Advancing the field: Sports cardiology, hypertrophic cardiomyopathy highlighted at ACC.23
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The American College of Cardiology Scientific Session featured three late-breaking clinical trials of particular interest to the sports cardiology and hypertrophic cardiomyopathy communities.
In this column, we provide highlights and clinical implications from those trials, plus two additional sports cardiology sessions.
LIVE-HCM
The goal of the LIVE-HCM study, led by Rachel Lampert, MD, FACC, the Robert W. Berliner Professor of Medicine (Cardiology) at Yale School of Medicine, Michael J. Ackerman, MD, PhD, the Windland Smith Rice Cardiovascular Genomics Research Professor and professor of medicine, pediatrics and pharmacology at Mayo Clinic in Rochester, Minnesota, and Sharlene M. Day, MD, director of translational research in the division of cardiovascular medicine and Cardiovascular Institute and Presidential Associate Professor at Penn Medicine, was to assess whether vigorous exercise was associated with an increased risk for life-threatening ventricular arrhythmias and/or death in individuals with hypertrophic cardiomyopathy (HCM).
The study enrolled 1,660 individuals (59% male, approximately 90% white) across five countries. Of those, 1,534 had overt phenotypic HCM and 126 had an associated genetic mutation but no left ventricular hypertrophy. Approximately 77% of the patients were older than 25 years, whereas 9% were younger than 18 years and 14% were aged 18 to 25 years. Exercise was determined via the Minnesota Leisure Time Questionnaire, with vigorous exercise defined as at least one activity with metabolic equivalents of task (METs) of at least 6 for at least 60 hours per year (42% of the cohort). Moderate-intensity exercise was defined as all activities of at least 4 and less than 6 METs for at least 60 hours per year (43% of the cohort), and sedentary activity was defined as not meeting the criteria for moderate or vigorous activity (16% of the cohort). The cohort was followed for 3 years and surveyed every 6 months for outcomes. The endpoints were death, resuscitated cardiac arrest, syncope (definitely or likely arrhythmic or undetermined) and appropriate shock from an implantable cardioverter defibrillator as reviewed by two electrophysiologists.
The results showed that the events per 1,000 person-years were not significantly different between the nonvigorous and vigorous exercisers (15.3 events vs. 15.9 events, respectively). The HR for the composite endpoint was not significantly different between the two groups (HR = 1.01; 90% CI, 0.68-1.48; P = .98), nor was it different in secondary and post hoc analyses. All events occurred in those with overt HCM and none occurred in those with a genetic mutation but no LV hypertrophy.
- Clinical implications: Vigorous exercise in individuals with HCM, including competitive sports, did not result in a heightened risk for death, cardiac arrest, appropriate ICD shocks or arrhythmic syncope compared with those engaging in low-to-moderate-intensity physical activity. This large data set provides further evidence against universal restriction of vigorous exercise in HCM patients.
Return-to-play for elite level athletes at risk for SCD
Katherine A. Martinez, an undergraduate at Loyola University, presented this study in coordination with Ackerman, Aaron Baggish, MD, professor of medicine at the University of Lausanne and former director of Massachusetts General Hospital’s Cardiovascular Performance Program, Dermot Phelan, MD, PhD, medical director of cardiovascular imaging, director of sports cardiology and co-director of the Hypertrophic Cardiomyopathy Center at Sanger Heart & Vascular Institute, Atrium Health, and Matthew W. Martinez, MD, director of Atlantic Health System Sports Cardiology at Morristown Medical Center. The goal of the retrospective study was to describe the experience and outcomes of elite college and professional athletes with genetic heart diseases at risk for sudden cardiac death (SCD) who underwent a return-to-play evaluation at four experienced institutions.
This study included 76 elite athletes (64% Division 1 college and 36% professional; 28% female). The most common conditions were HCM (53%), long QT syndrome (25%) and dilated cardiomyopathy (7%). Fifty-five percent had a positive genotype and 30% of athletes had an ICD. Initially, 72% of athletes were disqualified. Of the 76 athletes, 73 (96%) chose to return to play and three athletes chose not to return to play. Four of the athletes (5%) remained disqualified by their team. There were a total of four nonfatal breakthrough cardiac events among three athletes.
