Abstract

Background. Prognostic importance of pulmonary hypertension (PH) in patients with heart failure is well known, but its reversibility after restrictive mitral annuloplasty (RMA) is less well established. We assessed the potential reversibility of pulmonary vascular remodeling in relation to plasma B-type natriuretic peptide (BNP), a biomarker of left ventricular (LV) filling pressure and diastolic dysfunction, over time after RMA. Methods. We studied 98 patients with moderate to severe PH [systolic pulmonary artery pressure (SPAP) >40 mmHg] who underwent RMA for ischemic cardiomyopathy (ejection fraction <40%) and functional mitral regurgitation, and were followed up at least 12 months (mean, 49±26 months). Cardiac catheterization (baseline, 1month) and serial assessments of Doppler-derived SPAP (d-SPAP) and LV end-systolic dimension (ESD), with blood samples for plasma BNP measurement were performed. Results. At 1 month after RMA, pulmonary capillary wedge pressure (PCWP) and SPAP decreased from 22±7 to 16±6 mmHg and from 50±13 to 40±11 mmHg (p<0.0001 for both), respectively, while transpulmonary gradient (mean PAP minus PCWP) did not change (11±4 mmHg, p=0.56). Cardiac index increased from 2.5±0.6 to 2.7±0.6 l/min/m2 (p= 0.03), and pulmonary vascular resistance changed from 231±100 to 206±73 dynes sec cm-5 (p=0.03), suggesting partial reversibility of pulmonary vascular remodeling. Serial echocardiography showed that s d-SPAP changed from 55±14 at baseline to 37±11 at 1 month, to 40±14 at 1 year, and to 45±19 mmHg at 2 year (p<0.0001). LVESD decreased from 56±8 to 49±9, 48±10, and 48±10 mm, respectively (p<0.0001). Plasma BNP decreased from 741±372 to 283±234, 223±199, and 237±208 pg/ml, respectively (p<0.0001). The percent change from baseline to 1 month and 1 year in BNP were significantly associated with corresponding changes in the d-SPAP (r=0.314, p=0.009 and r=0.391, p=0.006, respectively). Conclusion. Following RMA, PA pressures commonly and significantly decreased, with a modest reverse pulmonary vascular remodeling in most patients after 2 years follow-up. Progression of pulmonary vascular abnormality may be a potential therapeutic target to reduce the prevalence of subsequent right ventricular dysfunction after RMA.

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