P5476Right ventricular - pulmonary vascular interaction predicts left ventricular remodelling after CRT: A prospective pressure volume loop study

Abstract

Objectives: The aim of the present study was to evaluate of the predictive value of baseline intrinsic right ventricular (RV) function and corresponding RV ‐ pulmonary artery (PA) coupling for the reverse left ventricular remodelling response after cardiac resynchronization therapy. Although large studies of cardiac resynchronization therapy (CRT) suggest consistent beneficial effects, results at an individual level are variable. CRT non‐responder rates of only 30‐50% using echocardiographic indices of reverse remodelling have been reported. RV dysfunction has been associated with adverse clinical outcomes in patients with systolic heart failure. However, the influence of baseline RV function and RV‐PA coupling on LV‐ CRT response has not been well described. Methods: One hundred fifteen patients, assigned to CRT, were enrolled in this prospective trial. At baseline, the RV volumes, the intrinsic load‐independent contractility of the RV, load‐dependent contraction performance and RV interaction with the pulmonary vascular tree was evaluated using a combined echocardiographic and invasive pressure‐volume loop catheter approach. A reverse left ventricular remodelling process (CRT response) was defined by the hard echocardiographic endpoint of a left ventricular end‐systolic volume (LVESV) decrease >15% after 6 months of CRT therapy. Results: The percentage decrease of LVESV in the CRT response group (n=56, 55%) was 29.1±12.7% vs. 4.5±5.4% (n=45, 45%, p<0.0001) in the non‐response group. Responders improved their NYHA class from 2.7 + 0.4 to 1.8 + 0.5 (p<0.001) vs. non‐responders from 2.9 + 0.3 to 2.4 + 0.8 (p<0.001) after 6‐ month CRT. At baseline, the echocardiographic responders markedly differed having a smaller RV size, lower extent of tricuspid regurgitation, a higher ejection fraction, and a lower total RV afterload (Ea), mainly driven by a lower pulmonary artery compliance and pulmonary vascular resistance (PVR). This resulted in a significant better RV‐PA coupling (Single‐Beat (SB)‐Ees/Ea) compared to non‐responders. After multivariate adjustment for hemodynamic, clinical, and echocardiographic variables, only the RV‐PA coupling ratio (SB‐Ees/Ea) (OR 14.37; 1.359‐151.99, p=0.027) and the baseline creatinine (OR 0.98; 0.965‐ 0.994, p=0.006), and the QRS duration (OR 1.044; 1.019‐1.071, p=0.001) predicted the echocardiographic response. In multivariate linear regression analysis only the baseline degree of mitral valve regurgitation was able to influence independently the ratio of RV‐PA coupling in addition to the RV intrinsic contractility (Ees) and its total afterload (Ea). Conclusions: Our data demonstrate that baseline right ventricular‐pulmonary artery coupling ratio (Ees/Ea) is an independent predictor of left ventricular reverse remodelling after 6‐month CRT.