Observational studyPhysiological reports2025
Increased contractility affects left ventricular kinetic energy in pulmonary hypertension.
Observational study in Physiological reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- CMR-derived left ventricular pressure-volume loops enhance individualized assessment of disease severity and prognosis in pulmonary arterial hypertension in adults.Physiological reports · 2026Article
- Increased contractility affects left ventricular kinetic energy in pulmonary hypertension.Physiological reports · 2025Observational
- Closure of atrial septal defect normalizes left and right ventricular hemodynamic forces in children and adolescents.Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic ResonanceArticle
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Precapillary pulmonary hypertension (PH) is characterized by increased pulmonary vascular resistance (PVR), with progressively altered right (RV) and left ventricular (LV) hemodynamics and function. Kinetic energy (KE) from 4D flow cardiovascular magnetic resonance (CMR) is a measure of intracardiac hemodynamics. In this observational case-control study, we investigate physiological mechanisms influencing RV-KE and LV-KE in PH. Twenty PH patients and 12 healthy controls underwent CMR including cine images and 4D flow. LV contractility was derived from noninvasive pressure-volume loops, and PVR from right heart catheterization. RV-KE and LV-KE were computed for systole, early and late diastolic filling, and indexed to stroke volume (SV). Systolic RV-KE did not differ between patients and controls. In patients, systolic RV-KE was associated with RV-SV but not with PVR, suggesting that the RV may still be able to compensate for the increased afterload. Systolic LV-KE indexed to LV-SV, LV contractility, and heart rate were all higher in patients than controls, suggesting sympathetic upregulation as a possible driving mechanism behind increased systolic LV-KE. LV contractility was negatively associated with systolic LV-KE and LV-SV. Late filling KE was increased in both ventricles in patients, suggesting an enhanced importance of the atrial kick to the filling of both ventricles.
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