Correlation Between Right Ventricular Free Wall Longitudinal Strain And Endothelin-1 Level In Patients With Exercise Induced Pulmonary Hypertension

Abstract

<h3>Background</h3> Exercise induced pulmonary hypertension (EI-PH) is defined as a resting pulmonary artery pressure > 25 mmHg which goes > 30 mmHg with exercise and PVR > 3 Woods unit. Endothelin-1 (ET-1) is a potent vasoconstrictor that is elevated in patients with pulmonary hypertension. Right ventricular free wall longitudinal strain (RVLS) has some prognostic role in patients with PH. However, little is known about correlation between RVLS and ET-1 level in those with EI-PH. <h3>Methods</h3> A prospective study measuring ET-1 level in patients with EI-PH both at rest and peak exercise in the Cath Lab. Patients data and demographic were summarized. Right heart cath was done to confirm diagnosis of EI-PH (pre-capillary vs. post-capillary) and measurement of mPA, RA, PW, PVR and CO were obtained. Blood samples were obtained to measure ET-1 level using ET-1 ELISA. Echocardiography data were obtained including RV function, size, TAPSE, S', FAC, RVLS, LV function and size. <h3>Results</h3> 100 patients were included in the study and divided into 2 groups. Group I had 50 patients with EI-PH and group II had 50 patient were control. ET-1 level in group was 3.1 fmol/m +/- 1.3 at rest and 3.6 fmol/m +/- 1.1 at peak exercise with a p value of 0.034. Whereas ET-1 level in group 2 was 2.6 fmol/m +/- 1.01 at rest and 2.9 fmol/m +/- 1.5 at peak exercise with p value of 0.11. In comparison, RVLS was -18% in group I compared to -22% in group 2 with a p value of 0.06. There was no statistical difference in other echocardiographic parameters of RV function. Although, non-statistically significant, but more signals of elevated ET-1 level with worse RVLS in group I. <h3>Conclusion</h3> This is the first study to show correlation (though statistically non-significant) between elevated ET-1 level with worse RV free wall longitudinal strain in patients with exercise induced pulmonary hypertension compared to control subjects. This probably indicates an intrinsic pathophysiological process involving RV and pulmonary vasculature tree in the setting of exercise induced pulmonary hypertension. A larger multi center trial is needed to confirm these findings.