Key result
Detraining reverses ECG abnormalities and apical LVH after 18 months of complete rest.
Why the study?
Differentiating athlete's heart from hypertrophic cardiomyopathy is challenging, and few data exist on the influence of aerobic training and detraining on morphological changes in athletes with apical hypertrophic cardiomyopathy.
Does detraining reverse electrocardiographic and morphological left ventricular hypertrophy in young athletes with familial hypertrophic cardiomyopathy?
Case Report (n=1)
No
Does detraining reverse electrocardiographic and morphological left ventricular hypertrophy in young athletes with familial hypertrophic cardiomyopathy?
Intensive aerobic training can trigger the phenotypic expression of apical hypertrophic cardiomyopathy in genetically predisposed young athletes, which may be fully reversible with complete detraining.
Answers are grounded in this paper and cite their sources.
Supports reversible training effects on apical hypertrophy in athletes; leaves open confirmation in prospective cohorts.
BACKGROUND Differential diagnosis between athlete's heart and hypertrophic cardiomyopathy is sometimes challenging in sport cardiology since endurance training can cause a distinct pattern of functional and structural changes of the cardiovascular system. It is of crucial importance to accurately diagnose it and stratify the arrhythmic risk since hypertrophic cardiomyopathy is one of the leading causes of sudden cardiac death in young athletes. Apical hypertrophic cardiomyopathy is a relatively rare form of hypertrophic cardiomyopathy that predominantly affects the apex of the left ventricle and usually has a nonobstructive physiology. Few data and studies are available on influence of aerobic training (and detraining) on morphological changes in athletes with apical hypertrophic cardiomyopathy. CASE REPORT We present the case of a 19-year-old male soccer athlete with family history for obstructive hypertrophic cardiomyopathy, with electrocardiographic and morphological left ventricular remodeling in association with sports activity. Intensive aerobic training led to marked T-wave inversion on 12-lead ECG and left ventricular hypertrophy compatible with apical hypertrophic cardiomyopathy. Genetic testing confirmed the presence of familial variant c853C>T, p.(Arg 285Cys) on TNNT2 gene. After 18 months detraining, we observed a complete regression of ECG abnormalities and a reverse remodeling of the left ventricular hypertrophy. No pharmacological therapy was indicated; periodic cardiological evaluations were advised. Monitoring devices or implantable cardioverter defibrillator were not recommended. CONCLUSIONS This case suggests that intensive aerobic training can affect the pathological hypertrophic cardiomyopathy substrate, facilitating the development of left ventricular hypertrophy and, more interesting, regression of structural changes after detraining.
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Gioia et al. (2023) conducted a case report in Apical hypertrophic cardiomyopathy (n=1). Intensive aerobic training and subsequent detraining was evaluated on Regression of electrocardiographic abnormalities and structural changes. Complete regression of electrocardiographic abnormalities and reverse remodeling of apical left ventricular hypertrophy was observed after 18 months of complete detraining.
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