Pulmonary blood volume measured by cardiovascular magnetic resonance: influence of pulmonary transit time methods and left atrial volume

Background Increased pulmonary blood volume (PBV) is a measure of congestion and is associated with an increased risk of cardiovascular events. PBV can be quantified using cardiovascular magnetic resonance (CMR) imaging as the product of cardiac output and pulmonary transit time (PTT), the latter measured from the contrast time-intensity curves in the right and left side of the heart from first-pass perfusion (FPP). Several methods of estimating PTT exist, including pulmonary transit beats (PTB), peak-to-peak, and center of gravity (CoG). The aim of this study was to determine the accuracy and precision for these methods of quantifying the PBV, taking the left atrium volume (LAV) into consideration. Methods Fifty-eight participants (64 ± 11 years, 24 women) underwent 1.5 T CMR. PTT was quantified from (1) a basal left ventricular short-axis image (FPP), and (2) the reference method with a separate contrast administration using an image intersecting the pulmonary artery (PA) and the LA (CoG(PA-LA)). Results Compared to the reference, PBV for (a) PTB(FPP) was 14 ± 17% larger, (b) peak-peak(FPP) was 17 ± 16% larger, and (c) CoG(FPP) was 18 ± 10% larger. Subtraction of the LAV (available for n = 50) decreased overall differences to − 1 ± 19%, 2 ± 18%, and 3 ± 12% for PTB(FPP), peak-peak(FPP), and CoG(FPP), respectively. Lowest interobserver variability was seen for CoG(FPP) (− 2 ± 7%). Conclusions CoG(PA-LA) and FPP methods measured the same PBV only when adjusting for the LAV, since FPP inherently quantifies a volume consisting of PBV + LAV. CoG(FPP) had the best precision and lowest interobserver variability among the FPP methods of measuring PBV. Graphical abstract

Pulmonary blood volume estimation in mice by magnetic particle imaging and magnetic resonance imaging

This methodical work describes the measurement and calculation of pulmonary blood volume in mice based on two imaging techniques namely by using magnetic particle imaging (MPI) and cardiac magnetic resonance imaging (MRI). Besides its feasibility aspects that may influence quantitative analysis are studied. Eight FVB mice underwent cardiac MRI to determine stroke volumes and anatomic MRI as morphological reference for functional MPI data. Arrival time analyses of boli of 1 µl of 1 M superparamagnetic tracer were performed by MPI. Pulmonary transit time of the bolus was determined by measurements in the right and left ventricles. Pulmonary blood volume was calculated out of stroke volume, pulmonary transit time and RR-interval length including a maximal error analysis. Cardiac stroke volume was 31.7 µl ± 2.3 µl with an ejection fraction of 71% ± 6%. A sharp contrast bolus profile was observed by MPI allowing subdividing the first pass into three distinct phases: tracer arrival in the right ventricle, pulmonary vasculature, and left ventricle. The bolus full width at half maximum was 578 ms ± 144 ms in the right ventricle and 1042 ms ± 150 ms in the left ventricle. Analysis of pulmonary transit time revealed 745 ms ± 81 ms. Mean RR-interval length was 133 ms ± 12 ms. Pulmonary blood volume resulted in 177 µl ± 27 µl with a mean maximal error limit of 27 µl. Non-invasive assessment of the pulmonary blood volume in mice was feasible. This technique can be of specific value for evaluation of pulmonary hemodynamics in mouse models of cardiac dysfunction or pulmonary disease. Pulmonary blood volume can complement cardiac functional parameters as a further hemodynamic parameter.

Functional respiratory imaging identifies redistribution of pulmonary blood flow in patients with COVID-19

An increasing observation is that some patients with COVID-19 have normal lung compliance but significant hypoxaemia different from typical acute respiratory distress syndrome (ARDS). We hypothesised that changes in pulmonary blood distribution may be partially responsible and used functional respiratory imaging on CT scans to calculate pulmonary blood volume. We found that patients with COVID-19 had significantly reduced blood volume in the smaller calibre blood vessels (here defined as <5 mm2 cross-sectional area) compared with matched ARDS patients and healthy controls. This suggests that using high levels of PEEP may not alone be enough to oxygenate these patients and that additional management strategies may be needed.

Assessment of small pulmonary blood vessels in COVID-19 patients using HRCT

BackgroundMounting evidence supports the role of pulmonary hemodynamic alternations in the pathogenesis of COVID-19. Previous studies have demonstrated that changes in pulmonary blood volumes measured on CT are associated with histopathological markers of pulmonary vascular pruning, suggesting that quantitative HRCT analysis may eventually be useful in the assessment pulmonary vascular dysfunction more broadly.MethodsBuilding upon previous work, automated HRCT measures of small blood vessel volume and pulmonary vascular density were developed. Scans from 103 COVID-19 patients and 108 healthy volunteers were analyzed and their results compared, with comparisons made both on lobar and global levels.ResultsCompared to healthy volunteers, COVID-19 patients showed significant reduction in BV5 (pulmonary blood volume contained in blood vessels of <5 mm2) expressed as BV5/(Total pulmonary blood volume) (p<0.0001), and significant increases in BV5_10 and BV 10 (pulmonary blood volumes contained in vessels between 5 and 10 mm2 and above 10 mm2, respectively) (p<0.0001). These changes were consistent across lobes.ConclusionsCOVID-19 patients display striking anomalies in the distribution of blood volume within the pulmonary vascular tree, consistent with increased pulmonary vasculature resistance in the pulmonary vessels below the resolution of HRCT.

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 (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 ~30% of the variation in PBVVSV. No correlation was found between PBVVSV and large vessel area. In conclusion, PBVVSV was higher in patients compared with 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 a small vessel level. Future studies are needed to show the clinical added value of PBVVSV 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.