Background: Pulmonary hypertension (PH) is defined as increased pulmonary artery pressure (PAP) and is associated with high risk of heart failure and mortality in general population. PH may serve as an underlying condition in patients with cardiopulmonary arrest.
Problem: TTE findings of PH in asymptomatic athletes during cardiovascular screening may cause restriction from training and competitive activity. Additional invasive methods in some cases are more helpful with precise diagnostics and making decision concerning further sports career.
Clinical case: An elite 21 year old athlete specializing in underwater swimming with 12 years of sports experience was admitted to cardiac functional diagnostics department. He had no complaints, no shortness of breath, no decrease of exercise performance. He denied heart disease family history or sudden cardiac arrest cases in relatives. 12-lead ECG was normal with sinus bradycardia with HR 49 bpm, (normal finding in endurance athletes). Regular CPET in our sports lab confirmed high level of exercise performance (VO2max 62 ml/kg/min, Pmax 414 W) with no decrease during previous months. Routine cardiovascular athletes’ TTE screening in 2016 revealed mild PH (rated PAP 47 mm Hg), mild RA enlargement of 60 ml, III degree of tricuspid regurgitation with no valve or myocardium lesion. Periodical TTE studies in 2016-2017 years, conducted each 3-4 months, confirmed PH diagnosis. Measured PAP was from 40 to 54 mm Hg, right heart chambers dilatation: RA volume up to 74 ml, RV size (apical view) 47 mm. None of any other TTE abnormal findings were observed. Values of myocardium structure, global and regional segment contractile function of RV and LV were within the physiologic norm. The preliminary diagnosis, based on PAP values, was idiopathic PH. In compliance with eligibility guidelines for competitive athletes, this diagnosis is a contradiction to training and competitive activity. Athlete was deeply concerned about his future sports career, as he was preparing to important international competitions. He had been aware of possible complications and risks associated with cardiac invasive measurements before his consent was obtained. Medical consultation referred a patient to further diagnostic catheterization of PA. Follow-up catheterization of right heart chambers with Svan-Hanse catheter placement and central haemodynamics evaluation was performed. Undertaken examinations revealed normal values of PAP – 10 mm Hg. As HP diagnosis based on data from diagnostic cardiac catheterization is defined by a mean PA value of 25 mm Hg or more at rest, PH diagnosis was not confirmed. Finally, sports cardiologist admitted athlete to training and competitive activity.
Conclusions: TTE findings of PH and RA enlargement in swimmers may be explained by physiological response and specific adaptation to aquatic environment. Diagnosis of PH in experienced swimmers is better confirmed with the use of invasive methods.