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.