Right ventricular improvement is associated with left ventricular diastolic function and size enhancement in PAH patients: an echocardiographic study

Abstract

Abstract Background While pulmonary vasodilation therapy improves right ventricular (RV) function in pulmonary arterial hypertension (PAH), data regarding left ventricular (LV) function remain sparse. Purpose We aimed to investigate whether PAH therapy improve LV function in PAH patients. Methods Between 2002 and 2020, all incident PAH patients from one PH referral centers were included, treated and followed-up according to current ESC/ERS guidelines. All patients had comprehensive echocardiography both investigating right and left ventricular function before and after 1-year of vasodilation therapy. In addition to RV echocardiographic evaluation, we focused on LV ejection fraction from Modified Simpson method, LV diameters by M-mode, transmitral pulsed-wave E/A ratio, Flow to tissue Doppler imaging E/e' ratio, and left atrial size. Results 126 patients were included (63% female, 57±17 yo), mainly from connectivite tissue associated and idiopathic PAH (24% and 28% respectively) causes. Compared to baseline, 1-year NYHA functional class (p<0.01), NTproBNP plasma level (p<0.001), invasive mean pulmonary arterial pressure (p<0.01) and cardiac index (p<0.01) significantly improved. While LV ejection fraction (p=0.68), LV end-diastolic diameter (p=0.11) as well as LA area and volume (p=0.09) were not significantly enhanced under vasodilation therapy, LV diastolic function, assessed by mitral E wave (p<0.01), tissue doppler imaging mitral e' wave (p=0.04), and E/A ratio (p=0.045) were significantly improved at 1-year. There was a significant correlation between LV end-diastolic diameter (p<0.001) and RV end-diastolic area (p<0.001) owing to the normalization of right- to left ventricular interdependence, as well as between mitral E wave and TAPSE (p=0.045). Conclusion By improving RV function, PAH vasodilation therapy enhances LV size and diastolic function and normalizes the biventricular interdependence. Funding Acknowledgement Type of funding sources: None.