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Circulation | 2012

Heart Disease and Stroke Statistics—2012 Update A Report From the American Heart Association

Véronique L. Roger; Alan S. Go; Donald M. Lloyd-Jones; Emelia J. Benjamin; Jarett D. Berry; William B. Borden; Dawn M. Bravata; Shifan Dai; Earl S. Ford; Caroline S. Fox; Heather J. Fullerton; Cathleen Gillespie; Susan M. Hailpern; John A. Heit; Virginia J. Howard; Brett Kissela; Steven J. Kittner; Daniel T. Lackland; Judith H. Lichtman; Lynda D. Lisabeth; Diane M. Makuc; Gregory M. Marcus; Ariane J. Marelli; David B. Matchar; Claudia S. Moy; Dariush Mozaffarian; Michael E. Mussolino; Graham Nichol; Nina P. Paynter; Elsayed Z. Soliman

Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .e3 1. About These Statistics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .e7 2. American Heart Associations 2020 Impact Goals. . . . . . . . . . . . . . . . .e10 3. Cardiovascular Diseases . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . .e21 4. Subclinical Atherosclerosis . . . . . . . . . . . . . . . . . . . . .e45 5. Coronary Heart Disease, Acute Coronary Syndrome, and Angina Pectoris . . . . . . . . .e54 6. Stroke (Cerebrovascular Disease) . . . . . . . . . . . . . . . . . . . . . . . . . . . .e68 7. High Blood Pressure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . .e88 8. Congenital Cardiovascular Defects . . . . . . . . . . . . . . . . . . . . . . . . . . . .e97 9. Cardiomyopathy and Heart Failure . . . . . . . . . . . . . . . . . . . . . . . . . . . .e102 10. Disorders …


Circulation | 2013

Heart Disease and Stroke Statistics—2013 Update A Report From the American Heart Association

Alan S. Go; Dariush Mozaffarian; Véronique L. Roger; Emelia J. Benjamin; Jarett D. Berry; William B. Borden; Dawn M. Bravata; Shifan Dai; Earl S. Ford; Caroline S. Fox; Sheila Franco; Heather J. Fullerton; Cathleen Gillespie; Susan M. Hailpern; John A. Heit; Virginia J. Howard; Mark D. Huffman; Brett Kissela; Steven J. Kittner; Daniel T. Lackland; Judith H. Lichtman; Lynda D. Lisabeth; David J. Magid; Gregory M. Marcus; Ariane J. Marelli; David B. Matchar; Darren K. McGuire; Emile R. Mohler; Claudia S. Moy; Michael E. Mussolino

Author(s): Go, Alan S; Mozaffarian, Dariush; Roger, Veronique L; Benjamin, Emelia J; Berry, Jarett D; Borden, William B; Bravata, Dawn M; Dai, Shifan; Ford, Earl S; Fox, Caroline S; Franco, Sheila; Fullerton, Heather J; Gillespie, Cathleen; Hailpern, Susan M; Heit, John A; Howard, Virginia J; Huffman, Mark D; Kissela, Brett M; Kittner, Steven J; Lackland, Daniel T; Lichtman, Judith H; Lisabeth, Lynda D; Magid, David; Marcus, Gregory M; Marelli, Ariane; Matchar, David B; McGuire, Darren K; Mohler, Emile R; Moy, Claudia S; Mussolino, Michael E; Nichol, Graham; Paynter, Nina P; Schreiner, Pamela J; Sorlie, Paul D; Stein, Joel; Turan, Tanya N; Virani, Salim S; Wong, Nathan D; Woo, Daniel; Turner, Melanie B; American Heart Association Statistics Committee and Stroke Statistics Subcommittee


Circulation | 2011

Heart Disease and Stroke Statistics—2011 Update A Report From the American Heart Association

Véronique L. Roger; Alan S. Go; Donald M. Lloyd-Jones; Robert J. Adams; Jarett D. Berry; Todd M. Brown; Mercedes R. Carnethon; Shifan Dai; Giovanni de Simone; Earl S. Ford; Caroline S. Fox; Heather J. Fullerton; Cathleen Gillespie; Kurt J. Greenlund; Susan M. Hailpern; John A. Heit; P. Michael Ho; Virginia J. Howard; Brett Kissela; Steven J. Kittner; Daniel T. Lackland; Judith H. Lichtman; Lynda D. Lisabeth; Diane M. Makuc; Gregory M. Marcus; Ariane J. Marelli; David B. Matchar; Mary M. McDermott; James B. Meigs; Claudia S. Moy

