Dataset Information

Predictive Value of Carotid Distensibility Coefficient for Cardiovascular Diseases and All-Cause Mortality: A Meta-Analysis.

ABSTRACT:

Aims

The aim of the present study is to determine the pooled predictive value of carotid distensibility coefficient (DC) for cardiovascular (CV) diseases and all-cause mortality.

Background

Arterial stiffness is associated with future CV events. Aortic pulse wave velocity is a commonly used predictor for CV diseases and all-cause mortality; however, its assessment requires specific devices and is not always applicable in all patients. In addition to the aortic artery, the carotid artery is also susceptible to atherosclerosis, and is highly accessible because of the surficial property. Thus, carotid DC, which indicates the intrinsic local stiffness of the carotid artery and may be determined using ultrasound and magnetic resonance imaging, is of interest for the prediction. However, the role of carotid DC in the prediction of CV diseases and all-cause mortality has not been thoroughly characterized, and the pooled predictive value of carotid DC remains unclear.

Methods

A meta-analysis, which included 11 longitudinal studies with 20361 subjects, was performed.

Results

Carotid DC significantly predicted future total CV events, CV mortality and all-cause mortality. The pooled risk ratios (RRs) of CV events, CV mortality and all-cause mortality were 1.19 (1.06-1.35, 95%CI, 9 studies with 18993 subjects), 1.09 (1.01-1.18, 95%CI, 2 studies with 2550 subjects) and 1.65 (1.15-2.37, 95%CI, 6 studies with 3619 subjects), respectively, for the subjects who had the lowest quartile of DC compared with their counterparts who had higher quartiles. For CV events, CV mortality and all-cause mortality, a decrease in DC of 1 SD increased the risk by 13%, 6% and 41% respectively, whereas a decrease in DC of 1 unit increased the risk by 3%, 1% and 6% respectively.

Conclusions

Carotid DC is a significant predictor of future CV diseases and all-cause mortality, which may facilitate the identification of high-risk patients for the early diagnosis and prompt treatment of CV diseases.

SUBMITTER: Yuan C

PROVIDER: S-EPMC4821582 | biostudies-literature | 2016

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Predictive Value of Carotid Distensibility Coefficient for Cardiovascular Diseases and All-Cause Mortality: A Meta-Analysis.

Yuan Chuang C Wang Jing J Ying Michael M

PloS one 20160405 4

<h4>Aims</h4>The aim of the present study is to determine the pooled predictive value of carotid distensibility coefficient (DC) for cardiovascular (CV) diseases and all-cause mortality.<h4>Background</h4>Arterial stiffness is associated with future CV events. Aortic pulse wave velocity is a commonly used predictor for CV diseases and all-cause mortality; however, its assessment requires specific devices and is not always applicable in all patients. In addition to the aortic artery, the carotid ...[more]

PMID: 27045958

Similar Datasets

Project description:With epigenome-wide mapping of DNA methylation, a number of novel smoking-associated loci have been identified.We aimed to assess dose-response relationships of methylation at the top hits from the epigenome-wide methylation studies with smoking exposure as well as with total and cause-specific mortality.In a population-based prospective cohort study in Germany, methylation was quantified in baseline blood DNA of 1,000 older adults by the Illumina 450K assay. Deaths were recorded during a median follow-up of 10.3 years. Dose-response relationships of smoking exposure with methylation at nine CpGs were modeled by restricted cubic spline regression. Associations of individual and aggregate methylation patterns with all-cause, cardiovascular, and cancer mortality were assessed by multiple Cox regression.Clear dose-response relationships with respect to current and lifetime smoking intensity were consistently observed for methylation at six of the nine CpGs. Seven of the nine CpGs were also associated with mortality outcomes to various extents. A methylation score based on the top two CpGs (cg05575921 and cg06126421) showed the strongest associations with all-cause, cardiovascular, and cancer mortality, with adjusted hazard ratios (95% CI) of 3.59 (2.10, 6.16), 7.41 (2.81, 19.54), and 2.48 (1.01, 6.08), respectively, for participants with methylation levels in the lowest quartile at both CpGs. Adding methylation at those two CpGs into a model that included the variables of the Systematic Coronary Risk Evaluation chart for fatal cardiovascular risk prediction improved the predictive discrimination.The novel methylation biomarkers are highly informative for both smoking exposure and smoking-related mortality outcomes. In particular, these biomarkers may substantially improve cardiovascular risk prediction. Nevertheless, the findings of the present study need to be further validated in additional large longitudinal studies.Zhang Y, Schöttker B, Florath I, Stock C, Butterbach K, Holleczek B, Mons U, Brenner H. 2016. Smoking-associated DNA methylation biomarkers and their predictive value for all-cause and cardiovascular mortality. Environ Health Perspect 124:67-74; http://dx.doi.org/10.1289/ehp.1409020.

