Carotid Endarterectomy Plaques: Correlations of Clinical and Anatomic Findings

Avril, G; Batt, Michel; Guidoin, Robert; Marois, M; Hassen-Khodja, Réda; Daune, B; Gagliardi, J M; Bas, Pierre

doi:10.1007/bf02021778

Cited by 75 publications

(43 citation statements)

References 12 publications

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“…This confirms previous findings [28,29], that atheromatous plaques are at higher risk of rupture than fibrous caps.…”

Section: Acknowledgementssupporting

confidence: 92%

The Effect of Carotid Plaque Morphology on Longitudinal Fibrous Cap Stress Levels

Thrysøe¹,

Stegmann²,

Eldrup³

et al. 2012

WJM

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Background and Purpose: Rupture of vulnerable carotid atherosclerotic plaques is a major cause of stroke. Stress levels may reflect risk of rupture in patients with carotid atherosclerotic plaques. Features thought to influence the risk of plaque rupture include the degree of stenosis, lipid-rich necrotic core (LR-NC) size, and thickness of the protective fibrous caps. We used computational models to investigate the effect of these variables on fibrous cap stress levels. Methods: Two-way coupled fluid-structure interaction longitudinal 2D simulations were performed on a bifurcation model based on idealized geometry derived from a symptomatic patient. Models with varying degrees of stenosis (50% -95%), fibrous cap thicknesses (0.05 -1 mm), and LR-NC sizes (2 × 1 mm -6 × 3 mm) were simulated. The stress distribution for each model was calculated and peak principal stresses extracted. Regression analysis was used for assessing the relationship between the variables and stress levels. Results: Mechanical stresses increased with decreasing fibrous cap thicknesses (ß = -0.905, p < 0.001) and increasing LR-NC sizes (ß = 0.262, p < 0.001). The degree of stenosis (ß = 0.024, p = 0.344) and LR-NC placement (ß = -0.001, p = 0.979) had insignificant effects on mechanical stress levels. Conclusions: Thin-capped plaques with large atheromas, known predictors of plaque vulnerability, were shown to exhibit the greatest mechanical stress levels.

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“…This confirms previous findings [28,29], that atheromatous plaques are at higher risk of rupture than fibrous caps.…”

Section: Acknowledgementssupporting

confidence: 92%

The Effect of Carotid Plaque Morphology on Longitudinal Fibrous Cap Stress Levels

Thrysøe¹,

Stegmann²,

Eldrup³

et al. 2012

WJM

View full text Add to dashboard Cite

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“…The strongest associations were found in studies during the 1980s. 7,13,66,67 Data from the mid-1990s and onward emerged on the beneficial effects of statins in the prevention of coronary heart disease. 79 Because cholesterol-lowering therapy might reduce risks of ischemic heart disease as well as extracranial and intracranial atherosclerosis, studies were accordingly dichotomized at 1995.…”

Section: Discussionmentioning

confidence: 99%

Correlation Between Carotid Intraplaque Hemorrhage and Clinical Symptoms

Gao

Chen

Bao

et al. 2007

Stroke

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Background and Purpose-We sought to investigate the association between carotid intraplaque hemorrhage (IPH) and ipsilateral symptoms of cerebral ischemia. Methods-A search was performed for clinical observational studies comparing the incidence of IPH between symptomatic and asymptomatic patients. Odds ratios (ORs) for IPH as a factor in the pathogenesis of neurologic events were calculated and combined by a meta-analysis. Interstudy heterogeneity, estimated effects, and methodologic quality of the studies were assessed. Results-Thirty-one studies were included for analysis. The reported ORs varied widely. Overall, the incidence of IPH in the symptomatic groups was significantly higher than in the asymptomatic group. However, there was an apparent trend for heterogeneity (PϽ0.00001) between studies. The random-effects summary estimator of ORs was 2.25 (95% CI, 1.57 to 3.22; PϽ0.00001). To identify potential sources of heterogeneity, subgroup analyses were performed. The pooled ORs varied greatly by stratification. Major heterogeneity was found among studies with low quality, microscopic methods of examination, significant effects, small sizes, early publication, and unequal severity of carotid stenosis in both groups. Large, recent, macroscopic, or high-quality studies, as well as studies with equal degrees of stenosis, tended to yield insignificant associations. The methods in defining and evaluating hemorrhage were very heterogeneous. Characterizations of the age, size, number, and location of hemorrhages were poorly reported and highly variable. In addition, a lack of control of confounders and selection bias were frequently identified among studies. Conclusions-Statistical inferences have suggested a plausible role in the production of cerebral ischemia; however, reliable interpretation was strongly undermined by poor methodologic quality, substantial heterogeneity, and suspicious publication bias. To preciously estimate the underlying correlation, a well-designed study with uniformity in definition and evaluation for IPH might be warranted.

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“…6 As the atherosclerotic lesion grows, this leads to formation of the so-called fibrous cap encapsulating the lipid-laden plaque core. 51 Asymptomatic carotid plaques are more commonly morphologically so-called fibrous "hard" plaques, whereas symptomatic plaques are more commonly lipid-laden "soft" plaques, 52,53 although this view has been disputed. 54 However, it is believed that the formation of a fibrous "cap" in human carotid arteries may be associated with increased intimal expression of adhesion molecules, 55 may protect the plaque from rupturing and in situ thrombosis, and perhaps may also inhibit inflammatory cell fluxes.…”

Section: Continuous Inflammation In Matured Atherosclerotic Plaquesmentioning

confidence: 99%

Inflammation and Infections as Risk Factors for Ischemic Stroke

Lindsberg

Grau

2003

Stroke

458

312

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Background-Inflammatory processes have fundamental roles in stroke in both the etiology of ischemic cerebrovascular disease and the pathophysiology of cerebral ischemia. We summarize clinical data on infection and inflammation as risk or trigger factors for human stroke and investigate current evidence for the hypothesis of a functional interrelation between traditional risk factors, genetic predisposition, and infection/inflammation in stroke pathogenesis. Summary of Review-Several traditional vascular risk factors are associated with proinflammatory alterations, including leukocyte activation, and predispose cerebral vasculature to thrombogenesis on inflammatory stimulation. Furthermore, accumulation of inflammatory cells, mainly monocytes/macrophages, within the vascular wall starts early during atherogenesis. During later disease stages, their activation can lead to plaque rupture and thrombus formation, increasing stroke risk. Inflammatory markers (eg, leukocytes, fibrinogen, C-reactive protein) are independent predictors of ischemic stroke. Chronic infections (eg, infection with Chlamydia pneumoniae or Helicobacter pylori) were found to increase the risk of stroke; however, study results are at variance, residual confounding is not excluded, and causality is not established at present. In case-control studies, acute infection within the preceding week was a trigger factor for ischemic stroke. Acute and exacerbating chronic infection may act by activating coagulation and chronic infections and may contribute to atherogenesis. Genetic predisposition of the inflammatory host response may be an important codeterminant for atherogenesis and stroke risk. Conclusions-Inflammation contributes to stroke risk via various interrelated mechanisms. Infectious diseases, traditional risk factors, and genetic susceptibility may cooperate in stimulating inflammatory pathways. Final proof of a causal role of infectious/inflammatory mechanisms in stroke pathogenesis is still lacking and will require interventional studies.

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Carotid Endarterectomy Plaques: Correlations of Clinical and Anatomic Findings

Cited by 75 publications

References 12 publications

The Effect of Carotid Plaque Morphology on Longitudinal Fibrous Cap Stress Levels

The Effect of Carotid Plaque Morphology on Longitudinal Fibrous Cap Stress Levels

Correlation Between Carotid Intraplaque Hemorrhage and Clinical Symptoms

Inflammation and Infections as Risk Factors for Ischemic Stroke

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