Dataset Information

Low grade inflammation and coronary heart disease: prospective study and updated meta-analyses.

ABSTRACT: OBJECTIVE:To assess associations between baseline values of four different circulating markers of inflammation and future risk of coronary heart disease, potential triggers of systemic inflammation (such as persistent infection), and other markers of inflammation. DESIGN:Nested case-control comparisons in a prospective, population based cohort. SETTING:General practices in 18 towns in Britain. PARTICIPANTS:506 men who died from coronary heart disease or had a non-fatal myocardial infarction and 1025 men who remained free of such disease until 1996 selected from 5661 men aged 40-59 years who provided blood samples in 1978-1980. MAIN OUTCOME MEASURES:Plasma concentrations of C reactive protein, serum amyloid A protein, and serum albumin and leucocyte count. Information on fatal and non-fatal coronary heart disease was obtained from medical records and death certificates. RESULTS:Compared with men in the bottom third of baseline measurements of C reactive protein, men in the top third had an odds ratio for coronary heart disease of 2.13 (95% confidence interval 1.38 to 3.28) after age, town, smoking, vascular risk factors, and indicators of socioeconomic status were adjusted for. Similar adjusted odds ratios were 1.65 (1.07 to 2.55) for serum amyloid A protein; 1.12 (0.71 to 1.77) for leucocyte count; and 0.67 (0.43 to 1.04) for albumin. No strong associations were observed of these factors with Helicobacter pylori seropositivity, Chlamydia pneumoniae IgG titres, or plasma total homocysteine concentrations. Baseline values of the acute phase reactants were significantly associated with one another (P<0.0001), although the association between low serum albumin concentration and leucocyte count was weaker (P=0.08). CONCLUSION:In the context of results from other relevant studies these findings suggest that some inflammatory processes, unrelated to the chronic infections studied here, are likely to be involved in coronary heart disease.

SUBMITTER: Danesh J

PROVIDER: S-EPMC27435 | biostudies-literature | 2000 Jul

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Low grade inflammation and coronary heart disease: prospective study and updated meta-analyses.

Danesh J J Whincup P P Walker M M Lennon L L Thomson A A Appleby P P Gallimore J R JR Pepys M B MB

BMJ (Clinical research ed.) 20000701 7255

<h4>Objective</h4>To assess associations between baseline values of four different circulating markers of inflammation and future risk of coronary heart disease, potential triggers of systemic inflammation (such as persistent infection), and other markers of inflammation.<h4>Design</h4>Nested case-control comparisons in a prospective, population based cohort.<h4>Setting</h4>General practices in 18 towns in Britain.<h4>Participants</h4>506 men who died from coronary heart disease or had a non-fat ...[more]

PMID: 10903648

Similar Datasets

Project description:ObjectiveTo clarify the role of dietary carbohydrate, glycemic index (GI), and glycemic load (GL) in progression from health to coronary heart disease (CHD) by determining disease-nutrient risk relation (RR) values needed for intake ranges within jurisdictions and across the globe.MethodsWe performed a literature search of MEDLINE and EMBASE for prospective cohort studies that used truly valid dietary instruments in heathy adults published from January 1, 2000, to June 5, 2018. Relevant observations were extracted by 2 reviewers independently. We used dose-response meta-analysis accounting for nonindependence of results within studies. Bradford-Hill criteria were used to assess causality.ResultsEligible studies had a mean follow-up of 11 years (range, 5-19 years), were conducted in North America, Europe, and East Asia, and yielded combined RRs of 1.44 (95% CI, 1.25-1.65) per 65 g/d GL (11 studies) and 1.24 (95% CI, 1.12-1.38) per 10 U GI (10 studies) (glucose scale). The CHD-carbohydrate RR on GI was 1.66 (95% CI, 1.23-2.25) per 98 g/d of carbohydrates per 10 units GI. The 65 g/d GL, 10 U GI, and 98 g/d carbohydrate values corresponded to oral intakes from the 10th to the 90th percentiles within sampled populations. Inconsistencies were minor (I 2 ≤20%), as were small-study effects (P=.61 for GL and P=.26 for GI). Funnel plots were symmetric. Cubic spline dose-response meta-analysis yielded RRs as follows: across the global range for GL (55-290 g/d), 5.5 (95% CI, 3.1-9.8) (I 2 =0); for GI (47-82 U), 2.71 (95% CI, 1.47-4.40) (I 2 =0); and for the CHD-carbohydrate dependence on GI (50-80 U), 4.57 (95% CI, 1.86-11.4) (I 2 =16%). Bradford-Hill criteria indicated that these relations were probably causal.ConclusionStrong and probably causal CHD-GL and GI RRs exist within populations. The RRs were remarkably higher across global exposures. The results support the consideration of these markers of carbohydrate food quality in dietary guidelines for general populations.Trial registrationPROSPERO Identifier: CRD42013004504.

