Increased pulmonary blood volume variation in patients with heart failure compared to healthy controls: a noninvasive, quantitative measure of heart failure.

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). Patients displayed higher PBVV than controls (58 ± 14 vs. 43 ± 7%, < 0.001). The change in PBVV could be explained by left ventricular (LV) longitudinal contribution to SV ( = 0.15, = 0.02) and the phase shift between in- and outflow ( = 0.31, < 0.001) in patients. Both variables contributed to the multiple regression analysis model and predicted PBVV ( = 0.38); however, the phase shift alone explained ~30% of the variation in PBVV. No correlation was found between PBVV and large vessel area. In conclusion, PBVV was higher in patients compared with controls. Approximately 40% of the variation of PBVV 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 compared with right-heart catheterization. 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.