Pulmonary artery pressure response to percutaneous mitral valvuloplasty: Associated factors and clinical implications

Abstract

Background: Pulmonary hypertension (PH) is a marker of poor outcome in mitral stenosis (MS), which improves after percutaneous mitral valvuloplasty (PMV). However, mechanical interventions for relief of valve obstruction often but not always reduce pulmonary pressures. This study aimed to assess the parameters associated with abnormal pulmonary artery pressure (PAP) response immediately after a successful PMV, and also its impact on long-term outcome.Methods: A total of 181 patients undergoing PMV for rheumatic MS were prospectively enrolled. Invasive hemodynamic and echocardiographic measures were examined in all patients. Abnormal PAP response was defined as the mean PAP (mPAP) values unchanged at the end of the procedure. Long-term outcome was a composite endpoint of death, mitral valve replacement, repeat PMV, new onset of atrial fibrillation (AF), or stroke. Results:The mean age was 44.1 ± 12.6 years, and 157 patients were women (86.7%). In the overall population, mPAP decreased from 33.4 ± 13.1 mmHg pre to 27.6 ± 9.8 mmHg post (p < 0.001). Following PMV, 52 patients (28.7%) did not have any reduction of mPAP immediately after the PMV. Multivariable analysis adjusting for baseline values of PAP and mitral valve area revealed that AF (Odds ratio[OR] 2.7, 95% [confidence interval] CI 1.3 to 6.7), maximum mitral valve leaflets displacement (OR 0.8, 95% CI 0.7 to 0.9), and post-procedural left ventricular compliance (OR 0.7, 95% CI 0.5 to 0.9) were predictors of a lack of improvement in mPAP.During a median follow-up of 4.4 years, the endpoint was reached in 56 patients (31%). The pulmonary pressure response to PMV was not an independent predictor of long-term events.

The 40th Anniversary of Percutaneous Balloon Valvuloplasty for Mitral Stenosis: Current Status

“…Our data, albeit in relatively young patients with ideal valve anatomy, has shown near-complete reversibility of elevated pulmonary artery pressures and pulmonary vascular resistance regardless of how high the baseline values 49 ; in older patients with chronic PHT, the data have been less convincing, likely because of irreversible changes in the pulmonary vasculature. 50 The LV dysfunction seen in some 30% of MS patients is likely secondary to altered hemodynamic load rather than primary myocardial involvement from RHD 51 ; although inconsistent, there is some evidence of left ventricular remodeling after successful PBMV, with improved global and regional LV function. 52 Reviews of trends in the United States 53 as well as in Europe 54 over the past several decades correlate with a continuing decline in patients undergoing PBMV.…”