Inherited cardiomyopathies and sports participation

Figures

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  Fig. a. Trends of sudden death for cardiomyopathies among athletes in the Veneto region of Italy after implementation of a national preparticipation screening programme. Adapted with permission from Corrado et al. [1]

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  Fig. 1. Trends of sudden death for cardiomyopathies among athletes in the Veneto region of Italy after implementation of a national preparticipation screening programme. Adapted with permission from Corrado et al. [1]

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  Fig. 2. Anterior T‑wave inversion in healthy athletes and patients with hypertrophic cardiomyopathy. Electrocardiographic (ECG) tracing (a) and close-up of lead V3 (b) of a 21-year-old healthy athlete with anterior T‑wave inversion confined to V1–V4. Note that negative T waves in V3–V4 are preceded by J‑point elevation and ST-segment elevation (suggesting early repolarisation variant) and there are no associated ECG abnormalities. ECG tracing (c) and close-up of lead V2 (d) of a 32-year-old patient with hypertrophic cardiomyopathy showing anterior T‑wave inversion. Negative T waves in V2–V4 are not preceded by J‑point elevation. Moreover, T‑wave inversions extend also to lateral leads and left axis deviation is also present. Modified with permission from Calore et al. [16]

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  Fig. 3. Differential diagnosis between athlete’s heart and hypertrophic cardiomyopathy. A subset of athletes exhibits an increase in left ventricular wall thickness that falls in the ‘grey zone’ of overlap between physiologic adaptation to exercise and pathologic hypertrophy. In these cases, the presence of positive family history of sudden cardiac death, cardiac arrest or inherited cardiac disease, electrocardiographic changes, echocardiographic abnormalities or late enhancement at cardiac magnetic resonance imaging suggests an underlying hypertrophic cardiomyopathy. On the other hand, symmetrical left ventricular hypertrophy with concomitant left ventricular dilatation compatible with gender (male > female), ethnicity (African/Afro-Caribbean > Caucasian) and intensity of training with no other abnormal features is suggestive of athlete’s heart

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  Fig. 4. Electrocardiographic and echocardiographic findings in a 15-year-old male soccer player with hypertrophic cardiomyopathy. The electrocardiogram shows T‑wave inversion in lateral leads (I and aVL) and pathological Q‑wave (duration >25% of the height of the ensuing R‑wave) in inferior leads (III and aVF) (a). The echocardiogram shows an asymmetric left ventricular hypertrophy with maximal septal thickness of 31 mm (b). (VS ventricular septal, LV left ventricle, LA left atrium, AO aorta). Reproduced with permission from Migliore et al. [28]

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  Fig. 5. Electrocardiographic and echocardiographic findings in a 14-year-old male soccer player with right ventricular dominant (classic phenotype) arrhythmogenic cardiomyopathy. The electrocardiogram shows T‑wave inversion in right precordial leads (V1–V2) (a). The echocardiogram reveals right ventricular dilatation (right ventricular outflow tract diameter of 39 mm on end-diastolic parasternal short-axis view) (b) and right ventricular dysfunction (akinesia of right ventricular outflow tract and posterobasal, subtricuspidal regions) (not shown). Reproduced with permission from Migliore et al. [28]

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  Fig. 6. Representative example of a left dominant arrhythmogenic cardiomyopathy. Post-contrast cardiac magnetic resonance findings of an asymptomatic 23-year-old female carrying a desmoplakin gene mutation. Four-chamber (a) and short-axis (b) views showing late gadolinium enhancement mostly involving the subepicardial layer of the posterolateral left ventricular wall at mid-basal level (white arrows), in the absence of other morpho-functional ventricular abnormalities. The electrocardiogram and echocardiogram of this patient were normal. Reproduced with permission from Zorzi et al. [40]

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  Fig. 7. Schematic representation of ARVC course from desmosomal gene mutation to phenotypic expression and cardiac arrest due to ventricular fibrillation. Sports activity may promote development of phenotypic expression, accelerate disease progression and trigger life-threatening ventricular arrhythmias. Reproduced with permission from Corrado et al. [47]. (ARVC arrhythmogenic right ventricular cardiomyopathy)