• infarto miocardico acuto

Background: after an acute myocardial infarction (AMI), many patients develop a progressive left ventricular (LV) dysfunction (remodeling) leading to the clinical scenario of heart failure. The global incidence of such pathology is progressively increasing: in fact it represents the leading cause of hospitalization in patients over 65 years old. Nevertheless, LV remodeling after AMI has very hard prognostic consequences if we considered that 40% of these patients will be dead at 5 years. We don't know the complex mechanisms responsible, in each patients, of the evolution toward ischemic dilated cardiomyopathy, but certainly a major role is played by myocardium conditions at the moment of coronary occlusion, by severity and duration of ischemia and, of course, by early reperfusion.
Aim: In patients with AMI we want to identify the optimal therapeutic strategy to limit the extension of infarcted area and the additional myocardial damage known as reperfusion injury, and to verify if this strategy is effective in preventing post ischemic cardiomyopathy.
Materials and Methods: patients admitted in the cath lab with a diagnosis of STEMI within 6 hours of ischemic symptoms onset who underwent primary PCI will be randomized to receive a pharmacological intervention (intracoronary administration of adenosine) or a mechanical intervention (ischemic post conditioning) to prevent reperfusion injury. The LV function is monitored during the hospital stay and up for 12 months with echocardiographic techniques, while microcirculation and infarct size will be estimated by Cardiac Magnetic Resonance (CMR) at 1 months from AMI, if possible, or by contrast echocardiography.
Objectives: Identification of optimal timing in the setting of AMI, Evaluation of reperfusion injury and its role In LV dysfunction, Identification of optimal strategies (pharmacological or mechanical) to avoid the development of dilated cardiomiopathy after AMI.
Conclusions: No Difference In Terms Of primary End Point Among adenosine and post-conditioning. Treatment with adenosine + postconditioning vs controls is statistically significative (p< 0.05) in terms of: WMSI, ST-resolution, Cardiac Markers, Delta%
Myocardial protection is feasible and well tolerated and adjunt to primary PCI ameliorate flow, prevents no reflow phenomenon, improves ventricular function and is associated with less edema of the infarcted wall.