Electrocardiographic changes in athletes are common and usually reflect benign, structural, and electrical remodeling of the heart as a consequence of regular and intensive physical activity, so called athlete's heart.1-3 However, differentiation between a physiological and a pathological process is important because abnormalities of an athlete's (electrocardiogram) ECG may be an expression of underlying cardiac disease, placing the athlete at risk of sudden cardiac death.4,5
A 33-year-old male international football player of South American origin presented for pre-participation cardiovascular screening. For the past 15 years, he has trained 5 days per week, with 2 hours per day, playing in ≥400 matches. He did not report any cardiac symptoms, denying any chest pain, palpitations, or syncope either at rest or during exercise. There was no family history (FH) of acquired cardiovascular disease, diabetes, or hypertension. However, he did report a FH of sudden death of a brother at 25 years of age, 14 years ago, with the ultimate cause of death unknown.
Physical examination was unremarkable (weight, 86 kg; height, 189 cm; and blood pressure, 126/69 mm Hg). A resting 12-lead ECG demonstrated deep T-wave inversions in leads I, II, III, aVF, and V4 to V6 (Figure 1). It should be noted that regardless of the inclusion or exclusion of electrocardiography in any pre-participation screening program, this player must receive a standard 12-lead ECG because of the FH of early sudden death. Due to his abnormal ECG and FH, an echocardiogram was performed revealing normal left ventricular (LV) dimensions and function (interventricular septum, 12 mm and LV posterior wall, 12 mm). The right ventricle (RV) and all valves were morphologically normal. The origins of coronary arteries were anatomically correct. An exercise stress test was negative for exercise-inducible arrhythmias. He completed 11 minutes 02 seconds of a ramped cycling protocol with a maximal heart rate of 181 beats per minute and a maximum minute power of 340 W. Blood pressure response was normal during and after exercise. Of note, baseline T-wave inversions normalized immediately at the onset of exercise but returned to negativity 3 minutes into recovery. Although the normalization of repolarization abnormalities is of better prognostic value than a lack of modification or a worsening of abnormalities, this isolated observation cannot exclude a pathologic cause and thus other investigations are warranted.
Due to the normal echocardiogram and exercise stress test, the player was referred for a cardiac magnetic resonance (CMR) scan. The CMR imaging revealed normal indexed LV volumes and ejection fraction. There were normal LV and RV wall thickness (maximum LV wall thickness, 11 mm at the basal anterior septum) and normal mass index. No regional LV or RV wall motion abnormalities existed at rest. The RV free wall and outflow tract appeared normal, and all valves appeared normal. In the late phase of gadolinium injection, there was a small area of subepicardial enhancement in the lateral wall at the mid-cavity level (Figure 2). Furthermore, the left upper pulmonary vein drained anomalously via a vertical vein into the innominate vein on the left side. The innominate and superior vena cava were mildly dilated, with a small left to right shunt. However, there was normal left lower and right-sided pulmonary venous drainage. Overall, there was no evidence of cardiomyopathy per se and no “classic” features of dilated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, or hypertrophic cardiomyopathy (HCM). Furthermore, the limited amount of subepicardial fibrosis was consistent with a previous episode of myocarditis rather than HCM.
In summary, this case report presents an asymptomatic male professional football player with a distinctly abnormal ECG and a FH of sudden death. This player presented a screening conundrum because the true cause of death of his brother was unknown, and despite an abnormal ECG, the player exhibited “nonattributable” secondary investigations. Although reflecting previous myocarditis, the finding of lateral wall fibrosis would not account for the pattern of ECG changes. Similarly, the anomalous pulmonary venous drainage represented a nonspecific incidental finding. Thus, he was provided medical clearance but was required to obtain yearly full clinical evaluation, including CMR, and given appropriate education to seek immediate medical attention if he became symptomatic.
Deep T-wave inversions in the lateral leads are of major concern because these ECG alterations are a recognized manifestation of HCM and arrhythmogenic right ventricular cardiomyopathy.6 Inverted T waves may represent the only sign of an inherited heart muscle disease even in the absence of any other features and before structural changes in the heart can be detected.6 However, recent studies examining cardiac adaptation in African/African-Caribbean male athletes have demonstrated that black athletes present with more striking repolarization changes than white athletes of similar age and size participating in identical sports.7,8 Indeed, up to 25% of black athletes exhibit repolarization changes that overlap with morphologically mild HCM.8 However, whether the repolarization abnormalities observed in this black South American football player reflect an adaptation due to regular and intensive exercise or are constant with his ethic origin remains unknown.
The football player identified in this case study presented physicians with a difficult scenario. Even after a comprehensive clinical work-up, the authors were unable to explain the clinical significance of his deep T-wave inversions. Recently, Pelliccia et al9 reported on 81 athletes (from a database of 12 550) with diffusely distributed and deeply inverted T waves, with no apparent cardiac disease, who had undergone serial ECG and echocardiographic studies for 9 ± 7 years (range, 1-27 years). From the 81 athletes identified, 5 (6%) ultimately proved to have cardiomyopathies. The authors suggest that these abnormal ECGs may represent the initial expression of genetic cardiac disease that may not be evident for many years. In line with these findings, it has been recommended that this player undergo an annual review, with genetic counseling for future mutation analysis. Furthermore, confirmed genotype positivity for a cardiomyopathy may change the medical clearance recommendations for physical activity.
Notwithstanding these observations, the uncertainty surrounding the cause of this player's repolarization abnormalities did not warrant disqualification from competitive sport, despite a FH of sudden death. This decision is based on the lack of any adrenergic arrhythmias or symptoms in more than 400 competitive matches, a normal echocardiogram, no hallmark abnormalities on the CMR, and the normalization of deep T-wave inversions to positivity with the immediate onset of exercise.8 However, the importance of continued clinical surveillance and follow-up for this football player, even in the absence of cardiac symptoms and/or clinically demonstrable heart disease, should be highlighted.9 Unfortunately, the risk of sudden cardiac death for this player cannot be quantified because the precise significance of such repolarization changes remains unresolved.
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