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  • Ovid Technologies (Wolters Kluwer Health)  (26)
  • 1
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    Causal Effect of Plasminogen Activator Inhibitor Type 1 on Coronary Heart Disease
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Journal of the American Heart Association Vol. 6, No. 6 ( 2017-11-06)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 6, No. 6 ( 2017-11-06)
    Abstract: Plasminogen activator inhibitor type 1 ( PAI ‐1) plays an essential role in the fibrinolysis system and thrombosis. Population studies have reported that blood PAI ‐1 levels are associated with increased risk of coronary heart disease ( CHD ). However, it is unclear whether the association reflects a causal influence of PAI ‐1 on CHD risk. Methods and Results To evaluate the association between PAI ‐1 and CHD , we applied a 3‐step strategy. First, we investigated the observational association between PAI ‐1 and CHD incidence using a systematic review based on a literature search for PAI ‐1 and CHD studies. Second, we explored the causal association between PAI ‐1 and CHD using a Mendelian randomization approach using summary statistics from large genome‐wide association studies. Finally, we explored the causal effect of PAI ‐1 on cardiovascular risk factors including metabolic and subclinical atherosclerosis measures. In the systematic meta‐analysis, the highest quantile of blood PAI ‐1 level was associated with higher CHD risk comparing with the lowest quantile (odds ratio=2.17; 95% CI: 1.53, 3.07) in an age‐ and sex‐adjusted model. The effect size was reduced in studies using a multivariable‐adjusted model (odds ratio=1.46; 95% CI : 1.13, 1.88). The Mendelian randomization analyses suggested a causal effect of increased PAI ‐1 level on CHD risk (odds ratio=1.22 per unit increase of log‐transformed PAI ‐1; 95% CI : 1.01, 1.47). In addition, we also detected a causal effect of PAI ‐1 on elevating blood glucose and high‐density lipoprotein cholesterol. Conclusions Our study indicates a causal effect of elevated PAI ‐1 level on CHD risk, which may be mediated by glucose dysfunction.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.116.004918
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 2653953-6
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  • 2
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    Multiethnic Exome-Wide Association Study of Subclinical Atherosclerosis
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Circulation: Cardiovascular Genetics Vol. 9, No. 6 ( 2016-12), p. 511-520
    Details
    In: Circulation: Cardiovascular Genetics, Ovid Technologies (Wolters Kluwer Health), Vol. 9, No. 6 ( 2016-12), p. 511-520
    Abstract: The burden of subclinical atherosclerosis in asymptomatic individuals is heritable and associated with elevated risk of developing clinical coronary heart disease. We sought to identify genetic variants in protein-coding regions associated with subclinical atherosclerosis and the risk of subsequent coronary heart disease. Methods and Results— We studied a total of 25 109 European ancestry and African ancestry participants with coronary artery calcification (CAC) measured by cardiac computed tomography and 52 869 participants with common carotid intima–media thickness measured by ultrasonography within the CHARGE Consortium (Cohorts for Heart and Aging Research in Genomic Epidemiology). Participants were genotyped for 247 870 DNA sequence variants (231 539 in exons) across the genome. A meta-analysis of exome-wide association studies was performed across cohorts for CAC and carotid intima–media thickness. APOB p.Arg3527Gln was associated with 4-fold excess CAC ( P =3×10 − 10 ). The APOE ε2 allele (p.Arg176Cys) was associated with both 22.3% reduced CAC ( P =1×10 − 12 ) and 1.4% reduced carotid intima–media thickness ( P =4×10 − 14 ) in carriers compared with noncarriers. In secondary analyses conditioning on low-density lipoprotein cholesterol concentration, the ε2 protective association with CAC, although attenuated, remained strongly significant. Additionally, the presence of ε2 was associated with reduced risk for coronary heart disease (odds ratio 0.77; P =1×10 − 11 ). Conclusions— Exome-wide association meta-analysis demonstrates that protein-coding variants in APOB and APOE associate with subclinical atherosclerosis. APOE ε2 represents the first significant association for multiple subclinical atherosclerosis traits across multiple ethnicities, as well as clinical coronary heart disease.
