Paul M Ridker

Brigham and Women's Hospital, Boston, Massachusetts, United States

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Publications (772)9370.98 Total impact

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    ABSTRACT: Background:Two recent genome-wide association studies (GWAS) identified SNPs related to circulating 25-hydroxyvitamin D [25(OH)D] concentration in or near four genes. To examine the hypothesized inverse relationship between vitamin D status and breast cancer, we studied the associations between SNPs in these genes and breast cancer risk in a large pooled study of 9,456 cases and 10,816 controls from six cohorts. Methods:SNP markers localized to each of four genes (GC, CYP24A1, CYP2R1, and DHCR7) previously associated with 25(OH)D were genotyped and examined both individually and as a 4-SNP polygenic score. Logistic regression was used to estimate the associations between the genetic variants and risk of breast cancer. Results:We found no association between any of the four SNPs or their polygenic score and breast cancer risk. Conclusions:Our findings do not support an association between vitamin D status, as reflected by 25(OH)D-related genotypes, and breast cancer risk. Impact: These findings may contribute to future meta-analyses and scientific review articles, and provide new data about the association between vitamin D-related genes and breast cancer. Copyright © 2014, American Association for Cancer Research.
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    ABSTRACT: Genome-wide association studies (GWASs) have identified multiple loci associated with cross-sectional eGFR, but a systematic genetic analysis of kidney function decline over time is missing. Here we conducted a GWAS meta-analysis among 63,558 participants of European descent, initially from 16 cohorts with serial kidney function measurements within the CKDGen Consortium, followed by independent replication among additional participants from 13 cohorts. In stage 1 GWAS meta-analysis, single-nucleotide polymorphisms (SNPs) at MEOX2, GALNT11, IL1RAP, NPPA, HPCAL1, and CDH23 showed the strongest associations for at least one trait, in addition to the known UMOD locus, which showed genome-wide significance with an annual change in eGFR. In stage 2 meta-analysis, the significant association at UMOD was replicated. Associations at GALNT11 with Rapid Decline (annual eGFR decline of 3 ml/min per 1.73 m(2) or more), and CDH23 with eGFR change among those with CKD showed significant suggestive evidence of replication. Combined stage 1 and 2 meta-analyses showed significance for UMOD, GALNT11, and CDH23. Morpholino knockdowns of galnt11 and cdh23 in zebrafish embryos each had signs of severe edema 72 h after gentamicin treatment compared with controls, but no gross morphological renal abnormalities before gentamicin administration. Thus, our results suggest a role in the deterioration of kidney function for the loci GALNT11 and CDH23, and show that the UMOD locus is significantly associated with kidney function decline.Kidney International advance online publication, 10 December 2014; doi:10.1038/ki.2014.361.
    Kidney international. 12/2014;
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    ABSTRACT: The value of aspirin in primary prevention of cancer and cardiovascular disease (CVD) remains unclear. The aim of this study was to identify women who benefit from alternate-day aspirin with regard to all relevant outcomes, including cancer, CVD and major gastrointestinal bleeding. Long term follow-up data of 27 939 healthy women with baseline plasma samples in the Women's Health Study, a randomised trial of 100 mg alternate-day aspirin versus placebo, were used to develop competing risks models for individualised prediction of absolute risk reduction of the combination of CVD, cancer and major gastrointestinal bleeding by aspirin. Although aspirin was associated with a modestly decreased 15-year risk of colorectal cancer, CVD, and in some women non-colorectal cancer, aspirin treatment resulted in a negative treatment effect in the majority of women if gastrointestinal bleeding was also taken into account. The excess risk of major gastrointestinal bleeding by aspirin increased with age, but the benefits for colorectal cancer and CVD risk were also greater at higher age. Decision curves indicated that selective treatment of women ≥65 years may improve net benefit compared to treating all, none and prediction-based treatment. The observed 15-year number needed to treat to prevent one event among women ≥65 years was 29 (95% CI 12 to 102). Concurrent evaluation of the absolute effects on cancer, CVD and major gastrointestinal bleeding showed that alternate-day use of low-dose aspirin is ineffective or harmful in the majority of women in primary prevention. Selective treatment of women ≥65 years with aspirin may improve net benefit. NCT00000479. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to
