TY  - JOUR
AB  - IMPORTANCE: Patients with heart failure may be particularly susceptible to nonoptimal temperature exposure, but the associations between short-term low and high temperature exposure and mortality in this population remain unclear, especially in Sweden-a high-latitude country where no nationwide study has been conducted. OBJECTIVE: To investigate the associations between short-term exposure to low and high ambient temperatures and all-cause and cardiovascular mortality among Swedish patients with heart failure. DESIGN, SETTING, AND PARTICIPANTS: This nationwide, time-stratified case-crossover study was conducted in Sweden among 250 640 patients with heart failure who died from any cause from 2006 to 2021, identified from the Swedish National Patient Register and the Cause of Death Register. EXPOSURE: Daily mean ambient temperature was assessed at 1 × 1-km spatial resolution. To account for regional adaptation, temperature exposures were defined using municipality-specific percentiles, with low and high temperatures corresponding to the 2.5th and 97.5th percentiles, respectively. MAIN OUTCOMES AND MEASURES: The primary outcome was all-cause and cardiovascular mortality among patients with heart failure. RESULTS: The mean (SD) age at death among patients with heart failure was 84.3 (9.4) years, with 121 061 female patients (48.3%). Short-term exposure to ambient temperature demonstrated a U-shaped association with both all-cause and cardiovascular mortality. For all-cause mortality, odds ratios (ORs) were 1.130 (95% CI, 1.074-1.189) for low temperatures and 1.054 (95% CI, 1.017-1.093) for high temperatures over the entire study period. For cardiovascular mortality, low temperatures were associated with an OR of 1.160 (95% CI, 1.083-1.242) over the entire study period, and high temperatures with an OR of 1.084 (95% CI, 1.014-1.159) during 2014-2021. The mortality risk associated with high temperatures was more pronounced during the 2014-2021 period compared to 2006-2013. Male patients, those with comorbid diabetes, and diuretic users were more susceptible to low temperatures, whereas high temperature was more strongly associated with mortality in patients with comorbid atrial fibrillation or flutter and those exposed to elevated ozone levels. CONCLUSIONS AND RELEVANCE: This nationwide Swedish time-stratified case-crossover study indicates that short-term exposure to both low and high temperatures was associated with increased risk of all-cause and cardiovascular mortality in patients with heart failure. The mortality risk associated with high temperatures appears to be increasing over time, emphasizing the need for adaptation, even in high-latitude regions.
AU  - Ni, W.*
AU  - Benson, L.*
AU  - Ljungman, P.*
AU  - Nobile, F.*
AU  - Breitner-Busch, S.
AU  - Zhang, S.*
AU  - de Bont, J.*
AU  - Lund, L.H.*
AU  - Savarese, G.*
AU  - Schneider, A.E.
AU  - Agewall, S.*
C1  - 75828
C2  - 58097
TI  - Short-term exposure to low and high temperatures and mortality among patients with heart failure in Sweden.
JO  - JAMA Cardiol.
PY  - 2025
SN  - 2380-6591
ER  - 

TY  - JOUR
AB  - Importance: Human genetics and studies in experimental models support a key role of monocyte-chemoattractant protein-1 (MCP-1) in atherosclerosis. Yet, the associations of circulating MCP-1 levels with risk of coronary heart disease and cardiovascular death in the general population remain largely unexplored. Objective: To explore whether circulating levels of MCP-1 are associated with risk of incident coronary heart disease, myocardial infarction, and cardiovascular mortality in the general population. Data Sources and Selection: Population-based cohort studies, identified through a systematic review, that have examined associations of circulating MCP-1 levels with cardiovascular end points. Data Extraction and Synthesis: Using a prespecified harmonized analysis plan, study-specific summary data were obtained from Cox regression models after excluding individuals with overt cardiovascular disease at baseline. Derived hazard ratios (HRs) were synthesized using random-effects meta-analyses. Main Outcomes and Measures: Incident coronary heart disease (myocardial infarction, coronary revascularization, and unstable angina), nonfatal myocardial infarction, and cardiovascular death (from cardiac or cerebrovascular causes). Results: The meta-analysis included 7 cohort studies involving 21401 individuals (mean [SD] age, 53.7 [10.2] years; 10012 men [46.8%]). Mean (SD) follow-up was 15.3 (4.5) years (326392 person-years at risk). In models adjusting for age, sex, and race/ethnicity, higher MCP-1 levels at baseline were associated with increased risk of coronary heart disease (HR per 1-SD increment in MCP-1 levels: 1.06 [95% CI, 1.01-1.11]; P =.01), nonfatal myocardial infarction (HR, 1.07 [95% CI, 1.01-1.13]; P =.02), and cardiovascular death (HR, 1.12 [95% CI, 1.05-1.20]; P <.001). In analyses comparing MCP-1 quartiles, these associations followed dose-response patterns. After additionally adjusting for vascular risk factors, the risk estimates were attenuated, but the associations of MCP-1 levels with cardiovascular death remained statistically significant, as did the association of MCP-1 levels in the upper quartile with coronary heart disease. There was no significant heterogeneity; the results did not change in sensitivity analyses excluding events occurring in the first 5 years after MCP-1 measurement, and the risk estimates were stable after additional adjustments for circulating levels of interleukin-6 and high-sensitivity C-reactive protein. Conclusions and Relevance: Higher circulating MCP-1 levels are associated with higher long-term cardiovascular mortality in community-dwelling individuals free of overt cardiovascular disease. These findings provide further support for a key role of MCP-1-signaling in cardiovascular disease..
