-
JACC. Cardiovascular Imaging Feb 2020The goal of this study was to compare the risk of stroke between patients with carotid artery disease with and without the presence of intraplaque hemorrhage (IPH) on... (Meta-Analysis)
Meta-Analysis
OBJECTIVES
The goal of this study was to compare the risk of stroke between patients with carotid artery disease with and without the presence of intraplaque hemorrhage (IPH) on magnetic resonance imaging.
BACKGROUND
IPH in carotid stenosis increases the risk of cerebrovascular events. Uncertainty remains whether risk of stroke alone is increased and whether stroke is predicted independently of known risk factors.
METHODS
Data were pooled from 7 cohort studies including 560 patients with symptomatic carotid stenosis and 136 patients with asymptomatic carotid stenosis. Hazards of ipsilateral ischemic stroke (primary outcome) were compared between patients with and without IPH, adjusted for clinical risk factors.
RESULTS
IPH was present in 51.6% of patients with symptomatic carotid stenosis and 29.4% of patients with asymptomatic carotid stenosis. During 1,121 observed person-years, 66 ipsilateral strokes occurred. Presence of IPH at baseline increased the risk of ipsilateral stroke both in symptomatic (hazard ratio [HR]: 10.2; 95% confidence interval [CI]: 4.6 to 22.5) and asymptomatic (HR: 7.9; 95% CI: 1.3 to 47.6) patients. Among patients with symptomatic carotid stenosis, annualized event rates of ipsilateral stroke in those with IPH versus those without IPH were 9.0% versus 0.7% (<50% stenosis), 18.1% versus 2.1% (50% to 69% stenosis), and 29.3% versus 1.5% (70% to 99% stenosis). Annualized event rates among patients with asymptomatic carotid stenosis were 5.4% in those with IPH versus 0.8% in those without IPH. Multivariate analysis identified IPH (HR: 11.0; 95% CI: 4.8 to 25.1) and severe degree of stenosis (HR: 3.3; 95% CI: 1.4 to 7.8) as independent predictors of ipsilateral stroke.
CONCLUSIONS
IPH is common in patients with symptomatic and asymptomatic carotid stenosis and is a stronger predictor of stroke than any known clinical risk factors. Magnetic resonance imaging might help identify patients with carotid disease who would benefit from revascularization.
Topics: Aged; Aged, 80 and over; Asymptomatic Diseases; Brain Ischemia; Carotid Stenosis; Female; Hemorrhage; Humans; Magnetic Resonance Imaging; Male; Middle Aged; Plaque, Atherosclerotic; Predictive Value of Tests; Prognosis; Risk Assessment; Risk Factors; Stroke
PubMed: 31202755
DOI: 10.1016/j.jcmg.2019.03.028 -
Circulation Journal : Official Journal... Jun 2019Statin therapy has been shown to result in coronary plaque regression, but the relationship between statin use and stabilization of coronary plaque has not been... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Statin therapy has been shown to result in coronary plaque regression, but the relationship between statin use and stabilization of coronary plaque has not been elucidated. We conducted a systematic review and meta-analysis to evaluate the effect of statin therapy on fibrous cap thickness (FCT) on optical coherence tomography (OCT).Methods and Results:Nine OCT studies (6 randomized controlled trials and 3 observational studies) were enrolled with a total of 341 patients (390 lesions). Arms of the studies were grouped according to statin type and/or dose. Random effects meta-analysis was used to estimate a pooled mean change in FCT from baseline to follow-up. The overall effect mean FCT change was 67.7 µm (95% CI: 51.4-84.1, I=95.0%, P<0.001). All statin groups had an increase in FCT, but the magnitude of the increase differed according to the statin. Two homogeneous subgroups with I=0 were identified: mean FCT change was 27.8 µm (for subgroup atorvastatin 5 mg and rosuvastatin), and 61.9 µm (for subgroup atorvastatin 20 mg, fluvastatin 30 mg, and pitavastatin 4 mg). On meta-regression modeling, statin therapy alone explained most of the change in FCT.
CONCLUSIONS
Statin therapy induced a significant increase in FCT as assessed on OCT, independent of coronary risk factors and other medications.
