Vulnerable Plaque, Characteristics, Detection, and Potential Therapies

Hafiane, Anouar

doi:10.3390/jcdd6030026

Cited by 79 publications

(56 citation statements)

References 200 publications

(264 reference statements)

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“…This was clearly shown by increased necrotic core area and regression of fibrous and fibrofatty areas. [13][14][15] These findings are supported by previous studies that showed high WSS as a contributor to plaque rupture in coronary and carotid arteries. [36][37][38][39] Similarly, a randomized clinical trial with 3 years follow-up showed that high WSS could predict myocardial infarction in stable CAD.…”

Section: Discussionsupporting

confidence: 86%

High Coronary Wall Shear Stress Worsens Plaque Vulnerability: A Systematic Review and Meta-Analysis

2021

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Aim: The aim of this meta-analysis is to assess the impact of wall shear stress (WSS) severity on arterial plaque vulnerability. Methods: We systematically searched electronic databases and selected studies which assessed the relationship between WSS measured by intravascular ultrasound and coronary artery plaque features. In 7 studies, a total of 615 patients with 28 276 arterial segments (median follow-up: 7.71 months) were identified. At follow-up, the pooled analysis showed high WSS to be associated with regression of plaque fibrous area, weighted mean difference (WMD) −0.11 (95% CI: −0.20 to −0.02, P = .02) and fibrofatty area, WMD −0.09 (95% CI: −0.17 to −0.01, P = .02), reduction in plaque total area, WMD −0.09 (95% CI: −0.14 to −0.04, P = .007) and increased necrotic core area, and WMD 0.04 (95% CI: 0.01-0.09, P = .03) compared with low WSS. Dense calcium deposits remained unchanged in high and low WSS (0.01 vs 0.02 mm2; P > .05). High WSS resulted in profound remodeling (40% vs 18%, P < .05) and with more constructive remodeling than low WSS (78% vs 40%, P < .01). Conclusions: High WSS in coronary arteries is associated with worsening plaque vulnerability and more profound arterial wall remodeling compared with low WSS.

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Section: Discussionsupporting

confidence: 86%

High Coronary Wall Shear Stress Worsens Plaque Vulnerability: A Systematic Review and Meta-Analysis

2021

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“…An elevated low-density lipoprotein (LDL) levels are an important predictor in the diagnosis of atherosclerosis. 2 The oxidation of LDL is the primary event that takes place in atherosclerosis. Studies have found that serum uric acid (UA) levels are directly proportional to the levels of triglycerides (TG), total cholesterol (TC), and LDLs.…”

Section: Introductionmentioning

confidence: 99%

“…The incidence of atherosclerosis occurs regardless of sex and ethnicity. An elevated low‐density lipoprotein (LDL) levels are an important predictor in the diagnosis of atherosclerosis 2 . The oxidation of LDL is the primary event that takes place in atherosclerosis.…”

Section: Introductionmentioning

confidence: 99%

Harnessing hyperuricemia to atherosclerosis and understanding its mechanistic dependence

Jayachandran

2020

Medicinal Research Reviews

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Atherosclerosis is regarded as the disease of the arterial vasculature. The main characteristics of atherosclerosis are the abnormal accumulation of lipids, increased inflammatory cells, matrix deposits, and proliferation of smooth muscle cells. Diabetes mellitus, obesity, and hyperlipidemia are the most studied risk factors of atherosclerosis. One least studied risk factor is the uric acid (UA), a high UA in circulation is interlinked with many pathological processes. Several epidemiological studies suggest elevated UA levels as an essential biomarker in the forecast of several cardiovascular diseases. Available evidence claims that UA upholds the atherosclerosis process via disturbing lipid metabolism, reducing the nitric oxide synthesis in endothelial cells, promoting the proliferation of vascular smooth muscle cells, and overwhelms inflammation. In endothelial dysfunction and coronary artery lesions, UA is considered as an independent predictor. The updated studies on the involvement of hyperuricemia in atherosclerosis prove that treatment with xanthine oxidase (XO) inhibitors not just benefits the treatment of hyperuricemia but also reduces the burden of atherosclerosis to a greater extent. In this review, we highlight how the hyperuricemia affects vascular integrity, causes atherosclerosis, and the mechanism of action of XO inhibitors on atherosclerosis.

