Abstract
Atherosclerotic prone-rupture plaque is mainly localized in the region of the entrance to the stenosis with high shear stress and the reasons are largely unknown. Our hypothesis is that such a distribution of cells in atherosclerotic plaque may depend on the angiogenesis. Silastic collars induced regions of high shear stress (20.68 ± 5.27 dynes/cm2) in the upstream flow and low shear stress (12.25 ± 1.28 dynes/cm2) in the downstream flow in carotid arteries. Compared with the low shear stress region, plaques in the high shear stress region showed more intraplaque haemorrhaging, less collagen and higher apoptotic rates of vascular smooth muscle cells; endothelial cells (ECs) in the high shear stress region were characterized with integrity and high endothelial nitric oxide synthase (eNOS) expression (1570.3 ± 345.5% vs 172.9 ± 49.9%). The number of intraplaque microvessels is very high in the high shear stress region (15 ± 1.8 n/mm2 vs 3.5 ± 0.4 n/mm2), and the microvessels in the plaque show ECs were abnormal, with membrane blebs, intracytoplasmic vacuoles and leukocyte infiltration. Our current study reveals that the integrity of the endothelium and the vulnerability of atherosclerotic plaques are simultaneously localized in high shear stress regions, and we provide evidence for the first time that microvessels in the intraplaque maybe responsible for rupture-prone plaque formation in the high shear stress region.
Highlights
Coronary artery diseases such as acute coronary syndromes (ACS), are the leading cause of death worldwide [1, 2]
High shear stress is well known to be endothelium-protective and the endothelium cells may obstruct the low-density lipoprotein(LDL)from entering into the vessel wall, and oxidized low-density lipoprotein (ox-LDL) is mainly accumulated within the downstream region
When the atherosclerotic plaques intrude into the lumen of artery, the shear stress in the area surrounding the plaque changes substantially and the upstream region becomes the region of high shear stress [13]
Summary
Coronary artery diseases such as acute coronary syndromes (ACS), are the leading cause of death worldwide [1, 2]. Ruptureprone plaques are characterized by their specific morphology and composition: a large lipid core separated from the vessel lumen by a thin fibrous cap and inflammation with higher macrophages counts [4]. It is well-known that local shear stress plays an essential role in plaque formation, progression and rupture. High shear stress is well known to be endothelium-protective and the endothelium cells may obstruct the low-density lipoprotein(LDL)from entering into the vessel wall, and ox-LDL is mainly accumulated within the downstream region
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
