The early course of pulmonary artery hypertension in patients undergoing mitral valve replacement with cardioplegic arrest.

In an effort to describe the immediate course of pulmonary hypertension following mitral valve replacement, we reviewed preoperative and postoperative data from 62 patients who underwent mitral valve replacement. Patients were divided based on the absence (Group I) or presence (Group II) of severe preoperative pulmonary hypertension, defined as a mean pulmonary artery pressure greater than or equal to 40 mm Hg. Group II patients were subdivided based on the absence (Group IIa) or presence ( Group IIb) of markedly elevated preoperative pulmonary vascular resistance indices, defined as a greater than or equal to 700 dynes . sec . cm-5 . m2. Pulmonary artery wedge pressures fell promptly following mitral valve replacement in all groups, but the course of other hemodynamic parameters varied among groups. Cardiac index increased significantly among Group I and IIb patients but not among Group IIa patients. Group I patients did not have significant changes in mean pulmonary artery pressure and pulmonary vascular resistance index. Group IIa patients had substantial reductions in mean pulmonary artery pressure while pulmonary vascular resistance index remained near 400 dynes . sec . cm-5 . m2. Group IIb patients had substantial reductions in mean pulmonary artery pressure while pulmonary vascular resistance index fell significantly to about 400 dynes . sec . cm-5 . m2. Primary valvular lesion and pharmacologic support were insignificant variables. Data from these hemodynamic groups suggest that at least three mechanisms contribute to the pulmonary hypertension seen in mitral valve disease: passive transmission of elevated left atrial pressures, reactive pulmonary arteriolar vasoconstriction, and morphologic changes in the pulmonary vasculature. The first two mechanisms appear to be rapidly reversed following mitral valve replacement. While others have described the regression of pulmonary hypertension several months following mitral valve operations, data presented here suggest that changes in pulmonary artery pressures and pulmonary vascular resistance index may occur much earlier.