Topics: Coronary Artery Disease; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Male; Observational Studies as Topic; Plaque, Atherosclerotic; Randomized Controlled Trials as Topic; Tomography, Optical Coherence
PubMed: 31118354
DOI: 10.1253/circj.CJ-18-1376 -
Atherosclerosis May 2019The relationship between plaque regression induced by dyslipidemia therapies and occurrence of major adverse cardiovascular events (MACE) is controversial. We performed...
BACKGROUND AND AIMS
The relationship between plaque regression induced by dyslipidemia therapies and occurrence of major adverse cardiovascular events (MACE) is controversial. We performed a systematic review and meta-regression of dyslipidemia therapy studies reporting MACE and intravascular ultrasound (IVUS) measures of change in coronary atheroma.
METHODS
Prospective studies of dyslipidemia therapies reporting percent atheroma volume (PAV) measured by IVUS and reporting death, myocardial infarction, stroke, unstable angina or transient ischemic attack (MACE) were included. The association between mean change in PAV and MACE was examined using meta-regression via mixed-effects binomial logistic regression models, unadjusted and adjusted for mean age, baseline PAV, baseline low density lipoprotein-cholesterol and study duration.
RESULTS
The study included 17 prospective studies published between 2001 and 2018 totaling 6333 patients. Study duration varied from 11 to 104 weeks. Mean change in PAV, across the study arms, ranged from -5.6% to 3.1%. MACE ranged from 0 to 72 events per study arm: 13 study arms (38%) reported no events, 8 (24%) reported 1-2 events and 13 (38%) reported 3 or more events. Meta-regression demonstrated a decline in the odds of MACE associated with reduction in mean PAV: unadjusted odds ratio (OR): 0.78, 95% Confidence Interval (CI): [0.63, 0.96], p = 0.018; adjusted OR: 0.82, 95% CI: [0.70, 0.95], p = 0.011, per 1% decrease in mean PAV.
CONCLUSIONS
A 1% reduction in mean PAV as induced by dyslipidemia therapies was associated with a 20% reduction in the odds of MACE.
Topics: Cardiovascular Diseases; Coronary Artery Disease; Humans; Hypolipidemic Agents; Plaque, Atherosclerotic; Regression Analysis; Remission Induction
PubMed: 30933694
DOI: 10.1016/j.atherosclerosis.2019.03.005 -
The Cochrane Database of Systematic... Mar 2019A possible strategy for increasing smoking cessation rates could be to provide smokers with feedback on the current or potential future biomedical effects of smoking... (Meta-Analysis)
Meta-Analysis
BACKGROUND
A possible strategy for increasing smoking cessation rates could be to provide smokers with feedback on the current or potential future biomedical effects of smoking using, for example, measurement of exhaled carbon monoxide (CO), lung function, or genetic susceptibility to lung cancer or other diseases.
OBJECTIVES
The main objective was to determine the efficacy of providing smokers with feedback on their exhaled CO measurement, spirometry results, atherosclerotic plaque imaging, and genetic susceptibility to smoking-related diseases in helping them to quit smoking.
SEARCH METHODS
For the most recent update, we searched the Cochrane Tobacco Addiction Group Specialized Register in March 2018 and ClinicalTrials.gov and the WHO ICTRP in September 2018 for studies added since the last update in 2012.
SELECTION CRITERIA
Inclusion criteria for the review were: a randomised controlled trial design; participants being current smokers; interventions based on a biomedical test to increase smoking cessation rates; control groups receiving all other components of intervention; and an outcome of smoking cessation rate at least six months after the start of the intervention.
DATA COLLECTION AND ANALYSIS
We used standard methodological procedures expected by Cochrane. We expressed results as a risk ratio (RR) for smoking cessation with 95% confidence intervals (CI). Where appropriate, we pooled studies using a Mantel-Haenszel random-effects method.