AU  - Georgakis, M.K.*
AU  - de Lemos, J.A.*
AU  - Ayers, C.*
AU  - Wang, B.*
AU  - Björkbacka, H.*
AU  - Pana, T.A.*
AU  - Thorand, B.
AU  - Sun, C.*
AU  - Fani, L.*
AU  - Malik, R.*
AU  - Dupuis, J.*
AU  - Engström, G.*
AU  - Orho-Melander, M.*
AU  - Melander, O.*
AU  - Boekholdt, S.M.*
AU  - Zierer, A.
AU  - Elhadad, M.A.
AU  - Koenig, W.*
AU  - Herder, C.*
AU  - Hoogeveen, R.C.*
AU  - Kavousi, M.*
AU  - Ballantyne, C.M.*
AU  - Peters, A.
AU  - Myint, P.K.*
AU  - Nilsson, J.*
AU  - Benjamin, E.J.*
AU  - Dichgans, M.*
C1  - 60534
C2  - 49340
CY  - 330 N Wabash Ave, Ste 39300, Chicago, Il 60611-5885 Usa
SP  - 587-592
TI  - Association of circulating monocyte chemoattractant protein-1 levels with cardiovascular mortality: A meta-analysis of population-based studies.
JO  - JAMA Cardiol.
VL  - 6
IS  - 5
PB  - Amer Medical Assoc
PY  - 2021
SN  - 2380-6591
ER  - 

TY  - JOUR
AB  - IMPORTANCE Risk stratification for coronary heart disease (CHD) remains challenging because of the complex causative mechanism of the disease. Metabolomic profiling offers the potential to detect new biomarkers and improve CHD risk assessment.OBJECTIVE To evaluate the association between circulating metabolites and incident CHD in a large European cohort.DESIGN, SETTING, AND PARTICIPANTS This population-based study used the Biomarkers for Cardiovascular Risk Assessment in Europe (BiomarCaRE) case-cohort to measure circulating metabolites using a targeted approach in serum samples from 10 741 individuals without prevalent CHD. The cohort consisted of a weighted, random subcohort of the original cohort of more than 70 000 individuals. The case-cohort design was applied to 6 European cohorts: FINRISK97 (Finland), Monitoring of Trends and Determinants in Cardiovascular Diseases/Cooperative Health Research in the Region of Augsburg (MONICA/KORA; Germany), MONICA-Brianza and Moli-Sani (Italy), DanMONICA (Denmark), and the Scottish Heart Health Extended Cohort (United Kingdom).MAIN OUTCOMES AND MEASURES Associations with time to CHD onset were assessed individually by applying weighted and adjusted Cox proportional hazard models. The association of metabolites with CHD onset was examined by C indices.RESULTS In 10 741 individuals (4157 women [38.7%]; median [interquartile range] age, 56.5 [49.2-62.2] years), 2166 incident CHD events (20.2%) occurred over a median (interquartile range) follow-up time of 9.2 (4.5-15.0) years. Among the 141 metabolites analyzed, 24 were significantly associated with incident CHD at a nominal P value of .05, including phosphatidylcholines (PCs), lysoPCs, amino acids, and sphingolipids. Five PCs remained significant after correction for multiple testing: acyl-alkyl-PC C40:6 (hazard ratio [HR], 1.13 [95% CI, 1.07-1.18]), diacyl-PC C40:6 (HR, 1.10 [95% CI, 1.04-1.15]), acyl-alkyl-PC C38:6 (HR, 1.11 [95% CI, 1.05-1.16]), diacyl-PC C38:6 (HR, 1.09 [95% CI, 1.04-1.14]) and diacyl-PC C38:5 (HR, 1.10 [95% CI, 1.05-1.16]). Lower levels of these metabolites were associated with increased risk of incident CHD. The strength of the associations competes with those of classic risk factors (C statistics: acyl-alkyl-PC C40:6, 0.756 [95% CI, 0.738-0.774], diacyl-PC C40:6, 0.754 [95% CI, 0.736-0.772], acyl-alkyl-PC C38:6, 0.755 [95% CI, 0.736-0.773], diacyl-PC C38:6, 0.754 [95% CI, 0.736-0.772]), diacyl-PC C38:5, 0.754 [95% CI, 0.736-0.772]). Adding metabolites to a base risk model including classic risk factors high-sensitivity C-reactive protein and high-sensitivity troponin I did not improve discrimination by C statistics.CONCLUSIONS AND RELEVANCE Five PCs were significantly associated with increased risk of incident CHD and showed comparable discrimination with individual classic risk factors. Although these metabolites do not improve CHD risk assessment beyond that of classic risk factors, these findings hold promise for an improved understanding of the pathophysiology of CHD.