Project description:Comparison of patients with coronary heart disease and controls in genome-wide association studies has revealed several single nucleotide polymorphisms (SNPs) associated with coronary heart disease. We aimed to establish the external validity of these findings and to obtain more precise risk estimates using a prospective cohort design.We tested 13 recently discovered SNPs for association with coronary heart disease in a case-control design including participants differing from those in the discovery samples (3829 participants with prevalent coronary heart disease and 48,897 controls free of the disease) and a prospective cohort design including 30,725 participants free of cardiovascular disease from Finland and Sweden. We modelled the 13 SNPs as a multilocus genetic risk score and used Cox proportional hazards models to estimate the association of genetic risk score with incident coronary heart disease. For case-control analyses we analysed associations between individual SNPs and quintiles of genetic risk score using logistic regression.In prospective cohort analyses, 1264 participants had a first coronary heart disease event during a median 10·7 years' follow-up (IQR 6·7-13·6). Genetic risk score was associated with a first coronary heart disease event. When compared with the bottom quintile of genetic risk score, participants in the top quintile were at 1·66-times increased risk of coronary heart disease in a model adjusting for traditional risk factors (95% CI 1·35-2·04, p value for linear trend=7·3×10(-10)). Adjustment for family history did not change these estimates. Genetic risk score did not improve C index over traditional risk factors and family history (p=0·19), nor did it have a significant effect on net reclassification improvement (2·2%, p=0·18); however, it did have a small effect on integrated discrimination index (0·004, p=0·0006). Results of the case-control analyses were similar to those of the prospective cohort analyses.Using a genetic risk score based on 13 SNPs associated with coronary heart disease, we can identify the 20% of individuals of European ancestry who are at roughly 70% increased risk of a first coronary heart disease event. The potential clinical use of this panel of SNPs remains to be defined.The Wellcome Trust; Academy of Finland Center of Excellence for Complex Disease Genetics; US National Institutes of Health; the Donovan Family Foundation.

Project description:Hyperuricemia, characterized by elevated serum uric acid levels, has garnered significant attention in cardiovascular research due to its potential association with coronary heart disease (CHD). While some studies suggest hyperuricemia as a risk factor of CHD, others present conflicting findings. A systematic review and dose-response meta-analysis is warranted to comprehensively summarize the previous studies and determine the association between hyperuricemia and CHD, thereby supporting clinical practice and future studies in this field. In this study, we will comprehensively search Medline, EMBase, Cochrane Central, ICTRP, and ClinicalTrials.gov, from inception to December 31, 2024. Prospective or retrospective cohort studies and case-control studies investigating the association between hyperuricemia and CHD will be included. Two independent reviewers will conduct study selection, data extraction, and risk of bias assessment. The primary outcome will be the pooled relative risk of CHD associated with hyperuricemia by using random-effect model. Dose-response meta-analysis will be performed with linear and non-linear model to explore the the magnitude and direction of the association between serum uric acid levels and CHD risk. Subgroup analyses will be conducted based on uric acid test approaches and corresponding cut-off values and human races. Sensitivity analyses will assess the robustness of the results with leave-one-out method, while publication bias will be evaluated using funnel plots, Egger's test, and Begg's test. We will further use GRADE to evaluate the quality of the evidences provided by our systematic review. From this systematic review and dose-response meta-analysis, we hope out findings will provide reliable conclusion and data support on the association between hyperuricemia and CHD. The transparent and replicable methodologies outlined in this protocol contribute to advancing understanding of hyperuricemia as a potentially modifiable risk factor for CHD, thus supporting evidence-based strategies for cardiovascular disease management. This protocol describes a rigorous plan to systematically review and analyze the quantitative association between hyperuricemia and CHD risk. In a word, we will help further clinical practice and scientific studies in this field. This protocol was registered in PROSPERO CRD42024538553.

Dataset Information

Low grade inflammation and coronary heart disease: prospective study and updated meta-analyses.

Publications

Low grade inflammation and coronary heart disease: prospective study and updated meta-analyses.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets