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Frontiers in Cardiovascular Medicine 2021Inflammation plays a key role in atherosclerotic plaque destabilization and adverse cardiac remodeling. Recent evidence has shown a promising role of colchicine in...
Inflammation plays a key role in atherosclerotic plaque destabilization and adverse cardiac remodeling. Recent evidence has shown a promising role of colchicine in patients with coronary artery disease. We evaluated the efficacy and safety of colchicine in post-acute myocardial infarction (MI) patients. We searched five electronic databases from inception to January 18, 2021, for randomized controlled trials (RCTs) evaluating colchicine in post-acute MI patients. Primary outcomes were cardiovascular mortality and recurrent MI. Secondary outcomes were all-cause mortality, stroke, urgent coronary revascularization, levels of follow-up high-sensitivity C-reactive protein (hs-CRP), and drug-related adverse events. All meta-analyses used inverse-variance random-effects models. Six RCTs involving 6,005 patients were included. Colchicine did not significantly reduce cardiovascular mortality [risk ratio (RR), 0.91; 95% confidence interval (95% CI), 0.52-1.61; = 0.64], recurrent MI (RR, 0.87; 95% CI, 0.62-1.22; = 0.28), all-cause mortality (RR, 1.06; 95% CI, 0.61-1.85; = 0.78), stroke (RR, 0.28; 95% CI, 0.07-1.09; = 0.05), urgent coronary revascularization (RR, 0.46; 95% CI, 0.02-8.89; = 0.19), or decreased levels of follow-up hs-CRP (mean difference, -1.95 mg/L; 95% CI, -12.88 to 8.98; = 0.61) compared to the control group. There was no increase in any adverse events (RR, 0.97; 95% CI, 0.89-1.07; = 0.34) or gastrointestinal adverse events (RR, 2.49; 95% CI, 0.48-12.99; = 0.20). Subgroup analyses by colchicine dose (0.5 vs. 1 mg/day), time of follow-up (<1 vs. ≥1 year), and treatment duration (≤30 vs. >30 days) showed no changes in the overall findings. In post-acute MI patients, colchicine does not reduce cardiovascular or all-cause mortality, recurrent MI, or other cardiovascular outcomes. Also, colchicine did not increase drug-related adverse events.
PubMed: 34169101
DOI: 10.3389/fcvm.2021.676771 -
Scientific Reports Apr 2021To assess the influence of lipid-lowering therapy on coronary plaque volume, and to identify the LDL and HDL targets for plaque regression to provide a comprehensive... (Meta-Analysis)
Meta-Analysis
To assess the influence of lipid-lowering therapy on coronary plaque volume, and to identify the LDL and HDL targets for plaque regression to provide a comprehensive overview. The databases searched (from inception to 15 July 2020) to identify prospective studies investigating the impact of lipid-lowering therapy on coronary plaque volume and including quantitative measurement of plaque volume by intravascular ultrasound after treatment. Thirty-one studies that included 4997 patients were selected in the final analysis. Patients had significantly lower TAV (SMD: 0.123 mm; 95% CI 0.059, 0.187; P = 0.000) and PAV (SMD: 0.123%; 95% CI 0.035, 0.212; P = 0.006) at follow-up. According to the subgroup analyses, TAV was significantly reduced in the LDL < 80 mg/dL and HDL > 45 mg/dL group (SMD: 0.163 mm; 95% CI 0.092, 0.234; P = 0.000), and PAV was significantly reduced in the LDL < 90 mg/dL and HDL > 45 mg/dL group (SMD: 0.186%; 95% CI 0.081, 0.291; P = 0.001).Thirty-one studies that included 4997 patients were selected in the final analysis. Patients had significantly lower TAV (SMD: 0.123 mm; 95% CI 0.059, 0.187; P = 0.000) and PAV (SMD: 0.123%; 95% CI 0.035, 0.212; P = 0.006) at follow-up. According to the subgroup analyses, TAV was significantly reduced in the LDL < 80 mg/dL and HDL > 45 mg/dL group (SMD: 0.163 mm; 95% CI 0.092, 0.234; P = 0.000), and PAV was significantly reduced in the LDL < 90 mg/dL and HDL > 45 mg/dL group (SMD: 0.186%; 95% CI 0.081, 0.291; P = 0.001). Our meta-analysis suggests that not only should LDL be reduced to a target level of < 80 mg/dL, but HDL should be increased to a target level of > 45 mg/dL to regress coronary plaques.Trial Registration PROSPERO identifier: CRD42019146170.
