Cardioprotective actions of acute HMG-CoA reductase inhibition in the setting of myocardial infarction

A known risk factor for the development of coronary artery disease and subsequent myocardial infarction is hypercholesterolaemia. The widespread nature of this phenomenon in the western world has led to the development of agents which reduce serum cholesterol levels. One such class of agents, HMG-CoA reductase inhibitors (statins) are very effective in cholesterol reduction. Recently, clinical and experimental evidence has amassed suggesting that patients taking statins receive cardiovascular benefits that occur independent of cholesterol reduction. Experimental data suggest that statins may increase levels of nitric oxide (NO) in vivo. This review will address the 'cholesterol-independent' vasculoprotective and cardioprotective effects of statins in animal models. Upon completion, the reader will be familiar with the proposed cholesterol-independent pathways of statins and understand that the cholesterol-independent benefits may arise from enhanced production of NO.