Sudden cardiac arrest of an apparently healthy athlete is an uncommon but feared event with an unclear incidence that has been reported to range from 0.4 to 6.8 per 100,000 athlete years depending on population and study methodology. Undiagnosed arrhythmogenic cardiomyopathy (AC) (previously known as arrhythmogenic right ventricular cardiomyopathy), is among the most common causes of sudden cardiac death in young athletes.
The physiological benefits of exercise are undisputed, and improved physical capacity reduces incident heart disease and mortality. Competitive athletes exercise in vast excess to the recommended health-promoting 150 mins per week. The “athlete’s heart” is widely recognized as a benign and reversible constellation of symmetrical heart chamber enlargement and relative bradycardia in the context of athletic activity. The athlete’s heart can fulfill structural and functional diagnostic criteria for AC. Genetic mutations causing AC have been reported to be surprisingly uncommon in athletes with ventricular arrhythmias. It has been suggested that the physiological adaptation to exercise can convert to irreversible cardiac changes and even induce an arrhythmogenic phenotype overlapping with AC even without a clear genetic vulnerability. However, little is known about this entity and the associated exercise doses, individual susceptibility and risk markers of arrhythmic remodeling in athletes.
Competitive athletes with ventricular arrhythmias had smaller LV volumes and worse systolic and diastolic function in both LV and RV by echocardiography compared to healthy athletes, but still within normal range (Table 2
). Regional contraction abnormalities were seen in none of the healthy athletes and in 4 athletes with ventricular arrhythmias. Of these, 3 fulfilled major criteria for AC by dilated RVOT and 1 fulfilled minor criteria by mildly reduced RV FAC.
Athletes with ventricular arrhythmias had impaired RV function and more myocardial fibrosis compared to healthy athletes. Athletes with life-threatening arrhythmic events had additional LV contraction abnormalities. These phenotypes mimic arrhythmogenic cardiomyopathy and may potentially be induced by high doses of exercise in susceptible individuals.
Cardiac Phenotypes and Markers of Adverse Outcome in Elite Athletes With Ventricular Arrhythmias - ScienceDirect
JACC Cardiovasc Imaging. 2021 Jan;14(1):148-158.
Øyvind H Lie, Lars Gunnar Klaboe, Lars A Dejgaard, Eystein T Skjølsvik, Jostein Grimsmo, Gerhard Bosse, Einar Hopp, Thor Edvardsen, Kristina H Haugaa
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