Key result
Coronary stent malapposition alters blood viscosity and wall shear stress, potentially promoting atherosclerosis.
Why the study?
Does incomplete stent apposition in tapered coronary arteries alter microrecirculation, wall shear stress, and blood viscosity?
Does incomplete stent apposition in tapered coronary arteries alter microrecirculation, wall shear stress, and blood viscosity?
Computational fluid dynamics demonstrate that incomplete stent apposition in tapered coronary arteries creates microrecirculations and alters wall shear stress and blood viscosity, providing a physical mechanism for tissue accumulation and stent thrombosis.
One particular complexity of coronary artery is the natural tapering of the vessel with proximal segments having larger caliber and distal tapering as the vessel get smaller. The natural tapering of a coronary artery often leads to proximal incomplete stent apposition (ISA). ISA alters coronary hemodynamics and creates pathological path to develop complications such as in-stent restenosis, and more worryingly, stent thrombosis (ST). By employing state-of-the-art computer-aided design software, generic stent hoops were virtually deployed in an idealized tapered coronary artery with decreasing malapposition distance. Pulsatile blood flow simulations were carried out using computational fluid dynamics (CFD) on these computer-aided design models. CFD results reveal unprecedented details in both spatial and temporal development of microrecirculation environments throughout the cardiac cycle (CC). Arterial tapering also introduces secondary microrecirculation. These primary and secondary microrecirculations provoke significant fluctuations in arterial wall shear stress (WSS). There has been a direct correlation with changes in WSS and the development of atherosclerosis. Further, the presence of these microrecirculations influence strongly on the local levels of blood viscosity in the vicinity of the malapposed stent struts. The observation of secondary microrecirculations and changes in blood rheology is believed to complement the wall (-based) shear stress, perhaps providing additional physical explanations for tissue accumulation near ISA detected from high resolution optical coherence tomography (OCT).
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Poon et al. (2018) studied this question. Coronary stent malapposition significantly alters blood viscosity and induces microrecirculation, influencing wall shear stress and potentially promoting atherosclerosis.
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