Background

The purpose of this study was to quantify right (RV) and left (LV) ventricular function, pulmonary artery flow (QP), tricuspid valve regurgitation velocity (TRV), and aorta flow (QS) from a single 4D flow cardiovascular magnetic resonance (CMR) (time-resolved three-directionally motion encoded CMR) sequence in a canine model of acute thromboembolic pulmonary hypertension (PH).

Methods

Acute PH was induced in six female beagles by microbead injection into the right atrium. Pulmonary arterial (PAP) and pulmonary capillary wedge (PCWP) pressures and cardiac output (CO) were measured by right heart catheterization (RHC) at baseline and following induction of acute PH. Pulmonary vascular resistance (PVRRHC) was calculated from RHC values of PAP, PCWP and CO (PVRRHC = (PAP-PCWP)/CO). Cardiac magnetic resonance (CMR) was performed on a 3 T scanner at baseline and following induction of acute PH. RV and LV end-diastolic (EDV) and end-systolic (ESV) volumes were determined from both CINE balanced steady-state free precession (bSSFP) and 4D flow CMR magnitude images. QP, TRV, and QS were determined from manually placed cutplanes in the 4D flow CMR flow-sensitive images in the main (MPA), right (RPA), and left (LPA) pulmonary arteries, the tricuspid valve (TRV), and aorta respectively. MPA, RPA, and LPA flow was also measured using two-dimensional flow-sensitive (2D flow) CMR.

Results

Biases between 4D flow CMR and bSSFP were 0.8 mL and 1.6 mL for RV EDV and RV ESV, respectively, and 0.8 mL and 4 mL for LV EDV and LV ESV, respectively. Flow in the MPA, RPA, and LPA did not change after induction of acute PAH (p = 0.42-0.81). MPA, RPA, and LPA flow determined with 4D flow CMR was significantly lower than with 2D flow (p < 0.05). The correlation between QP/TRV and PVRRHC was 0.95. The average QP/QS was 0.96 ± 0.11.

Conclusions

Using both magnitude and flow-sensitive data from a single 4D flow CMR acquisition permits simultaneous quantification of cardiac function and cardiopulmonary hemodynamic parameters important in the assessment of PH.

Cardiovascular disease is the leading cause of death worldwide. Many cardiovascular diseases are better diagnosed during a cardiac stress test. Current approaches include either exercise or pharmacological stress echocardiography and pharmacological stress magnetic resonance imaging (MRI). MRI is the most accurate noninvasive method of assessing cardiac function. Currently there are very few exercise devices that allow collection of cardiovascular MRI data during exercise. We developed a low-cost exercise device that utilizes adjustable weight resistance and is compatible with magnetic resonance (MR) imaging. It is equipped with electronics that measure power output. Our device allows subjects to exercise with a leg-stepping motion while their torso is in the MR imager. The device is easy to mount on the MRI table and can be adjusted for different body sizes. Pilot tests were conducted with 5 healthy subjects (3 male and 2 female, 29.2 ± 3.9 yr old) showing significant exercise-induced changes in heart rate (+42%), cardiac output (+40%) and mean pulmonary artery (PA) flow (+%49) post exercise. These data demonstrate that our MR compatible stepper exercise device successfully generated a hemodynamically stressed state while allowing for high quality imaging. The adjustable weight resistance allows exercise stress testing of subjects with variable exercise capacities. This low-cost device has the potential to be used in a variety of pathologies that require a cardiac stress test for diagnosis and assessment of disease progression.

Purpose

To compare pulmonary artery flow using Cartesian and radially sampled four-dimensional flow-sensitive (4D flow) MRI at two institutions.

Methods

Nineteen healthy subjects and 17 pulmonary arterial hypertension (PAH) subjects underwent a Cartesian 4D flow acquisition (institution 1) or a three-dimensional radial acquisition (institution 2). The diameter, peak systolic velocity (Vmax), peak flow (Qmax), stroke volume (SV), and wall shear stress (WSS) were computed in two-dimensional analysis planes at the main, right, and left pulmonary artery. Interobserver variability, interinstitutional differences, flow continuity, and the hemodynamic measurements in healthy and PAH subjects were assessed.

Results

Vmax, Qmax, SV, and WSS at all locations were significantly lower (P < 0.05) in PAH compared with healthy subjects. The limits of agreement were 0.16 m/s, 2.4 L/min, 10 mL, and 0.31 N/m(2) for Vmax, Qmax, SV, and WSS, respectively. Differences between Qmax and SV using Cartesian and radial sequences were not significant. Plane placement and acquisition exhibited isolated, site-based differences between Vmax and WSS.

Conclusions

4D flow MRI was used to detect differences in pulmonary artery hemodynamics for PAH subjects. Flow and WSS in healthy and PAH subject cohorts were similar between Cartesian- and radial-based 4D flow MRI acquisitions with minimal interobserver variability.

A low relative area change (RAC) of the proximal pulmonary artery (PA) over the cardiac cycle is a good predictor of mortality from right ventricular failure in patients with pulmonary hypertension (PH). The relationship between RAC and local mechanical properties of arteries, which are known to stiffen in acute and chronic PH, is not clear, however. In this study, we estimated elastic moduli of three PAs (MPA, LPA and RPA: main, left and right PAs) at the physiological state using mechanical testing data and correlated these estimated elastic moduli to RAC measured in vivo with both phase-contrast magnetic resonance imaging (PC-MRI) and M-mode echocardiography (on RPA only). We did so using data from a canine model of acute PH due to embolization to assess the sensitivity of RAC to changes in elastic modulus in the absence of chronic PH-induced arterial remodeling. We found that elastic modulus increased with embolization-induced PH, presumably a consequence of increased collagen engagement, which corresponds well to decreased RAC. Furthermore, RAC was inversely related to elastic modulus. Finally, we found MRI and echocardiography yielded comparable estimates of RAC. We conclude that RAC of proximal PAs can be obtained from either MRI or echocardiography and a change in RAC indicates a change in elastic modulus of proximal PAs detectable even in the absence of chronic PH-induced arterial remodeling. The correlation between RAC and elastic modulus of proximal PAs may be useful for prognoses and to monitor the effects of therapeutic interventions in patients with PH.