ABC | Volume 112, Nº3, March 2019

Updated The Brazilian Society of Cardiology and Brazilian Society of Exercise and Sports Medicine Updated Guidelines for Sports and Exercise Cardiology - 2019 Arq Bras Cardiol. 2019; 112(3):326-368 undergo anamnesis, a physical examination, echocardiography (to evaluate disease progression), and exercise testing to ensure that their exercise tolerance is compatible with their physical activity, that no episodes of hypotension occur during exercise, and that there is no electrocardiographic evidence of complex ischemia/arrhythmia. 6.2.1.1. Recommendations and Evidence Level Athletes with aortic stenosis should be evaluated annually to continue participating in sports. Recommendation grade: I. Evidence level: C. Athletes with discrete aortic stenosis (stage B) and an appropriate physiological response to a maximal exercise testing may participate in any sport. Recommendation grade: IIa. Evidence level: C. Athletes with moderate aortic stenosis (stage B) can participate in competitive sports with low-to-moderate static and dynamic components (classes IA, IB and IIA) if the exercise testing results are sufficient for the activity level required in competition, with clinical, hemodynamic and ECG responses to exercise and without ventricular tachyarrhythmias. Recommendation grade: IIa. Evidence level: C. Asymptomatic athletes with severe aortic stenosis (stage C) should not participate in competitive sports, except for those with low static and dynamic components (class IA). Symptomatic athletes with aortic stenosis (stage D) should not participate in competitive sports. Recommendation grade: III. Evidence level: C. 6.2.2. Aortic Regurgitation The prevalence of aortic regurgitation increases with age, although it is very low (1%) in individuals less than 70 years of age. After that age, its prevalence increases to over 2%. 219 In the native valve, aortic regurgitation may be the result of abnormalities of the valve leaflets, the aortic root or both. The main causes of aortic regurgitation are diseases that affect the aortic ring or root without directly involving the aortic valve: BAV, connective tissue genetic disorders (Marfan, Ehlers-Danlos and Loeys-Dietz syndromes), inflammatory diseases (in particular syphilitic aortitis, Takayasu arteritis and giant cell arteritis), rheumatic heart disease and hypertensive dilation. In fact, so-called “idiopathic” aneurysms of the ascending aorta have a genetic diagnosis in at least 30% of the cases. 210,219 Aortic regurgitation is invariably well tolerated and asymptomatic for years; however, eccentric hypertrophy progressively develops and LV systolic and diastolic volumes increase, which could lead to LV systolic dysfunction. Aortic regurgitation is diagnosed in asymptomatic athletes when physical examination reveals wide arterial pulse pressure, a diastolic murmur in the aortic area or Erb’s point, or a systolic murmur related to increased systolic volume. An echocardiogram is definitive for diagnostic confirmation and classifying aortic regurgitation. With color Doppler echocardiography, the size of the regurgitant jet and the flow convergence can be determined, allowing the regurgitant orifice area to be calculated. 210,220 CMRI may be used as a complement to echocardiography when quantifying aortic regurgitation. In fact, it has been reported that quantitative volume and regurgitant fraction can be calculated with better reproducibility through CRMI than echocardiography. 221,222 Because the pathophysiology of aortic regurgitation leads to LV dilation in elite athletes, it must be differentiated from the physiological alterations in athlete’s heart syndrome. Therefore, when evaluating increased LV volume in elite athletes with suspected or diagnosed aortic regurgitation, only LV volumes that exceed normal physiological response to sports training should be considered. Although up to 45% of male athletes have a LV end-diastolic diameter (LVDD) > 55 mm, only 14% of elite male athletes have a LVDD > 60 mm, and LVDD rarely exceeds 70 mm. A LVDD > 55 mm occurs in < 10% of elite female athletes, while only 1% have a LVDD > 60 mm. 223-225 The same is true for LV end-systolic diameter (LVSD): in elite athletes, the upper limit for LVSD is 49 mm for males and 38 mm for females. Only index data on body surface area and height are available regarding LVDD, which indicate upper limits of 35.3 mm/m 2 and 40.8 mm/m 2 for male female athletes, respectively. 223-226 A normal LV ejection fraction response to exercise is observed in aortic regurgitation patients until there is significant LV dilation. When evaluating the progressive effects of severe aortic impairment in athletes with normal LV ejection fraction, serial analysis of LVSD is of great value. The American Heart Association/American College of Cardiology define preserved systolic function (stage C1) in patients with significant aortic impairment as a LV ejection fraction ≥ 50% and LVSD ≤ 50 mm or index LVSD ≤ 25 mL/m 2 . 210,227 Thus, in athletes with significant aortic impairment and a LVDD that exceeds the above- mentioned reference values. There is a higher probability that severe aortic impairment contributes to LV dilation. Such athletes require a more careful evaluation to verify that no ventricular increase has occurred and whether signs and/or symptoms occur during exercise, such as dyspnea on exertion or reduced functional capacity. 6.2.2.1. Recommendations and Evidence Level Athletes with aortic regurgitation should be evaluated annually to continue participating in sports. To confirm that athletes with aortic regurgitation are truly asymptomatic, they should undergo an exercise testing involving at least the activity level achieved during training and competition and have a physiological hemodynamic response. Athletes with mild-to-moderate aortic impairment (stage B), a physiological response to a maximal exercise testing, normal 349