AU  - Cavus, E.*
AU  - Karakas, M.*
AU  - Ojeda, F.M.*
AU  - Kontto, J.*
AU  - Veronesi, G.*
AU  - Ferrario, M.M.*
AU  - Linneberg, A.*
AU  - Jørgensen, T.*
AU  - Meisinger, C.
AU  - Thorand, B.
AU  - Iacoviello, L.*
AU  - Börnigen, D.*
AU  - Woodward, M.*
AU  - Schnabel, R.*
AU  - Costanzo, S.*
AU  - Tunstall-Pedoe, H.*
AU  - Koenig, W.*
AU  - Kuulasmaa, K.*
AU  - Salomaa, V.*
AU  - Blankenberg, S.*
AU  - Zeller, T.*
C1  - 57216
C2  - 47616
CY  - 330 N Wabash Ave, Ste 39300, Chicago, Il 60611-5885 Usa
SP  - 1270-1279
TI  - Association of circulating metabolites with risk of coronary heart disease in a European population results from the biomarkers for cardiovascular risk assessment in Europe (BiomarCaRE) consortium.
JO  - JAMA Cardiol.
VL  - 4
IS  - 12
PB  - Amer Medical Assoc
PY  - 2019
SN  - 2380-6591
ER  - 

TY  - JOUR
AB  - IMPORTANCE It is uncertain to what extent established cardiovascular risk factors are associated with venous thromboembolism (VTE).OBJECTIVE To estimate the associations of major cardiovascular risk factors with VTE, ie, deep vein thrombosis and pulmonary embolism.DESIGN, SETTING, AND PARTICIPANTS This study included individual participant data mostly from essentially population-based cohort studies from the Emerging Risk Factors Collaboration (ERFC; 731728 participants; 75 cohorts; years of baseline surveys, February 1960 to June 2008; latest date of follow-up, December 2015) and the UK Biobank (421537 participants; years of baseline surveys, March 2006 to September 2010; latest date of follow-up, February 2016). Participants without cardiovascular disease at baseline were included. Data were analyzed from June 2017 to September 2018.EXPOSURES A panel of several established cardiovascular risk factors.MAIN OUTCOMES AND MEASURES Hazard ratios (HRs) per 1-SD higher usual risk factor levels (or presence/absence). Incident fatal outcomes in ERFC (VTE, 1041; coronary heart disease [CND], 25131) and incident fatal/nonfatal outcomes in UK Biobank (VTE, 2321; CHD, 3385). Hazard ratios were adjusted for age, sex, smoking status, diabetes, and body mass index (BMI).RESULTS Of the 731728 participants from the ERFC. 403 396 (55.1%) were female, and the mean (SD) age at the time of the survey was 51.9 (9.0) years; of the 421537 participants from the UK Biobank, 233 699 (55.4%) were female, and the mean (SD) age at the time of the survey was 56.4 (8.1) years. Risk factors for VTE included older age (ERFC: HR per decade, 2.67; 95% CI, 2.45-2.91; UK Biobank: HR, 1.81; 95% CI, 1.71-1.92), current smoking (ERFC: HR, 1.38; 95% CI, 1.20-1.58; UK Biobank: HR, 1.23; 95% CI, 1.08-1.40), and BMI (ERFC: HR per 1-SD higher BMI, 1.43; 95% CI, 1.35-1.50; UK Biobank: HR, 1.37; 95% CI, 1.32-1.41). For these factors, there were similar HRs for pulmonary embolism and deep vein thrombosis in UK Biobank (except adiposity was more strongly associated with pulmonary embolism) and similar HRs for unprovoked vs provoked VTE. Apart from adiposity, these risk factors were less strongly associated with VTE than CHD. There were inconsistent associations of VTEs with diabetes and blood pressure across ERFC and UK Biobank, and there was limited ability to study lipid and inflammation markers.CONCLUSIONS AND RELEVANCE Older age, smoking, and adiposity were consistently associated with higher VTE risk.