Topics: Aged; Coronary Artery Disease; Female; Follow-Up Studies; Humans; Hypolipidemic Agents; Male; Middle Aged; Plaque, Atherosclerotic; Regression Analysis
PubMed: 33846492
DOI: 10.1038/s41598-021-87528-w -
Arteriosclerosis, Thrombosis, and... Apr 2021[Figure: see text]. (Meta-Analysis)
Meta-Analysis
[Figure: see text].
Topics: Carotid Arteries; Carotid Stenosis; Coronary Artery Disease; Coronary Stenosis; Coronary Vessels; Humans; Plaque, Atherosclerotic; Prognosis; Risk Assessment; Risk Factors; Severity of Illness Index; Vascular Calcification
PubMed: 33626907
DOI: 10.1161/ATVBAHA.120.315747 -
World Journal of Nuclear Medicine 2020Stroke and other thromboembolic events in the brain are often due to carotid artery atherosclerosis, and atherosclerotic plaques with inflammation are considered... (Review)
Review
Stroke and other thromboembolic events in the brain are often due to carotid artery atherosclerosis, and atherosclerotic plaques with inflammation are considered particularly vulnerable, with an increased risk of becoming symptomatic. Positron emission tomography (PET) with 2-deoxy-2-[Fluorine-18] fluoro-D-glucose (F-FDG) provides valuable metabolic information regarding arteriosclerotic lesions and may be applied for the detection of vulnerable plaque. At present, however, patients are selected for carotid surgical intervention on the basis of the degree of stenosis alone, and not the vulnerability or inflammation of the lesion. During the past decade, research using PET with the glucose analog tracer F-fluor-deoxy-glucose, has been implemented for identifying increased tracer uptake in symptomatic carotid plaques, and tracer uptake has been shown to correlate with plaque inflammation and vulnerability. These findings imply that F-FDG PET might hold the promise for a new and better diagnostic test to identify patients eligible for carotid endarterectomy. The rationale for developing diagnostic tests based on molecular imaging with F-FDG PET, as well as methods for simple clinical PET approaches, are discussed. This is a systematic review, following Preferred Reporting Items for Systematic Reviews guidelines, which interrogated the PUBMED database from January 2001 to November 2019. The search combined the terms, "atherosclerosis," "inflammation," "FDG," and "plaque imaging." The search criteria included all types of studies, with a primary outcome of the degree of arterial vascular inflammation determined by F-FDG uptake. This review examines the role of F-FDG PET imaging in the characterization of atherosclerotic plaques.
PubMed: 33623500
DOI: 10.4103/wjnm.WJNM_26_20 -
High Coronary Wall Shear Stress Worsens Plaque Vulnerability: A Systematic Review and Meta-Analysis.Angiology Sep 2021The aim of this meta-analysis is to assess the impact of wall shear stress (WSS) severity on arterial plaque vulnerability. (Meta-Analysis)
Meta-Analysis
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, = .02) and fibrofatty area, WMD -0.09 (95% CI: -0.17 to -0.01, = .02), reduction in plaque total area, WMD -0.09 (95% CI: -0.14 to -0.04, = .007) and increased necrotic core area, and WMD 0.04 (95% CI: 0.01-0.09, = .03) compared with low WSS. Dense calcium deposits remained unchanged in high and low WSS (0.01 vs 0.02 mm; > .05). High WSS resulted in profound remodeling (40% vs 18%, < .05) and with more constructive remodeling than low WSS (78% vs 40%, < .01).
