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Increased contractility affects left ventricular kinetic energy in pulmonary hypertension

Bergström, E. LU orcid ; Pola, K. LU ; Kjellström, B. LU ; Töger, J. LU orcid ; Arvidsson, P. M. LU ; Carlsson, M. LU ; Rådegran, G. LU ; Arheden, H. LU and Ostenfeld, E. LU orcid (2025) In Physiological Reports 13(17).
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).... (More)

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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author
; ; ; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
4D flow, cardiac hemodynamics, contractility, kinetic energy, pulmonary hypertension
in
Physiological Reports
volume
13
issue
17
article number
e70563
publisher
John Wiley & Sons Inc.
external identifiers
  • scopus:105015895117
  • pmid:40939108
ISSN
2051-817X
DOI
10.14814/phy2.70563
language
English
LU publication?
yes
id
4d98ae7a-87a3-4283-ad19-fcf1def59dea
date added to LUP
2025-10-15 15:26:11
date last changed
2025-10-16 03:00:08
@article{4d98ae7a-87a3-4283-ad19-fcf1def59dea,
  abstract     = {{<p>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.</p>}},
  author       = {{Bergström, E. and Pola, K. and Kjellström, B. and Töger, J. and Arvidsson, P. M. and Carlsson, M. and Rådegran, G. and Arheden, H. and Ostenfeld, E.}},
  issn         = {{2051-817X}},
  keywords     = {{4D flow; cardiac hemodynamics; contractility; kinetic energy; pulmonary hypertension}},
  language     = {{eng}},
  number       = {{17}},
  publisher    = {{John Wiley & Sons Inc.}},
  series       = {{Physiological Reports}},
  title        = {{Increased contractility affects left ventricular kinetic energy in pulmonary hypertension}},
  url          = {{http://dx.doi.org/10.14814/phy2.70563}},
  doi          = {{10.14814/phy2.70563}},
  volume       = {{13}},
  year         = {{2025}},
}