Key result
RAAS interruption and pulsatile insulin target nonhemodynamic microvascular fibrosis and inflammation in diabetes.
Highlights the potential of targeting angiotensin-aldosterone mechanisms and physiologic glycemic control to improve macrovascular outcomes in diabetic patients.
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May support RAAS blockade and pulsatile insulin in diabetic microvascular disease; hypothesis-generating, requiring randomized trials before practice change.
The results of recent outcome trials challenge hypotheses that tight control of both glycohemoglobin and blood pressure diminishes macrovascular events and survival among type 2 diabetic patients. Relevant questions exist regarding the adequacy of glycohemoglobin alone as a measure of diabetes control. Are we ignoring mechanisms of vasculotoxicity (profibrosis, altered angiogenesis, hypertrophy, hyperplasia, and endothelial injury) inherent in current antihyperglycemic medications? Is the polypharmacy for lowering cholesterol, triglyceride, glucose, and systolic blood pressure producing drug interactions that are too complex to be clinically identified? We review angiotensin-aldosterone mechanisms of tissue injury that magnify microvascular damage caused by hyperglycemia and hypertension. Many studies describe interruption of these mechanisms, without hemodynamic consequence, in the preservation of function in type 1 diabetes. Possible interactions between the renin-angiotensin-aldosterone system and physiologic glycemic control (through pulsatile insulin release) suggest opportunities for further clinical investigation.
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Weinrauch et al. (2010) conducted a review in Diabetic microvascular and macrovascular complications. Angiotensin-aldosterone blockade and pulsatile insulin therapy was evaluated. Nonhemodynamic effects on renal, cardiac, and ocular microvasculature, particularly through renin-angiotensin-aldosterone system interruption and pulsatile insulin delivery, present important targets for reducing profibrotic and proinflammatory forces in diabetes.
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