CONCLUSIONS
High WSS in coronary arteries is associated with worsening plaque vulnerability and more profound arterial wall remodeling compared with low WSS.
Topics: Adult; Aged; Coronary Artery Disease; Coronary Circulation; Coronary Vessels; Female; Hemodynamics; Humans; Male; Middle Aged; Plaque, Atherosclerotic; Prognosis; Risk Assessment; Risk Factors; Rupture, Spontaneous; Stress, Mechanical; Ultrasonography, Interventional; Vascular Remodeling
PubMed: 33535802
DOI: 10.1177/0003319721991722 -
American Journal of Physiology. Heart... Apr 2021Atherosclerosis is a dynamic process starting with endothelial dysfunction and inflammation and eventually leading to life-threatening arterial plaques. Exercise...
Atherosclerosis is a dynamic process starting with endothelial dysfunction and inflammation and eventually leading to life-threatening arterial plaques. Exercise generally improves endothelial function in a dose-dependent manner by altering hemodynamics, specifically by increased arterial pressure, pulsatility, and shear stress. However, athletes who regularly participate in high-intensity training can develop arterial plaques, suggesting alternative mechanisms through which excessive exercise promotes vascular disease. Understanding the mechanisms that drive atherosclerosis in sedentary versus exercise states may lead to novel rehabilitative methods aimed at improving exercise compliance and physical activity. Preclinical tools, including in vitro cell assays, in vivo animal models, and in silico computational methods, broaden our capabilities to study the mechanisms through which exercise impacts atherogenesis, from molecular maladaptation to vascular remodeling. Here, we describe how preclinical research tools have and can be used to study exercise effects on atherosclerosis. We then propose how advanced bioengineering techniques can be used to address gaps in our current understanding of vascular pathophysiology, including integrating in vitro, in vivo, and in silico studies across multiple tissue systems and size scales. Improving our understanding of the antiatherogenic exercise effects will enable engaging, targeted, and individualized exercise recommendations to promote cardiovascular health rather than treating cardiovascular disease that results from a sedentary lifestyle.
Topics: Animals; Arteries; Atherosclerosis; Bioengineering; Cells, Cultured; Computer Simulation; Disease Models, Animal; Endothelium, Vascular; Exercise Therapy; Hemodynamics; Humans; Microfluidic Analytical Techniques; Models, Cardiovascular; Plaque, Atherosclerotic; Sedentary Behavior
PubMed: 33385323
DOI: 10.1152/ajpheart.00719.2020 -
Stroke Jan 2021Intracranial atherosclerotic disease is a common cause of stroke worldwide. Intracranial vessel wall magnetic resonance imaging may be able to identify imaging... (Meta-Analysis)
Meta-Analysis
BACKGROUND AND PURPOSE
Intracranial atherosclerotic disease is a common cause of stroke worldwide. Intracranial vessel wall magnetic resonance imaging may be able to identify imaging biomarkers of symptomatic plaque. We performed a meta-analysis to evaluate the strength of association of imaging features of symptomatic plaque leading to downstream ischemic events. Effects on the strength of association were also assessed accounting for possible sources of bias and variability related to study design and magnetic resonance parameters.
METHODS
PubMed, Scopus, Web of Science, EMBASE, and Cochrane databases were searched up to October 2019. Two independent reviewers extracted data on study design, vessel wall magnetic resonance imaging techniques, and imaging end points. Per-lesion odds ratios (OR) were calculated and pooled using a bivariate random-effects model. Subgroup analyses, sensitivity analysis, and evaluation of publication bias were also performed.
RESULTS
Twenty-one articles met inclusion criteria (1750 lesions; 1542 subjects). Plaque enhancement (OR, 7.42 [95% CI, 3.35-16.43]), positive remodeling (OR, 5.60 [95% CI, 2.23-14.03]), T1 hyperintensity (OR, 2.05 [95% CI, 1.27-3.32]), and surface irregularity (OR, 4.50 [95% CI, 1.39-8.57]) were significantly associated with downstream ischemic events. T2 signal intensity was not significant (=0.59). Plaque enhancement was significantly associated with downstream ischemic events in all subgroup analyses and showed stronger associations when measured in retrospectively designed studies (=0.02), by a radiologist as a rater (<0.001), and on lower vessel wall magnetic resonance imaging spatial resolution sequences (=0.02).