    Type of Medium: Online Resource
    ISSN: 1942-325X , 1942-3268
    URL: Article
    DOI: 10.1161/CIRCGENETICS.116.001572
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 2927603-2
    detail.hit.zdb_id: 2457085-0
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  • 3
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    Genome-Wide Association Study for Coronary Artery Calcification With Follow-Up in Myocardial Infarction
    Ovid Technologies (Wolters Kluwer Health) ; 2011
    In:  Circulation Vol. 124, No. 25 ( 2011-12), p. 2855-2864
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 124, No. 25 ( 2011-12), p. 2855-2864
    Abstract: Coronary artery calcification (CAC) detected by computed tomography is a noninvasive measure of coronary atherosclerosis, which underlies most cases of myocardial infarction (MI). We sought to identify common genetic variants associated with CAC and further investigate their associations with MI. Methods and Results— Computed tomography was used to assess quantity of CAC. A meta-analysis of genome-wide association studies for CAC was performed in 9961 men and women from 5 independent community-based cohorts, with replication in 3 additional independent cohorts (n=6032). We examined the top single-nucleotide polymorphisms (SNPs) associated with CAC quantity for association with MI in multiple large genome-wide association studies of MI. Genome-wide significant associations with CAC for SNPs on chromosome 9p21 near CDKN2A and CDKN2B (top SNP: rs1333049; P =7.58×10 −19 ) and 6p24 (top SNP: rs9349379, within the PHACTR1 gene; P =2.65×10 −11 ) replicated for CAC and for MI. Additionally, there is evidence for concordance of SNP associations with both CAC and MI at a number of other loci, including 3q22 ( MRAS gene), 13q34 ( COL4A1/COL4A2 genes), and 1p13 ( SORT1 gene). Conclusions— SNPs in the 9p21 and PHACTR1 gene loci were strongly associated with CAC and MI, and there are suggestive associations with both CAC and MI of SNPs in additional loci. Multiple genetic loci are associated with development of both underlying coronary atherosclerosis and clinical events.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/CIRCULATIONAHA.110.974899
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2011
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  • 4
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    Abstract P207: Nonalcoholic Fatty Liver Disease Interacts With Diabetes Increasing The Risk Of Atherosclerosis In The Family Heart Study
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Circulation Vol. 125, No. suppl_10 ( 2012-03-13)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 125, No. suppl_10 ( 2012-03-13)
    Abstract: Nonalcoholic fatty liver disease (NAFLD) is associated with obesity and type 2 diabetes (T2D), which are risk factors for atherosclerosis. However, it is not clear whether NAFLD has an independent contribution to atherosclerosis. The burden of calcification in the coronary artery (CAC) can be measured by computed tomography (CT) and is a measure of atherosclerosis. CT measured liver attenuation (in Hounsfield Units) is inversely related to the amount of fat in the liver (FL), while elevated alanine aminotransferse (ALT, in U/L) levels indicate hepatic damage and is often used as a marker of NAFLD. We investigated whether NAFLD, defined by FL and ALT levels, is a significant predictor of the presence of CAC independent of insulin resistance (HOMA-IR: fasting glucose* fasting insulin/22.5) and overall obesity (BMI, kg/m 2 ) in 2,550 European-American individuals. We employed a linear mixed model to account for the non-independence of family members, and included age, age 2 , sex, current cigarette smoking (yes/no), alcohol intake (yes/no) and clinical center in each model. Heavy drinkers (men: ≥ 21 drinks/week, women: ≥ 14 drinks/week) and subjects who tested positive for hepatitis-C antibodies were excluded from the analyses. In the multivariate model including FL, ALT, BMI, HOMA-IR, and T2D, neither FL nor ALT was associated with CAC; while BMI (p 〈 0.0001), HOMA-IR (p= 0.0150) and T2D (p= 0.0008) were significant. Also, we employed a similar multivariate regression model separately in subjects without T2D (not taking hypoglycemic medications and/or fasting glucose 〈 126 ml/dL) and with T2D (but excluding subject taking insulin medication). In subjects without T2D, we found that ALT (p=0.0385, OR=1.126, 95% CI:1.006–1.260) was a significant predictor of CAC together with BMI (p 〈 0.0001) and HOMA-IR (p= 0.0082). In subjects with T2D, ALT (p=0.0376, OR= 0.590, 95% CI:0.361–0.964) was a significant predictor of CAC but not FL, BMI or HOMA-IR which may reflect the effect of other T2D medication. Further, we investigated whether T2D interacts with ALT modifying the risk of CAC independent of BMI and HOMA-IR. In the combined T2D and non-T2D subsets, we included the interaction term (T2D*ALT) in the multivariate model and found significant association of CAC with T2D*ALT (p= 0.0018, OR= 0.555, 95% CI: 0.0384–0.802), ALT (p= 0.0315, OR= 1.134, 95% CI: 1.011–1.271), and T2D (p=0.0001), together with BMI (p 〈 0.0001) and HOMA-IR (p= 0.0156). In summary, we found that: (i) the association of NAFLD steatosis (FL) with CAC is mediated by overall obesity (BMI) and insulin resistance (HOMA-IR); (ii) ALT, indicating hepatic damage, is a significant predictor of atherosclerosis independent of BMI and HOMA-IR; and (iii) having hepatic damage along with T2D augments the risk of atherosclerosis.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.125.suppl_10.AP207
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
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  • 5
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    Abstract P328: Genetic Variants Involved in Postprandial Triglyceride Metabolism are Modified by Fenofibrate Treatment in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) Study
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Circulation Vol. 125, No. suppl_10 ( 2012-03-13)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 125, No. suppl_10 ( 2012-03-13)
    Abstract: Genetic variants associated with fasting plasma triglycerides (TG) have been reported in the literature. Less is known about genetic variants influencing TG response to dietary factors, specifically a fat challenge (postprandial lipemia, PPL). Additionally, little is known about genetic variants associated with response to pharmacologic agents, such as fenofibrate (FFB), which are used to reduce plasma levels of TG. Preliminary genome-wide association (GWA) analyses on three interventions: 1) FFB; 2) PPL before FFB; and 3) PPL after FFB, implicated different genetic variants associated with the TG response. Therefore, we hypothesized that FFB treatment modifies gene effects on TG response to a dietary postprandial fat challenge. We analyzed participants (N=693) from the GOLDN study who ingested a standardized high-fat meal containing 83% fat and 700 calories/m2 both before and after 3 weeks of daily FFB treatment, thereby having two postprandial plasma TG assessments. Plasma TG was measured at baseline, 3.5 hrs, and 6 hrs after each high-fat meal. The area under the curve (AUC) describing the change in plasma TG concentration over the PPL period was calculated using the trapezoid method. Standardized TG AUC residuals were obtained by using a growth curve method and a stepwise regression approach, retaining covariate terms (age, age2, age3, sex, field center, baseline TG, and principle components (EIGENSTRAT)) that were significant at 5% level. A GWA scan of ∼2.5 million typed or imputed single nucleotide polymorphisms (SNPs) was undertaken to identify gene by FFB treatment interaction effects on the TG AUC PPL response using a repeated measures mixed model with a random effect to adjust for family relatedness. The GWA model included a SNP effect, FFB effect (before or after treatment), and an interaction term (SNP*FFB). For TG AUC residuals, we found GWA significant associations with 8 variants in LDLRAD3 (11p13) for the SNP*FFB term (p 〈 5E-08), and the accompanying main effect terms had suggestive (p 〈 1E-05) associations. These 8 variants are in one linkage disequilibrium block, and indicate that FFB interacts with these variants to decrease their independent effects on TG AUC. In analyses using only the SNP, these 8 variants had p-values 〈 0.005 for TG response to PPL both before and after FFB. SNPs in this group associate with expression of CD44, a molecule which binds osteopontin which is an activator of human adipose tissue macrophages and adipocyte function. This analysis highlights a new gene implicated in TG metabolism whose effect on dietary TG responses to fat ingestion is modified by FFB, possibly by acting through CD44. Further investigation into this gene region is needed in order to enhance our understanding of the underlying mechanistic processes involved in TG metabolism during the postprandial state and the effect of FFB treatment.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.125.suppl_10.AP328
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
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  • 6
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    Abstract 002: Race and Sex Influence the Associations of Subcutaneous and Visceral Adipose Tissues with Calcified Plaque of the Coronary and Abdominal Aortic Arteries: The Family Heart Study
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Circulation Vol. 125, No. suppl_10 ( 2012-03-13)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 125, No. suppl_10 ( 2012-03-13)
    Abstract: Previous research suggests that visceral adipose tissue (VAT) increases risk for atherosclerosis and specifically arterial calcification, yet the association of subcutaneous adipose tissue (SAT) with calcification is less substantiated. Studies have also noted important race and sex differences in risk of atherosclerosis. In the Family Heart Study, we examined race and sex differences in the pattern of associations of abdominal fat depots with coronary (CAC) and abdominal aorto-iliac (AAC) calcified plaque measured using computed tomography (CT). Methods- We used CT to measure abdominal fat volume and arterial calcified plaque in 2,748 participants of European American descent (EA; n=1512 females) and 626 participants of African American descent (AA; n=412 females) in the Family Heart Study. CAC and AAC were defined as present (≥1) or absent (0) based on Agatston scores. Odds ratios (OR) and 95% confidence intervals (95% CI) were determined using logistic regression models adjusted for age, field center, family pedigree, race, and history of coronary heart disease (CHD), diabetes, hypertension, hypercholesterolemia, and smoking. Results- The association of SAT and VAT with prevalent CAC and AAC varied with sex and race in multivariable logistic regression models. In males, SAT was strongly associated with both CAC (p=0.001) and AAC (p 〈 0.001) in multivariable models and there was evidence that the associations of SAT with CAC and AAC differed by race (each p interaction SAT*race p 〈 0.01). The associations of SAT with CAC and AAC appeared to be stronger in EA males than in AA males. In EA, the OR for CAC for a single SD increase in SAT was 2.17 (95% CI 1.37-3.45) whereas for AA the OR was 1.42 (95% CI 1.17-1.72) per SD increase in SAT. Also, in EA males the OR for AAC per SD increase in SAT was 2.69 (95% CI 1.61-4.50) compared to 1.39 (95% CI 1.11-1.73) in AA males. VAT was significantly associated with prevalent CAC in both EA males (OR=1.96 per SD increase, p=0.02) and AA males (OR=1.26 per SD increase, p=0.02) though there were no significant associations of VAT with AAC among males. In females, both SAT (OR=1.18 per SD increase, p=0.004) and VAT (OR=1.21 per SD increase, p=0.003) were associated with prevalent CAC, but not AAC, in multivariable models and associations did not vary by race. Conclusions- Abdominal SAT was associated with both CAC and AAC prevalence in males, and associations appeared to be stronger in EA compared to AA participants. VAT was predictive of CAC in both EA and AA males. In contrast, SAT and VAT were only associated with CAC in females and no differences by race were noted. Our findings suggest that SAT, and by inference obesity, along with VAT may be an important contributors to prevalence of arterial calcification and that race plays a role in associations among males.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.125.suppl_10.A002
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
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  • 7
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    A novel healthy blood pressure phenotype in the Long Life Family Study
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Journal of Hypertension Vol. 36, No. 1 ( 2018-01), p. 43-53
    Details
    In: Journal of Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 36, No. 1 ( 2018-01), p. 43-53
    Type of Medium: Online Resource
    ISSN: 0263-6352
    URL: Article
    DOI: 10.1097/HJH.0000000000001514
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
    detail.hit.zdb_id: 2017684-3
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  • 8
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    Sex and race differences in the prevalence of fatty liver disease as measured by computed tomography liver attenuation in European American and African American participants of the NHLBI family heart study
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  European Journal of Gastroenterology & Hepatology Vol. 24, No. 1 ( 2012-01), p. 9-16
    Details
    In: European Journal of Gastroenterology & Hepatology, Ovid Technologies (Wolters Kluwer Health), Vol. 24, No. 1 ( 2012-01), p. 9-16
    Type of Medium: Online Resource
    ISSN: 0954-691X
    URL: Article
    DOI: 10.1097/MEG.0b013e32834a94fb
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 2030291-5
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  • 9
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    Heterogeneity of the Predictive Polygenic Risk Scores for Coronary Heart Disease Age-at-Onset in Three Different Coronary Heart Disease Family-Based Ascertainments
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Circulation: Genomic and Precision Medicine Vol. 14, No. 3 ( 2021-06)
    Details
    In: Circulation: Genomic and Precision Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 14, No. 3 ( 2021-06)
