Abstract Athlete’s heart is the condition of cardiac remodeling as a result of physiologic stress induced by regular strenuous physical activity by professional or elite amateur individuals. The literature describes several characteristics of the athletic heart, including left ventricular hypertrophy, increased left ventricular mass, right ventricular dilatation, atrial enlargement, electrocardiographic changes, and abnormalities on cardiac magnetic resonance imaging. We present a case of athletic heart in an exceptionally physically fit active duty naval aviator who experienced syncope and underwent extensive cardiac testing. He was found to have borderline hypertrophic changes as well as delayed gadolinium enhancement initially concerning for myocarditis. Cardiopulmonary exercise testing revealed an exercise capacity of 120% above the maximum measurable value for his age and gender. He was then diagnosed with athlete’s heart and released to active duty with no limitations to his flight status. A challenge is posed to the practicing clinician in differentiating the athletic heart from the heart of an athlete suffering from underlying pathophysiology. Athlete’s heart is an elusive diagnosis and may be associated with findings concerning for more insidious pathology, including hypertrophic cardiomyopathy and dilated cardiomyopathy. Additionally, patients with athlete’s heart have been noted to have delayed gadolinium enhancement similar to that seen in patients with a history of myocarditis; the clinical significance of this finding is yet to be fully elucidated. In a military setting, distinguishing the heart of the healthy and athletic service member from the unfortunate one who has cardiomyopathy remains an important clinical distinction warranting further study. INTRODUCTION Athlete’s heart is a condition characterized by cardiac remodeling that is the result of physiologic stress induced by regular strenuous physical activity. Electrophysiologic and anatomic changes characteristic of the athlete’s heart are readily identified on electrocardiogram (ECG), transthoracic echocardiogram (TTE), and cardiac magnetic resonance imaging (cMRI)1. A common clinical dilemma posed to the military healthcare provider is the differentiation of the athletic heart from the heart of an athlete suffering from underlying pathology. We present a case of athlete’s heart diagnosed during evaluation of syncope in an active duty naval aviator. CASE DISCUSSION A 40-year-old active duty naval aviator was referred to the Brooke Army Medical Center (BAMC) Cardiology Service for evaluation of recurrent syncope. The patient reported being very physically active; his usual regimen includes a 2-mile run in the morning and a 4-mile run in the afternoon, approximately 6 d a week. He additionally performs weight training for 45–60 min 5 d weekly. The patient’s first episode of syncope occurred while seated and was associated with a prodrome of diaphoresis, flushing, and tunnel vision; this occurred in the setting of extensive caffeine and energy supplement use. Given his high-risk occupation, he underwent a thorough cardiovascular diagnostic evaluation consisting of a resting 12 lead ECG, a TTE, exercise nuclear stress test, and a 28-d ambulatory ECG monitor. Resting 12 lead ECG was normal. TTE revealed mild concentric left ventricular hypertrophy (LVH) with intraventricular septal thickness of 1.5 cm, dilation of the left atrium to 4.1 cm, normal filling pressure with E/A ratio 0.93, and left ventricular ejection fraction (LVEF) of 56%. Twenty eight-day ECG monitor was normal. An exercise nuclear stress test revealed a partially reversible defect in the distribution of the left anterior descending artery. He was then referred for coronary angiography, which revealed mild non-obstructive coronary artery atherosclerosis and started on Metoprolol Tartrate 12.5 mg twice daily. He subsequently underwent tilt-table testing twice; on the first occasion, he had a positive result attributed to beta blockade. Metoprolol was discontinued and repeat tilt-table testing was negative. At this point, he was diagnosed with orthostatic syncope attributed to poor oral intake and heavy coffee use the day of the event, and he was released to full duty without limitation. One year later, the patient experienced a second episode of syncope, again while seated, in the setting of decreased sleep, moderate alcohol consumption, and low oral intake over the course of a day. His blood alcohol level on arrival was 110 mg/dL. He regained consciousness and, upon standing, experienced syncope a third time. He was subsequently referred to cardiology at Brooke Army Medical Center. On initial evaluation, his cardiac exam and ECG were normal. Given prior findings of scar on prior nuclear study, cMRI was performed which revealed a mildly dilated left ventricle, dilated left atrium, a normal ejection fraction of 60%, and a mid-wall late gadolinium enhancement (LGE) (51–75% involvement) of the basal inferior wall. To objectively quantify the patient’s cardiovascular conditioning, he underwent cardiopulmonary exercise testing which revealed excellent exercise capacity with a VO2 max of 47.7 mL/kg/min, which represents 120% of the maximum measurable