    Heart (British Cardiac Society) 12/2014; · 6.02 Impact Factor
  • Gregory Piazza, Paul M Ridker
    Clinical Chemistry 12/2014; · 7.77 Impact Factor
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    ABSTRACT: Osteoporosis and cardiovascular disease may share common biological pathways, with inflammation playing a role in the development of both. Although observational studies have suggested that statin use is associated with a lower risk of fractures, randomized trial data addressing this issue are scant. To determine whether statin therapy reduces the risk of fracture and, in a secondary analysis, whether baseline levels of the inflammatory biomarker high-sensitivity C-reactive protein (hs-CRP) are associated with the risk of fracture. The JUPITER (Justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin) trial was an international, randomized, double-blind, placebo-controlled study enrolling 17 802 men older than 50 years and women older than 60 years with hs-CRP level of at least 2 mg/L. Participants were screened from 2003 to 2006 and observed prospectively for up to 5 years (median follow-up, 1.9 years). Rosuvastatin calcium, 20 mg daily, or placebo. Incident fracture was a prespecified secondary end point of JUPITER. Fractures were confirmed by radiographs, computed tomography, bone scan, or other methods. Cox proportional hazards models were used to calculate hazard ratios (HRs) and associated 95% confidence intervals for the risk of fracture according to randomized treatment assignment, as well as increasing tertiles of hs-CRP, controlling for potential confounders. During the study, 431 incident fractures were reported and confirmed. Among participants allocated to rosuvastatin, 221 fractures were confirmed, compared with 210 among those allocated to placebo, such that the incidence of fracture in the rosuvastatin and placebo groups was 1.20 and 1.14 per 100 person-years, respectively (adjusted HR, 1.06 [95% CI, 0.88-1.28]; P = .53). Overall, increasing baseline hs-CRP level was not associated with an increased risk of fractures (adjusted HR for each unit increase in hs-CRP tertile, 1.06 [95% CI, 0.94-1.20]; P for trend, .34). Among men and women with elevated hs-CRP level enrolled in a large trial of rosuvastatin therapy for cardiovascular disease, statin therapy did not reduce the risk of fracture. Higher baseline hs-CRP level was not associated with an increased risk of incident fracture. Identifier: NCT00239681.
    JAMA Internal Medicine 12/2014; · 13.25 Impact Factor
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    ABSTRACT: BACKGROUND: Ezetimibe lowers plasma levels of low-density lipoprotein (LDL) cholesterol by inhibiting the activity of the Niemann-Pick C1-like 1 (NPC1L1) protein. However, whether such inhibition reduces the risk of coronary heart disease is not known. Human mutations that inactivate a gene encoding a drug target can mimic the action of an inhibitory drug and thus can be used to infer potential effects of that drug. METHODS: We sequenced the exons of NPC1L1 in 7364 patients with coronary heart disease and in 14,728 controls without such disease who were of European, African, or South Asian ancestry. We identified carriers of inactivating mutations (nonsense, splice-site, or frameshift mutations). In addition, we genotyped a specific inactivating mutation (p.Arg406X) in 22,590 patients with coronary heart disease and in 68,412 controls. We tested the association between the presence of an inactivating mutation and both plasma lipid levels and the risk of coronary heart disease. RESULTS: With sequencing, we identified 15 distinct NPC1L1 inactivating mutations; approximately 1 in every 650 persons was a heterozygous carrier for 1 of these mutations. Heterozygous carriers of NPC1L1 inactivating mutations had a mean LDL cholesterol level that was 12 mg per deciliter (0.31 mmol per liter) lower than that in noncarriers (P=0.04). Carrier status was associated with a relative reduction of 53% in the risk of coronary heart disease (odds ratio for carriers, 0.47; 95% confidence interval, 0.25 to 0.87; P=0.008). In total, only 11 of 29,954 patients with coronary heart disease had an inactivating mutation (carrier frequency, 0.04%) in contrast to 71 of 83,140 controls (carrier frequency, 0.09%). CONCLUSIONS: Naturally occurring mutations that disrupt NPC1L1 function were found to be associated with reduced plasma LDL cholesterol levels and a reduced risk of coronary heart disease. (Funded by the National Institutes of Health and others.).
