Athletes with scar and arrhythmia: better double-check?

Previous data have documented an increased prevalence of ventricular ectopy and complex ventricular tachyarrhythmias in endurance-trained veteran athletes. It has also been previously suggested that the increased ventricular irritability may be caused, at least partially, by the predominance of sympathetic modulation. Frequent and complex ventricular tachyarrhythmias might not be ominous in well-trained athletes without overt cardiovascular abnormalities however, thorough assessment is necessary to clarify potential underlying cardiomyopathic background, but also any evidence of myocardial fibrosis [1]. An important question is, how much evidence is there currently, and how should we go about this in our current clinical practice?

The Italian group led by Domenico Corrado [2] tested non-ischaemic left ventricular fibrosis as a substrate for ventricular arrhythmia (VA) but also its reproducibility at repeated exercise testing (ET). They included consecutive athletes who underwent CMR for evaluation of ventricular arrhythmias (VA) and two consecutive ETs off-therapy within 12 months. Those with positive family history for premature sudden death, cardiomyopathy, significant symptoms, ECG or abnormalities in echocardiography as well as low-risk VA were excluded. CMR fibrosis was defined as subepicardial or mid-myocardial stria of late gadolinium enhancement involving >5% of the LV mass. Reproducibility was defined as the occurrence of VA with the same pattern and behaviour during repeated ET.

Of 325 athletes who underwent CMR for evaluation of VA, 75 were included, and 30 showed fibrosis involving 2-4 LV segments. On the first ET, athletes with fibrosis showed a higher prevalence of exercise-induced VA (93% versus 53%, p<0.001). On the second, reproducibility was observed in 97% of athletes versus 13% without fibrosis (p<0.001). Of note, reproducibility yielded a positive predictive value of 83% and negative predictive value of 98%. The remaining 87% of athletes with normal CMR either did not show any VA at repeated ET (59%) or showed arrhythmias with different patterns, mostly benign ones.

In light of this study and despite its limitations, it seems reasonable to consider a repeat evaluation of VA by means of ET checking for reproducibility, particular in athletes with non-typical for athletic adaptation scars, but otherwise normal clinical work-up. It may improve risk stratification with apparently idiopathic VA and guide these patients’ challenging management.