Three-Dimensional Echocardiography for the Assessment of Right Ventriculo-Arterial Coupling.

ABSTRACT

BACKGROUND: The analysis of right ventriculo-arterial coupling (RVAC) from pressure-volume loops is not routinely performed. RVAC may be approached by the combination of right heart catheterization (RHC) pressure data and cardiac magnetic resonance (CMR)-derived right ventricular (RV) volumetric data. RV pressure and volume measurements by Doppler and three-dimensional echocardiography (3DE) allows another way to approach RVAC. METHODS: Ninety patients suspected of having pulmonary hypertension underwent RHC, 3DE, and CMR (RHC mean pulmonary artery pressure [mPAP] 37.9 ± 11.3 mm Hg; range, 15-66 mm Hg). Three-dimensional (3D) echocardiography was performed in 30 normal patients (echocardiographic mPAP 18.4 ± 3.1 mm Hg). Pulmonary artery (PA) effective elastance (Ea), RV maximal end-systolic elastance (Emax), and RVAC (PA Ea/RV Emax) were calculated from RHC combined with CMR and from 3DE using simplified formulas including mPAP, stroke volume, and end-systolic volume. RESULTS: Three-dimensional echocardiographic and RHC-CMR measures for PA Ea (3DE, 1.27 ± 0.94; RHC-CMR, 0.71 ± 0.52; r = 0.806, P < .001), RV Emax (3DE, 0.72 ± 0.37; RHC-CMR, 0.38 ± 0.19; r = 0.798, P < .001), and RVAC (3DE, 2.01 ± 1.28; RHC-CMR, 2.32 ± 1.77; r = 0.826, P < .001) were well correlated despite a systematic overestimation of 3DE elastance parameters. Among the whole population, 3D echocardiographic PA Ea and 3D echocardiographic RVAC but not 3D echocardiographic RV Emax were significantly lower in patients with mPAP < 25 mm Hg (n = 41) than in others (n = 79). Among the 90 patients who underwent RHC, 3D echocardiographic PA Ea and 3D echocardiographic RVAC but not 3D echocardiographic RV Emax increased significantly with increasing levels of pulmonary vascular resistance. CONCLUSIONS: Three-dimensional echocardiography-derived PA Ea, RV Emax, and RVAC correlated well with the reference RHC-CMR measurements. Ea and RVAC but not Emax were significantly different between patients with different levels of afterload, suggesting failure of the right ventricle to maintain coupling in severe pulmonary hypertension.