Background: Mitral Regurgitation (MR) is a severe complication after percutaneous valvulopalsty for Mitral Stenosis (MS). Objective: To study some predictors, mechanisms and outcome of MR immediately and 3 months after percutaneous valvuloplasty (PMV) by the Inoue technique for mitral stenosis.Subjects and method: 43 patients with MS were followed up for 3 months after PMV by the Inoue technique in the Viet Nam National Heart Institute at Bach Mai Hospital between Jan 2007 to Oct 2007. Results: Uneven mitral leaflets and calcium commissures with Padial\u2019s criteria scoring over 10 was a significant predicator of influence of severe MR after PMV.According to Wilkins\u2019 score, only the calcium commissures affected the MR after PMV (p<0.05). Conclusion: Patients with aortic regurgitation and/or mild MR who\u2019s Wilkins\u2019 scores less than 8 and Padial's scores less than 10 had not be influenced by severe MR after PMV.
Mitral stenosis ; Percutaneous valvuloplasty (PMV)

Objective: To examine the in vitro and in vivo anti-inflammatory effects of the alkaloid enriched extract (ELA) from the roots of Eurycoma longifolia. Methods: The in vitro antiinflammatory effects of ELA were evaluated by examining its inhibitory activities against nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) expressions in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. The level of NO produced in the culture media was determined by Griess method. The iNOS and COX-2 protein expressions were analyzed by Western blot. The in vivo effect of ELA was evaluated on LPS-induced septic shock in mice model. Mice mortality was monitored for 5 days after injection of LPS. The chemical contents of the ELA were determined by using various chromatographic and spectroscopic techniques. Results: The ELA was found to exhibit a significant anti-inflammatory effect in both in vitro and in vivo models. The results demonstrated that ELA dose-dependently inhibited LPS-induced NO production as well as the protein iNOS and COX-2 expressions. In the septic shock model, ELA dose-dependently protected mice from LPS-induced mortality. Further study on the isolated components of ELA indicated that 9,10-dimethoxycanthin-6-one may contribute significantly to the anti-inflammatory effects of the extract. Conclusions: These results suggest that ELA exhibits the anti-inflammatory activity via suppression of pro-inflammatory mediators such as NO, iNOS, and COX-2 and protects mice from LPS-induced mortality in septic shock model.