show enhanced thickening of capillary basement membrane, myocellular atrophy and hypertrophy with myocardial and, interstitial fibrosis, which further reduces the function of the myocardium. In this review the author have looked into various cardiovascular complications in diabetic condition and the pathophysiological mechanisms lying behind each.