Stress analysis using anatomically realistic coronary tree

Abstract

Plaque rupture with superimposed thrombosis is the main cause of the acute coronary syndromes of unstable angina, myocardial infarction, and sudden death. Endothelial disruption leading to plaque rupture may relate to mechanical fatigue associated with cyclic flexion of plaques. A novel method is proposed to assess stress and strain distribution using the finite element (FE) analysis and in vivo patient-specific dynamic 3D coronary arterial tree reconstruction from cine angiographic images. The local stresses were calculated on the diseased arterial wall which was modeled as consisting of a central fibrotic cap subjected to the cyclic flexion from cardiac contraction. Various parameters characterizing the plaque were chosen including vessel diameter, percentage narrowing, and lesion length. According to the FEA simulations, the results show that the smaller vessel diameter, greater percentage narrowing, and/or larger lesion size may result in higher stress on the plaque cap, with the vessel diameter as the dominant factor.

Materials, fluid dynamics, and solid mechanics aspects of coronary artery stents: A state‐of‐the‐art review

“…For both CFD and FEA studies, improved methods for generating (1) geometrically accurate 3D vessel geometry through reconstructions derived from contrast‐enhanced magnetic resonance angiography scans obtained during clinical procedures on patients253 and/or (2) patient‐specific in vivo moving 3D coronary arterial trees from cine angiographic images254 should be utilized. Improved methods for generating geometrically accurate flow domains within a stented region that can then be used in CFD studies should be developed, an example being post‐processing procedures used in conjunction with microfocal X‐ray computed tomography imaging and reconstruction 255…”

Three-dimensional analysis of vulnerable segments in the left anterior descending artery

“…Two more factors may also contribute to plaque rupture and thrombosis at bifurcation sites. A highly localized circumferential wall stress concentration of approximately nine to 14 times the proximal circumferential wall stress occurs at bifurcation sites [28], which, in addition, undergo a larger deformation during cyclic flexion of the coronary artery, yielding a higher circumferential stress than those further to bifurcations [21]. Second, pulsating flow results in oscillatory and vorticity-stream flow patterns at sites of bifurcations with demonstration of backflow in the presence of even minimal atheromatosis [29].…”

“…In addition, our findings indicate that the longer the lesion, the higher the probability of plaque rupture and subsequent thrombosis. In experimental models, it has been demonstrated that the larger lesion length results in higher strain on the plaque cap [21].…”

Ruptured versus stable plaques in human coronary arteries

“…Ruptured coronary plaques Katritsis et al 349 circumferential wall stress concentration of approximately 9-14 times the proximal circumferential wall stress occurs at bifurcation sites [20], which, in addition, undergo a larger deformation during cyclic flexion of the coronary artery, yielding a higher circumferential stress [21]. Second, pulsating flow conditions as those of coronary circulation result in oscillatory and vorticity-stream flow patterns at sites of bifurcations, with demonstration of back flow in the presence of even minimal atheromatosis [22].…”