DE during p-PCI occurs more often in the presence of high thrombus burden lesion. It reduces the effectiveness of myocardial reperfusion within 6 h and enhances myocardial damage within 3 h after symptom onset. Afterwards, it does not affect myocardial reperfusion or the extent of myocardial damage.

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We describe the clinical case of a 48–year–old master athlete, runner (marathon runner), always asymptomatic at rest and during effort, with a family history of ischemic heart disease and no other known cardiovascular risk factors. On the occasion of the pre–partecipation screening visit, he presented an altered baseline electrocardiogram with low peripheral voltages and T wave inversion in V1–V5 leads and inferior leads. The echocardiogram documented morphofunctional alterations in the right ventricle and raises the suspicion of arrhythmogenic cardiomyopathy, later confirmed by cardiac magnetic resonance with Gadolinium. During effort, even repetitive premature ventricular beats LBBB with superior axis morphology appeared. Also, torsade de pointes episode with presyncopal sensation. He was hospitalized with a diagnosis of threatening arrhythmias in right ventricular arrhythmogenic heart disease. Coronary angiography was negative. We recommend beta–blocker therapy, genetic analysis, screening of family members. A subcutaneus defibrillator has been placed. The patient, against the advice of the Physicians, continued to train even at high intensity until he has a syncopal episode with correct intervention of the device on ventricular fibrillation. Since the patient has requested specific indications to continue training independently, an exercise test in beta–blocker therapy is repeated and the training thresholds are calculated. The case of this master athlete highlights the issue of the difficulty of screening the master athlete with frequent omission of symptoms (the patient already had syncopal/presyncopal episodes at home which he had omitted), poor adherence to therapeutic indications, possible negative effects of high intensity physical training on the evolution of arrhythmogenic cardiomyopathy.

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