MAIN RESULTS
We included 20 trials using a variety of biomedical tests interventions; one trial included two interventions, for a total of 21 interventions. We included a total of 9262 participants, all of whom were adult smokers. All studies included both men and women adult smokers at different stages of change and motivation for smoking cessation. We judged all but three studies to be at high or unclear risk of bias in at least one domain. We pooled trials in three categories according to the type of biofeedback provided: feedback on risk exposure (five studies); feedback on smoking-related disease risk (five studies); and feedback on smoking-related harm (11 studies). There was no evidence of increased cessation rates from feedback on risk exposure, consisting mainly of feedback on CO measurement, in five pooled trials (RR 1.00, 95% CI 0.83 to 1.21; I = 0%; n = 2368). Feedback on smoking-related disease risk, including four studies testing feedback on genetic markers for cancer risk and one study with feedback on genetic markers for risk of Crohn's disease, did not show a benefit in smoking cessation (RR 0.80, 95% CI 0.63 to 1.01; I = 0%; n = 2064). Feedback on smoking-related harm, including nine studies testing spirometry with or without feedback on lung age and two studies on feedback on carotid ultrasound, also did not show a benefit (RR 1.26, 95% CI 0.99 to 1.61; I = 34%; n = 3314). Only one study directly compared multiple forms of measurement with a single form of measurement, and did not detect a significant difference in effect between measurement of CO plus genetic susceptibility to lung cancer and measurement of CO only (RR 0.82, 95% CI 0.43 to 1.56; n = 189).
AUTHORS' CONCLUSIONS
There is little evidence about the effects of biomedical risk assessment as an aid for smoking cessation. The most promising results relate to spirometry and carotid ultrasound, where moderate-certainty evidence, limited by imprecision and risk of bias, did not detect a statistically significant benefit, but confidence intervals very narrowly missed one, and the point estimate favoured the intervention. A sensitivity analysis removing those studies at high risk of bias did detect a benefit. Moderate-certainty evidence limited by risk of bias did not detect an effect of feedback on smoking exposure by CO monitoring. Low-certainty evidence, limited by risk of bias and imprecision, did not detect a benefit from feedback on smoking-related risk by genetic marker testing. There is insufficient evidence with which to evaluate the hypothesis that multiple types of assessment are more effective than single forms of assessment.
Topics: Adult; Biofeedback, Psychology; Breath Tests; Carbon Monoxide; Female; Genetic Predisposition to Disease; Humans; Male; Randomized Controlled Trials as Topic; Risk Assessment; Smoking; Smoking Cessation; Spirometry
PubMed: 30912847
DOI: 10.1002/14651858.CD004705.pub5 -
Frontiers in Neurology 2018Vessel-wall magnetic resonance imaging (MRI) has been suggested as a valuable tool for assessing intracranial arterial stenosis with additional diagnostic features....
Vessel-wall magnetic resonance imaging (MRI) has been suggested as a valuable tool for assessing intracranial arterial stenosis with additional diagnostic features. However, there is limited conclusive evidence on whether vessel-wall MR imaging of intracranial atherosclerotic plaques provides valuable information for predicting vulnerable lesions. We conducted this systematic review and meta-analysis to evaluate which characteristics of intracranial-plaque on vessel-wall MRI are markers of culprit lesions. The MEDLINE, EMBASE, and Cochrane Library of Clinical Trials databases were searched for studies reporting the association between vessel-wall MRI characteristics of intracranial plaque and corresponding stroke events. Odds ratios (ORs) for the prevalence of stroke with intracranial-plaque MRI characteristics were pooled in a meta-analysis using a random-effects model. Twenty studies were included in this review. We found a significant association between plaque enhancement (OR, 10.09; 95% CI, 5.38-18.93), positive remodeling (OR, 6.19; 95% CI, 3.22-11.92), and plaque surface irregularity (OR, 3.94; 95% CI, 1.90-8.16) with stroke events. However, no significant difference was found for the presence of eccentricity (OR, 1.22; 95% CI, 0.51-2.91). Based on current evidence, intracranial plaque contrast enhancement, positive remodeling, and plaque irregularity on MRI are associated with increased risk of stroke events. Our findings support the design of future studies on intracranial-plaque MRI and decision making for the management of intracranial atherosclerotic plaques.
PubMed: 30559708
DOI: 10.3389/fneur.2018.01032 -
Pharmacology & Therapeutics Apr 2019Atherosclerosis, the principal cause of cardiovascular death worldwide, is a pathological disease characterized by fibro-proliferation, chronic inflammation, lipid...
