FIGURE 4.

Schematic demonstration of changes in tissue, fiber, and myocyte-level RV biomechanical properties at different stages of PAH. The adaptation/maladaptation stages in this figure are defined based on the time-course of changes in organ-level hemodynamics (maintained/reduced cardiac output, ejection fraction, RV-PA coupling). The RV initially responds to elevated afterload in PAH via hypertrophy (increased myocyte cross-sectional area) and increased myocyte contractile forces (maximum Ca²⁺ activated tension), which results in increased organ-level contractility (E_es). This is accompanied by myofiber stiffening (increased passive stiffness) and capillary rarefaction, leading to RV fibrosis. Passive myocyte mechanical properties, cross-sectional area and RV free wall capillary density remain relatively constant at later stages of PAH. The RV undergoes fiber reorientation with further progression of PAH, which is accompanied by impaired myocyte-level contractility and reduced ejection fraction and RV-PA coupling efficiency. RV: Right ventricle; PAH: Pulmonary arterial hypertension; PA: Pulmonary artery.