Background
Endurance athletes commonly exhibit larger cardiac dimensions than the rest of the athletic population, with cardiac enlargement representing a physiological adaptation to intensive training(1). However, relevant enlargement of the aorta cannot be considered a common consequence of the athlete’s heart, with aortic dilatation being associated with an increased risk of adverse aortic events(2).
Risk factors for aortic dilation include advancing age, male sex, large body size, hypertension (particularly if not controlled), genetic syndromes including bicuspid aortic valve (BAV), connective tissue disorders, such as Marfan Syndrome(3,4).
Aortic root dilation is the leading cause of aortic insufficiency, whereby the aortic valve does not provide adequate closure to prevent regurgitation of blood from the aorta into the left ventricle. Aortic root dilation can also lead to aortic dissection because increased wall forces in the area of dilation lead to a tear in the aortic wall that can extend retrograde into coronary vessels or anterograde into the ascending and descending aorta.
Introduction
We present a case of a 42-year-old practicing competitive cycling and running for 8 hours per week. He was admitted to our Center for Sports Cardiology for a complete clinical assessment, including physical examination, resting ECG, ambulatory ECG monitoring, and transthoracic echocardiography (TTE) because of uncommon premature ventricular beats (PVBs) during the recovery step of an exercise testing performed for pre-participation screening. The athlete has no relevant prior medical history, no cardiovascular risk factors, or syncope. Family history was negative for coronary artery disease or sudden cardiac death. Physical examination was normal, and 12-lead ECG revealed common training-related findings, including bradycardia and incomplete right bundle branch block. The echocardiographic examination was performed according to the current standards(5).