Mechanism of reducing platelet activity by percutaneous transluminal mitral valvuloplasty in patients with rheumatic mitral stenosis

Background: Previous studies have demonstrated that platelet activity significantly decreased after optimal percutaneous transluminal mitral valvuloplasty (PTMV) in patients with rheumatic mitral stenosis (MS). However, the mechanism of reducing platelet activity by valvuloplasty remains unclear. Methods and results: We studied 19 patients with symptomatic NIS who were undergoing PTMV. The fractions of unstimulated platelets expressing P-selectin in the venous blood obtained before, and at the 1-week and 4-week follow-ups after PTMV were determined by flow cytometry. The mitral valve areas, measured before and at the 1-week follow-up after PTMV, were calculated by means of the Doppler pressure half-time method. The mean (+/- SD) area of the mitral valve increased significantly after PTMV (1.05 +/- 0.17 vs 1.44 +/- 0.27 cm(2), respectively; p < 0.0001). The mean left atrial area was reduced in size significantly after PTMV (36.6 +/- 11.4 vs 33.9 +/- 13.4 em 2, respectively; p < 0.05). The mean left atrial pressure (23.3 +/- 5.1 vs 18.0 +/- 5.8 mm Hg, respectively; p < 0.0001) and the mean pulmonary arterial pressure (31.4 +/- 7.8 vs 26.1 +/- 7.7 mm Hg, respectively; p < 0.0001) fell significantly after PTMV. The fraction of platelets expressing P-selectin in the venous blood fell significantly after PTMV (before PTMV, 4.7 t 2.4%; 1 week after PTMV, 2.2 +/- 2.1%; 4 weeks after PTMV, 2.0 +/- 1.7%; p < 0.0001). Correlation analysis demonstrated that there was a significantly direct relationship between the magnitude of increase in mitral valve area and the magnitude of decrease in the fraction of platelets expressing P-selectin in the venous blood 4 weeks after PTMV (p = 0.0013; r = 0.682). However, there was no significant correlation between the magnitude of decrease in the fraction of platelets expressing P-selectin in the venous blood and the magnitude of decrease in the left atrial area, the decrease in left atrial pressure, or the decrease in the pulmonary artery pressure after PTMV. Conclusions: In patients with moderate-to-severe NIS, increased platelet activation fell significantly after PTNIV. It was the increase in mitral valve area by PTMV, instead of hemodynamic and echocardiographic factors, that accounted for the decrease in the fraction of venous platelets expressing P-selectin after PTMV.