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“…Third, correlation coefficients are effect sizes, so in real terms, we do not need a p-value to interpret them. Finally, currently various techniques and biomarkers (e.g., biochemical, genetic, imaging) have been proposed to assess the characteristics of atherosclerotic plaques (e.g., to identify vulnerable plaques) [47]. Among imaging biomarkers for vulnerable plaques, echography/virtual histology, computed tomography, spectroscopy, optical coherence tomography, high-frequency intravascular ultrasound and magnetic resonance imaging were described [47].…”

Section: Strengths and Limitationsmentioning

confidence: 99%

“…Finally, currently various techniques and biomarkers (e.g., biochemical, genetic, imaging) have been proposed to assess the characteristics of atherosclerotic plaques (e.g., to identify vulnerable plaques) [47]. Among imaging biomarkers for vulnerable plaques, echography/virtual histology, computed tomography, spectroscopy, optical coherence tomography, high-frequency intravascular ultrasound and magnetic resonance imaging were described [47]. In our work we opted for using B-Mode echography/virtual histology, since (a) we worked with peripheral plaques (non-coronary), and (b) we proposed to consider selecting a non-invasive and innocuous technique widely used in clinical practice [27,28].…”

Section: Strengths and Limitationsmentioning

confidence: 99%

Carotid and Femoral Atherosclerotic Plaques in Asymptomatic and Non-Treated Subjects: Cardiovascular Risk Factors, 10-Years Risk Scores, and Lipid Ratios’ Capability to Detect Plaque Presence, Burden, Fibro-Lipid Composition and Geometry

Marin

Bia

Zócalo

2020

JCDD

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Carotid and/or femoral atherosclerotic plaques (AP) assessment through imaging studies is an interesting strategy for improving individual cardiovascular risk (CVR) stratification and cardiovascular disease (CVD) and/or events prediction. There is no consensus on who would benefit from image screening aimed at determining AP presence, burden, and characteristics. Aims: (1) to identify, in asymptomatic and non-treated subjects, demographic factors, anthropometric characteristics and cardiovascular risk factors (CRFs), individually or grouped (e.g., CVR equations, pro-atherogenic lipid ratios) associated with carotid and femoral AP presence, burden, geometry, and fibro-lipid content; (2) to identify cut-off values to be used when considering the variables as indicators of increased probability of AP presence, elevated atherosclerotic burden, and/or lipid content, in a selection scheme for subsequent image screening. Methods: CRFs exposure and clinical data were obtained (n = 581; n = 144 with AP; 47% females). Arterial (e.g., ultrasonography) and hemodynamic (central [cBP] and peripheral blood pressure; oscillometry/applanation tonometry) data were obtained. Carotid and femoral AP presence, burden (e.g., AP number, involved territories), geometric (area, width, height) and fibro-lipid content (semi-automatic, virtual histology analysis, grayscale analysis and color mapping) were assessed. Lipid profile was obtained. Lipid ratios (Total cholesterol/HDL-cholesterol, LDL-cholesterol/HDL-cholesterol, LogTryglicerides(TG)/HDL-cholesterol) and eight 10-years [y.]/CVR scores were quantified (e.g., Framingham Risk Scores [FRS] for CVD). Results: Age, 10-y./CVR and cBP showed the highest levels of association with AP presence and burden. Individually, classical CRFs and lipid ratios showed almost no association with AP presence. 10-y./CVR levels, age and cBP enabled detecting AP with large surfaces (˃p75th). Lipid ratios showed the largest association with AP fibro-lipid content. Ultrasound evaluation could be considered in asymptomatic and non-treated subjects aiming at population screening of AP (e.g., ˃ 45 y.; 10-y./FRS-CVD ˃ 5–8%); identifying subjects with high atherosclerotic burden (e.g., ˃50 y., 10-y./FRS-CVD ˃ 13–15%) and/or with plaques with high lipid content (e.g., LogTG/HDL ˃ 0.135).

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Vulnerable Plaque, Characteristics, Detection, and Potential Therapies

Cited by 79 publications

References 200 publications

High Coronary Wall Shear Stress Worsens Plaque Vulnerability: A Systematic Review and Meta-Analysis

High Coronary Wall Shear Stress Worsens Plaque Vulnerability: A Systematic Review and Meta-Analysis

Harnessing hyperuricemia to atherosclerosis and understanding its mechanistic dependence

Carotid and Femoral Atherosclerotic Plaques in Asymptomatic and Non-Treated Subjects: Cardiovascular Risk Factors, 10-Years Risk Scores, and Lipid Ratios’ Capability to Detect Plaque Presence, Burden, Fibro-Lipid Composition and Geometry

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