Intraventricular vortex properties in nonischemic dilated cardiomyopathy

Abstract

Vortices may have a role in optimizing the mechanical efficiency and blood mixing of the left ventricle (LV). We aimed to characterize the size, position, circulation, and kinetic energy (KE) of LV main vortex cores in patients with nonischemic dilated cardiomyopathy (NIDCM) and analyze their physiological correlates. We used digital processing of color-Doppler images to study flow evolution in 61 patients with NIDCM and 61 age-matched control subjects. Vortex features showed a characteristic biphasic temporal course during diastole. Because late filling contributed significantly to flow entrainment, vortex KE reached its maximum at the time of the peak A wave, storing 26 ± 20% of total KE delivered by inflow (range: 1-74%). Patients with NIDCM showed larger and stronger vortices than control subjects (circulation: 0.008 ± 0.007 vs. 0.006 ± 0.005 m(2)/s, respectively, P = 0.02; KE: 7 ± 8 vs. 5 ± 5 mJ/m, P = 0.04), even when corrected for LV size. This helped confining the filling jet in the dilated ventricle. The vortex Reynolds number was also higher in the NIDCM group. By multivariate analysis, vortex KE was related to the KE generated by inflow and to chamber short-axis diameter. In 21 patients studied head to head, Doppler measurements of circulation and KE closely correlated with phase-contract magnetic resonance values (intraclass correlation coefficient = 0.82 and 0.76, respectively). Thus, the biphasic nature of filling determines normal vortex physiology. Vortex formation is exaggerated in patients with NIDCM due to chamber remodeling, and enlarged vortices are helpful for ameliorating convective pressure losses and facilitating transport. These findings can be accurately studied using ultrasound.

Keywords: diastolic function; doppler echocardiography; fluid dynamics.

Figures

Fig. 1.

Overview of the methods used for image processing.

Fig. 2.

Geometric reference systems. A: main (Smain) and secondary (Ssec) vortex sections as well as the asymmetric toroidal geometric model used to estimate out-of-plane vortex distribution for the calculation of total vortex energy, overlaid on the two-dimensional (2-D) velocity distributions of a patient with nonischemic dilated cardiomyopathy (NIDCM; see text for details). B: internal moving coordinate system used for the analysis of vortex trajectories along the cardiac cycle. v, flow velocity.

Fig. 3.

A–F: head-by-head comparison between echocardiography and phase-contrast magnetic resonance (PC-MR) for vortex size and position in a patient with NIDCM for early filling (A and D), late filling (B and E), and ejection (C and F) phases. A–C: results of the ultrasound-based 2-D velocity fields. The distributions of flow velocity and longitudinal myocardial strain are overlaid on the raw B-mode tissue images. D–F: time-matched PC-MR frames. The endocardial boundary from the MR is overlaid in white, whereas the endocardial boundary from the ultrasound is overlaid in cyan, normalized for the same long-axis length. Automatically identified vortex structures are overlaid as yellow and cyan for the PC-MR and ultrasound methods, respectively. The secondary vortex structure could only be identified during late filling (B and E). G–K: vortex properties along the cardiac cycle, as measured by ultrasound (blue line) and PC-MR (red squares) in another patient with NIDCM.

Fig. 4.

Mean (solid curves) and SD (light ribbons) values of vortex properties along the cardiac cycle for patients with NIDCM (left) and control subjects (right). Properties are shown for the main and secondary vortex cores (red and blue, respectively). The horizontal axes have been scaled for average times of cardiac events in each population. The number of subjects in which the main (red) and secondary (blue) cores were identified in each phase is shown at the bottom. Qonset, onset of the Q wave; MVC, mitral valve closure; AVO, aortic valve opening; AVC, aortic valve closure; MVO, mitral valve opening; Epeak, peak of the E wave; Aonset, onset of the A wave; Apeak, peak of the A wave; LAx, long axis.

Fig. 5.

Snapshots of 2-D intraventricular flow along the cardiac cycle in a representative NIDCM patient and a control subject. The position and radius of the main vortex core section is indicated by the white circle; the position and radius of the secondary vortex core section is indicated by the green circle.

Fig. 6.

Physiological analysis of vortex energy during diastole in a patient with NIDCM (A, C, and E) and a control subject (B, D, and F). Waveforms are shown for transmitral filling velocity (A and B), the intraventricular pressure difference (C and D), and vortex kinetic energy (E and F). Vertical lines represent mitral valve opening and closing. Notice the impact of late filling flow on vortex kinetic energy.