Sports-related sudden cardiac death is reduced by pre-participation cardiovascular screening

August 31, 2008

Young competitive athletes are perceived by the general population to be the healthiest members of society. The possibility that highly trained athletes may have a potentially serious cardiac condition that can predispose to life-threatening tachyarrhythmias or sudden cardiac death seems paradoxical. However, high-risk ventricular tachyarrhythmias and sudden cardiac death in the athlete although uncommon, are extremely visible events due to the high profile of elite and professional athletes. In athletes under the age of 35 years, the incidence of sudden death is low and in most cases occurs in individuals with inherited heart disease, such as hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasia and congenital anomalies of coronary arteries. In older athletes, sudden death is more common and is generally due to arrhythmias in the context of coronary artery disease.

A crucial point is the role played by physical exercise and training in the genesis of ventricular arrhythmias and, therefore, whether exercise can enhance the risk of arrhythmic cardiac arrest in athletes. Indeed, regular exercise training is associated with morphologic and functional cardiac changes that may create ambiguity with cardiac pathologic conditions and differentiating the benign, exercise-induced physiologic changes from true pathological conditions with risk of sudden death is critical to developing appropriate screening strategies to reduce such adverse events.

Recent studies showed that the risk for sudden death in young competitive athletes with cardiovascular disease was 2.5-fold greater than in non-athletes. These data suggest that sports activity itself may act as a trigger for life-threatening ventricular tachyarrhythmias in susceptible individuals with underlying, even silent cardiovascular disease, thereby predisposing to cardiac arrest. Therefore, polymorphic and malignant ventricular tachycardia triggered by intensive athletic conditioning should raise suspicion and greater scrutiny for an underlying inherited electrophysiological disorder (such as channelopathies), or an underlying structural disease (like arrhythmogenic right ventricular dysplasia or hypertrophic cardiomyopathy). These findings are in agreement with results of our previous study on physical de conditioning, in which we observed that none of the athletes with frequent and complex ventricular arrhythmias (with or without cardiovascular abnormalities) disqualified from training and competition, experienced clinical events or cardiac arrest in the follow-up and all showed a marked reduction, or even disappearance of the premature ventricular depolarizations.

Therefore, the reduction/disappearance of ventricular arrhythmias is a potential mechanism by which disqualification from competitive sports may reduce the risk for sudden cardiac death. These data support the restriction from competitive sport and intense exercise training in athletes with frequent and complex ventricular arrhythmias and structural heart disease and explains the 89% decline in the incidence rate of sudden cardiovascular death among young competitive athletes aged 12 to 35 years in the Veneto region of Italy over a 26-year period.

These data support the conclusion that the reduction in the incidence of sudden cardiovascular death is the result of the introduction in 1982 of a nationwide pre participation screening program. There was coincident timing between decline of sudden cardiovascular death in young competitive athletes and implementation of pre participation cardiovascular screening in Italy. Athletes with cardiovascular abnormalities need a thorough clinical assessment and therapeutic options for sudden cardiac death prevention, such as ICD. However, in athletes with documented malignant ventricular tachyarrhythmias, competitive sports are contraindicated. A possible exception is represented by ventricular arrhythmias occurring in the context of acute and transient myocardial lesion, such as myocarditis, commotio cordis, acute electrolytic depletion, when the cause has proven to be completely resolved.
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European Society of Cardiology

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