Atherosclerosis, the principal cause of cardiovascular death worldwide, is a pathological disease characterized by fibro-proliferation, chronic inflammation, lipid accumulation, and immune disorder in the vessel wall. As the atheromatous plaques develop into advanced stage, the vulnerable plaques are prone to rupture, which causes acute cardiovascular events, including ischemic stroke and myocardial infarction. Emerging evidence has suggested that atherosclerosis is also an epigenetic disease with the interplay of multiple epigenetic mechanisms. The epigenetic basis of atherosclerosis has transformed our knowledge of epigenetics from an important biological phenomenon to a burgeoning field in cardiovascular research. Here, we provide a systematic and up-to-date overview of the current knowledge of three distinct but interrelated epigenetic processes (including DNA methylation, histone methylation/acetylation, and non-coding RNAs), in atherosclerotic plaque development and instability. Mechanistic and conceptual advances in understanding the biological roles of various epigenetic modifiers in regulating gene expression and functions of endothelial cells (vascular homeostasis, leukocyte adhesion, endothelial-mesenchymal transition, angiogenesis, and mechanotransduction), smooth muscle cells (proliferation, migration, inflammation, hypertrophy, and phenotypic switch), and macrophages (differentiation, inflammation, foam cell formation, and polarization) are discussed. The inherently dynamic nature and reversibility of epigenetic regulation, enables the possibility of epigenetic therapy by targeting epigenetic "writers", "readers", and "erasers". Several Food Drug Administration-approved small-molecule epigenetic drugs show promise in pre-clinical studies for the treatment of atherosclerosis. Finally, we discuss potential therapeutic implications and challenges for future research involving cardiovascular epigenetics, with an aim to provide a translational perspective for identifying novel biomarkers of atherosclerosis, and transforming precision cardiovascular research and disease therapy in modern era of epigenetics.
Topics: Animals; Atherosclerosis; Epigenesis, Genetic; Humans; Immunity; RNA, Untranslated; Risk Factors
PubMed: 30439455
DOI: 10.1016/j.pharmthera.2018.11.003 -
Cardiovascular Research Dec 2018
Meta-Analysis
Topics: Animals; Arteries; Atherosclerosis; Diet, High-Fat; Disease Models, Animal; Disease Progression; Genetic Predisposition to Disease; Lipids; Mice, Knockout, ApoE; Phenotype; Plaque, Atherosclerotic; Proprotein Convertase 9; Receptors, LDL; Severity of Illness Index; Time Factors
PubMed: 29878146
DOI: 10.1093/cvr/cvy140 -
Revista de Neurologia May 2018The concept of embolic stroke of undetermined source (ESUS) has recently appeared to better characterise patients with cryptogenic stroke.
INTRODUCTION
The concept of embolic stroke of undetermined source (ESUS) has recently appeared to better characterise patients with cryptogenic stroke.
PATIENTS AND METHODS
A systematic review of studies published since 2014 was performed to evaluate the epidemiology, clinical features and prognosis of patients with ESUS and their proportion among patients with cryptogenic stroke.
RESULTS
Ten studies were identified with a total of 14,810 patients. The frequency of ESUS varied between 6% and 42%. We observed a high percentage of patients with cryptogenic stroke who met ESUS criteria (37-82%). The mean age of these patients was 65-68 years. The mean severity of the stroke, as measured using the National Institutes of Health Stroke Scale, was found to be 3-7 points. A high degree of variability was seen in the proportion of atrial fibrillation (detected during follow-up) related to the electrocardiogram monitoring technique. In five studies, some minor source of cardioembolism was observed in one out of every two patients, the most frequent being the persistence of patent foramen ovale. The risk of recurrence was 5-14.5%.
CONCLUSION
The application of the new ESUS criteria provides a better definition of patients with cryptogenic stroke. Applying the concept of ESUS requires not only adequate electrocardiogram monitoring, but also routine complementary examinations to rule out the presence of minor sources of cardioembolism and other sources of embolism other than atrial fibrillation.