value for the patient’s age and gender. His episode of syncope was favored to again be orthostatic, and he was diagnosed with athlete’s heart with no cardiogenic etiology of syncope identified. ATHLETE’S HEART The term “Athlete’s Heart” is used to describe the structural, functional, and electrical remodeling of the heart in response to physical stimuli placed on it by regular athletic training. In the late 19th century, a hypertrophied heart and bradycardia were noted to be more common in highly trained athletes.2 Today, advanced imaging modalities, particularly echocardiography, have allowed for more precise measurements and diagnostic criteria. In the athlete’s heart, LVEF is usually that of the normal healthy population, though in extreme cases, world-class endurance athletes such as cyclists may experience left ventricular dilation to the point of decreasing LVEF to abnormal values; importantly, these athletes demonstrate appropriate response and augmentation during activity.3 Right ventricular dilatation may also be noted, and the atria generally enlarge proportional to ventricular growth.1 A 2003 review of athlete’s heart demonstrated that significant increases in peak VO2, left ventricular mass, and decreases in resting heart rate occurred only in those athletes who exercised greater than 3 h per week.4 In athletic individuals, form determines function – a meta-analysis of almost 1,500 athletes divided into endurance-, strength-, and combination-trained athletes compared to controls noted that while all athletes had an increased left ventricular internal diameter, interventricular septal thickness, and posterior wall thickness, there were notable differences between diverging training styles. Specifically, exclusively strength-trained athletes had a much higher mean relative LV wall thickness (44 mm) than endurance athletes (39 mm) and controls (36 mm). Similarly, strength-trained athletes achieved a septal thickness 11.8 mm, compared to 10.5 mm in endurance-trained athletes and 8.8 mm in controls.5 Healthcare providers must differentiate between the physiologic changes characteristic of the athlete’s heart and pathologic abnormalities signaling underlying disease. A thorough history and physical examination should be obtained; specifically, the precise amount of exercise undertaken. A physical exam may reveal bradycardia and possibly a displaced point of maximal impulse (PMI). An ECG should follow with attention paid to known findings in athlete’s heart including sinus bradycardia, increased voltage in the precordial leads, early repolarization, incomplete right bundle branch block, and first degree atrioventricular block.6 An echocardiogram is indicated with attention paid to the dimensions of the LV, the interventricular septum, and ejection fraction. An increased LV wall thickness must be distinguished from hypertrophic cardiomyopathy (HCM), as the latter would lead to an increased risk of sudden cardiac death and the recommendation to cease strenuous exercise.7 A series of criteria for individuals with an increased LV thickness of 13–15 mm have been proposed to distinguish HCM and athlete’s heart. Higher risk characteristics include unusual LVH pattern, diastolic dysfunction, left atrial enlargement, female sex, a family history of HCM, bizarre ECG pattern, and LV end-diastolic diameter below 45 mm should suggest a diagnosis of HCM rather than athlete’s heart.8 More recently, advanced imaging with cMRI has been undertaken to further elucidate characteristics of the athlete’s heart, with the increasingly common finding of LGE1,2,4,5,9 in the competitive athlete. In a study of veteran male endurance athletes with a mean age of 65 compared with both age-matched healthy controls and young athletes with a mean age of 30. Expected findings were confirmed: athletes demonstrated increased left and right ventricular volumes, preserved systolic function, and increased septal thickness compared to healthy controls. Notably, 50% of evaluated veteran athletes displayed LGE indicating myocardial fibrosis, as was noted in the patient presented in this case. Of the six cases, one had a probable past myocarditis, one had a probable previous silent myocardial infarction, and four were of undetermined etiology. Neither younger athletes nor age-matched controls demonstrated LGE, and the distribution of LGE among those in which it was found was not associated with age, height, weight, or body surface area, but was associated with number of years trained and number of marathons ran. The researchers noted a link between lifelong endurance exercise and myocardial fibrosis with an etiology still to be determined.10 Additionally, a 2008 study compared Framingham Risk Score, coronary artery calcium, and LGE in 102 marathon runners over the age of 50 compared to age-matched controls. Interestingly, the number of marathons run was again found to be an independent predictor of increasing incidence of LGE, which was noted in 12% of athletes. Of the 12 patients with LGE, 5 had a scar pattern typical of ischemia and 7 displayed a non-ischemic patchy pattern, suggesting again that regular athletic training carries with it a risk of cardiac remodeling.11 This is further supported by a rat model that has