Hemodynamic effects of inhaled nitric oxide in women with mitral stenosis and pulmonary hypertension

Mitral stenosis (MS) is associated with elevated left atrial pressure, increased pulmonary vascular resistance (PVR), and pulmonary hypertension (PH). The hemodynamic effects of inhaled nitric oxide (NO) in adults with MS are unknown. We sought to determine the acute hemodynamic effects of inhaled NO in adults with MS and PH. Eighteen consecutive women (mean age 58 ± 15 years) with MS and PH underwent heart catheterization. Hemodynamic measurements were recorded at baseline, after NO inhalation at 80 ppm, and after percutaneous balloon valvuloplasty (n = 10). NO reduced pulmonary artery systolic pressure (62 ± 14 mm Hg [baseline] vs 54 ± 15 mm Hg [NO]; p <0.001) and PVR (3.7 ± 2.5 Wood U [baseline] vs 2.2 ± 1.4 Wood U [NO]; p <0.001). NO had no effect on mean aortic pressure, left ventricular end-diastolic pressure, left atrial pressure, cardiac output, or systemic vascular resistance. Mitral valve area increased after valvuloplasty (0.9 ± 0.2 cm2 [baseline] vs 1.6 ± 0.3 cm2 [postvalvuloplasty]; p <0.001). A decrease in left atrial pressure (25 ± 4 mm Hg [baseline] vs 17 ± 4 mm Hg [after valvuloplasty]; p <0.001) and pulmonary artery systolic pressure (58 ± 12 mm Hg [baseline] vs 45 ± 8 mm Hg [after valvuloplasty]; p <0.001) was observed after valvuloplasty. No change in cardiac output or PVR was observed. Thus inhaled NO, but not balloon valvuloplasty, acutely reduced PVR in women with MS and PH. This suggests that a reversible, endothelium-dependent regulatory abnormality of vascular tone is an important mechanism of elevated PVR in MS.