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BACKGROUND: Several aetiologies account for exercise intolerance, with cardiac sarcoidosis (CS) constituting a rare cause thereof. The pathogenesis of CS is still unresolved and its diagnosis still difficult to establish, in the absence of any extracardiac manifestations in particular. CASE SUMMARY: A 49-year-old amateur athlete presented with exercise intolerance during running over a 3-week period. Coronary artery and structural lung disease were excluded by coronary angiography and computer tomography. The symptoms could be reproduced during spiroergometry during which an exercise-induced high-degree atrioventricular (AV) block was documented. During electrocardiographic monitoring, a 2:1 AV block was observed. Different imaging modalities showed inferobasal septal inflammation and fibrosis. Transthoracic and transoesophageal echocardiography-guided endomyocardial biopsies were inconclusive and only subsequent epicardial biopsy performed by transdiaphragmatic minimally invasive surgery lead to the histological diagnosis of non-caseating granuloma, confirming CS. The patient was treated with high-dose steroids 1 week after implantation of a primary prevention dual-chamber implantable cardioverter-defibrillator (ICD). While tapering steroids, recurrence of myocardial inflammation occurred. However, no tachytherapies and <0.1% right ventricular pacing were needed after 2 years of follow-up. DISCUSSION: Differential diagnoses were either an infiltrative disease, a tumour, or an infectious disease. Due to the different treatment options, we had to establish definite diagnosis by myocardial biopsy. Retrospectively, the implantation of the ICD can be discussed. However, cardiac magnetic resonance imaging showed fibrosis which is usually irreversible and substrate for potentially lethal ventricular arrhythmia. Confirming the diagnosis of isolated CS is challenging. Long-term management should be guided individually based on clinical and imaging findings.
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INTRODUCTION: Prolonged strenuous exercise training may result in structural, functional and electrical cardiac remodelling, as well as vascular and myocardial injuries. However, the extent to which high-volume, intense exercise is associated with arrhythmias, myocardial fibrosis, coronary heart disease and pathological alterations of the vasculature remains unknown. In addition, there is no clear consensus on the clinical significance of these exercise-induced changes. Previous studies typically used cross-sectional designs and examined exercise-induced cardiovascular changes in small cohorts of athletes for up to 3-7 days of recovery. Long-term longitudinal studies investigating cardiovascular changes induced by prolonged strenuous exercise in large cohorts of athletes are needed to improve scientific understanding in this area. METHODS AND ANALYSIS: In this prospective observational monocenter study, 277 participants of the Beer, Marathon, Genetics, Inflammation and the Cardiovascular System (Be-MaGIC) study (ClinicalTrials.gov: NCT00933218) will be invited to participate in this 10-year follow-up study. A minimum target sample size of 130 participants will be included in the study. Participating athletes will be examined via the following: anthropometry, resting electrocardiography and echocardiography, blood sampling, retinal vessel diameters, carotid sonography and cardiopulmonary exercise testing, including exercise electrocardiography. DISCUSSION: This longitudinal study will provide comprehensive data on physiological changes in the cardiovascular system and the development of pathologies after a 10-year period of prolonged and strenuous endurance exercise. Since the participants will have engaged in a wide range of training loads and competitive race events, this study will provide useful risk factor determinants and training load cut-off values. The primary endpoint is the association between the exercise-induced increase in cardiac troponin during the Munich marathon 2009 and the decline in right ventricular ejection fraction over the next 10 years. TRIAL REGISTRATION NUMBER: NCT04166903.
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PURPOSE OF REVIEW: In this review, our aim is to summarize the evidence of exercise interventions in heart failure. Addressing pathophysiology, we discuss training modalities and optimal dose finding in exercising patients with reduced (HFrEF) and preserved ejection fraction (HFpEF). RECENT FINDINGS: While smaller studies showed a trend towards improved exercise capacity by high-intensity interval training in comparison with moderate continuous training in HFrEF, recent multicenter randomized trials were unable to confirm these findings. Considering the lack of effective drug therapies in HFpEF, exercise training plays an even more important role in this particular population. Exercise training in heart failure is beneficial in addition to medical and device therapy. Data are still mostly limited to HFrEF. Intensity should primarily be moderate at a daily base. The concept of "the higher the better" could not be confirmed for HFrEF. The overall concept of training is to maximally strain the periphery without straining the myocardium.
