06 March 2023
: Case report
[In Press] Reversible Apical Hypertrophy in a Young Competitive Athlete with Familiar Hypertrophic Cardiomyopathy
Unusual clinical course, Challenging differential diagnosis, Unusual setting of medical care
Giuseppe Di Gioia123ABE, Viviana Maestrini14CDF, Alessandra Colella1BEF, Ruggiero Mango1CDF, Andrea Segreti23DEF, Maria Rosaria Squeo1ADF, Erika Lemme
DOI: 10.12659/AJCR.939058
Am J Case Rep In Press; DOI: 10.12659/AJCR.939058
Available online: 2023-03-06, In Press, Corrected Proof
Publication in the "In-Press" formula aims at speeding up the public availability of the pending manuscript while waiting for the final publication. The assigned DOI number is active and citable. The availability of the article in the Medline, PubMed and PMC databases as well as Web of Science will be obtained after the final publication according to the journal schedule
Abstract
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.
Keywords: Cardiomyopathy; Sport Cardiology; Athlete
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