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Increased pulmonary blood volume variation in patients with heart failure compared to healthy controls; a non-invasive, quantitative measure of heart failure

Al-Mashat, Mariam LU ; Jögi, Jonas LU orcid ; Carlsson, Marcus LU ; Borgquist, Rasmus LU orcid ; Ostenfeld, Ellen LU orcid ; Magnusson, Martin LU orcid ; Bachus, Erasmus LU ; Rådegran, Göran LU ; Arheden, Hakan LU and Kanski, Mikael LU (2020) In Journal of Applied Physiology 128(2). p.324-337
Abstract

Variation of the blood content of the pulmonary vascular bed during a heartbeat can be quantified by pulmonary blood volume variation (PBVV) using magnetic resonance imaging (MRI). The aim was to evaluate if PBVV differs in patients with heart failure compared to healthy controls and investigate the mechanisms behind the PBVV. Forty-six patients and 10 controls underwent MRI. PBVV was calculated from blood flow measurements in the main pulmonary artery and a pulmonary vein, defined as the maximum difference in cumulative PBV over one heartbeat. PBVV was indexed to stroke volume (SV) in the main pulmonary artery (PBVVSV). Patients displayed higher PBVVSV than controls (58±14% vs 43±7%, p<0.001). The change in PBVVSV could be explained... (More)

Variation of the blood content of the pulmonary vascular bed during a heartbeat can be quantified by pulmonary blood volume variation (PBVV) using magnetic resonance imaging (MRI). The aim was to evaluate if PBVV differs in patients with heart failure compared to healthy controls and investigate the mechanisms behind the PBVV. Forty-six patients and 10 controls underwent MRI. PBVV was calculated from blood flow measurements in the main pulmonary artery and a pulmonary vein, defined as the maximum difference in cumulative PBV over one heartbeat. PBVV was indexed to stroke volume (SV) in the main pulmonary artery (PBVVSV). Patients displayed higher PBVVSV than controls (58±14% vs 43±7%, p<0.001). The change in PBVVSV could be explained by left ventricular (LV) longitudinal contribution to SV (R2=0.15, p=0.02) and the phase shift between in- and outflow (R2=0.31, p<0.001) in patients. Both variables contributed to the multiple regression analysis model and predicted PBVVSV (R2=0.38), however, the phase shift alone explained about ~30% of the variation in PBVVSV. No correlation was found between PBVVSV and large vessel area. In conclusion, PBVVSV was higher in patients compared to controls. Approximately 40% of the variation of PBVVSV in patients can be explained by the LV longitudinal contribution to SV and the phase shift between pulmonary in- and outflow, where the phase shift alone accounts for ~30%. The remaining variation, (60-70%), most likely occurs on small vessel level. Future studies are needed to show the clinical added value of PBVVSV compared to right heart catheterization.

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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Applied Physiology
volume
128
issue
2
pages
14 pages
publisher
American Physiological Society
external identifiers
  • pmid:31873068
  • scopus:85079345287
ISSN
1522-1601
DOI
10.1152/japplphysiol.00507.2019
language
English
LU publication?
yes
id
0b88cdcc-e068-47c8-b80b-9164d6d2f967
date added to LUP
2019-12-27 13:58:58
date last changed
2024-03-20 02:24:34
@article{0b88cdcc-e068-47c8-b80b-9164d6d2f967,
  abstract     = {{<p>Variation of the blood content of the pulmonary vascular bed during a heartbeat can be quantified by pulmonary blood volume variation (PBVV) using magnetic resonance imaging (MRI). The aim was to evaluate if PBVV differs in patients with heart failure compared to healthy controls and investigate the mechanisms behind the PBVV. Forty-six patients and 10 controls underwent MRI. PBVV was calculated from blood flow measurements in the main pulmonary artery and a pulmonary vein, defined as the maximum difference in cumulative PBV over one heartbeat. PBVV was indexed to stroke volume (SV) in the main pulmonary artery (PBVVSV). Patients displayed higher PBVVSV than controls (58±14% vs 43±7%, p&lt;0.001). The change in PBVVSV could be explained by left ventricular (LV) longitudinal contribution to SV (R2=0.15, p=0.02) and the phase shift between in- and outflow (R2=0.31, p&lt;0.001) in patients. Both variables contributed to the multiple regression analysis model and predicted PBVVSV (R2=0.38), however, the phase shift alone explained about ~30% of the variation in PBVVSV. No correlation was found between PBVVSV and large vessel area. In conclusion, PBVVSV was higher in patients compared to controls. Approximately 40% of the variation of PBVVSV in patients can be explained by the LV longitudinal contribution to SV and the phase shift between pulmonary in- and outflow, where the phase shift alone accounts for ~30%. The remaining variation, (60-70%), most likely occurs on small vessel level. Future studies are needed to show the clinical added value of PBVVSV compared to right heart catheterization.</p>}},
  author       = {{Al-Mashat, Mariam and Jögi, Jonas and Carlsson, Marcus and Borgquist, Rasmus and Ostenfeld, Ellen and Magnusson, Martin and Bachus, Erasmus and Rådegran, Göran and Arheden, Hakan and Kanski, Mikael}},
  issn         = {{1522-1601}},
  language     = {{eng}},
  month        = {{02}},
  number       = {{2}},
  pages        = {{324--337}},
  publisher    = {{American Physiological Society}},
  series       = {{Journal of Applied Physiology}},
  title        = {{Increased pulmonary blood volume variation in patients with heart failure compared to healthy controls; a non-invasive, quantitative measure of heart failure}},
  url          = {{http://dx.doi.org/10.1152/japplphysiol.00507.2019}},
  doi          = {{10.1152/japplphysiol.00507.2019}},
  volume       = {{128}},
  year         = {{2020}},
}