Coronary vasospasm and aborted sudden death treated with an implantable defibrillator and stenting.

Cardiac troponins are highly sensitive and specific markers of early detection of myocardial injury. The incidence of cardiac troponin increase is of 5-40% after percutaneous coronary interventions and is significantly higher in patients undergoing stenting than in patients with balloon angioplasty only. Four mechanisms are responsible for myocardial necrosis during coronary angioplasty: 1) distal embolization of small fragments of the atherosclerotic plaque; 2) side branch occlusion; 3) intimal dissection, and 4) temporary vessel occlusion. The multiple and/or complex lesions, the diabetic status and plaque instability increase the probability of troponin elevation during coronary angioplasty. Moreover, the long time needed for interventional as well as atherectomy procedures may induce myocardial necrosis. In conclusion, after successful percutaneous coronary interventions, minor elevation of troponin may occur. In this setting cardiac troponin I is a highly specific marker of myocardial injury.