Echocardiographic Pulmonary to Left Atrial Ratio (ePLAR): A Comparison Study between Ironman Athletes, Age Matched Controls and A General Community Cohort

Background: During exercise there is a proportionally lower rise in systemic and pulmonary pressures compared to cardiac output due to reduced vascular resistance. Invasive exercise data suggest that systemic vascular resistance reduces more than pulmonary vascular resistance. The aim of this study was the non-invasive assessment of exercise hemodynamics in ironman athletes, compared with an age matched control group and a larger general community cohort. Methods: 20 ironman athletes (40 +/- 11 years, 17 male) were compared with 20 age matched non-athlete controls (43 +/- 7 years, 10 male) and a general community cohort of 230 non-athletes individuals (66 +/- 11 years, 155 male), at rest and after maximal-symptom limited treadmill exercise stress echocardiography. Left heart parameters (mitral E-wave, e'-wave and E/e') and right heart parameters (tricuspid regurgitation maximum velocity and right ventricular systolic pressure), were used to calculate the echocardiographic Pulmonary to Left Atrial Ratio (ePLAR) value of the three groups. Results: Athletes exercised for 12.2 +/- 0.53 min, age matched controls for 10.1 +/- 2.8 min and general community cohort for 8.3 +/- 2.6 min. Mitral E/e' rose slightly for athletes (0.9 +/- 1.8), age matched controls (0.6 +/- 3.0) and non-athletes (0.4 +/- 3.2). Right ventricular systolic pressure increased significantly more in athletes than in both non-athlete cohorts (35.6 +/- 17 mmHg vs. 20.4 +/- 10.8 mmHg and 18 +/- 9.6 mmHg). The marker of trans-pulmonary gradient, ePLAR, rose significantly more in athletes than in both non-athlete groups (0.15 +/- 0.1 m/s vs. 0.07 +/- 0.1 m/s). Conclusions: Pulmonary pressures increased proportionally four-fold compared with systemic pressures in ironman athletes. This increase in pulmonary vascular resistance corresponded with a two-fold increase in ePLAR. These changes were exaggerated compared with both non-ironman cohorts. Such changes have been previously suggested to lead to right ventricle dysfunction, arrhythmias and sudden cardiac death