CONCLUSIONS
Plaque enhancement, positive remodeling, T1 hyperintensity, and surface irregularity emerged as strong imaging biomarkers of symptomatic plaque in patients with ischemic events. Plaque enhancement remained significant accounting for sources of bias and variability in both study design and instrument. Future studies evaluating plaque enhancement as a predictive marker for stroke recurrence with larger sample sizes would be valuable.
Topics: Biomarkers; Blood Vessels; Humans; Intracranial Arteriosclerosis; Magnetic Resonance Imaging; Plaque, Atherosclerotic; Sensitivity and Specificity
PubMed: 33370193
DOI: 10.1161/STROKEAHA.120.031480 -
Journal of Vascular Surgery Jun 2021Restenosis after carotid endarterectomy (CEA) limits its long-term efficacy for stroke prevention. Thus, it is of utmost importance to identify the factors that...
OBJECTIVE
Restenosis after carotid endarterectomy (CEA) limits its long-term efficacy for stroke prevention. Thus, it is of utmost importance to identify the factors that predispose a patient to restenosis after CEA. This systemic review aims to survey the current literature regarding restenosis after CEA and discuss the predictive value of carotid plaque features.
METHODS
A systemic review of studies on the predictive value of carotid plaque features for restenosis after CEA was conducted according to the PRISMA guidelines. PubMed/MEDLINE and Embase databases were searched up to March 20, 2020. Two authors independently extracted the data and assessed the risk of bias with the Quality in Prognosis Studies tool. Given the heterogeneity in the measurement of prognostic factors, types of CEA, and clinical outcomes, a qualitative synthesis was performed.
RESULTS
Twenty-one articles with a sample size that ranged from 11 to 1203 were included in this systematic review. Based on the presence of calcification in original carotid plaques, two progression patterns of restenosis were hypothesized: patients with calcified plaques may experience a temporary increase in the intima-media thickness (IMT) followed by a decrease in IMT after CEA, whereas patients with noncalcified plaques may experience a gradual increase in IMT after CEA. Accordingly, patients with a high calcium score may have a high restenosis rate within 6 months after CEA and a low restenosis rate thereafter. Thus, the late restenosis rate in patients with uniformly echogenic plaques was lower than that in patients with uniformly echolucent plaques. Pathologically, a lipid-rich, inflammatory carotid plaque is associated with a decreased risk of restenosis within 1 year after CEA, mainly owing to the relatively mild reactive intimal hyperplasia at the surgical site and active inflammation in the remaining media and adventitia. Molecular predictors for restenosis included a Mannose-binding lectin 2 genotype, preoperative C-reactive protein, serum homocysteine, apolipoprotein J, vitamin C, and telomere length of carotid plaques.
CONCLUSIONS
This review demonstrated that carotid plaque features, including imaging features, cellular composition, and molecular features, are correlated with the risk of restenosis after CEA. A comprehensive evaluation of plaque characteristics may help to stratify the risk of restenosis after CEA.
Topics: Adult; Aged; Aged, 80 and over; Biomarkers; Carotid Stenosis; Endarterectomy, Carotid; Female; Humans; Male; Middle Aged; Neointima; Plaque, Atherosclerotic; Recurrence; Risk Assessment; Risk Factors; Time Factors; Treatment Outcome; Vascular Calcification
PubMed: 33253876
DOI: 10.1016/j.jvs.2020.10.084 -
Imaging endpoints of intracranial atherosclerosis using vessel wall MR imaging: a systematic review.Neuroradiology Jun 2021The vessel wall MR imaging (VWI) literature was systematically reviewed to assess the criteria and measurement methods of VWI-related imaging endpoints for symptomatic...
