Abstract

Cardiac magnetic resonance (CMR) is a second-line imaging test in cardiology. Balanced enlargement of heart chambers called athlete’s heart (AH) is a part of physiological adaptation to regular physical activity. The aim of this study was to evaluate the diagnostic utility of CMR in athletes with suspected structural heart disease (SHD) and to analyse the relation between the coexistence of AH and SHD. We wanted to assess whether the presence of AH phenotype could be considered as a sign of a healthy heart less prone to development of SHD. This retrospective, single centre study included 154 consecutive athletes (57 non-amateur, all sports categories, 87% male, mean age 34 ± 12 years) referred for CMR because of suspected SHD. The suspicion was based on existing guidelines including electrocardiographic and/or echocardiographic changes suggestive of abnormality but without a formal diagnosis. CMR permitted establishment of a new diagnosis in 66 patients (42%). The main diagnoses included myocardial fibrosis typical for prior myocarditis (n = 21), hypertrophic cardiomyopathy (n = 17, including 6 apical forms), other cardiomyopathies (n = 10) and prior myocardial infarction (n = 6). Athlete’s heart was diagnosed in 59 athletes (38%). The presence of pathologic late gadolinium enhancement (LGE) was found in 41 patients (27%) and was not higher in athletes without AH (32% vs. 19%, p = 0.08). Junction-point LGE was more prevalent in patients with AH phenotype (22% vs. 9%, p = 0.02). Patients without AH were not more likely to be diagnosed with SHD than those with AH (49% vs. 32%, p = 0.05). Based on the results of CMR and other tests, three patients (2%) were referred for ICD implantation for the primary prevention of sudden cardiac death with one patient experiencing adequate intervention during follow-up. The inclusion of CMR into the diagnostic process leads to a new diagnosis in many athletes with suspicion of SHD and equivocal routine tests. Athletes with AH pattern are equally likely to be diagnosed with SHD in comparison to those without AH phenotype. This shows that the development of AH and SHD can occur in parallel, which makes differential diagnosis in this group of patients more challenging.

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