Abstract

As discussed in Chapter 7 of this book, the right ventricle (RV) undergoes a disproportionate increase in load during exercise. This leads to acute changes like dilatation and temporary dysfunction, and may be associated with minor cell damage as evidenced by cardiac enzyme elevations that are very commonly observed after endurance competition. In general, these changes seem to recover within a few days. This chapter reflects on the thesis that the RV can develop chronic sports injury, based on our hypothesis that was originally put forward in 2003. We speculate that repetitive acute injury may culminate in a chronic overload syndrome of the RV, which is very reminiscent of what is observed in patients with familial arrhythmogenic RV cardiomyopathy (ARVC), despite the absence of underlying demonstrable genetic abnormalities. The syndrome of ‘exercise-induced ARVC’ may easily be overlooked. It may even become more prevalent now that modern sports tries to push the limits of human performance in a much more ‘professionalised’ way and on a much larger scale. The aim of this chapter is to describe the pathophysiological findings of ‘exercise-induced ARVC’ and its relation with desmosomal ARVC.

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