AU  - Gregson, J.*
AU  - Kaptoge, S.*
AU  - Bolton, T.*
AU  - Pennells, L.*
AU  - Willeit, P.*
AU  - Burgess, S.*
AU  - Bell, S.*
AU  - Sweeting, M.*
AU  - Rimm, E.B.*
AU  - Kabrhel, C.*
AU  - Zöller, B.*
AU  - Assmann, G.*
AU  - Gudnason, V.*
AU  - Folsom, A.R.*
AU  - Arndt, V.*
AU  - Fletcher, A.*
AU  - Norman, P.E.*
AU  - Nørdestgaard, B.G.*
AU  - Kitamura, A.*
AU  - Mahmoodi, B.K.*
AU  - Whincup, P.H.*
AU  - Knuiman, M.*
AU  - Salomaa, V.*
AU  - Meisinger, C.
AU  - Koenig, W.*
AU  - Kavousi, M.*
AU  - Völzke, H.*
AU  - Cooper, J.A.*
AU  - Ninomiya, T.*
AU  - Casiglia, E.*
AU  - Rodriguez, B.*
AU  - Ben-Shlomo, Y.*
AU  - Després, J.P.*
AU  - Simons, L.*
AU  - Barrett-Connor, E.*
AU  - Björkelund, C.*
AU  - Notdurfter, M.*
AU  - Kromhout, D.*
AU  - Price, J.*
AU  - Sutherland, S.E.*
AU  - Sundström, J.*
AU  - Kauhanen, J.*
AU  - Gallacher, J.*
AU  - Beulens, J.W.J.*
AU  - Dankner, R.*
AU  - Cooper, C.*
AU  - Giampaoli, S.*
AU  - Deen, J.F.*
AU  - Gómez de la Cámara, A.*
AU  - Kuller, L.H.*
AU  - Rosengren, A.*
AU  - Svensson, P.J.*
AU  - Nagel, D.*
AU  - Crespo, C.J.*
AU  - Brenner, H.*
AU  - Albertorio-Diaz, J.R.*
AU  - Atkins, R.*
AU  - Brunner, E.J.*
AU  - Shipley, M.*
AU  - Njølstad, I.*
AU  - Lawlor, D.A.*
AU  - van der Schouw, Y.T.*
AU  - Selmer, R.M.*
AU  - Trevisan, M.*
AU  - Verschuren, W.M.M.*
AU  - Greenland, P.*
AU  - Wassertheil-Smoller, S.*
AU  - Lowe, G.D.O.*
AU  - Wood, A.M.*
AU  - Butterworth, A.S.*
AU  - Thompson, S.G.*
AU  - Danesh, J.*
AU  - di Angelantonio, E.*
AU  - Meade, T.*
C1  - 55322
C2  - 46274
CY  - 330 N Wabash Ave, Ste 39300, Chicago, Il 60611-5885 Usa
SP  - 163-173
TI  - Cardiovascular risk factors are associated with venous thromboembolism.
JO  - JAMA Cardiol.
