Abstract
ABSTRACT Right ventricular (RV) intrinsic contractility and its response to afterload defined as pulmonary arterial (PA) elastance, is referred to as RV-PA coupling. RV contractility can be estimated by end-systolic elastance (Ees), the slope of the line through the end-systolic pressure-volume point. Afterload or arterial elastance (Ea) can be estimated from RV end-systolic pressure divided by stroke volume. A ratio of Ees/Ea of 1.5-2 reflects an optimal balance between RV mechanical work and oxygen consumption. In left-sided heart failure (HF), chronically elevated left‐sided filling pressures result in secondary pulmonary hypertension (PH). In the early stages of PH, RV contractility and load are adequately coupled through mainly RV hypertrophy, but as the disease advances, ventricular dilatation and failure takes place. The degree of RV coupling (or lack thereof) to the pulmonary circulation can be measured either invasively or through noninvasive imaging. Several non-invasive surrogate indexes for Ees and Ea have been associated with decreased functional status and mortality in patients with HF and valvular disease. Abbreviations: RV: Right ventricle; LV: Left ventricle; CMR: Cardiac magnetic resonance; Ees: End-systolic elastance; Ea: Arterial elastance; PVR: Pulmonary vascular resistance; PH: Pulmonary hypertension; TAPSE: Tricuspid annular plane systolic excursion; TR: Tricuspid regurgitation; SPAP; RV systolic pulmonary artery pressure; RVLS: RV free wall longitudinal strain; TAVR: Transcatheter aortic valve replacement; HF: Heart failure; HFpEF: Heart failure with persevered ejection fraction; HFrEF: Heart failure with reduced ejection fraction; AS=aortic stenosis.
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