Do the Different Types of Pulmonary Hypertension Cause the Same Effect on Right Heart and Serum Asymmetrical Dimethylarginine Levels in Female Patients?

ABSTRACT Objective: Right-heart function is a major determinant of clinical outcome in patients with elevated pulmonary artery pressure due to pulmonary venous hypertension (PVH) and pulmonary arterial hypertension (PAH). Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase. This study aimed to evaluate if different types of pulmonary hypertension (PH) would cause the same effect on right-heart functions and serum ADMA levels in female patients. Methods: This study included patients with PAH as group I, patients with PVH due to mitral stenosis (mitral valve area ≤ 1.5 cm2, without any additional valve or left-heart disease and systolic pulmonary artery pressure ≥ 50 mmHg in transthoracic echocardiography) as group II, and healthy control subjects as group III. Transthorasic echocardiographic evaluations for right-heart functions were performed according to the guidelines of the American Society of Echocardiography. Venous blood samples were collected, and the serum ADMA concentrations were obtained with the ELISA kit (DRG® International Inc., Springfield, NJ, USA). Results: Patients in groups I and II had higher ADMA levels than healthy control subjects. Right-atrium area and dimensions, right-ventricular (RV) volumes, grade of tricuspid regurgitation, systolic pulmonary arterial pressure, RV wall thickness, and RV outflow tract diameters were significantly higher in group I patients than in group II patients. Right-ventricular myocardial performance index was lower, and RV fractional area change and tricuspid valve systolic tissue Doppler velocity were higher in group II patients than in group I patients. Conclusion: This study demonstrated that both PAH and PVH caused increase in right-heart dimensions and impairment in right-heart functions.

Inhaled levosimendan versus intravenous levosimendan in patients with pulmonary hypertension undergoing mitral valve replacement

Context: Inhaled levosimendan may act as selective pulmonary vasodilator and avoid systemic side effects of intravenous levosimendan, which include decrease in systemic vascular resistance (SVR) and systemic hypotension, but with same beneficial effect on pulmonary artery pressure (PAP) and right ventricular (RV) function. Aim: The aim of this study was to compare the effect of inhaled levosimendan with intravenous levosimendan in patients with pulmonary hypertension undergoing mitral valve replacement. Settings and Design: The present prospective randomized comparative study was conducted in a tertiary care hospital. Subjects and Methods: Fifty patients were randomized into two groups (n = 25). Group A: Levosimendan infusion was started immediately after coming-off of cardiopulmonary bypass and continued for 24 h at 0.1 mcg/kg/min. Group B: Total dose of levosimendan which would be given through intravenous route over 24 h was calculated and then divided into four equal parts and administered through inhalational route 6th hourly over 24 h. Hemodynamic profile (pulse rate, mean arterial pressure, pulmonary artery systolic pressure [PASP], SVR) and RV function were assessed immediately after shifting, at 1, 8, 24, and 36 h after shifting to recovery. Statistical Analysis Used: Intragroup analysis was done using paired student t-test, and unpaired student t-test was used for analysis between two groups. Results: PASP and RV-fractional area change (RV-FAC) were comparable in the two groups at different time intervals. There was a significant reduction in PASP and significant improvement in RV-FAC with both intravenous and inhalational levosimendan. SVR was significantly decreased with intravenous levosimendan, but no significant decrease in SVR was observed with inhalational levosimendan. Conclusions: Inhaled levosimendan is a selective pulmonary vasodilator. It causes decrease in PAP and improvement in RV function, without having a significant effect on SVR.