Sensitivity of coronary hemodynamics to vascular structure variations in health and disease

Abstract

Local hemodynamics play an essential role in the initiation and progression of coronary artery disease. While vascular geometry alters local hemodynamics, the relationship between vascular structure and hemodynamics is poorly understood. Previous computational fluid dynamics (CFD) studies have explored how anatomy influences plaque-promoting hemodynamics. For example, areas exposed to low wall shear stress (ALWSS) can indicate regions of plaque growth. However, small sample sizes, idealized geometries, and simplified boundary conditions have limited their scope. We generated 230 synthetic models of left coronary arteries and simulated coronary hemodynamics with physiologically realistic boundary conditions. We measured the sensitivity of hemodynamic metrics to changes in bifurcation angles, positions, diameter ratios, tortuosity, and plaque topology. Our results suggest that the diameter ratio between left coronary branches plays a substantial role in generating adverse hemodynamic phenotypes and can amplify the effect of other geometric features such as bifurcation position and angle, and vessel tortuosity. Introducing mild plaque in the models did not change correlations between structure and hemodynamics. However, certain vascular structures can induce ALWSS at the trailing edge of the plaque. Our analysis demonstrates that coronary artery vascular structure can provide key insight into the hemodynamic environments conducive to plaque formation and growth.

Fig. 1

(a) Baseline LCA structure. The diagram of the LCA is from a lateral, or looking towards the myocardium, view. (b) Histograms of average population distributions for the segment lengths, angles, and diameters varied in this study. Most features were referenced from Medrano-Gracia et al.. Patient-specific models from the Vascular Model Repository were used to estimate anatomical characteristics not established in the literature, such as left main branch segment lengths. Terminal branch lengths were kept constant in all models.

Fig. 2

Automated computational pipeline to generate models, meshes, and simulation files, perform simulations, and extract hemodynamic metrics. Geometric changes imposed on the baseline LCA were defined by a numerical description of the geometric parameters considered: diameters (), lengths() angles (), tortuosity (), and plaque (). Specialized coronary LPNs were coupled to the 3D geometry flow outlets () and a coronary inflow waveform was prescribed at the inlet (I). Dirichlet no-slip conditions were applied on , and a parabolic inlet velocity profile was prescribed on .

Fig. 3

Sensitivity of ALWSS at the LAD/LCx bifurcation to bifurcation position and angle in (a) healthy and (b) diseased models at a neutral LAD/LCx diameter ratio ( = 0.94). TAWSS contours are observed from a proximal view, as in looking underneath the myocardium. (a) More proximal bifurcation positions increased ALWSS at the LAD/LCx bifurcation. Proximal bifurcation positions consistently induced ALWSS for small (case 1) and large (case 2) angles in the proximal LAD. (b) ALWSS at the LAD/LCx bifuraction in models with proximal LCx plaque. Trends observed in the healthy model are conserved, except for a significant reduction in ALWSS in the proximal LCx. ALWSS measured in the LAD did not significantly differ between healthy and diseased models, as shown by comparing cases 1 and 3, as well as cases 2 and 4. Case 5 is referred to in Fig. 7.

Fig. 4

Sensitivity of ALWSS at the LAD/LCx bifurcation to varying diameter ratio in healthy male and female models. The same trends were observed in both sexes, with the skewed LAD and LCx dominance increasing ALWSS. ALWSS was maximized in the proximal LAD for geometries with the largest LCx and smallest LAD diameter (cases 2 and 4). Similarly, dominant LAD models with the largest LAD and smallest LCx diameter (cases 1 and 3) led to a ALWSS formation exclusively in the proximal LCx.

Fig. 5

Sensitivity of ALWSS at the LAD/LCx bifurcation to varying LAD/LCx bifurcation angle and position in LAD dominant (=0.65) and in LCx dominant (=1.40) (a) healthy and (b) diseased models. (a) LCx dominant models had greater ALWSS than the LAD dominant ones (p < 0.001). Large bifurcation angles led to the largest ALWSS magnitude in LCx dominant models (case 3). However, the LAD dominant cases exhibited the opposite behavior (case 1); smaller angles increased ALWSS at the bifurcation (cases 2 and 6). Changing the bifurcation position only moderately changed ALWSS. (b) The same trends were observed in both the healthy and diseased models. However, ALWSS at the LAD/LCx bifurcation was significantly lower in the diseased cases.

Fig. 6

Sensitivity of ALWSS at the LAD/LCx bifurcation to tortuosity and branch dominance. With LAD dominant models, ALWSS increased at the LAD/LCx bifurcation with both LAD and LCx tortuosity (case 2). In the LCx dominant models, weaker trends were observed between tortuosity and ALWSS.

Fig. 7

Time-averaged streamlines colored by velocity magnitude for various geometries from Figs. 3 and 6. At the same bifurcation position (2.2 cm), changes in bifurcation angle and diameter ratio induced different flow patterns. The effect of the bifurcation on the local flow is more pronounced in LCx dominant models.

Fig. 8

Sensitivity of ALWSS at the LAD/LCx bifurcation to varying diameter ratio in diseased models. Compared to its healthy counterpart, ALWSS in the proximal LCx is reduced when compared to healthy geometries due to the presence of plaque (case 1). Similarly, ALWSS in the proximal LAD is reduced in comparison to healthy cases due to the presence of proximal LAD plaque (case 2).