Rosamond, Paul D. Sorlie, Randall S. Stafford, Tanya N. Turan, Melanie B. Turner, Nathan D. Dariush Mozaffarian, Michael E. Mussolino, Graham Nichol, Nina P. Paynter, Wayne D. Ariane Marelli, David B. Matchar, Mary M. McDermott, James B. Meigs, Claudia S. Moy, Lackland, Judith H. Lichtman, Lynda D. Lisabeth, Diane M. Makuc, Gregory M. Marcus, John A. Heit, P. Michael Ho, Virginia J. Howard, Brett M. Kissela, Steven J. Kittner, Daniel T. Caroline S. Fox, Heather J. Fullerton, Cathleen Gillespie, Kurt J. Greenlund, Susan M. Hailpern, Todd M. Brown, Mercedes R. Carnethon, Shifan Dai, Giovanni de Simone, Earl S. Ford, Véronique L. Roger, Alan S. Go, Donald M. Lloyd-Jones, Robert J. Adams, Jarett D. Berry, Association 2011 Update : A Report From the American Heart −− Heart Disease and Stroke Statistics


Circulation | 2014

Heart Disease and Stroke Statistics—2014 Update A Report From the American Heart Association

Alan S. Go; Dariush Mozaffarian; Véronique L. Roger; Emelia J. Benjamin; Jarett D. Berry; Michael J. Blaha; Shifan Dai; Earl S. Ford; Caroline S. Fox; Sheila Franco; Heather J. Fullerton; Cathleen Gillespie; Susan M. Hailpern; John A. Heit; Virginia J. Howard; Mark D. Huffman; Suzanne E. Judd; Brett Kissela; Steven J. Kittner; Daniel T. Lackland; Judith H. Lichtman; Lynda D. Lisabeth; Rachel H. Mackey; David J. Magid; Gregory M. Marcus; Ariane J. Marelli; David B. Matchar; Darren K. McGuire; Emile R. Mohler; Claudia S. Moy

Author(s): Go, Alan S; Mozaffarian, Dariush; Roger, Veronique L; Benjamin, Emelia J; Berry, Jarett D; Blaha, Michael J; Dai, Shifan; Ford, Earl S; Fox, Caroline S; Franco, Sheila; Fullerton, Heather J; Gillespie, Cathleen; Hailpern, Susan M; Heit, John A; Howard, Virginia J; Huffman, Mark D; Judd, Suzanne E; Kissela, Brett M; Kittner, Steven J; Lackland, Daniel T; Lichtman, Judith H; Lisabeth, Lynda D; Mackey, Rachel H; Magid, David J; Marcus, Gregory M; Marelli, Ariane; Matchar, David B; McGuire, Darren K; Mohler, Emile R; Moy, Claudia S; Mussolino, Michael E; Neumar, Robert W; Nichol, Graham; Pandey, Dilip K; Paynter, Nina P; Reeves, Matthew J; Sorlie, Paul D; Stein, Joel; Towfighi, Amytis; Turan, Tanya N; Virani, Salim S; Wong, Nathan D; Woo, Daniel; Turner, Melanie B; American Heart Association Statistics Committee and Stroke Statistics Subcommittee


The Lancet | 2010

Association of estimated glomerular filtration rate and albuminuria with all-cause and cardiovascular mortality in general population cohorts: a collaborative meta-analysis.

Kunihiro Matsushita; Marije van der Velde; Brad C. Astor; Mark Woodward; Andrew S. Levey; Paul E. de Jong; Josef Coresh; Ron T. Gansevoort; Meguid El-Nahas; Kai-Uwe Eckardt; Bertram L. Kasiske; Marcello Tonelli; Brenda R. Hemmelgarn; Yaping Wang; Robert C. Atkins; Kevan R. Polkinghorne; Steven J. Chadban; Anoop Shankar; Ronald Klein; Barbara E. K. Klein; Haiyan Wang; Fang Wang; Zhang L; Lisheng Liu; Michael G. Shlipak; Mark J. Sarnak; Ronit Katz; Linda P. Fried; Tazeen H. Jafar; Muhammad Islam

BACKGROUND Substantial controversy surrounds the use of estimated glomerular filtration rate (eGFR) and albuminuria to define chronic kidney disease and assign its stages. We undertook a meta-analysis to assess the independent and combined associations of eGFR and albuminuria with mortality. METHODS In this collaborative meta-analysis of general population cohorts, we pooled standardised data for all-cause and cardiovascular mortality from studies containing at least 1000 participants and baseline information about eGFR and urine albumin concentrations. Cox proportional hazards models were used to estimate hazard ratios (HRs) for all-cause and cardiovascular mortality associated with eGFR and albuminuria, adjusted for potential confounders. FINDINGS The analysis included 105,872 participants (730,577 person-years) from 14 studies with urine albumin-to-creatinine ratio (ACR) measurements and 1,128,310 participants (4,732,110 person-years) from seven studies with urine protein dipstick measurements. In studies with ACR measurements, risk of mortality was unrelated to eGFR between 75 mL/min/1.73 m(2) and 105 mL/min/1.73 m(2) and increased at lower eGFRs. Compared with eGFR 95 mL/min/1.73 m(2), adjusted HRs for all-cause mortality were 1.18 (95% CI 1.05-1.32) for eGFR 60 mL/min/1.73 m(2), 1.57 (1.39-1.78) for 45 mL/min/1.73 m(2), and 3.14 (2.39-4.13) for 15 mL/min/1.73 m(2). ACR was associated with risk of mortality linearly on the log-log scale without threshold effects. Compared with ACR 0.6 mg/mmol, adjusted HRs for all-cause mortality were 1.20 (1.15-1.26) for ACR 1.1 mg/mmol, 1.63 (1.50-1.77) for 3.4 mg/mmol, and 2.22 (1.97-2.51) for 33.9 mg/mmol. eGFR and ACR were multiplicatively associated with risk of mortality without evidence of interaction. Similar findings were recorded for cardiovascular mortality and in studies with dipstick measurements. INTERPRETATION eGFR less than 60 mL/min/1.73 m(2) and ACR 1.1 mg/mmol (10 mg/g) or more are independent predictors of mortality risk in the general population. This study provides quantitative data for use of both kidney measures for risk assessment and definition and staging of chronic kidney disease. FUNDING Kidney Disease: Improving Global Outcomes (KDIGO), US National Kidney Foundation, and Dutch Kidney Foundation.Background A comprehensive evaluation of the independent and combined associations of estimated glomerular filtration rate (eGFR) and albuminuria with mortality is required for assessment of the impact of kidney function on risk in the general population, with implications for improving the definition and staging of chronic kidney disease (CKD).


Circulation | 2007

Abdominal Visceral and Subcutaneous Adipose Tissue Compartments Association With Metabolic Risk Factors in the Framingham Heart Study

Caroline S. Fox; Joseph M. Massaro; Udo Hoffmann; Karla M. Pou; Pál Maurovich-Horvat; Chunyu Liu; Joanne M. Murabito; James B. Meigs; L. Adrienne Cupples; Ralph B. D’Agostino; Christopher J. O’Donnell

Background— Visceral adipose tissue (VAT) compartments may confer increased metabolic risk. The incremental utility of measuring both visceral and subcutaneous abdominal adipose tissue (SAT) in association with metabolic risk factors and underlying heritability has not been well described in a population-based setting. Methods and Results— Participants (n=3001) were drawn from the Framingham Heart Study (48% women; mean age, 50 years), were free of clinical cardiovascular disease, and underwent multidetector computed tomography assessment of SAT and VAT volumes between 2002 and 2005. Metabolic risk factors were examined in relation to increments of SAT and VAT after multivariable adjustment. Heritability was calculated using variance-components analysis. Among both women and men, SAT and VAT were significantly associated with blood pressure, fasting plasma glucose, triglycerides, and high-density lipoprotein cholesterol and with increased odds of hypertension, impaired fasting glucose, diabetes mellitus, and metabolic syndrome (P range <0.01). In women, relations between VAT and risk factors were consistently stronger than in men. However, VAT was more strongly correlated with most metabolic risk factors than was SAT. For example, among women and men, both SAT and VAT were associated with increased odds of metabolic syndrome. In women, the odds ratio (OR) of metabolic syndrome per 1–standard deviation increase in VAT (OR, 4.7) was stronger than that for SAT (OR, 3.0; P for difference between SAT and VAT <0.0001); similar differences were noted for men (OR for VAT, 4.2; OR for SAT, 2.5). Furthermore, VAT but not SAT contributed significantly to risk factor variation after adjustment for body mass index and waist circumference (P ≤0.01). Among overweight and obese individuals, the prevalence of hypertension, impaired fasting glucose, and metabolic syndrome increased linearly and significantly across increasing VAT quartiles. Heritability values for SAT and VAT were 57% and 36%, respectively. Conclusions— Although both SAT and VAT are correlated with metabolic risk factors, VAT remains more strongly associated with an adverse metabolic risk profile even after accounting for standard anthropometric indexes. Our findings are consistent with the hypothesized role of visceral fat as a unique, pathogenic fat depot. Measurement of VAT may provide a more complete understanding of metabolic risk associated with variation in fat distribution.