- Clinical implications: This landmark multicenter trial is the first in elite athletes to show a safety signal in those with genetic heart diseases after careful evaluation by an expert, risk stratification and shared decision-making into both Division I and professional athletes for whom return to play should be considered. The next steps will be to follow these individuals longitudinally and add similar patients to the database for future study.
Master@Heart
This clinical trial was led by Ruben De Bosscher, MD, PhD, and Guido Claessen, MD, PhD, both from the University of Leuven, Belgium. Given prior data suggesting that exercise may be associated with an increased burden of coronary plaque, the aim of the Master@Heart study was to evaluate the impact of long-term endurance sport participation, in addition to a healthy lifestyle, on coronary atherosclerosis. This prospective, observational cohort study enrolled 558 participants (median age, 55 years) who were divided into three groups: lifelong masters endurance athletes (34%); late-onset athletes, defined as endurance sports started after age 30 years (34%); and healthy nonathletes (32%). All participants were white men with low CV risk profiles. The investigators used peak VO2 to quantify fitness.
The primary endpoint was the prevalence of coronary plaques (calcified, mixed and noncalcified) on coronary CT. The investigators found that lifelong and late-onset athletes had higher VO2 peaks than nonathletes (lifelong, 159% predicted [95% CI, 143-177]; late-onset, 155% predicted [95% CI, 138-169]; nonathletes, 122% predicted [95% CI, 108-138]). The study also found that lifelong endurance sport participation was associated with having coronary plaque, proximal coronary plaque, noncalcified plaque and proximal noncalcified plaque as well as mixed plaque compared with healthy controls. Vulnerable plaques were uncommon, but a lifelong athletic lifestyle was associated with a lower prevalence. Importantly, the overall plaque burden was low.
- Clinical implications: The study identified a higher-than-expected plaque burden in endurance sport athletes compared with healthy controls. No outcome data were reported. This is a relatively small study compared with previously published much larger data sets indicating improved outcomes with endurance exercise. There are many confounding factors that can affect these data given the small sample size, such as diet (present and past), prior statin use and previously known CAD risk factors that are now controlled. It underscores that diet, past and present, and exercise do not completely negate the risk for CAD and that better evaluation tools for active exercisers are needed with improved outcome data to support its use.
Other sports cardiology sessions
Nathaniel Moulson, MD, clinical assistant professor at the University of British Columbia, Vancouver, Canada, discussed a case presented by Bradley J. Petek, MD, cardiology fellow at Massachusetts General Hospital, on late gadolinium enhancement (LGE).
Persistent LGE on cardiac MRI after an episode of myocarditis often creates a clinical conundrum when evaluating an athlete for RTP shared decision-making. The clinical context must be taken into consideration, including presence of symptoms and underlying CVD. When evaluating the pattern of LGE on cardiac MRI, it is important to remember that highly trained older endurance athletes can have a 10-fold increase in right ventricular insertion site LGE.
COVID-19 increased the cohort of young athletes evaluated with cardiac MRI used to screen for myocarditis. Although COVID-19-associated myocarditis was reported as rare, two large studies found that persistent LGE after COVID-19 myocarditis was not uncommon when reevaluated around 90 days after infection. Interestingly, upon reevaluation, normalization of T1 and T2 signals was common, suggesting resolution of active inflammation and edema.
The clinical significance of persistent LGE in asymptomatic athletes remains unknown. However, data evaluating LGE in other settings (HCM, dilated cardiomyopathy, arrhythmia) is associated with increased risk for adverse events. Therefore, current guidelines are conservative and recommend that athletes with probable or definite myocarditis not participate in sports for 3 to 6 months. Return to play is considered in those with resolution of LV systolic function, normalization of cardiac biomarkers (troponin and N-terminal pro-B-type natriuretic peptide) and no evidence of clinically relevant arrhythmia on ambulatory ECG monitoring and exercise treadmill testing. The role of repeat cardiac MRI with or without persistent LGE in return to play is unclear. Current guidelines do not provide clear guidance on the utility of cardiac MRI to identify resolution of LGE in athletes, and an update to the guidelines is overdue.
Ankit Shah, MD, MPH, sports cardiologist at MedStar Heart & Vascular Institute, director of MedStar Sports & Performance Cardiology and assistant professor of medicine at Georgetown University Medical Center, discussed a case presented by Douglas Darden, MD, a cardiac electrophysiologist at Kansas City Heart Rhythm Institute of HCA Midwest Health, on premature ventricular contractions (PVC).
