Myocardial injury during coronary intervention occurs in 10-40% of cases and is often characterized by a slight increase of markers of myocardial necrosis, without symptoms, electrocardiographic changes or impairment of cardiac function. However, even small increases of creatine kinase-MB levels are expression of a true and detectable infarction, and may be associated with higher follow-up mortality. The cause of CK-MB elevation in case of procedural complications (dissection, transient vessel closure, no reflow, side branch occlusion etc.) is obvious; however, most cases of minor CK-MB elevation occur in patients with uncomplicated procedure with excellent final angiographic results. It has been suggested that the main mechanism explaining occurrence of myocardial necrosis during otherwise successful coronary interventions may be distal microembolization of plaque components, an enhanced inflammatory state or due to total plaque burden and/or to plaque instability. Different treatments have been proposed to prevent myocardial injury during coronary intervention, including nitrate infusion, intracoronary beta-blockers, adenosine, clopidogrel and IIb/IIIa inhibitors, but none of those (apart from the use of IIb/IIIa inhibitors) has been routinely introduced in clinical practice. We performed the ARMYDA (Atorvastatin for Reduction of MYocardial Damage during Angioplasty) trial, i.e. the first prospective, randomised, placebo controlled study to evaluate effects of 7 days of pre-treatment with a fixed dose of atorvastatin (40 mg/day) on post-procedural release of markers of myocardial damage in patients with stable angina undergoing percutaneous intervention. In this study therapy with atorvastatin has been associated with 80% risk reduction on the occurrence of peri-procedural myocardial infarction, as well as with significant reduction of post-intervention peak levels of all markers of myocardial damage. The mechanisms underlying the beneficial effects of atorvastatin may be an inflammatory action reducing myocardial necrosis due to microembolization, an improvement of endothelial function on microcirculation, and direct protection of myocardium.