The pathophysiological role of exercise and nonsteroidal anti-inflammatory drugs (NSAIDs) in the development of (left ventricular) myocardial fibrosis during viral myocarditis.

Despite exercise being our oldest and most efficacious medicine, animal and human data suggest that excessive exercise may contribute to pathological cardiac remodelling in some, resulting in increased susceptibility for atrial and ventricular arrhythmias and sudden cardiac death. One hallmark of this pathological remodelling is the development of myocardial fibrosis (MF). In two specific types of MF in athletes (i.e. insertion point MF and right ventricular fibrosis in the context of arrhythmogenic cardiomyopathy), exercise contributes as a causal factor. We hypothesise that exercise also contributes to the development of MF in the left ventricle after (silent) myocarditis, which could explain its higher incidence in athletes. We will verify this hypothesis in a murine coxsackie B virus-induced myocarditis and exercise model. MF will be evaluated by standard histology, as well as by whole mount 3D microscopic imaging. Further, innovative serial multiplex immunohistochemistry (IHC) will be used for detailed cellular and molecular phenotyping, providing unrivalled insights into (patho)physiological remodelling during myocaditis. In addition, the modulating effect of NSAIDs will be evaluated. In parallel, clinical studies are conducted to gain insight into the aetiology and evolution of MF in athletes. Ultimately, our results will contribute to the development of guidelines on safe sport participation and NSAIDs use in the setting of viral syndromes.

Keywords:ARRYTHMIAS, CARDIOLOGY, EXERCISE PHYSIOLOGY, FIBROSIS

Disciplines:Cardiology, Exercise physiology, Sports sciences, Pharmacotherapy, Pathophysiology

Project type:Collaboration project