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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 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.
Highlights
Heart failure (HF) is a clinical syndrome associated with high mortality [26]
The lower right pulmonary vein was used in 32 patients and 4 controls, the upper right pulmonary vein was used in 7 patients and 4 controls, the lower left pulmonary vein was used in 3 patients and 2 controls, and the upper left pulmonary vein was used in 4 patients
There was no significant difference in PBVV indexed to effective stroke volume (PBVVSV) between patients with NYHA class I-II (n ϭ 26) and patients with NYHA class III-IV (n ϭ 10) (56 Ϯ 15 vs. 61 Ϯ 9%, P ϭ 0.15). This is the first study to investigate PBVVSV using magnetic resonance imaging (MRI) in patients with HF and show that PBVVSV was higher in patients with HF compared with healthy controls
Summary
Heart failure (HF) is a clinical syndrome associated with high mortality [26]. A cornerstone feature in HF is that cardiac output can only be maintained at increased filling pressures. The most accurate method to estimate left ventricular (LV) filling pressure is by measuring pulmonary artery wedge pressure from right-heart catheterization [20]. HF has been shown to be associated with alterations in the pulmonary venous flow pattern, related to increased left atrial (LA) and LV filling pressure. This has been shown as decreased pulmonary venous flow during ventricular systole using echocardiography [30] [16]. Several aspects of the pulmonary venous velocity patterns as possible surrogate measures of LA pressure have been suggested: the so-called systolic fraction (%venous flow during systole), the systolic velocity-time integral, and peak systolic-to-peak diastolic ratio [18]. There is a need for a better noninvasive and quantitative method for HF diagnosis
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