Project description:ObjectivesTo assess evidence for 'legacy' (post-trial) effects on cardiovascular disease (CVD) mortality and all-cause mortality among adult participants of placebo-controlled randomised controlled trials (RCTs) of statins.DesignMeta-analysis of aggregate data.Setting/participantsPlacebo-controlled statin RCTS for primary and secondary CVD prevention.MethodsData sources: PubMed, Embase from inception and forward citations of Cholesterol Treatment Trialists' Collaborators RCTs to 16 June 2016.Study selectionTwo independent reviewers identified all statin RCT follow-up reports including ?1000 participants, and cardiovascular and all-cause mortality.Data extraction and synthesisTwo independent reviewers extracted data in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines.Main outcomesPost-trial CVD and all-cause mortality.ResultsWe included eight trials, with mean post-trial follow-up ranging from 1.6 to 15.1 years, and including 13?781 post-trial deaths (6685 CVD). Direct effects of statins within trials were greater than legacy effects post-trials. The pooled data from all eight studies showed no evidence overall of legacy effects on CVD mortality, but some evidence of legacy effects on all-cause mortality (p=0.01). Exploratory subgroup analysis found possible differences in legacy effect for primary prevention trials compared with secondary prevention trials for both CVD mortality (p=0.15) and all-cause mortality (p=0.02). Pooled post-trial HR for the three primary prevention studies demonstrated possible post-trial legacy effects on CVD mortality (HR=0.87; 95%?CI 0.79 to 0.95) and on all-cause mortality (HR=0.90; 95%?CI 0.85 to 0.96).ConclusionsPossible post-trial statin legacy effects on all-cause mortality appear to be driven by the primary prevention studies. Although these relative benefits were smaller than those observed within the trial, the absolute benefits may be similar for the two time periods. Analysis of individual patient data from follow-up studies after placebo-controlled statin RCTs in lower-risk populations may provide more definitive evidence on whether early treatment of subclinical atherosclerosis is likely to be beneficial.

Project description:ObjectivesTo investigate the associations between echocardiographic left atrial (LA) size and incident stoke and stroke cause mortality among a rural population in China.DesignA prospective study.Setting and participantsBased on the Northeast China Rural Cardiovascular Health Study, we selected a total of 10 041 participants aged ≥35 years who agreed to have transthoracic echocardiography at baseline and were successfully followed up for incident stoke and stroke cause mortality.Primary outcome measureThe outcomes were stroke and stroke cause death according to medical records and death certificates during the follow-up period.ResultsLA enlargement (LAE) group had a higher prevalence of cardiovascular disease than normal LA diameter (LAD) group. After excluding individuals who had a prior stroke, subjects with LAE showed higher incident rates of stroke and its mortality in the overall and specific stratified analyses (all p<0.05). Kaplan-Meier analysis revealed that LAE could predict stroke incidence and stroke-free survival, but the association was no longer observed after the adjustment for potential confounding factors. Cox regression analysis reported that per 1 SD increment in LAD and LAD/body surface area (BSA) was associated with an increased incidence of stroke (LAD: HR=1.20, 95% CI 1.08 to 1.33, p<0.001; LAD/BSA: HR=1.22, 95% CI 1.11 to 1.35, p<0.001) and stroke cause mortality (LAD: HR=1.27, 95% CI 1.08 to 1.50, p<0.01; LAD/BSA: HR=1.41, 95% CI 1.20 to 1.65, p<0.001) in the total population, and similar trends were found in both genders (all p<0.05). LAD or LAD/BSA was related to ischaemic and haemorrhagic stroke incidence, and the risk of ischaemic and haemorrhagic stroke mortality (all p<0.05). The dose-response curves further suggested linear associations between LAD, LAD/BSA and the incidence of stroke and subsequent mortality in the general population (all p<0.05).ConclusionsOur population-based study implied that LA size, especially LAD and LAD/BSA, might be useful echocardiographic biomarkers that had the potential to predict incident stroke and stroke cause mortality.

Dataset Information

Predictive Value of Carotid Distensibility Coefficient for Cardiovascular Diseases and All-Cause Mortality: A Meta-Analysis.

Aims

Background

Methods

Results

Conclusions

Publications

Predictive Value of Carotid Distensibility Coefficient for Cardiovascular Diseases and All-Cause Mortality: A Meta-Analysis.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure