Abstract

Mitral regurgitation represents a volume load on the left ventricle leading to congestion and symptoms of heart failure. The aim of this study was to characterize early hemodynamic adaptions after percutaneous mitral valve (MV) repair. Forty-six consecutive patients with symptomatic high-grade MV insufficiency (mean age, 72years; 54% men) were prospectively included in the study and examined before and after successful catheter-based clip implantation. Seventy percent of patients had secondary mitral regurgitation. Noninvasive pressure-volume loops were reconstructed from echocardiography with simultaneous blood pressure measurements. MV repair reduced left ventricular end-diastolic volume index from 87±41 to 80±40mL/m(2) (P<.0001). End-systolic volume index was 55±37mL/m(2) before versus 54±37mL/m(2) after repair (P=.52). Hence, total stroke volume decreased from 60±23 to 49±16mL (P<.0001), as did total ejection fraction (from 41±14% to 37±13%, P=.002) and global longitudinal strain (from -11±4.9% to -9.1±4.4%, P=.0001). Forward stroke volume, forward ejection fraction, and forward cardiac output remained constant (43±12mL vs 42±11mL, 33±17% vs 35±18%, and 3.2±0.9L/min vs 3.4±0.8L/min, respectively). Parameters of left ventricular contractility (end-systolic elastance and peak power index) and measurements of afterload (arterial elastance, end-systolic wall stress, and total peripheral resistance) were similar before and after MV repair. Forward ejectionfraction correlated more strongly with end-systolic elastance (r=0.61, P<.0001) than did total ejection fraction (r=0.35, P=.0007) or global longitudinal strain (r=-0.38, P=.0002). Total mechanical energy (pressure-volume area) decreased from10,903±4,410 to 9,124±2,968mmHg×mL (P=.0007) because of reduced stroke work (5,546±2,241mmHg×mL vs 4,414±1,412mmHg×mL, P<.0001). At 3months, symptom statushad improved (76% of patients in New York Heart Association classes I and II), and 97% of patients had mitral regurgitation grade ≤2+. Left ventricular contractility and forward cardiac output remained unchanged after percutaneous MV repair despite decreases in total ejection fraction and global longitudinal strain. The left ventricle was unloaded through reduced end-diastolic volume. Thus, MV repair is associated with an improved hemodynamic state in noninvasive pressure-volume analysis.

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