Nature Medicine | 2011

Metabolite profiles and the risk of developing diabetes

Thomas J. Wang; Martin G. Larson; Susan Cheng; Eugene P. Rhee; Elizabeth L. McCabe; Gregory D. Lewis; Caroline S. Fox; Paul F. Jacques; Céline Fernandez; Christopher J. O'Donnell; Stephen A Carr; Vamsi K. Mootha; Jose C. Florez; Amanda Souza; Olle Melander; Clary B. Clish; Robert E. Gerszten

Emerging technologies allow the high-throughput profiling of metabolic status from a blood specimen (metabolomics). We investigated whether metabolite profiles could predict the development of diabetes. Among 2,422 normoglycemic individuals followed for 12 years, 201 developed diabetes. Amino acids, amines and other polar metabolites were profiled in baseline specimens by liquid chromatography–tandem mass spectrometry (LC-MS). Cases and controls were matched for age, body mass index and fasting glucose. Five branched-chain and aromatic amino acids had highly significant associations with future diabetes: isoleucine, leucine, valine, tyrosine and phenylalanine. A combination of three amino acids predicted future diabetes (with a more than fivefold higher risk for individuals in top quartile). The results were replicated in an independent, prospective cohort. These findings underscore the potential key role of amino acid metabolism early in the pathogenesis of diabetes and suggest that amino acid profiles could aid in diabetes risk assessment.


Nature Genetics | 2009

Genome-wide association study of blood pressure and hypertension

Daniel Levy; Georg B. Ehret; Kenneth Rice; Germaine C. Verwoert; Lenore J. Launer; Abbas Dehghan; Nicole L. Glazer; Alanna C. Morrison; Andrew D. Johnson; Thor Aspelund; Yurii S. Aulchenko; Thomas Lumley; Anna Köttgen; Fernando Rivadeneira; Gudny Eiriksdottir; Xiuqing Guo; Dan E. Arking; Gary F. Mitchell; Francesco Mattace-Raso; Albert V. Smith; Kent D. Taylor; Robert B. Scharpf; Shih Jen Hwang; Eric J.G. Sijbrands; Joshua C. Bis; Tamara B. Harris; Santhi K. Ganesh; Christopher J. O'Donnell; Albert Hofman; Jerome I. Rotter

Blood pressure is a major cardiovascular disease risk factor. To date, few variants associated with interindividual blood pressure variation have been identified and replicated. Here we report results of a genome-wide association study of systolic (SBP) and diastolic (DBP) blood pressure and hypertension in the CHARGE Consortium (n = 29,136), identifying 13 SNPs for SBP, 20 for DBP and 10 for hypertension at P < 4 × 10−7. The top ten loci for SBP and DBP were incorporated into a risk score; mean BP and prevalence of hypertension increased in relation to the number of risk alleles carried. When ten CHARGE SNPs for each trait were included in a joint meta-analysis with the Global BPgen Consortium (n = 34,433), four CHARGE loci attained genome-wide significance (P < 5 × 10−8) for SBP (ATP2B1, CYP17A1, PLEKHA7, SH2B3), six for DBP (ATP2B1, CACNB2, CSK-ULK3, SH2B3, TBX3-TBX5, ULK4) and one for hypertension (ATP2B1). Identifying genes associated with blood pressure advances our understanding of blood pressure regulation and highlights potential drug targets for the prevention or treatment of hypertension.


Circulation | 2010

Executive Summary: Heart Disease and Stroke Statistics—2013 Update

Alan S. Go; Dariush Mozaffarian; Véronique L. Roger; Emelia J. Benjamin; Jarett D. Berry; William B. Borden; Dawn M. Bravata; Shifan Dai; Earl S. Ford; Caroline S. Fox; Sheila Franco; Heather J. Fullerton; Cathleen Gillespie; Susan M. Hailpern; John A. Heit; Virginia J. Howard; Mark D. Huffman; Brett Kissela; Steven J. Kittner; Daniel T. Lackland; Judith H. Lichtman; Lynda D. Lisabeth; David J. Magid; Gregory M. Marcus; Ariane J. Marelli; David B. Matchar; Darren K. McGuire; Emile R. