Coronary heart disease risk, aspirin use, and apolipoprotein(a) 4399Met allele in the Atherosclerosis Risk in Communities (ARIC) study.
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ABSTRACT:
SUBMITTER: Shiffman D
PROVIDER: S-EPMC4351745 | biostudies-literature | 2009 Jul
REPOSITORIES: biostudies-literature
Publications
Coronary heart disease risk, aspirin use, and apolipoprotein(a) 4399Met allele in the Atherosclerosis Risk in Communities (ARIC) study.
Shiffman Dov D Chasman Daniel I DI Ballantyne Christie M CM Nambi Vijay V Devlin James J JJ Boerwinkle Eric E
Thrombosis and haemostasis 20090701 1
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Project description:ObjectiveThe cytochromes P450 epoxygenases CYP2J2 and CYP2C8 synthesize epoxyeicosatrienoic acids, which regulate endothelial function. We sought to determine if genetic variation in CYP2J2 and CYP2C8 was associated with coronary heart disease risk.MethodsWe genotyped 2065 Atherosclerosis Risk in Communities study participants (1085 incident coronary heart disease cases, 980 noncases) for polymorphisms in CYP2J2 and CYP2C8. Using a case-cohort design, associations between genotype and incident coronary heart disease risk were evaluated using proportional hazards regression. The influence of cigarette smoking on these associations was also evaluated. False discovery rate q-values were estimated to minimize the impact of the multiple statistical comparisons completed. All analyses were race stratified.ResultsThe CYP2J2 G-50T polymorphism variant -50T allele was associated with significantly lower risk of incident coronary heart disease in African-Americans (adjusted hazard rate ratio 0.58, 95% confidence interval 0.35-0.96, P=0.036, q=0.051); however, no significant association was observed in Caucasians. Overall, the I264M, I269F, and K399R polymorphisms in CYP2C8 were not significantly associated with risk of incident coronary heart disease. In Caucasians, the relationship between the I264M and K399R polymorphisms and incident coronary heart disease risk was significantly modified by cigarette smoking status (P for interaction=0.008, q=0.064), with the highest risk observed in smokers carrying at least one variant allele.ConclusionsThe G-50T polymorphism in CYP2J2 may be an important risk factor for the development of coronary heart disease events in African-Americans, whereas cigarette smoking may modify the relationship between the I264M and K399R polymorphisms in CYP2C8 and coronary heart disease risk in Caucasians. Confirmation of these findings in an independent population is warranted.
| S-EPMC1947003 | biostudies-literature
Project description:This study was designed to assess the relationship between insulin resistance and incident heart failure (HF) in a community-based cohort.Diabetes mellitus increases the risk for HF, but the association between insulin resistance and HF in individuals without diabetes is unclear.We prospectively analyzed 12,606 participants without diabetes mellitus, prevalent HF, or history of myocardial infarction at baseline (1987 to 1989) from the ARIC (Atherosclerosis Risk in Communities) study. We assessed the relationship between insulin resistance and incident HF using the homeostatic model assessment of insulin resistance (HOMA-IR) equation, adjusting for age, sex, race, body mass index, smoking, hypertension, center, and interim myocardial infarction. We tested for interactions by age, sex, obesity, and race.Participants with insulin resistance, defined as HOMA-IR ≥2.5 (n = 4,810, 39%), were older, more likely female, African American, hypertensive, and had a higher body mass index as compared with those without insulin resistance. There were 1,455 incident HF cases during a median of 20.6 years of follow-up. Insulin resistance defined by this threshold was not significantly associated with an increased risk for incident HF after adjustment (hazard ratio: 1.08, 95% confidence interval: 0.95 to 1.23). However, when analyzed continuously, this relationship was nonlinear, which indicated that risk increased, and was significantly associated with incident HF between HOMA-IR of 1.0 to 2.0, adjusting for baseline covariates; however, values over 2.5 were not associated with additional increased risk in adjusted models.In a community cohort, insulin resistance, defined by lower levels of HOMA-IR than previously considered, was associated with an increased risk for HF.
| S-EPMC3893700 | biostudies-other
Project description:ObjectiveTo investigate the relationship between plasma levels of small dense low-density lipoprotein-cholesterol (sdLDL-C) and risk for incident coronary heart disease (CHD) in a prospective study among Atherosclerosis Risk in Communities (ARIC) study participants.Approach and resultsPlasma sdLDL-C was measured in 11 419 men and women of the biracial ARIC study using a newly developed homogeneous assay. A proportional hazards model was used to examine the relationship among sdLDL-C, vascular risk factors, and risk for CHD events (n=1158) for a period of ≈11 years. Plasma sdLDL-C levels were strongly correlated with an atherogenic lipid profile and were higher in patients with diabetes mellitus than non-diabetes mellitus (49.6 versus 42.3 mg/dL; P<0.0001). In a model that included established risk factors, sdLDL-C was associated with incident CHD with a hazard ratio of 1.51 (95% confidence interval, 1.21-1.88) for the highest versus the lowest quartile, respectively. Even in individuals considered to be at low cardiovascular risk based on their LDL-C levels, sdLDL-C predicted risk for incident CHD (hazard ratio, 1.61; 95% confidence interval, 1.04-2.49). Genome-wide association analyses identified genetic variants in 8 loci associated with sdLDL-C levels. These loci were in or close to genes previously associated with risk for CHD. We discovered 1 novel locus, PCSK7, for which genetic variation was significantly associated with sdLDL-C and other lipid factors.ConclusionssdLDL-C was associated with incident CHD in ARIC study participants. The novel association of genetic variants in PCSK7 with sdLDL-C and other lipid traits may provide new insights into the role of this gene in lipid metabolism.
| S-EPMC3999643 | biostudies-literature
Project description:Endothelial dysfunction contributes to the development of coronary heart disease (CHD). Soluble epoxide hydrolase metabolizes epoxyeicosatrienoic acids in the vasculature and regulates endothelial function. We sought to determine whether genetic variation in soluble epoxide hydrolase (EPHX2) was associated with the risk of CHD. We genotyped 2,065 Atherosclerosis Risk in Communities study participants (1,085 incident CHD cases, 980 non-cases) for 10 previously identified polymorphisms in EPHX2. Using a case-cohort design, associations between incident CHD risk and both non-synonymous EPHX2 polymorphisms and phase-reconstructed haplotypes were evaluated using proportional hazards regression. Individuals carrying the K55R polymorphism variant allele demonstrated higher apparent soluble epoxide hydrolase activity in vivo. Presence of the K55R variant allele was significantly more common among Caucasian CHD cases when compared with non-cases (20.8% versus 15.3%, respectively, P=0.012), and was associated with significantly higher risk of incident CHD (adjusted hazard rate ratio 1.45, 95% confidence interval 1.05-2.01, P=0.026). A significant association between the K55R variant allele and risk of CHD was not observed in African-Americans. The distribution of reconstructed haplotypes were significantly different in Caucasian cases when compared with non-cases (P=0.021). Significant differences in haplotype distribution were not observed in African-Americans (P=0.315). Genetic variation in EPHX2 was significantly associated with risk of incident CHD in Caucasians, implicating EPHX2 as a potential cardiovascular disease-susceptibility gene.
| S-EPMC2040335 | biostudies-literature
Project description:Atherosclerosis Risk in Communities (ARIC) Cohort
| PRJNA75713 | ENA
Project description:In an entirely African-American cohort, we compared clinical characteristics, cardiac structure and function, and all-cause mortality in patients with heart failure (HF) with preserved ejection fraction (HFpEF) in relation to patients with heart failure with reduced ejection fraction (HFrEF) and those without HF.African Americans are at increased risk for HF. Nevertheless, there are limited phenotypic and prognostic data in African Americans with HFpEF compared with those with HFrEF and those without HF.Middle-aged African Americans from the Jackson, Mississippi, cohort of the ARIC (Atherosclerosis Risk In Communities) study (n = 2,445) underwent echocardiography between 1993 and 1995. HF prevalence was available in 1,962 patients for whom left ventricular ejection fraction (LVEF) could be quantified. Participants with HF were categorized as having HFpEF (LVEF ≥50%), HFrEF (LVEF <50%), or no HF, with comparisons made between groups.HF was identified in 116 (5.9%) participants (HFpEF n = 85 [73%]; HFrEF n = 31 [27%]). Compared with those without HF, those with HFpEF were older, were more likely to be female, and had more frequent comorbidities and concentric hypertrophy. In relation to HFrEF, those with HFpEF were more likely to be female but less likely to have coronary heart disease, diabetes mellitus, chronic kidney disease, left atrial enlargement, and eccentric hypertrophy. Over a median 13.7 years of follow-up, risk of death differed between groups, with age- and sex-adjusted hazard ratios of 1.51 (95% confidence interval: 1.01 to 2.25) for HFpEF versus those without HF and 2.50 (95% confidence interval: 1.37 to 4.58) for HFrEF versus HFpEF.In this cohort of middle-aged African Americans, HFpEF was the most common form of HF and was associated with a substantially better prognosis than HFrEF but worse than those without HF.
| S-EPMC3650857 | biostudies-other
Project description:ObjectiveThe aim of this work was to estimate agreement of self-reported heart failure (HF) with physician-diagnosed HF and compare the prevalence of HF according to method of ascertainment.Methods and resultsARIC cohort members (60-83 years of age) were asked annually whether a physician indicated that they have HF. For those self-reporting HF, physicians were asked to confirm their patients' HF status. Physician-diagnosed HF included surveillance of hospitalized HF and hospitalized and outpatient HF identified in administrative claims databases. We estimated sensitivity, specificity, positive predicted value, kappa, prevalence and bias-adjusted kappa (PABAK), and prevalence. Compared with physician-diagnosed HF, sensitivity of self-report was low (28%-38%) and specificity was high (96%-97%). Agreement was poor (kappa 0.32-0.39) and increased when adjusted for prevalence and bias (PABAK 0.73-0.83). Prevalence of HF measured by self-report (9.0%), ARIC-classified hospitalizations (11.2%), and administrative hospitalization claims (12.7%) were similar. When outpatient HF claims were included, prevalence of HF increased to 18.6%.ConclusionsFor accurate estimates HF burden, self-reports of HF are best confirmed by means of appropriate diagnostic tests or medical records. Our results highlight the need for improved awareness and understanding of HF by patients, because accurate patient awareness of the diagnosis may enhance management of this common condition.
| S-EPMC5671356 | biostudies-literature
Project description:BackgroundThe influence of diabetes on progression from preclinical heart failure (HF) stages to overt HF is poorly understood.ObjectivesThe purpose of this study was to characterize the influence of diabetes on the progression from preclinical HF stages (A or B based on the 2021 Universal Definition) to overt HF.MethodsWe included 4,774 adults with preclinical HF (stage A [n = 1,551] or B [n = 3,223]) who attended the ARIC (Atherosclerosis Risk In Communities) study Visit 5 (2011-2013). Within each stage (A or B), we assessed the associations of diabetes and glycemic control (hemoglobin A1C [HbA1C] <7% vs ≥7%) with progression to HF, and of cross-categories of HF stages (A vs B), diabetes, and glycemic control with incident HF.ResultsAmong the participants (mean age 75.4 years, 58% women, 20% Black), there were 470 HF events during 8.6 years of follow-up. Stage B participants with HbA1C ≥7% experienced clinical HF at a younger age than those with controlled diabetes or without diabetes (mean age 80 years vs 83 years vs 82 years; P < 0.001). HbA1C ≥7% was more strongly associated with HF in stage B (HR: 1.83; 95% CI: 1.33-2.51) compared with stage A (HR: 1.52; 95% CI: 0.53-4.38). In cross-categories of preclinical HF stage and HbA1C, participants with stage B and HbA1C ≥7% had increased risk of HF progression compared with stage A without diabetes (HR: 7.56; 95% CI: 4.68-12.20).ConclusionsAmong older adults with preclinical HF stages, uncontrolled diabetes was associated with substantial risk of HF progression. Our results suggest that targeting diabetes early in the HF process is critical.
| S-EPMC10125541 | biostudies-literature
Project description:BackgroundPrevious studies suggest that heart failure (HF) is an independent risk factor for cognitive decline. A better understanding of the relationship between HF, cognitive status, and cognitive decline in a community-based sample may help clinicians understand disease risk.ObjectiveTo examine whether persons with HF have a higher prevalence of cognitive impairment and whether persons developing HF have more rapid cognitive decline.DesignThis observational cohort study of American adults in the Atherosclerosis Risk in Communities (ARIC) study has two components: cross-sectional analysis examining the association between prevalent HF and cognition using multinomial logistic regression, and change over time analysis detailing the association between incident HF and change in cognition over 15 years.ParticipantsAmong visit 5 (2011-2013) participants (median age 75 years), 6495 had neurocognitive information available for cross-sectional analysis. Change over time analysis examined the 5414 participants who had cognitive scores and no prevalent HF at visit 4 (1996-1998).MeasurementsThe primary outcome was cognitive status, classified as normal, mild cognitive impairment [MCI], and dementia on the basis of standardized cognitive tests (delayed word recall, word fluency, and digit symbol substitution). Cognitive change was examined over a 15-year period. Control variables included socio-demographic, vascular, and smoking/drinking measures.ResultsAt visit 5, participants with HF had a higher prevalence of dementia (adjusted relative risk ratio [RRR] = 1.60 [95% CI 1.13, 2.25]) and MCI (RRR = 1.36 [1.12, 1.64]) than those without HF. A decline in cognition between visits 4 and 5 was - 0.07 standard deviation units [- 0.13, - 0.01] greater among persons who developed HF compared to those who did not. Results did not differ by ejection fraction.ConclusionHF is associated with neurocognitive dysfunction and decline independent of other co-morbid conditions. Further study is needed to determine the underlying pathophysiology.
| S-EPMC6153245 | biostudies-literature
Project description:Prospective data examining the relationship between dietary protein intake and incident coronary heart disease (CHD) are inconclusive. Most evidence is derived from homogenous populations such as health professionals. Large community-based analyses in more diverse samples are lacking.We studied the association of protein type and major dietary protein sources and risk for incident CHD in 12,066 middle-aged adults (aged 45-64 at baseline, 1987-1989) from four U.S. communities enrolled in the Atherosclerosis Risk in Communities (ARIC) Study who were free of diabetes mellitus and cardiovascular disease at baseline. Dietary protein intake was assessed at baseline and after 6 years of follow-up by food frequency questionnaire. Our primary outcome was adjudicated coronary heart disease events or deaths with following up through December 31, 2010. Cox proportional hazard models with multivariable adjustment were used for statistical analyses.During a median follow-up of 22 years, there were 1,147 CHD events. In multivariable analyses total, animal and vegetable protein were not associated with an increased risk for CHD before or after adjustment. In food group analyses of major dietary protein sources, protein intake from red and processed meat, dairy products, fish, nuts, eggs, and legumes were not significantly associated with CHD risk. The hazard ratios [with 95% confidence intervals] for risk of CHD across quintiles of protein from poultry were 1.00 [ref], 0.83 [0.70-0.99], 0.93 [0.75-1.15], 0.88 [0.73-1.06], 0.79 [0.64-0.98], P for trend = 0.16). Replacement analyses evaluating the association of substituting one source of dietary protein for another or of decreasing protein intake at the expense of carbohydrates or total fats did not show any statistically significant association with CHD risk.Based on a large community cohort we found no overall relationship between protein type and major dietary protein sources and risk for CHD.
| S-EPMC4193805 | biostudies-other