Topics: Aged; Aortic Diseases; Arteriosclerosis; Atrial Fibrillation; Brain Damage, Chronic; Female; Humans; Intracranial Embolism; Male; Plaque, Atherosclerotic; Prognosis; Recovery of Function
PubMed: 29749592
DOI: No ID Found -
European Journal of Vascular and... Aug 2018The role of positron emission tomography (PET)/computed tomography (CT) in the determination of inflammation in arterial disease is not well defined. This can provide... (Meta-Analysis)
Meta-Analysis Review
INTRODUCTION
The role of positron emission tomography (PET)/computed tomography (CT) in the determination of inflammation in arterial disease is not well defined. This can provide information about arterial wall inflammation in atherosclerotic disease, and may give insight into plaque stability. The aim of this review was to perform a meta-analysis of PET/CT with F-FDG (fluorodeoxyglucose) uptake in symptomatic and asymptomatic carotid artery disease.
METHODS
This was a systematic review, following PRISMA guidelines, which interrogated the MEDLINE database from January 2001 to May 2017. The search combined the terms, "inflammation", "FDG", and "stroke". The search criteria included all types of studies, with a primary outcome of the degree of arterial vascular inflammation determined by F-FDG uptake. Analysis involved an inverse weighted variance estimate of pooled data, using a random effects model.
RESULTS
A total of 14 articles (539 patients) were included in the meta-analysis. Comparing carotid artery F-FDG uptake in symptomatic versus asymptomatic disease yielded a standard mean difference of 0.94 (95% CI 0.58-1.130; p < .0001; I = 65%).
CONCLUSIONS
PET/CT using F-FDG can demonstrate carotid plaque inflammation, and is a marker of symptomatic disease. Further studies are required to understand the clinical implication of PET/CT as a risk prediction tool.
Topics: Aged; Asymptomatic Diseases; Carotid Arteries; Carotid Artery Diseases; Chi-Square Distribution; Female; Fluorodeoxyglucose F18; Humans; Male; Plaque, Atherosclerotic; Positron Emission Tomography Computed Tomography; Predictive Value of Tests; Prognosis; Radiopharmaceuticals
PubMed: 29730127
DOI: 10.1016/j.ejvs.2018.03.028 -
Clinical and Experimental Rheumatology 2018Acute systemic inflammation and chronic systemic vasculitis are associated with endothelial dysfunction and atherosclerotic plaque formation. Studies on cardiovascular... (Meta-Analysis)
Meta-Analysis Review
OBJECTIVES
Acute systemic inflammation and chronic systemic vasculitis are associated with endothelial dysfunction and atherosclerotic plaque formation. Studies on cardiovascular or cerebrovascular events in primary Sjögren's syndrome (pSS) are limited, with conflicting results. This meta-analysis aimed to explore the risk of cardiovascular and cerebrovascular disease in pSS.
METHODS
A comprehensive search of the MEDLINE and EMBASE databases was performed from date of inception through August 2017. The inclusion criterion was observational studies evaluating the association between pSS and cardiovascular disease or cerebrovascular event. Outcomes are diagnosis of ischaemic heart disease, myocardial infarction, ischaemic stroke or haemorrhagic stroke. The pooled odds ratio (OR) of the cerebrovascular event or cardiovascular disease and their 95% confidence interval (CI) were calculated using a random-effect meta-analysis to compare risk between patients with pSS and controls. The between-study heterogeneity of effect-size was quantified using the Q statistic and I2.
RESULTS
Data were extracted from 10 observational studies involving 165,291 subjects. Pooled result demonstrated a significant increase in risk of having cardiovascular disease or cerebrovascular event in pSS patients compared with controls (OR=1.28; 95% CI: 0.11-1.46, p value<0.01, I2=68%). Subgroup analyses showed no difference in risk for cerebrovascular event (OR=1.31; 95% CI: 0.96-1.79, p value=0.09, I2=71%), but an increased risk of cardiovascular disease (OR=1.30; 95% CI: 1.09-1.55, p value=0.003, I2=74%).
CONCLUSIONS
Our study has shown an increased risk of cardiovascular or cerebrovascular disease in patients with pSS. These results support multiple studies' finding of increased arterial stiffness in patients with pSS.
Topics: Adult; Aged; Cardiovascular Diseases; Cerebrovascular Disorders; Chi-Square Distribution; Female; Humans; Male; Middle Aged; Observational Studies as Topic; Odds Ratio; Prognosis; Risk Assessment; Risk Factors; Sjogren's Syndrome
PubMed: 29600936
DOI: No ID Found