Local Hemodynamic Forces After Stenting

Abstract

Local hemodynamic forces are well-known to modulate atherosclerotic evolution, which remains one of the largest cause of death worldwide. Percutaneous coronary interventions with stent implantation restores blood flow to the downstream myocardium and is only limited by stent failure caused by restenosis, stent thrombosis, or neoatherosclerosis. Cumulative evidence has shown that local hemodynamic forces affect restenosis and the platelet activation process, modulating the pathophysiological mechanisms that lead to stent failure. This article first covers the pathophysiological mechanisms through which wall shear stress regulates arterial disease formation/neointima proliferation and the role of shear rate on stent thrombosis. Subsequently, the article reviews the current evidence on (1) the implications of stent design on the local hemodynamic forces, and (2) how stent/scaffold expansion can influence local flow, thereby affecting the risk of adverse events.

Characteristics of Wall Shear Stress and Pressure of Intracranial Atherosclerosis Analyzed by a Computational Fluid Dynamics Model: A Pilot Study

“…Furthermore, the scatterplots also show the inter-subject variability, indicating the fact that the hemodynamic damage of ICAS was partly determined by percent stenosis, as proved by previous studies on coronary heart disease (24,25). Other factors may also involve, such as the presence of collaterals and the plaque characteristics (26).…”

The impact of plaque type on strut embedment/protrusion and shear stress distribution in bioresorbable scaffold

“…Despite breathtaking advances in stent/scaffold designs over the last decades, restenosis and stent/scaffold thrombosis continue to be the 'Achilles heel' of the percutaneous coronary intervention (PCI). 5 PCI outcomes depend on several factors including implantation techniques, treated vessel segment features, particularly plaque characteristics and the design properties of the stent/scaffold. While the normal vessel wall is incompressible, the diseased vessel wall, including atherosclerotic plaque, is compressible and exhibits viscoelasticity while subjected to a pressure load.…”

“…These disrupted flow areas yield low wall shear stress (WSS) triggering various pathobiological reactions in platelets and endothelial layer of the vessel wall that may result in excessive neointimal hyperplasia. 5 The histomorphometric properties of the treated vessel segments, in particularly the underlying atherosclerotic plaque properties determine strut apposition and penetration status. 6 In the present study, we investigated the strut embedment/protrusion patterns in different plaque types treated with BRS and its effect on the local WSS distribution in treated segments.…”

Screening of biopolymeric materials for cardiovascular surgery toxicity—Evaluation of their surface relief with assessment of morphological aspects of monocyte/macrophage polarization in atherosclerosis patients

“…At the histological level an atherosclerotic plaque consists of a) MN-MPh and lipid-loaded foam cells, originating from the MN-MPh; b) actively proliferating smooth muscle cells; c) lymphocytes; d) developed extracellular matrix with lipid inclusions, and e) a vascular network, developed to a different degree [[34], [35], [36]].…”