High shear stress relates to intraplaque haemorrhage in asymptomatic carotid plaques

Tuenter, Annelies; Selwaness, Mariana; Lorza, Andrés Arias; Schuurbiers, Johan C.H.; Speelman, Lambert; Cibiş, Merih; Lugt, Aad van der; Bruijne, Marleen de; Steen, Antonius F.W. van der; Franco, Oscar H.; Vernooij, Meike W.; Wentzel, Jolanda J.

doi:10.1016/j.atherosclerosis.2016.05.018

Cited by 82 publications

(75 citation statements)

References 42 publications

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“…Previous studies have shown that the intensity of neovasculature within plaques and the blood pressure were associated with carotid IPH. Beyond these risk factors, investigators demonstrated that local mechanical conditions may play important role in the occurrence of carotid IPH . In contrast, the normal vessel wall of intracranial arteries is lacking of vasa vasorum and the local hemodynamics are complex which may be different from the extracranial carotid arteries.…”

Section: Discussionmentioning

confidence: 99%

Association of severity between carotid and intracranial artery atherosclerosis

Yuan

et al. 2018

Ann Clin Transl Neurol

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ObjectiveThis study sought to investigate the relationship of atherosclerosis between intracranial and extracranial carotid arteries using three‐dimensional multicontrast magnetic resonance (MR) vessel wall imaging.MethodsPatients with recent cerebrovascular symptoms in anterior circulation were recruited and underwent MR vessel wall imaging for intracranial and extracranial carotid arteries. The plaque burden, including maximum wall thickness (Max WT) and stenosis, and presence of intraplaque hemorrhage (IPH) were assessed. The correlation of the plaque characteristics between intracranial and extracranial carotid arteries was determined.ResultsIn total, 107 patients (mean age: 57.0 ± 11.1 years, 69 males) were recruited. In discriminating intracranial severe stenosis (≥50% stenosis), the odds ratio (OR) of Max WT of extracranial carotid arteries was 1.41 (95% confidence interval [CI], 0.94–2.11, P = 0.095) and 1.72 (95% CI, 1.04–2.83, P = 0.034) before and after adjusting for confounding factors, respectively. The OR of stenosis of extracranial carotid arteries with increment of 10% was 1.26 (95% CI, 0.99–1.60, P = 0.054) and 1.37 (95% CI, 1.03–1.82, P = 0.033) before and after adjusting for confounding factors, in discriminating intracranial severe stenosis respectively. Receiver operating characteristic analysis revealed that the area under the curve (AUC) of Max WT, stenosis, and IPH of extracranial carotid artery plaques was 0.641, 0.605, and 0.603 in discriminating intracranial severe stenosis, respectively. After adjusting for confounding factors, the AUC of Max WT, stenosis, and presence of IPH in extracranial carotid artery plaques increased to 0.812, 0.817 and 0.781, respectively.InterpretationCarotid artery plaque burden is significantly associated with severe intracranial artery stenosis, suggesting that extracranial carotid plaque burden might be an independent indicator for severity of intracranial artery atherosclerosis.

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Section: Discussionmentioning

confidence: 99%

Association of severity between carotid and intracranial artery atherosclerosis

Yuan

et al. 2018

Ann Clin Transl Neurol

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“…In the carotid circulation, ulceration of carotid plaques, visible on angiography or on pathological examination, was seen most often in regions where WSS was highest [43] and the inflammatory burden was severe [44]. In line with the experimental and autopsy studies, longitudinal and cross-sectional human coronary and carotid studies have shown an increase in plaque necrotic core, calcium [35], and strain [45], development of expansive remodeling [35,46], presence of IPH [47], large necrotic core [34,46,48], a necrotic core in contact with the lumen [48], and napkin-ring sign [46] in areas exposed to high WSS. Meanwhile, some data show that WSS might not have the same role in development of plaque erosion as it has in the development of plaque rupture [9,10].…”

Section: High Wall Shear Stressmentioning

confidence: 97%

“…High WSS at baseline was associated with subsequent ulceration at follow-up imaging. The relationship between WSS and IPH was further explored in a relatively large cross-sectional study in 93 carotid arteries of 74 asymptomatic participants from the Rotterdam Study who underwent magnetic resonance imaging for CFD simulations and plaque composition assessment [47]. The investigators found a relationship between higher maximum WSS and the presence of IPH and calcification, independent of plaque thickness, age, and sex.…”

Section: High Wss and Individual Characteristics Of High-risk Plaquementioning

confidence: 99%

High wall shear stress and high-risk plaque: an emerging concept

Eshtehardi

Brown

Bhargava

et al. 2017

Int J Cardiovasc Imaging

106

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In recent years, there has been a significant effort to identify high-risk plaques in vivo prior to acute events. While number of imaging modalities have been developed to identify morphologic characteristics of high-risk plaques, prospective natural-history observational studies suggest that vulnerability is not solely dependent on plaque morphology and likely involves additional contributing mechanisms. High wall shear stress (WSS) has recently been proposed as one possible causative factor, promoting the development of high-risk plaques. High WSS has been shown to induce specific changes in endothelial cell behavior, exacerbating inflammation and stimulating progression of the atherosclerotic lipid core. In line with experimental and autopsy studies, several human studies have shown associations between high WSS and known morphological features of high-risk plaques. However, despite increasing evidence, there is still no longitudinal data linking high WSS to clinical events. As the interplay between atherosclerotic plaque, artery, and WSS is highly dynamic, large natural history studies of atherosclerosis that include WSS measurements are now warranted. This review will summarize the available clinical evidence on high WSS as a possible etiological mechanism underlying high-risk plaque development.

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“…At the shoulder area, however, stresses increase considerably attributed to blood incompressibility. Thus, not only are ROS production and inflammation stimulated in the underlying tissue (as a result of high, rather than low, stresses in this area), but an abrupt transition between mildly and highly stressed areas occurs, favoring plaque rupture and neovessel formation and rupture . Similarly, at the downstream shoulder, flow turbulence leads to decrease of transmural pressure attributed to vortex‐formation–related energy dissipation, mirroring the events of the upstream region.…”

Section: On the Genesis Of Atherosclerotic Plaquementioning

confidence: 99%