We read the report published by Rowin et al in the American Journal of Cardiology. The authors demonstrated that screening of athletes based solely on 12-lead electrocardiography (interpreted using the European Society of Cardiology 2010 guidelines ) would fail to detect 10% of all asymptomatic persons with hypertrophic cardiomyopathy (HC). Although conceding that their data were not intended to assess the overall screening process, the authors nevertheless use their findings to promote a position against the inclusion of electrocardiography in screening protocols for athletes. We believe this argument is fundamentally flawed.
All preparticipation screening protocols are first and foremost based on a full history and physical examination, with electrocardiography adding complementary information thereafter. Thus, taking the authors’ cohort as an example, all 11 patients with HC and normal electrocardiographic findings would have been considered for additional imaging investigations because of the positive family history and/or physical examination findings; indeed, it is precisely these findings that led to their initial evaluation.
Importantly, the authors demonstrate that an electrocardiogram alone would positively identify 90% of the patients with HC. A prospective cardiac screening study among young competitive athletes in Italy showed that >80% of all those with HC required an electrocardiogram to raise suspicion of the diagnosis in the absence of history or physical examination abnormalities. Although a small minority of patients would be missed by electrocardiography, it has been demonstrated that those patients with HC phenotypes with a normal electrocardiographic appearance usually exhibit a mild phenotype and have a good prognosis. Although unproved, one could hypothesize that the risk from participation in athletic activity might be lower in this group than in the cohorts with abnormal electrocardiographic findings, considering the more severe phenotype in the latter.
Finally, the World Health Organization has clearly stated that screening should be a continuous process, rather than an isolated event. It is therefore probable that those patients with HC and initially normal electrocardiographic findings will develop electrocardiographic changes and/or symptoms over time as a part of the natural history of the condition, thus triggering additional investigations, either independently or as a part of an ongoing screening program.
Given these points, we conclude that preparticipation screening using 12-lead electrocardiography is likely to have a low false-negative rate when combined with the history, physical examination, and periodic repetition. Therefore, although an understanding of the false-negative rate of electrocardiography is important, this must be taken in the context of “real-world” screening protocols. It seems absurd that the ability to identify 90% of those with a potentially lethal cardiovascular disorder using electrocardiography, particularly in adolescents and young adults, should be used as an argument against its use.