    Abstract: Polygenic risk scores (PRS) for coronary heart disease (CHD) may contribute to assess the overall risk of CHD. We evaluated how PRS may influence CHD risk when the distribution of age-at-onset, sex, and family health history differ significantly. Methods: Our study included 3 family-based ascertainments: LLFS (Long Life Family Study, N Individuals =4572), which represents a low CHD risk, and Family Heart Study, which consists of randomly selected families (FamHS-random, N Individuals =1806), and high CHD risk families (FamHS-high risk, N Individuals =2301). We examined the effects of PRS, sex, family ascertainment, PRS interaction with sex (PRS*sex) and with family ascertainment (PRS*LLFS and PRS*FamHS-high risk) on CHD, corrected for traditional cardiovascular risk factors using Cox proportional hazard regression models. Results: Healthy-aging LLFS presented ≈17 years delayed for CHD age-at-onset compared with FamHS-high risk ( P 〈 1.0×10 −4 ). Sex-specific association ( P 〈 1.0×10 −17 ) and PRS*sex ( P =2.7×10 −3 ) predicted prevalent CHD. CHD age-at-onset was associated with PRS (hazard ratio [HR], 1.57; P =1.3×10 −5 ), LLFS (HR, 0.54; P =2.6×10 −5 ), and FamHS-high risk (HR, 2.86; P =6.70x10 −15 ) in men, and with PRS (HR, 1.76; P =7.70×10 −3 ), FamHS-high risk (HR, 4.88; P =8.70×10 −10 ), and PRS×FamHS-high risk (HR, 0.61; P =3.60×10 −2 ) in women. In the PRS extreme quartile distributions, CHD age-at-onset was associated ( P 〈 0.05) with PRS, FamHS-high risk, and PRS interactions with both low and high CHD risk families for women. For men, the PRS quartile results remained similar to the whole distribution. Conclusions: Differences in CHD family-based ascertainments show evidence of PRS interacting with sex to predict CHD risk. In women, CHD age-at-onset was associated with PRS, CHD family history, and interactions of PRS with family history. In men, PRS and CHD family history were the major effects on the CHD age-at-onset. Understanding the heterogeneity of risks associated with CHD end points at both the personal and familial levels may shed light on the underlying genetic effects influencing CHD and lead to more personalized risk prediction.
    Type of Medium: Online Resource
    ISSN: 2574-8300
    URL: Article
    DOI: 10.1161/CIRCGEN.120.003201
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
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  • 10
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    Abstract MP79: Identification of Novel Loci Associated with Anthropometric Traits in African Ancestry Populations
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Circulation Vol. 133, No. suppl_1 ( 2016-03)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 133, No. suppl_1 ( 2016-03)
    Abstract: Introduction: African Americans have the highest prevalence of obesity in the U.S. Our prior work on HapMap imputed genome-wide association studies (GWAS) from the African Ancestry Anthropometry Genetics Consortium (AAAGC) revealed seven genome-wide significant loci for body mass index (BMI). Hypothesis: In this study, we extended to use genome-wide imputation to the cosmopolitan 1000 Genomes Phase 1 reference panel to examine individuals of African ancestry for association with BMI (N=53,493), waist-to-hip ratio adjusted for BMI (WHRadjBMI) (N=23,692) and height (N=53,362) in the discovery and replication stages. Methods: In each study, traits were stratified by gender and transformed to normality and adjusted for age, study specific covariates and principal components for single variant association test under an additive model. In the discovery stage, meta-analyses using fixed-effects inverse variance weighted method were performed to combine association results in all and sex-stratified samples. Variants with P 〈 1E-4 were selected for subsequent replications in both individuals of African ancestry and European ancestry, the latter results were obtained by imputation of summary statistics from the GIANT consortium (N=322,154 for BMI, 210,062 for WHRadjBMI, and 253,252 for height). Results: For BMI, we observed genome-wide significant associations (P 〈 5E-8) at seven established loci (near SEC16B, TMEM18, GNPDA2, GALNT10, KLHL32, FTO and MC4R) in meta-analysis of all African ancestry individuals from the discovery and replication stages. Sex-stratified meta-analysis revealed two novel loci near IRX4-IRX2 in women, and near MLC1 in men, respectively. Meta-analysis of all individuals from African and European ancestry revealed an additional novel locus near ARAP1. For WHRadjBMI, we observed genome-wide significant associations at one established locus (ADAMTS9) in all African ancestry individuals, and three novel loci (near SSX2IP, RREB1 and PDE3B) in women. For height, we observed 29 established loci and three novel loci (near NCOA2, P4HA1 and TGFB3) in all African ancestry individuals, and three novel loci (near CRB1, MIR4268 and LINC00704) in women. Among 12 lead variants at novel loci associated with anthropometry traits, four variants are low frequencies in our African ancestry populations (0.005 〈 MAF 〈 0.05). On the contrary, all but one of the lead variants at established loci were common. Conclusions: We identified 12 novel loci associated with anthropometry traits in sex-combined and sex-stratified analyses of African ancestry populations and additional European populations. Our findings support that imputation to higher density reference panels such as 1000 Genomes improves the power to detect associations at low frequency variants, which is particularly useful for African ancestry populations with a low degree of linkage disequilibrium.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.133.suppl_1.mp79
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
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