Right ventricle in acute and chronic pulmonary embolism (2013 Grover Conference series)

Abstract

Venous thromboembolism (VTE) encompasses deep-vein thrombosis and pulmonary embolism (PE). It is the third-most-frequent cardiovascular disease, with an overall annual incidence of 1-2 per 1,000 population. Chronic thromboembolic pulmonary hypertension (CTEPH) is regarded as a late sequela of PE, with a reported incidence varying between 0.1% and 9.1% of those surviving acute VTE. Right ventricular (RV) function is dependent on afterload. The most precise technique to describe RV function is invasive assessment of the RV-to-pulmonary vascular coupling. However, assessments of RV afterload (i.e., steady and pulsatile flow components and their product, the RC-time) may be useful hemodynamic surrogates of coupling. RV load is different in acute and chronic PE. In acute PE, more than 60% occlusion of the cross-sectional area of the pulmonary artery within a short period of time leads to abrupt hemodynamic collapse. If the time of occlusion is limited to ∼15 seconds, significant decreases in fractional area change, tricuspid annulus systolic excursion, and RV free-wall deformation (strain) occur, with the latter showing significant postsystolic shortening. These changes have similarities to ischemic stunning, and they recover within minutes. In CTEPH, studies of pulmonary vascular resistance (PVR) and pulmonary arterial compliance demonstrated low RC-times that were further lowered after pulmonary endarterectomy (PEA). Immediate postoperative PVR was the only predictor of long-term survival/freedom from lung transplantation, suggesting that the effect of PEA on opening vascular territories to flow outweighs its effect on proximal stiffness. This review summarizes the current knowledge on vascular and intrinsic RV adaptation to VTE, including CTEPH, and the role of imaging.

Keywords: hemodynamics; pulmonary embolism; pulmonary heart disease; right ventricle.

Figure 1

Prediction of right ventricular–to–pulmonary vascular (RV-PV) coupling by the single-beat method. Left, maximal ventricular pressure (P_max) as encountered in an isovolumetric nonejecting beat, which is estimated by fitting a sinus wave over a right ventricular pressure (P_RV) curve during the isovolumetric contraction-and-relaxation phase. P_PA: pulmonary artery pressure. Right, end-systolic ventricular elastance (E_es) can be derived from P_max by dividing the difference between P_max and mean pulmonary artery pressure (mPAP) by the stroke volume (SV). Arterial elastance (E_a) can be estimated as mPAP/SV. Adapted from Trip et al.

Figure 2

Quadrants summarizing vectors that depict changes in both pulmonary vascular resistance (PVR) and pulmonary arterial compliance (C_PA) between catheterizations at baseline and immediately after pulmonary endarterectomy, to discriminate “PVR and C_PA responders” from “PVR and C_PA nonresponders.” All patients’ vectors with persistent/recurrent pulmonary hypertension in the upper-left quadrant are localized within the circled area (representing cases with only a minor improvement in C_PA and PVR). Hemodynamic changes that are associated with improved survival are all within the green quadrant.