European Journal of Cardiovascular Medicine

Statins exert beneficial effects on the endothelium, inflammation and the coagulation cascade that are independent of cholesterol lowering. The main mechanism underlying these effects is inhibi- tion of isoprenoid synthesis, modulating the inflammatory cascade and the endothelial activation reliable of atherosclerosis. Different studies demonstrated that statins improve endothelial function in patients with stable atherosclerotic plaque and that this effect is dose-dependent. Statins may modulate endothelial expression of adhesion molecules, as demonstrated in the ARMYDA-CAMS, and may enhance mobilisation of endothelial progenitor cells. Elevated C-reactive protein levels, an inflammatory marker that also plays a direct pathogenetic role in the atherosclerotic process, have been correlated with worse outcome in patients with cardio- vascular disease. Multiple studies demonstrated that statin attenuates the rise of inflammatory markers and improves clinical outcome in patients with stable angina, unstable angina and non-Q wave acute myocardial infarction. During percutaneous coronary intervention randomised trials showed a benefical effect of statin pre-treatment in reducing peri-procedural myocardial damage probably by plaque stabilisation and inhibition of microembolisation phenomena during stent implantation. The ARMYDA study and the NAPLES II trial demonstrated this beneficial effect in patients undergoing coronary revascularisation for stable angina. Also in patients with ACS, receiving invasive strategy, the role of statins in preventing peri-procedural damage was demonstrated in the ARMYDA-ACS study by the administration of an acute high loading-dose with atorvastatin. In patients already on chronic statin therapy at the time of the procedure, an acute drug reload before stenting would have cardio- protective effects, like demonstrated in the ARMYDA RECAPTURE study.