    New England Journal of Medicine 11/2014; 371(22):2072-82. · 54.42 Impact Factor
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    ABSTRACT: Very long-chain saturated fatty acids (VLSFA) are saturated fatty acids with 20 or more carbons. In contrast to the more abundant saturated fatty acids, such as palmitic acid, there is growing evidence that circulating VLSFA may have beneficial biological properties. Whether genetic factors influence circulating levels of VLSFA is not known. We investigated the association of common genetic variation with plasma phospholipid/erythrocyte levels of three VLSFA by performing genome-wide association studies in seven population-based cohorts comprising 10,129 subjects of European ancestry. We observed associations of circulating VLSFA concentrations with common variants in two genes, SPTLC3 (serine palmitoyl-transferase, long-chain base subunit 3), a gene involved in the rate-limiting step of de novo sphingolipid synthesis, and CERS4 (ceramide synthase 4). The SPTLC3 variant at rs680379 was associated with higher 20:0 (arachidic acid, p = 5.81x10-13). The CERS4 variant at rs2100944 was associated with higher levels of 20:0 (p = 2.65x10-40) and in analyses that adjusted for 20:0, with lower levels of 22:0 (behenic acid, p = 4.22x10-26) and 24:0 (lignoceric acid, p = 3.20x10-21). These novel associations highlight the inter-relationship of circulating VLSFA and sphingolipid synthesis.
    Journal of lipid research. 11/2014;
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    ABSTRACT: AimWhile prevalent periodontal disease associates with cardiovascular risk, little is known about how incident periodontal disease influences future vascular risk. We compared effects of incident versus prevalent periodontal disease in developing major cardiovascular diseases (CVD), myocardial infarction (MI), ischemic stroke and total CVD.Material and Methods In a prospective cohort of 39863 predominantly white women, age > 45 years and free of cardiovascular disease at baseline were followed for an average of 15.7 years. Cox proportional hazard models with time-varying periodontal status (prevalent [18%], incident [7.3%] vs. never [74.7%]) were used to assess future cardiovascular risks.ResultsIncidence rates of all CVD outcomes were higher in women with prevalent or incident periodontal disease. For women with incident periodontal disease, risk factor adjusted hazard ratios (HRs) were 1.42 (95% CI, 1.14-1.77) for major CVD, 1.72 (1.25-2.38) for MI, 1.41(1.02-1.95) for ischemic stroke, and 1.27(1.06-1.52) for total CVD. For women with prevalent periodontal disease, adjusted HRs were 1.14 (1.00-1.31) for major CVD, 1.27 (1.04-1.56) for MI, 1.12(0.91-1.37) for ischemic stroke, and 1.15(1.03-1.28) for total CVD.Conclusion New cases of periodontal disease, not just those that are pre-existing, place women at significantly elevated risks for future cardiovascular events.This article is protected by copyright. All rights reserved.
    Journal Of Clinical Periodontology 11/2014; · 3.61 Impact Factor
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    ABSTRACT: Statins effectively lower LDL cholesterol levels in large studies and the observed interindividual response variability may be partially explained by genetic variation. Here we perform a pharmacogenetic meta-analysis of genome-wide association studies (GWAS) in studies addressing the LDL cholesterol response to statins, including up to 18,596 statin-treated subjects. We validate the most promising signals in a further 22,318 statin recipients and identify two loci, SORT1/CELSR2/PSRC1 and SLCO1B1, not previously identified in GWAS. Moreover, we confirm the previously described associations with APOE and LPA. Our findings advance the understanding of the pharmacogenetic architecture of statin response.
