Myocardial injury during coronary intervention occurs in 10-40% of cases and is often characterized by a slight increase in the markers of myocardial necrosis, without symptoms, electrocardiographic changes or impairment of cardiac function. However, even small increases in creatine kinase (CK)-MB levels are an expression of a true and detectable infarction and may be associated with a higher follow-up mortality. The cause of CK-MB elevation in case of procedural complications is obvious; however, most cases of minor CK-MB elevation occur in patients with uncomplicated procedures with excellent final angiographic results. It has been suggested that the main mechanism explaining the occurrence of myocardial necrosis during otherwise successful coronary intervention may be distal microembolization of plaque components, an enhanced inflammatory state or total plaque burden and/or instability. Different treatments have been proposed to prevent myocardial injury during coronary intervention, including nitrate infusion, intracoronary beta-blockers, adenosine and IIb/IIa inhibitors, but none of these (apart from the use of IIb/IIIa inhibitors) have been routinely introduced into clinical practice. Previous observational studies suggested a beneficial effect of pre-treatment with statins in this setting; the ARMYDA (Atorvastatin for Reduction of Myocardial Damage During Angioplasty) trial is the first prospective, randomized, placebo-controlled study, evaluating the effects of 7-day therapy with 40 mg/day of atorvastatin on post-procedural release of markers of myocardial damage in patients with stable angina undergoing percutaneous intervention. In this study therapy with atorvastatin was associated with an 80% risk reduction in the occurrence of periprocedural myocardial infarction, as well as with a significant reduction in 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 injury necrosis due to microembolization, an improvement in endothelial function on microcirculation, and direct myocardial protection.