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Increased pulmonary blood volume variation in patients with heart failure compared to healthy controls: a noninvasive, quantitative measure of heart failure
Author(s) -
Mariam AlMashat,
Jonas Jögi,
Marcus Carlsson,
Rasmus Borgquist,
Ellen Ostenfeld,
Martin Magnusson,
Erasmus Bachus,
Göran Rådegran,
Håkan Arheden,
Mikael Kanski
Publication year - 2019
Publication title -
journal of applied physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.253
H-Index - 229
eISSN - 8750-7587
pISSN - 1522-1601
DOI - 10.1152/japplphysiol.00507.2019
Subject(s) - cardiology , stroke volume , medicine , heart failure , pulmonary artery , blood flow , magnetic resonance imaging , blood volume , hemodynamics , nuclear medicine , ejection fraction , radiology
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 whether PBVV differs in patients with heart failure compared with 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 (PBVV SV ). Patients displayed higher PBVV SV than controls (58 ± 14 vs. 43 ± 7%, P < 0.001). The change in PBVV SV could be explained by left ventricular (LV) longitudinal contribution to SV ( R 2  = 0.15, P = 0.02) and the phase shift between in- and outflow ( R 2  = 0.31, P < 0.001) in patients. Both variables contributed to the multiple regression analysis model and predicted PBVV SV ( R 2  = 0.38); however, the phase shift alone explained ~30% of the variation in PBVV SV . No correlation was found between PBVV SV and large vessel area. In conclusion, PBVV SV was higher in patients compared with controls. Approximately 40% of the variation of PBVV SV 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 a small vessel level. Future studies are needed to show the clinical added value of PBVV SV compared with right-heart catheterization. NEW & NOTEWORTHY This study shows that the pulmonary blood volume variation indexed to the stroke volume is higher in patients with heart failure compared with controls. The mechanisms behind this are lack of systolic suction from the left ventricular atrioventricular plane descent and increased phase shift between the in- and outflow to the pulmonary circulation (~40%), where the phase shift alone accounts for ~30%. The remaining variation (60–70%) is suggested to occur on a small vessel level.

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