Athletes with mild hypertrophic cardiomyopathy (HCM) at low risk of sudden cardiac death (SCD) can safely continue to exercise at competitive levels, a retrospective study suggests.
During a mean follow-up of 4.5 years, athletes who continued to engage in high-intensity competitive sports after a mild HCM diagnosis were free of cardiac symptoms, and there were no deaths, incidents of sustained ventricular tachycardia or syncope, or changes in cardiac electrical, structural, or functional phenotypes.
“This study supports emerging evidence that HCM individuals with a low-risk profile and mild hypertrophy may engage in vigorous exercise and competitive sport,” Sanjay Sharma, MD, of St. George’s University of London, UK, told theheart.org | Medscape Cardiology. Current guidelines from the European Society of Cardiology and the American College of Cardiology support a more liberal approach to exercise for these individuals, he noted.
That said, he added, “It is important to emphasize that our cohort consisted of a group of adult competitive athletes who had probably been competing for several years before the diagnosis was made and therefore represented a self-selected, low-risk cohort. It is difficult to extrapolate this data to adolescent athletes, who appear to be more vulnerable to exercise-related SCD from HCM.”
The study was published online today in the Journal of the American College of Cardiology.
Vigorous Exercise OK for Some
Sharma and colleagues analyzed data from 53 athletes with HCM who continued to participate in competitive sports. The mean age was 39 years, 98% were men, and 72% were White. About half (53%) competed as professionals, and were most commonly engaged in cycling, football, running, and rugby.
Participants underwent 6 to 12 monthly assessments that included electrocardiograms (ECGs), echocardiograms, cardiopulmonary exercise testing, Holter monitoring (≥ 24 hours), and cardiac magnetic resonance (CMR) imaging. A majority (64.2%) were evaluated because of an abnormal ECG, and one presented with an incidental abnormal echocardiogram.
About a quarter (24.5%) were symptomatic and 5 (9.4%) were identified on family screening. Eight (15%) had a family history of HCM, and six (11.3%) of SCD.
At the baseline evaluation, all athletes had a “low” European Society of Cardiology 5-year SCD risk score for HCM (1.9% ± 0.9%). None had syncope. Mean peak VO2 was 40.7 ± 6.8 mL/kg/min.
The mean left ventricular (LV) wall thickness was 14.6 ± 2.3 mm. All had normal LV systolic and diastolic function and no LV outflow tract obstruction at rest or on provocation testing. In addition, none had an LV apical aneurysm.
Twenty-two (41%) showed late gadolinium enhancement on baseline CMR.
A total of 19 participants underwent genotyping; 4 (21.1%) had a pathogenic/likely pathogenic sarcomeric variant. None took cardiovascular medication or had an implantable cardioverter defibrillator (ICD).
During a mean follow-up of 4.5 years, all participants continued to exercise at the same level as before their diagnosis; none underwent detraining. All stayed free of cardiac symptoms, and there were no deaths, sustained ventricular tachycardia episodes, or syncope.
Four demonstrated new, nonsustained ventricular tachycardia (NSVT) during follow-up, one of whom underwent ICD implantation because of an increased risk score and subsequently moderated exercise levels.
One participant had a >30-second atrial fibrillation (AF) episode, started on a beta-blocker and oral anticoagulation, and also moderated exercise levels.
The event rate was 2.1% per year for asymptomatic arrhythmias (NSVT and AF). No changes were observed in the cardiac electrical, structural, or functional phenotype during follow-up.
Sharma and colleagues state, “Our sample size is small; however, it is nearly double the size of a previously studied Italian athletic cohort, and one half were professional athletes. Furthermore, 17% of our cohort comprised Black athletes who are perceived to be at higher risk of SCD than White athletes.”
Daniele Massera, MD, assistant professor in the HCM Program, Department of Medicine, Charney Division of Cardiology, NYU Langone Health, New York City, commented on the study for theheart.org | Medscape Cardiology. “Of note, these were athletes/patients at the very low end of phenotypic severity of HCM…It is also notable that diastolic function was normal in all of them, an uncommon finding in patients with HCM.”
Like Sharma, he said the findings are in line with recent guidelines, and cautioned, “This small study applies only to a very small subset of patients who are being evaluated at specialized HCM programs: asymptomatic male individuals who have mild, low-risk HCM and are on no medicines.
“The findings cannot be generalized to the population of symptomatic individuals with (or without) outflow obstruction, more severe hypertrophy, and who have ICDs and/or take medication for symptoms, nor to younger patients or adolescents, who may be at higher risk for adverse outcomes,” he concluded.
Individualized Approach Urged
Sharma was a coauthor of the recent JACC article challenging the traditional restrictive approach to exercise for athletes diagnosed with HCM and other inherited cardiovascular diseases. The article suggested that individualized recommendations, taking risks into consideration, can help guide those who want to exercise or participate in competitive sports.
Sharma also is a coauthor of a 6-month follow-up to the SAFE-HCM study, which compared the effects of a supervised 12-week high-intensity exercise program to usual care in low-risk individuals with HCM (mean age, 45.7).
In the 6-month follow-up study, published as an abstract in the European Journal of Preventive Cardiology 2021 supplement, “exercising individuals had improved functional capacity and atherosclerotic risk profile and there were no differences in the composite safety outcomes (CV death; cardiac arrest; device therapy; exercise-induced syncope; sustained VT; NSVT or sustained atrial arrhythmias) between exercising individuals and usual care individuals,” Sharma said.
The full study will soon be ready to submit for publication, he added.
No commercial funding or relevant conflicts of interest were disclosed.
J Am Coll Cardiol. Published online October 3, 2022. Letter
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