    Nature Communications 10/2014; · 10.74 Impact Factor
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    ABSTRACT: Background Although N-terminal pro–B-type natriuretic peptide (NT-proBNP) has a strong relationship with incident cardiovascular disease (CVD), few studies have examined whether NT-proBNP adds to risk prediction algorithms, particularly in women. Objectives This study sought to evaluate the relationship between NT-proBNP and incident CVD in women. Methods Using a prospective case-cohort within the WHI (Women’s Health Initiative) observational study, we selected 1,821 incident cases of CVD (746 myocardial infarctions, 754 ischemic strokes, 160 hemorrhagic strokes, and 161 other cardiovascular [CV] deaths) and a randomly selected reference cohort of 1,992 women without CVD at baseline. Results Median levels of NT-proBNP were higher at study entry among incident cases (120.3 ng/l [interquartile range (IQR): 68.1 to 219.5 ng/l]) than among control subjects (100.4 ng/l [IQR: 59.7 to 172.6 ng/l]; p < 0.0001). Women in the highest quartile of NT-proBNP (≥140.8 ng/l) were at 53% increased risk of CVD versus those in the lowest quartile after adjusting for traditional risk factors (1.53 [95% confidence interval (CI): 1.21 to 1.94]; p for trend <0.0001). Similar associations were observed after adjustment for Reynolds Risk Score covariables (1.53 [95% CI: 1.20 to 1.95]; p for trend <0.0001); the association remained in separate analyses of CV death (2.66 [95% CI: 1.48 to 4.81]; p for trend <0.0001), myocardial infarction (1.39 [95% CI: 1.02 to 1.88]; p for trend = 0.008), and stroke (1.60 [95% CI: 1.22 to 2.11]; p for trend <0.0001). When added to traditional risk covariables, NT-proBNP improved the c-statistic (0.765 to 0.774; p = 0.0003), categorical net reclassification (0.08; p < 0.0001), and integrated discrimination (0.0105; p < 0.0001). Similar results were observed when NT-proBNP was added to the Reynolds Risk Score. Conclusions In this multiethnic cohort of women with numerous CV events, NT-proBNP modestly improved measures of CVD risk prediction.
    Journal of the American College of Cardiology 10/2014; 64(17):1789–1797. · 15.34 Impact Factor
  • Circulation 10/2014; 130(17):e152. · 14.95 Impact Factor
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    ABSTRACT: Coffee, a major dietary source of caffeine, is among the most widely consumed beverages in the world and has received considerable attention regarding health risks and benefits. We conducted a genome-wide (GW) meta-analysis of predominately regular-type coffee consumption (cups per day) among up to 91 462 coffee consumers of European ancestry with top single-nucleotide polymorphisms (SNPs) followed-up in ~30 062 and 7964 coffee consumers of European and African-American ancestry, respectively. Studies from both stages were combined in a trans-ethnic meta-analysis. Confirmed loci were examined for putative functional and biological relevance. Eight loci, including six novel loci, met GW significance (log10Bayes factor (BF)>5.64) with per-allele effect sizes of 0.03-0.14 cups per day. Six are located in or near genes potentially involved in pharmacokinetics (ABCG2, AHR, POR and CYP1A2) and pharmacodynamics (BDNF and SLC6A4) of caffeine. Two map to GCKR and MLXIPL genes related to metabolic traits but lacking known roles in coffee consumption. Enhancer and promoter histone marks populate the regions of many confirmed loci and several potential regulatory SNPs are highly correlated with the lead SNP of each. SNP alleles near GCKR, MLXIPL, BDNF and CYP1A2 that were associated with higher coffee consumption have previously been associated with smoking initiation, higher adiposity and fasting insulin and glucose but lower blood pressure and favorable lipid, inflammatory and liver enzyme profiles (P<5 × 10(-8)).Our genetic findings among European and African-American adults reinforce the role of caffeine in mediating habitual coffee consumption and may point to molecular mechanisms underlying inter-individual variability in pharmacological and health effects of coffee.Molecular Psychiatry advance online publication, 7 October 2014; doi:10.1038/mp.2014.107.
    Molecular Psychiatry 10/2014; · 15.15 Impact Factor
  • Nancy R Cook, Paul M Ridker
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    ABSTRACT: While the pooled cohort equations from the recent American College of Cardiology/American Heart Association (ACC/AHA) Guideline on the Assessment of Cardiovascular Risk have overestimated cardiovascular risk in multiple external cohorts, the reasons for the discrepancy are unclear.
    JAMA Internal Medicine 10/2014; · 13.25 Impact Factor
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    ABSTRACT: Using genome-wide data from 253,288 individuals, we identified 697 variants at genome-wide significance that together explained one-fifth of the heritability for adult height. By testing different numbers of variants in independent studies, we show that the most strongly associated approximately 2,000, approximately 3,700 and approximately 9,500 SNPs explained approximately 21%, approximately 24% and approximately 29% of phenotypic variance. Furthermore, all common variants together captured 60% of heritability. The 697 variants clustered in 423 loci were enriched for genes, pathways and tissue types known to be involved in growth and together implicated genes and pathways not highlighted in earlier efforts, such as signaling by fibroblast growth factors, WNT/beta-catenin and chondroitin sulfate-related genes. We identified several genes and pathways not previously connected with human skeletal growth, including mTOR, osteoglycin and binding of hyaluronic acid. Our results indicate a genetic architecture for human height that is characterized by a very large but finite number (thousands) of causal variants.
