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Diabetes and Vascular Disease http://circ.ahajournals.org/content/108/12/1527.full.pdf Vascular diseases are the principal causes of death and disability in people with diabetes. There is a strong correlation between cardiovascular disease (CVD) and diabetes. Heart disease and stroke are the No. 1 causes of death and disability among people with type 2 diabetes. At least 65 % of people of diabetics die from some form of heart disease/stroke. Adults with diabetes are two to four times more likely to have heart disease or a stroke than adults without diabetes. The American Heart Association considers diabetes to be one of the six major controllable risk factors for cardiovascular disease. Over time, the excess glucose damages blood vessels throughout the body and vascular disease may result such as retinopathy and nephropathy which are major causes of blindness and end-stage renal failure respectively. Pathophysiology of diabetic vascular disease Effective endothelial and vascular smooth muscle cell function within vascular walls is vital and an abnormality may contribute to and exacerbate atherosclerosis and its complications. In normal endothelial cells, biologically active substances are synthesised and released to maintain vascular homeostasis to ensure adequate blood flow and nutrient delivery. One important substance synthesised by the endothelial cell is nitric oxide (NO). The bioavailability of NO represents a key marker in vascular health because it; causes vasodilation of smooth muscle cells, protects from endogenous injury. Also the loss of endothelial-derived NO leads to increased activity of pro-inflammatory transcription factors that results in greater expression of chemokines and cytokines that promote formation of macrophage foam cells (initial morphological changes of atherosclerosis). NO also is a key mediator of molecular signals that prevent platelet and leukocyte interaction with vascular wall and an inhibitor of vascular smooth muscle cell proliferation and migration. These abnormalities in endothelial cell function are mediated by the metabolic derangements which include: Hyperglycaemia: studies show hyperglycemia directly decreases endothelium derived NO and endothelial relaxation is impaired. Leads to a series of events that produces superoxide anion whilst inactivating NO increased oxidative stress. Excess free fatty acid deposition: impair endothelial function by increased production of oxygen-derived free radicals, exacerbation of dyslipidemiaIncrease oxidative stress. Insulin resistance: Insulin normally stimulates NO by a complex mechanism from endothelial cells Endothelial cell dysfunction also results in not only a decreased NO but also an increased synthesis of vasoconstrictors prostanoids and endothelin. These promote inflammation and cause vascular smooth muscle cell contraction and growth. Figure: The metabolic abnormalities that characterize diabetes, particularly hyperglycemia, free fatty acids, and insulin resistance, provoke molecular mechanisms that alter the function and structure of blood vessels. Abnormalities of the cardiovascular system specific to diabetes What is it? Microangiopathy Autonomic neuropathy Damage to small blood vessels and capillary circulation Damage to the nerve supply of the internal organs of the body Problems with the Retinopathy Nephropathy Neuropathy Clinical outcome pulse rate Diabetic foot Other blood vessel damage Damage to the inner or outer lining of blood vessels Impaired regulation of blood flow Weakened vessel walls Postural fall in blood Aggravated microangiopathy and pressure atherosclerosis/macroangiopathy Foot ulcers Impotence Gastro-intestinal dysfunction