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Exercise Training and Cardiac Remodeling in Hypertrophic Cardiomyopathy: A Systematic Review and Meta-Analysis
Maddison Weber1, Mohammed Azouz1, Ella Young2
1From the Creighton University Medical Center, Omaha, NE.
Insights
Structured exercise is safe for individuals with hypertrophic cardiomyopathy (HCM), showing no adverse cardiac remodeling or increased arrhythmia risk. Personalized exercise plans may offer functional benefits for HCM patients.
Area of Science:
- Cardiology
- Genetics
- Sports Medicine
Background:
- Hypertrophic cardiomyopathy (HCM) is a common inherited heart condition and a leading cause of sudden cardiac death in young people.
- Historically, exercise was restricted in HCM patients due to concerns about arrhythmias and obstruction, but recent evidence suggests otherwise.
Conclusions:
- Structured and habitual exercise are safe for HCM patients, without increased risk of adverse remodeling or arrhythmias.
- Individualized, supervised exercise prescriptions and patient-centered counseling are recommended for potential functional benefits.
Abstract:
Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiomyopathy and a leading cause of sudden cardiac death in young individuals and athletes. Historically, exercise restrictions were advised because of concerns about arrhythmias, left ventricular outflow tract (LVOT) obstruction, and adverse remodeling; however, emerging evidence challenges these recommendations. To systematically evaluate the effects of structured and habitual exercise on cardiac structure, function, biomarkers, functional capacity, and safety in individuals with HCM. We performed a systematic review and meta-analysis in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 guidelines. Randomized and observational studies including patients ≥12 years with confirmed HCM participating in structured exercise or habitual physical activity were eligible. Comparators included usual care, lower-intensity exercise, or sedentary controls. Outcomes included cardiac remodeling parameters (wall thickness, chamber volumes, LVOT gradient, and diastolic function), left ventricular ejection fraction, B-type natriuretic peptide, peak oxygen consumption (VO 2 peak), body mass index, and major adverse clinical events. Random-effects models were used for pooled analyses. Eleven studies (1457 participants) were included. Exercise was not associated with adverse changes in wall thickness, chamber volumes, left ventricular ejection fraction, LVOT gradient, diastolic indices, B-type natriuretic peptide, or body mass index. VO 2 peak changes were heterogeneous, with some trials demonstrating individualized functional improvement. No study reported excess adverse events, including sudden cardiac death, ventricular arrhythmias, syncope, or appropriate implantable cardioverter-defibrillator therapy. Structured and habitual exercise appear safe in HCM, without evidence of adverse remodeling or increased arrhythmic risk. Functional benefits vary, supporting individualized, supervised exercise prescriptions and more patient-centered counseling.
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