    Nature Genetics 10/2014; · 29.65 Impact Factor
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    ABSTRACT: Background Statins increase the risk of new-onset type 2 diabetes mellitus. We aimed to assess whether this increase in risk is a consequence of inhibition of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), the intended drug target. Methods We used single nucleotide polymorphisms in the HMGCR gene, rs17238484 (for the main analysis) and rs12916 (for a subsidiary analysis) as proxies for HMGCR inhibition by statins. We examined associations of these variants with plasma lipid, glucose, and insulin concentrations; bodyweight; waist circumference; and prevalent and incident type 2 diabetes. Study-specific effect estimates per copy of each LDL-lowering allele were pooled by meta-analysis. These findings were compared with a meta-analysis of new-onset type 2 diabetes and bodyweight change data from randomised trials of statin drugs. The effects of statins in each randomised trial were assessed using meta-analysis. Findings Data were available for up to 223 463 individuals from 43 genetic studies. Each additional rs17238484-G allele was associated with a mean 0·06 mmol/L (95% CI 0·05–0·07) lower LDL cholesterol and higher body weight (0·30 kg, 0·18–0·43), waist circumference (0·32 cm, 0·16–0·47), plasma insulin concentration (1·62%, 0·53–2·72), and plasma glucose concentration (0·23%, 0·02–0·44). The rs12916 SNP had similar effects on LDL cholesterol, bodyweight, and waist circumference. The rs17238484-G allele seemed to be associated with higher risk of type 2 diabetes (odds ratio [OR] per allele 1·02, 95% CI 1·00–1·05); the rs12916-T allele association was consistent (1·06, 1·03–1·09). In 129 170 individuals in randomised trials, statins lowered LDL cholesterol by 0·92 mmol/L (95% CI 0·18–1·67) at 1-year of follow-up, increased bodyweight by 0·24 kg (95% CI 0·10–0·38 in all trials; 0·33 kg, 95% CI 0·24–0·42 in placebo or standard care controlled trials and −0·15 kg, 95% CI −0·39 to 0·08 in intensive-dose vs moderate-dose trials) at a mean of 4·2 years (range 1·9–6·7) of follow-up, and increased the odds of new-onset type 2 diabetes (OR 1·12, 95% CI 1·06–1·18 in all trials; 1·11, 95% CI 1·03–1·20 in placebo or standard care controlled trials and 1·12, 95% CI 1·04–1·22 in intensive-dose vs moderate dose trials). Interpretation The increased risk of type 2 diabetes noted with statins is at least partially explained by HMGCR inhibition. Funding The funding sources are cited at the end of the paper.
    The Lancet. 09/2014;
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    ABSTRACT: Recent US guidelines expand the indications for high-intensity statin therapy, yet data on the safety of attaining very low-density lipoprotein cholesterol (LDL-C) levels are scarce. Among 16,304 participants in the Justification for the Use of Statins in Prevention: An Intervention Trial Evaluating Rosuvastatin (JUPITER) with on-treatment LDL-C levels, we identified 767 who did and 7,387 who did not achieve LDL-C <30 mg/dl on rosuvastatin 20 mg daily and 718 participants who did and 7,436 who did not achieve LDL-C reductions of ≥70% on rosuvastatin, and 8,150 allocated to placebo. In participants with an LDL-C <30 mg/dl, we observed an increase in the risk of physician-reported type 2 diabetes with an adjusted hazard ratio (95% confidence interval) of 1.56 (1.09 to 2.23, p = 0.01) and physician-reported hematuria (hazard ratio 2.10 [1.39 to 3.19], p <0.001) compared with rosuvastatin-treated participants with LDL-C ≥30 mg/dl. There was also an increased risk of certain musculoskeletal, hepatobiliary, and psychiatric disorders. No difference in renal failure, cancer, memory impairment, or hemorrhagic stroke was observed, although there were few events in these categories. In rosuvastatin-treated participants, achieving LDL-C reduction ≥70% versus <70% did not appear to be associated with increased risk of hepatobiliary, renal, or urinary disorders. In conclusion, in this post hoc analysis in the JUPITER, achieving LDL-C levels <30 mg/dl with high-intensity statin therapy appeared to be generally well tolerated but associated with certain adverse events, including more physician-reported diabetes, hematuria, hepatobiliary disorders, and insomnia. These data may guide the monitoring of patients on intensive statin therapy and adverse events in trials of therapies that lead to very low LDL-C levels. Copyright © 2014 Elsevier Inc. All rights reserved.
