We need better data on how to manage myocarditis in athletes

Abstract

One of us (PDT) recently complained to one of our clinical cardiology trainees that there was little advice on how to manage athletes with myocarditis. That comment was made as we were discussing a young female triathlete who had suffered two episodes of myocarditis, and had just returned with symptomatic ventricular tachycardia induced by exercise. Almost on cue after that complaint, the current issue of the European Journal of Preventive Cardiology (EJPC)1 and a recent edition of the Journal of the American College of Cardiology – Cardiovascular Imaging (JACC-Img)2 presented two excellent articles addressing this issue. The EJPC article summarizes the role of exercise and exercise training in developing acute myocarditis and provides recommendations for sport and exercise participation once myocarditis is diagnosed. The JACC-Img article provides guidance on managing athletes primarily using cardiac magnetic resonance (cMR) imaging. The JACC-Img article’s premise is that cMR’s sensitivity and specificity, especially using novel techniques such as T1 and T2 weighting, can be used to update standard recommendations and to provide more accurate guidance as to when an athlete can return to vigorous exercise training and competition. Both articles are well-written and provide some guidance, but both emphasize that their recommendations are based on very limited data in athletes. So what prompts this recent interest in myocarditis in athletes? There are several possible reasons. Myocarditis is estimated to cause ≈6% of exercise-related sudden cardiac deaths (SCDs) in athletes.3 SCD due to myocarditis is more difficult to prevent than other more frequent causes of SCD in athletes, such as hypertrophic cardiomyopathy, because myocarditis is not inherited so leaves no familial trail, is an acute versus chronic condition so less likely to be detected, and often has no or only subtle electrocardiogram (ECG) findings. It is possible, but not certain, that athletes are more vulnerable to viral infections and to myocarditis. The EJPC article discusses the possibility of enhanced virus susceptibility in athletes because many, but not all, animal models of myocarditis document an increase in viral load, myocardial necrosis and mortality in animals forced to exercise after infection.1 Alternatively, athletes may simply appear to be more vulnerable to myocarditis because they are aware of decreases in their exercise performance prompting them to seek medical treatment and to be more readily diagnosed than non-athletes. Regardless as to whether or not athletes are more susceptible, it is highly likely that athletes with myocarditis are more vulnerable to SCD because of the probability that vigorous exercise increases the risk of symptomatic and even fatal arrhythmias. Establishing an unequivocal diagnosis of myocarditis appears to be more difficult in athletes. ECG variants are common in athletes4 as are post-exercise increases in the myocardial band of creatine kinase,5 cardiac troponins6 and even brain natriuretic protein.7 Healthy endurance athletes demonstrate left ventricular enlargement, but may also demonstrate reduced or borderline left ventricular ejection fractions (LVEFs). Eleven percent of cyclists competing in the Tour de France had echocardiographically determined LVEFs <52%.8 Lifelong endurance athletes may also demonstrate late gadolinium enhancement (LGE) predominantly, but not exclusively, at the “hinge points,” where the right ventricle inserts into the interventricular septum.9 Why the predilection for this area is not clear, but it may be because there is a greater relative increase in right ventricular shear stress and systolic pressure during exertion compared with rest than in the left ventricle.9 The “overtraining syndrome” or the exercise intolerance, listlessness and slight increase in resting heart rate that can occur in athletes who have performed too much intense exercise for too long also mimics the symptoms of myocarditis. Both articles present excellent flow charts on how to manage myocarditis in athletes. In brief, the diagnosis of acute myocarditis requires considering the possibility in athletes with decreased exercise tolerance and other symptoms, looking for ECG and cardiac biomarkers of myocardial injury/inflammation, performing an echocardiogram and cMR to exclude wall motion abnormalities, pericardial effusion and LGE evidence of myocardial scar. T1 and T2 can be used to assess myocardial relaxation and extracellular volume indicative of myocardial edema, but the sensitivity and specificity of these new test modalities remains uncertain. There is no role for endomyocardial biopsy unless giant cell myocarditis is suspected due to a rapid decline in left ventricular function or life-threatening ventricular arrhythmias. No test alone provides absolute diagnostic accuracy, especially in athletes, so the diagnosis requires assessing a clinical constellation of factors, and remembering that each of these tests can be falsely abnormal in athletes. The acute management of myocarditis in athletes requires exercise restriction. Neither article addresses drug management in detail because there are no established treatment guidelines. Non-steroidal anti-inflammatory drugs (NSAIDs) and colchicine are useful if there is chest pain and evidence of pericardial involvement. Some cardiologists use NSAIDs and colchicine for a month based on the unproven hypothesis that these anti-inflammatory medications reduce inflammation and accelerate healing, and possibly longer if cardiac biomarkers remain abnormal. Many cardiologists use low dose beta blocker in those patients with preserved LVEF for several months in the hope of lowering arrhythmia risk, but again there are no data documenting benefit. Both European10 and American11 guidelines exist on when athletes with myocarditis can return to exercise training and competition. Our clinical experience is that athletes resist attempts to restrict their exercise training, and they return to hard training too soon. The authors of the EJPC article allow return to low-level exercise training at one month in those with normal biomarkers and a normal echo and cMR and return to full competition at three months. The issue is more difficult in those with persistent biomarker elevations or other evidence of myocardial injury. The authors suggest restricting these athletes with persistent biomarker abnormalities for at least six months, but both articles note that there are few data on the safety of return to competition in such patients. Maximal exercise testing should be performed prior to a return to training and competition to ensure that exercise does not provoke any important arrhythmias. Both articles recommended establishing patient registries for athletes with myocarditis to ultimately provide the data for such decisions. We are enthusiastic about exercise, but do think that vigorous exercise training increases the risk for cardiac events in those with persistent injury. We encourage such patients to be active, but do encourage them to avoid strenuous training and competition. Data from the proposed registries may ultimately prove this approach to be needlessly conservative. We understand that hard training and competition is a critical part of athletes’ lives and that they must be included in this shared decision. Nevertheless, until better data are available, we encourage athletes with persistent evidence of myocardial injury to avoid competitive, physically demanding athletics. Exercise and exercise training are an important part of life, but doing no harm is even more important. The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article. The author(s) received no financial support for the research, authorship, and/or publication of this article. The opinions expressed in this article are not necessarily those of the Editors of the European Journal of Preventive Cardiology or of the European Society of Cardiology.

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