PVCs are a common finding in most individuals undergoing Holter monitoring or ambulatory ECG evaluation. In general, the prevalence of PVCs in athletes mirrors that of the general population. However, the clinician should consider additional workup when a 12-lead ECG reveals two PVCs in an asymptomatic athlete or when one PVC is present with additional ECG abnormalities. When evaluated with 24-hour ECG monitoring, 2,000 PVCs per day are associated with a higher likelihood of an underlying abnormality. It is important to note that there can be normal day-to-day variations in the PVC burden. Therefore, 24-hour monitoring may not give a true representation of the actual number of PVCs over time.
PVC morphology is an important consideration. Darden noted that PVCs can be characterized as benign or more concerning based on the morphology and coupling interval (PVC proximity to QRS and T waves).
When evaluating an athlete with a high burden of PVCs, it is important to start with a thorough history and physical exam. A family history of SCD should prompt further investigation. Athletes should also be asked about supplement use, sleep, nutrition and hydration. Temporary exercise restrictions may be necessary until the workup is completed. This generally involves exercise treadmill testing, ambulatory ECG monitoring and an echocardiogram. Expanded workup may include cardiac MRI with rare utility of a coronary angiogram, electrophysiology study and genetic testing.
For patients identified as having structural heart disease, disease specific management is recommended. For athletes without structural heart disease, management is based on the presence or absence of symptoms. In an asymptomatic athlete, return to play without exercise restrictions may be reasonable with serial follow-up exams. For the symptomatic athlete, medical management (usually with beta-blockers or calcium channel blockers) and/or antiarrhythmics or an ablation may be considered. Additional return-to-play guidelines for the management of PVCs in athletes are provided by ACC/American Heart Association and European Society of Cardiology guidelines.
- References:
- Daniels CJ, et al. JAMA Cardiol. 2021;doi:10.1001/jamacardio.2021.2065.
- De Bosscher R, et al. Featured Clinical Research III. Presented at: American College of Cardiology Scientific Session; March 4-6, 2023; New Orleans.
- Domenech-Ximenos B, et al. J Cardiovasc Magn Reson. 2020;doi:10.1186/s12968-020-00660-w.
- Drezner JA, et al. Br J Sports Med. 2017;doi:10.1136/bjsports-2016-097331.
- Lampert R, et al. Late-Breaking Clinical Trials V. Presented at: American College of Cardiology Scientific Session; March 4-6, 2023; New Orleans.
- Lee DH, et al. Circulation. 2022;doi:10.1161/CIRCULATIONAHA.121.058162.
- Maron BJ, et al. Circulation. 2015;doi:10.1161/CIR.0000000000000239.
- Martinez KA, et al. Late-Breaking Clinical Trials V. Presented at: American College of Cardiology Scientific Session; March 4-6, 2023; New Orleans.
- Martinez MW. Clin Sports Med. 2015;doi:10.1016/j.csm.2015.02.005.
- Martinez MW, et al. JAMA Cardiol. 2021;doi:10.1001/jamacardio.2021.0565.
- Moulson N, et al. Circulation. 2021;doi:10.1161/CIRCULATIONAHA.121.054824.
- Pelliccia A, et al. Eur Heart J. 2021;doi:10.1093/eurheartj/ehaa605.
- Petek BJ, et al. Circulation. 2022;doi.10.1161/CIRCULATIONAHA.121.058272.
- Zipes DP, et al. Circulation. 2015;doi:10.1161/CIR.0000000000000245.
- For more information:
- Bradley S. Lander, MD, is a HCM/sports cardiology fellow at Morristown Medical Center and an advanced echocardiography fellow at Columbia University Irving Medical Center. Twitter: @bradlander18.
- Robyn E. Bryde, MD, is an incoming HCM/sports cardiology fellow at Morristown Medical Center and current cardiology fellow at Mayo Clinic Jacksonville. Twitter: @robynbrydemd.
- Matthew W. Martinez, MD, is director of Atlantic Health System Sports Cardiology at Morristown Medical Center. He can be reached at matthew.martinez@atlantichealth.org; Twitter: @mmartinezheart.
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