    The American Journal of Cardiology 09/2014; · 3.43 Impact Factor
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    ABSTRACT: To evaluate the impact of preoperative sepsis on risk of postoperative arterial and venous thromboses.
    BMJ Clinical Research 09/2014; 349:g5334. · 14.09 Impact Factor
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    ABSTRACT: Glycosylated proteins partake in multiple cellular processes including inflammation. We hypothesized that GlycA, a novel biomarker of protein glycan N-acetyl groups, is related to incident cardiovascular disease (CVD), and we compared it with high-sensitivity C-reactive protein (hsCRP).
    Journal of the American Heart Association. 09/2014; 3(5).
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    ABSTRACT: -Healthy levels of lifestyle factors can reduce risk of CVD. However, except for smoking status, often considered a traditional risk factor, their effect on cardiovascular risk prediction is unclear.
    Circulation 08/2014; · 14.95 Impact Factor
  • Paul M Ridker
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    ABSTRACT: Lifelong exposure to raised concentrations of LDL cholesterol increases cardiovascular event rates, and the use of statin therapy as an adjunct to diet, exercise, and smoking cessation has proven highly effective in reducing the population burden associated with hyperlipidaemia. Yet, despite consistent biological, genetic, and epidemiological data, and evidence from randomised trials, there is controversy among national guidelines and clinical practice with regard to LDL cholesterol, its measurement, the usefulness of population-based screening, the net benefit-to-risk ratio for different LDL-lowering drugs, the benefit of treatment targets, and whether aggressive lowering of LDL is safe. Several novel therapies have been introduced for the treatment of people with genetic defects that result in loss of function within the LDL receptor, a major determinant of inherited hyperlipidaemias. Moreover, the usefulness of monoclonal antibodies that extend the LDL-receptor lifecycle (and thus result in substantial lowering of LDL cholesterol below the levels achieved with statins alone) is being assessed in phase 3 trials that will enrol more than 60 000 at-risk patients worldwide. These trials represent an exceptionally rapid translation of genetic observations into clinical practice and will address core questions of how low LDL cholesterol can be safely reduced, whether the mechanism of LDL-cholesterol lowering matters, and whether ever more aggressive lipid-lowering provides a safe, long-term mechanism to prevent atherothrombotic complications.
    The Lancet 08/2014; 384(9943):607–617. · 39.21 Impact Factor

Publication Stats

73k Citations
9,370.98 Total Impact Points


  • 1991–2014
    • Brigham and Women's Hospital
      • • Center for Cardiovascular Disease Prevention
      • • Department of Medicine
      • • Center for Brain Mind Medicine
      • • Division of Preventive Medicine
      • • Division of Cardiovascular Medicine
      Boston, Massachusetts, United States
  • 1990–2014
    • Harvard Medical School
      • Department of Medicine
      Boston, Massachusetts, United States
  • 2013
    • University of Exeter
      Exeter, England, United Kingdom
  • 2012–2013
    • Academisch Medisch Centrum Universiteit van Amsterdam
      • • Academic Medical Center
      • • Department of Cardiology and Cardio-thoracic Surgery
      Amsterdam, North Holland, Netherlands
    • St. Michael's Hospital
      Toronto, Ontario, Canada
    • McGill University
      • Department of Epidemiology, Biostatistics and Occupational Health
      Montréal, Quebec, Canada
    • Soroka Medical Center
      Be'er Sheva`, Southern District, Israel
    • University of Amsterdam
      Amsterdamo, North Holland, Netherlands
  • 2010–2013
    • University of Massachusetts Boston
      Boston, Massachusetts, United States
    • University of Chicago
      Chicago, Illinois, United States
    • Universität Ulm
      • Clinic of Internal Medicine II
      Ulm, Baden-Wuerttemberg, Germany
    • McMaster University
      • Department of Pathology and Molecular Medicine
      Hamilton, Ontario, Canada
