Persistent Pulmonary Hypertension After Percutaneous Mitral Commissurotomy

Predictors of Persistent Pulmonary Hypertension After Percutaneous Mitral Commissurotomy and Its Impact on Clinical Outcomes

To identify clinical, echocardiographic, and hemodynamic parameters which can predict persistent PH after PMC, and also to determine the impact of persistent PH on the clinical outcomes.

Pure mitral Stenosis develops in approximately 40% of all patients with rheumatic heart disease, and is frequently complicated by Pulmonary hypertension (PH). Pulmonary hypertension influences symptomatology and long-term prognosis. Percutaneous Mitral Commissurotomy (PMC), was first described in 1984, has good results and is performed by antegrade access to the mitral valve through trans-septal puncture by one of various techniques (e.g. Inuoe, and multitrack system). Pulmonary artery pressures (PAP) decrease following PMC. The improvement in pulmonary hypertension after PMC is explained by the improvement in the mitral valve area and subsequent decompression of left atrium (LA) and pulmonary venous beds. Even though there have been studies showing excellent results following PMC in all grades of PH, nonregression of PH following PMC is not uncommon. The component of PAP contributed by the passive transmission of the elevated LA pressure regresses immediately after a successful PMC proportional to the reduction in transmitral gradient. The PH contributed by pulmonary arteriolar constriction slowly comes down over weeks or a few months, But a "fixed" component due to pulmonary vascular disease usually persists.

Inclusion Criteria:

• Severe mitral stenosis (mitral valve area ≤1.5cm).
• Significant dyspnea.
• Favorable anatomical characteristics for PMC as assessed by transthoracic echocardiography

Exclusion Criteria:

• Significant mitral regurgitation (≥ grade II/IV). Bilateral commissural calcification.
• Presence of other lesions which need open heart surgery.
• Wilkins' score > 12.
• Persistent LA thrombus despite adequate anticoagulation.
• End stage renal or liver disease.
• Patients with severe COPD and other chest problems that might be complicated by pulmonary hypertension per se.