Left-Ventricular Energetics in Pulmonary Arterial Hypertension-Induced Right-Ventricular Hypertrophic Failure.

摘要: Pulmonary arterial hypertension (PAH) alters the geometries of both ventricles heart. While right ventricle (RV) hypertrophies, left (LV) atrophies. Multiple lines clinical and experimental evidence lead us to hypothesize that impaired stroke volume systolic pressure LV are a direct consequence effect overload in RV, atrophy plays only minor role. In this study, we tested hypothesis by examining mechanoenergetic response atrophied RV hypertrophy rats treated with monocrotaline. Experiments were performed across multiple-scales: whole-heart vivo ex vivo, its trabeculae vitro. Under state where was pressure-overloaded, measured reduced systemic blood ventricular pressure. contrast, under vitro conditions, circumvented, found capable developing normal stress. Nevertheless, played role remained lower, thereby contributing lower mechanical work output. Concomitantly oxygen consumption change enthalpy observed, hence energy efficiency unchanged. Our internally consistent findings between working-heart trabecula experiments explain rapid improvement function observed patients chronic pulmonary following surgical relief overload.