    • National Heart, Lung, and Blood Institute
      • Division of Cardiovascular Sciences (DCVS)
      Maryland, United States
  • 2007–2013
    • Beth Israel Deaconess Medical Center
      • • Division of General Medicine and Primary Care
      • • Cardiovascular Epidemiology Research Unit
      Boston, MA, United States
    • Schepens Eye Research Institute
      Boston, Massachusetts, United States
    • Boston Medical Center
      Boston, Massachusetts, United States
  • 2000–2013
    • Partners HealthCare
      Boston, Massachusetts, United States
    • University of California, San Francisco
      • Division of Cardiology
      San Francisco, CA, United States
  • 2010–2012
    • Indiana University-Purdue University Indianapolis
      • Department of Public Health
      Indianapolis, IN, United States
  • 2001–2012
    • Harvard University
      • • Department of Nutrition
      • • Department of Epidemiology
      Cambridge, Massachusetts, United States
    • Concordia University–Ann Arbor
      Ann Arbor, Michigan, United States
  • 2011
    • University of Alberta
      Edmonton, Alberta, Canada
    • Memorial Sloan-Kettering Cancer Center
      New York City, New York, United States
    • Universitätsspital Basel
      Bâle, Basel-City, Switzerland
    • Vanderbilt University
      • Division of Cardiovascular Medicine
      Nashville, MI, United States
    • AstraZeneca
      Tukholma, Stockholm, Sweden
    • University Medical Center Utrecht
      • Julius Center for Health Sciences and Primary Care
      Utrecht, Utrecht, Netherlands
    • University of Texas Southwestern Medical Center
      • Department of Internal Medicine
      Dallas, TX, United States
  • 2010–2011
    • Duke University Medical Center
      • Division of Cardiology
      Durham, NC, United States
  • 2009–2011
    • University of Cambridge
      • Department of Public Health and Primary Care
      Cambridge, ENG, United Kingdom
    • Broad Institute of MIT and Harvard
      Cambridge, Massachusetts, United States
    • Albert Einstein College of Medicine
      New York City, New York, United States
  • 2008–2011
    • University of Texas Medical School
      • Department of Internal Medicine
      Houston, TX, United States
    • Alpert Medical School - Brown University
      • Department of Family Medicine
      Providence, RI, United States
    • Erasmus MC
      Rotterdam, South Holland, Netherlands
    • Celera
      Alameda, California, United States
    • Karolinska Institutet
      • Institutionen för medicin, Huddinge
      Solna, Stockholm, Sweden
  • 2007–2011
    • Northwestern University
      • • Department of Medicine
      • • Department of Preventive Medicine
      Evanston, IL, United States
  • 2009–2010
    • Johns Hopkins University
      • Department of Epidemiology
      Baltimore, MD, United States
    • University of Notre Dame
      South Bend, Indiana, United States
  • 2005–2010
    • University of California, San Diego
      • Department of Family and Preventive Medicine
      San Diego, CA, United States
    • University of California, Los Angeles
      • Department of Epidemiology
      Los Angeles, CA, United States
    • University of Toronto
      • Division of Cardiac Surgery
      Toronto, Ontario, Canada
  • 2001–2010
    • Beverly Hospital, Boston MA
      Beverly, Massachusetts, United States
    • University of Michigan
      • Department of Biostatistics
      Ann Arbor, MI, United States
  • 2006
    • University of Vermont
      • Department of Medicine
      Burlington, VT, United States
  • 2004–2005
    • University of Pittsburgh
      • Department of Epidemiology
      Pittsburgh, PA, United States
    • Texas Heart Institute
      Houston, Texas, United States
  • 2003
    • Institut Català de la Salut
      Cerdanyola del Vallès, Catalonia, Spain
    • Mater Misericordiae University Hospital
      Dublin, Leinster, Ireland
  • 2001–2003
    • Boston Children's Hospital
      • Department of Laboratory Medicine
      Boston, MA, United States
  • 2002
    • St. Vincent's Hospital Sydney
      Sydney, New South Wales, Australia
  • 1999
    • Massachusetts Department of Public Health
      Boston, Massachusetts, United States