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There is an increasing number of patients receiving an ICD due to a hereditary and/or electrical cardiomyopathy [1, 2]. These patients often have the ability to practice competitive sports despite their disease as performance capacity is at most marginally affected. Because of this situation, sports physicians are increasingly confronted with the evaluation of athletes with ICD concerning competitive sports participation. Current guidelines almost invariably prohibit competitive sports participation of ICD patients [3]. However, these recommendations are critically questioned due to their low level of evidence [4]. Here, we present the case of a professional soccer player with hypertrophic cardiomyopathy (HCM) and ICD implanted for primary prevention of sudden cardiac death. Contrary to current recommendations [3, 5, 6], we certified ability for competitive sports participation, whereupon establishment of a close meshed follow-up using Home Monitoring [7] was one important prerequisite for our decision. A 23-year old professional soccer player (third German football league, formerly U21 national team) was introduced by the team doctor due to resting ECG abnormalities. The patient negated any current leading cardiovascular symptoms. However, he reported of three syncopal events within the last 5 years, detailed description rather pointed to a non-cardiac cause. Family history for sudden cardiac death was inconspicuous. Resting ECG showed preterminal T-wave negativity of precordial leads. Ergometry up to 360 W revealed a normal RR-regulation, no arrhythmias, an erection of the negative T-waves and no ECG-alterations suspicious for cardiac ischemia. Echocardiographically, basal septum was mildly hypertrophied (13 mm end-diastolic) with implied apical accentuation. Left ventricular diameter (53 mm end-diastolic), size of the atria, total heart volume (880 ml, respectively, 11.0 ml/kg bodyweight) and left ventricular systolic and diastolic function were normal. Evaluation of right ventricular morphology and function resulted in a slight enlargement and no evidence for impaired systolic function. Because of our findings, we arranged further cardiac imaging. Cardiac MRI revealed an asymmetrical, midventricular to apical septal hypertrophy up to 18 mm (enddiastolic) with an atypical scar within the center consistent to hypertrophic cardiomyopathy (Fig. 1). In the first instance, based on the diagnosis, we did not certify ability for competitive sports participation [5]. Prognosis was estimated to be good due to a hypertrophy \30 mm, normal blood pressure regulation during exercise, negative family history concerning sudden cardiac death and absence of left ventricular outflow tract obstruction [8]. In our opinion, arrhythmia risk seemed to be rather low at this time-point, as additional 7-day Holter ECG showed no abnormalities. For further risk stratification, we recommended the implantation of an event recorder. However, the patient was told to visit an arrhythmia center for a second opinion and thereafter, he should re-visit us to organize further treatment. Our suggested procedure was confirmed by the center. Thereafter, the patient obtained a third opinion in another hospital on his own initiative. In this clinic—unfortunately without contacting us before—an ICD was & Roman Laszlo roman.laszlo@uniklinik-ulm.de

Catheter ablation is of growing importance in patients with an ischemic cardiomyopathy and recurrent episodes of ventricular tachyarrhythmias. Most ablation strategies in these patients are based on the detection of areas of scar and border zones to normal myocardium. However, the mapping criteria for identifying these areas have not been validated sufficiently so far. Therefore, we have performed a comparison between electroanatomical bipolar voltage maps obtained during substrate-based VT ablation procedures and [18 F]fluoro-2-deoxyglucose PET studies performed prior to these procedures.Seven patients suffering from severe coronary artery disease and repetitive ventricular tachycardias were enrolled in this study. In all patients, there was a history of myocardial infarction and the left ventricular function was severely impaired. A FDG PET was performed at least 1 day prior to the ablation procedure in all patients. Then, a substrate-based VT ablation procedure was performed using the CARTO system (Biosense Webster, Diamond Bar, CA, USA). Finally, the FDG PET images and the bipolar voltage maps were compared in all patients.The ablation procedures could be performed successfully in all patients and 1-5 monomorphic VTs could be eliminated in each patient. There were no major complications. At 1-year follow-up, five out of seven patients (71.4%) remained free from any arrhythmia recurrence. In all patients, there were extensive areas of scar and adjacent low-voltage areas could be identified in the CARTO bipolar voltage maps. In areas commonly defined as "dense scar" (bipolar voltage amplitude0.5 mV), the mean FDG uptake was 43.1% (SD ±18.2%) indicating predominantly scar tissue. In the so-called low-voltage border zones the mean FDG uptake ranged between 49.5% [(SD ±15.8%);0.5-1 mV] and 60.1% [(SD ±14.8%);1-1.5 mV], thereby indicating the presence of predominantly viable myocardium. In areas with a bipolar voltage amplitude1.5 mV the presence of viable myocardium was confirmed by a mean FDG uptake of approximately 60%.The results of our study demonstrate that there is a significant amount of viable myocardium in the low-voltage border zones of scars frequently targeted as ablation sites. Therefore, RF current delivery in these areas should be restricted to the minimum assumed to be necessary for successful catheter ablation because extensive RF applications might result in a further deterioration of the left ventricular function. Larger studies are needed to validate our results and to develop more reliable criteria for distinguishing areas of scar from viable myocardium in CARTO bipolar voltage maps.