reported inflammatory and pro-fibrotic infiltrates in the myocardium of rats undergoing an intensive exercise regimen. Indeed, ventricular tachycardia could be induced in a statistically higher percentage of “athletic” rats than controls.12 Such a relationship has yet to be definitively demonstrated in humans. DISCUSSION The case in question highlights several interesting points regarding athletic heart. First, the patient could be described as being at an elite amateur level of fitness. His personal and family history was unrevealing of any cardiac disease, physical exam was unremarkable, and ECG was normal. His evaluation revealed characteristics of the athlete’s heart on echocardiography with mild concentric LVH, an enlarged LV cavity, borderline left atrial dilation, and a normal ejection fraction. Ambulatory ECG monitoring was normal and a myocardial perfusion scan demonstrated a partially reversible defect suggestive of scar alongside viable ischemic myocardium in the distribution of the distal left anterior descending artery. Subsequent coronary angiography revealed non-obstructive coronary artery atherosclerosis. A second episode of syncope prompted further workup with cardiac MRI which revealed an area of LGE radiologically consistent with prior myocarditis, however the patient adamantly denied any past symptoms consistent with such. He then displayed a robust response to exercise with a VO2 max above the measurable limit. Thus, the patient neatly demonstrates the entire recommended algorithm for workup of athlete’s heart without sign of underlying cardiac disease; this algorithm is provided as Figure 1. His finding of LGE is an interesting incidental note that warrants further study as the definite cause – and implication – of this in the adult athlete has yet to be elucidated. FIGURE 1. View largeDownload slide Recommended evaluation for patients with cardinal manifestations of cardiac disease (chest pain, palpitations, dyspnea, syncope). Seattle criteria refer to criteria considered normal in athletes (7), hx, history; LVID, LV internal diameter; AH, athlete’s heart; LA, left atrium; VO2 max, maximal oxygen consumption; rx, treatment. Adapted from Prior and La Gerche 2 and B J Maron.8 FIGURE 1. View largeDownload slide Recommended evaluation for patients with cardinal manifestations of cardiac disease (chest pain, palpitations, dyspnea, syncope). Seattle criteria refer to criteria considered normal in athletes (7), hx, history; LVID, LV internal diameter; AH, athlete’s heart; LA, left atrium; VO2 max, maximal oxygen consumption; rx, treatment. Adapted from Prior and La Gerche 2 and B J Maron.8 REFERENCES 1 La Gerche A, Taylor AJ, Prior DL: Athlete’s heart: the potential for multimodality imaging to address the critical remaining questions. JACC Cardiovasc Imaging 2009; 2( 3): 350– 63. Google Scholar CrossRef Search ADS PubMed 2 Prior DL, La Gerche A: The athlete’s heart. Heart 2012; 98: 947– 55. Google Scholar CrossRef Search ADS PubMed 3 Abergele E, Chatellier G, Hagege A, et al. : Serial left ventricular adaptations in world-class professional cyclists. J Am Coll Cardiol 2004; 44: 144– 9. Google Scholar CrossRef Search ADS PubMed 4 Fagard R: Athlete’s heart. Heart 2003; 89: 1455– 61. Google Scholar CrossRef Search ADS PubMed 5 Pluim BM, Zwinderman AH, van der Laarse A, et al. : The athlete’s heart: a meta-analysis of structure and function. Circulation 2000; 101: 336– 44. Google Scholar CrossRef Search ADS PubMed 6 Drezner JA, Ackerman MJ, Anderson J, et al. : Electrocardiographic interpretation in athletes: the ‘Seattle criteria. Br J Sports Med 2013; 47: 122– 4. Google Scholar CrossRef Search ADS PubMed 7 Elliot PM, Gimeno JR, Thaman R, et al. : Historical trends in reported survival rates in patients with hypertrophic cardiomyopathy. Heart 2006; 92: 785– 91. Google Scholar CrossRef Search ADS PubMed 8 Maron BJ: Distinguishing hypertrophic cardiomyopathy from athlete’s heart: a clinical problem of increasing magnitude and significance. Heart 2005; 91: 1380– 2. Google Scholar CrossRef Search ADS PubMed 9 Baggish AL, Wood MJ: Athlete’s heart and cardiovascular care of the athlete, scientific and clinical update. Circulation 2011; 123: 2723– 35. Google Scholar CrossRef Search ADS PubMed 10 Mohlenkamp S, Lehmann N, Breuckmann F, et al. : Running: the risk of coronary events. Prevalence and prognostic relevance of coronary atherosclerosis in marathon runners. Eur Heart J 2008; 29: 1903– 10. Google Scholar CrossRef Search ADS PubMed 11 Wilson M, O’Hanlon R, Prasad S, et al. : Diverse patterns of myocardial fibrosis in lifelong, endurance veteran athletes. J Appl Physiol 2011; 110( 6): 1622– 6. Google Scholar CrossRef Search ADS PubMed 12 Benito B, Gay-Jordi G, Serrano-Mollar A, et al. : Cardiac arrhythmogenic remodeling in a rat model of long-term intensive exercise training. Circulation 2011; 123: 13– 22. Google Scholar CrossRef Search ADS PubMed Published by Oxford University Press on behalf of the Association of Military Surgeons of the United States 2018. This work is written by (a) US Government employee(s) and is in the public domain in the US.
Military Medicine – Oxford University Press
Published: May 31, 2018
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