VL  - 4
IS  - 2
PB  - Amer Medical Assoc
PY  - 2019
SN  - 2380-6591
ER  - 

TY  - JOUR
AB  - IMPORTANCE Genetic and epidemiologic data suggest that lipoprotein(a) (Lp[a]) is one of the strongest genetically determined risk factors for coronary heart disease (CHD). Specific therapies to lower Lp(a) are on the horizon, but the required reduction of Lp(a) to translate into clinically relevant lowering of CHD outcomes is a matter of debate.OBJECTIVE To estimate the required Lp(a)-lowering effect size that may be associated with a reduction of CHD outcomes compared with the effect size of low-density lipoprotein cholesterol (LDL-C)-lowering therapies.DESIGN, SETTING, AND PARTICIPANTS Genetic epidemiologic study using a mendelian randomization analysis to estimate the required Lp(a)-lowering effect size for a clinically meaningful effect on outcomes. We used the effect estimates for Lp(a) from a genome-wide association study (GWAS) and meta-analysis on Lp(a) published in 2017 of 5 different primarily population-based studies of European ancestry. All Lp(a) measurements were performed in 1 laboratory. Genetic estimates for 27 single-nucleotide polymorphisms on Lp(a) concentrations were used. Odds ratios for these 27 single-nucleotide polymorphisms associated with CHD risk were retrieved from a subsample of the CHD Exome+ consortium.EXPOSURES Genetic LPA score, plasma Lp(a) concentrations, and observations of statin therapies on CHD outcomes.MAIN OUTCOMES AND MEASURES Coronary heart disease.RESULTS The study included 13 781 individuals from the Lp(a)-GWAS-Consortium from 5 primarily population-based studies and 20 793 CHD cases and 27 540 controls from a subsample of the CHD Exome+ consortium. Four of the studies were similar in age distribution (means between 51 and 59 years), and 1 cohort was younger; mean age, 32 years. The frequency of women was similar between 51% and 55%. We estimated that the required reduction in Lp(a) effect size would be 65.7mg/dL (95% CI, 46.3-88.3) to reach the same potential effect on clinical outcomes that can be reached by lowering LDL-C by 38.67mg/dL (to convert to millimoles per liter, multiply by 0.0259).CONCLUSIONS AND RELEVANCE This mendelian randomization analysis estimated a required Lp(a)-lowering effect size of 65.7mg/dL to reach the same effect as a 38.67-mg/dL lowering of LDL-C. However, this estimate is determined by the observed effect estimates of single-nucleotide polymorphisms on Lp(a) concentrations and is therefore influenced by the standardization of the Lp(a) assay used. As a consequence, calculations of the required Lp(a)-lowering potential of a drug to be clinically effective might have been overestimated in the past.
AU  - Lamina, C.*
AU  - Kronenberg, F.*
AU  - Mack, S.*
AU  - Coassin, S.*
AU  - Rueedi, R.*
AU  - Yousri, N.A.*
AU  - Seppälä, I.*
AU  - Lp(a)-GWAS-Consortium (Gieger, C.)
AU  - Schönherr, S.*
AU  - Forer, L.*
AU  - Erhart, G.*
AU  - Marques-Vidal, P.*
AU  - Lp(a)-GWAS-Consortium (Ried, J.S.)
AU  - Waeber, G.*
AU  - Bergmann, S.*
AU  - Daehnhardt, D.*
AU  - Stoeckl, A.*
AU  - Raitakari, O.T.*
AU  - Kähönen, M.*
AU  - Lp(a)-GWAS-Consortium (Peters, A.)
AU  - Lp(a)-GWAS-Consortium (Meitinger, T.)
AU  - Lp(a)-GWAS-Consortium (Strauch, K.)
AU  - Kedenko, L.*
AU  - Paulweber, B.*
AU  - Lehtimäki, T.*
AU  - Hunt, S.C.*
AU  - Vollenweider, P.*
C1  - 56526
C2  - 47081
CY  - 330 N Wabash Ave, Ste 39300, Chicago, Il 60611-5885 Usa
SP  - 575-579
TI  - Estimation of the required lipoprotein(a)-lowering therapeutic effect size for reduction in coronary heart disease outcomes a mendelian randomization analysis.
JO  - JAMA Cardiol.