PURPOSE
The vessel wall MR imaging (VWI) literature was systematically reviewed to assess the criteria and measurement methods of VWI-related imaging endpoints for symptomatic intracranial plaque in patients with ischemic events.
METHODS
PubMed, Scopus, Web of Science, EMBASE, and Cochrane databases were searched up to October 2019. Two independent reviewers extracted data from 47 studies. A modified Guideline for Reporting Reliability and Agreement Studies was used to assess completeness of reporting.
RESULTS
The specific VWI-pulse sequence used to identify plaque was reported in 51% of studies. A VWI-based criterion to define plaque was reported in 38% of studies. A definition for culprit plaque was reported in 40% of studies. Frequently scored qualitative imaging endpoints were plaque quadrant (21%) and enhancement (21%). Frequently measured quantitative imaging endpoints were stenosis (19%), lumen area (15%), and remodeling index (14%). Reproducibility for all endpoints ranged from good to excellent (range: ICC = 0.451 to ICC = 0.983). However, rater specialty and years of experience varied among studies.
CONCLUSIONS
Investigators are using different criteria to identify and measure VWI-imaging endpoints for culprit intracranial plaque. Early awareness of these differences to address methods of acquisition and measurement will help focus research resources and efforts in technique optimization and measurement reproducibility. Consensual definitions to detect plaque will be important to develop automatic lesion detection tools particularly in the era of radiomics.
Topics: Humans; Intracranial Arteriosclerosis; Magnetic Resonance Angiography; Magnetic Resonance Imaging; Plaque, Atherosclerotic; Reproducibility of Results
PubMed: 33029735
DOI: 10.1007/s00234-020-02575-w -
AJNR. American Journal of Neuroradiology Aug 2020Severe carotid stenosis carries a high risk of stroke. However, the risk of stroke with nonstenotic carotid plaques (<50%) is increasingly recognized. (Meta-Analysis)
Meta-Analysis
BACKGROUND
Severe carotid stenosis carries a high risk of stroke. However, the risk of stroke with nonstenotic carotid plaques (<50%) is increasingly recognized.
PURPOSE
We aimed to summarize the risk of TIA or stroke in patients with nonstenotic carotid plaques.
DATA SOURCES
We performed a comprehensive systematic review and meta-analysis in patients with acute ischemic stroke in whom carotid imaging was performed using MEDLINE and the Cochrane Database, including studies published up to December 2019.
STUDY SELECTION
Included studies had >10 patients with <50% carotid plaques on any imaging technique and reported the incidence or recurrence of ischemic stroke/TIA. High-risk plaque features and the risk of progression to stenosis >50% were extracted if reported.
DATA SYNTHESIS
We identified 31 studies reporting on the risk of ipsilateral stroke/TIA in patients with nonstenotic carotid plaques. Twenty-five studies ( = 13,428 participants) reported on first-ever stroke/TIA and 6 studies ( = 122 participants) reported on the recurrence of stroke/TIA.
DATA ANALYSIS
The incidence of first-ever ipsilateral stroke/TIA was 0.5/100 person-years. The risk of recurrent stroke/TIA was 2.6/100 person-years and increased to 4.9/100 person-years if intraplaque hemorrhage was present. The risk of progression to severe stenosis (>50%) was 2.9/100 person-years (8 studies, = 448 participants).
LIMITATIONS
Included studies showed heterogeneity in reporting stroke etiology, the extent of stroke work-up, imaging modalities, and classification systems used for characterizing carotid stenosis.
CONCLUSIONS
The risk of recurrent stroke/TIA in nonstenotic carotid plaques is not negligible, especially in the presence of high-risk plaque features. Further research is needed to better define the significance of nonstenotic carotid plaques for stroke etiology.
Topics: Aged; Carotid Arteries; Female; Humans; Incidence; Ischemic Attack, Transient; Male; Middle Aged; Plaque, Atherosclerotic; Risk Factors; Stroke
PubMed: 32646945
DOI: 10.3174/ajnr.A6613