VL  - 4
IS  - 6
PB  - Amer Medical Assoc
PY  - 2019
SN  - 2380-6591
ER  - 

TY  - JOUR
AB  - IMPORTANCE Tumor necrosis factor α (TNF-α) is a proinflammatory cytokine with manifold consequences for mammalian pathophysiology, including cardiovascular disease. A deeper understanding of TNF-α biologymay enhance treatment precision. OBJECTIVE To conduct an epigenome-wide analysis of blood-derived DNA methylation and TNF-α levels and to assess the clinical relevance of findings. DESIGN, SETTING, AND PARTICIPANTS This meta-analysis assessed epigenome-wide associations in circulating TNF-α concentrations from 5 cohort studies and 1 interventional trial, with replication in 3 additional cohort studies. Follow-up analyses investigated associations of identified methylation loci with gene expression and incident coronary heart disease; this meta-analysis included 11 461 participants who experienced 1895 coronary events. EXPOSURES Circulating TNF-α concentration. MAIN OUTCOMES AND MEASURES DNA methylation at approximately 450 000 loci, neighboring DNA sequence variation, gene expression, and incident coronary heart disease. RESULTS The discovery cohort included 4794 participants, and the replication study included 816 participants (overall mean [SD] age, 60.7 [8.5] years). In the discovery stage, circulating TNF-α levels were associated with methylation of 7 cytosine-phosphate-guanine (CpG) sites, 3 of which were located in or near DTX3L-PARP9 at cg00959259 (β [SE] = -0.01 [0.003]; P = 7.36 × 10-8), cg08122652 (β [SE] = -0.008 [0.002]; P = 2.24 × 10-7), and cg22930808(β [SE] = -0.01 [0.002]; P = 6.92 × 10-8); NLRC5 at cg16411857 (β [SE] = -0.01 [0.002]; P = 2.14 × 10-13) and cg07839457 (β [SE] = -0.02 [0.003]; P = 6.31 × 10-10); or ABO, at cg13683939 (β [SE] = 0.04 [0.008]; P = 1.42 × 10-7) and cg24267699 (β [SE] = -0.009 [0.002]; P = 1.67 × 10-7), after accounting for multiple testing. Of these, negative associations between TNF-α concentration and methylation of 2 loci in NLRC5 and 1 in DTX3L-14 PARP9 were replicated. Replicated TNF-α-linked CpG sites were associated with 9% to 19% decreased risk of incident coronary heart disease per 10% higher methylation per CpG site (cg16411857: hazard ratio [HR], 0.86; 95%CI, 0.78-1.95; P = .003; cg07839457: HR, 0.89; 95%CI, 0.80-0.94; P = 3.1 × 10-5; cg00959259: HR, 0.91; 95%CI, 0.84-0.97; P = .002; cg08122652: HR, 0.81; 95%CI, 0.74-0.89; P = 2.0 × 10-5). CONCLUSIONS AND RELEVANCE We identified and replicated novel epigenetic correlates of circulating TNF-α concentration in blood samples and linked these loci to coronary heart disease risk, opening opportunities for validation and therapeutic applications.
AU  - Aslibekyan, S.*
AU  - Agha, G.*
AU  - Colicino, E.*
AU  - Do, A.N.*
AU  - Lahti, J.*
AU  - Ligthart, S.*
AU  - Marioni, R.E.*
AU  - Marzi, C.
AU  - Mendelson, M.M.*
AU  - Tanaka, T.*
AU  - Wielscher, M.*
AU  - Absher, D.M.*
AU  - Ferrucci, L.*
AU  - Franco, O.H.*
AU  - Gieger, C.
AU  - Grallert, H.
AU  - Hernandez, D.*
AU  - Huan, T.*
AU  - Iurato, S.*
AU  - Joehanes, R.*
AU  - Just, A.C.*
AU  - Kunze, S.
AU  - Lin, H.*
AU  - Liu, C.*
AU  - Meigs, J.B.*
AU  - van Meurs, J.B.J.*
AU  - Moore, A.Z.*
AU  - Peters, A.
AU  - Prokisch, H.
AU  - Räikkönen, K.*
AU  - Rathmann, W.*
AU  - Roden, M.*
AU  - Schramm, K.
AU  - Schwartz, J.D.*
AU  - Starr, J.M.*
AU  - Uitterlinden, A.G.*
AU  - Vokonas, P.*
AU  - Waldenberger, M.
AU  - Yao, C.*
AU  - Zhi, D.*
AU  - Baccarelli, A.A.*
AU  - Bandinelli, S.*
AU  - Deary, I.J.*
AU  - Dehghan, A.*
AU  - Eriksson, J.*
AU  - Herder, C.*
AU  - Järvelin, M.R.*
AU  - Levy, D.*
AU  - Arnett, D.K.*
C1  - 53742
C2  - 44983
SP  - 463-472
TI  - Association of methylation signals with incident coronary heart disease in an epigenome-wide assessment of circulating tumor necrosis factor.
JO  - JAMA Cardiol.
VL  - 3
IS  - 6
PY  - 2018
SN  - 2380-6591
ER  -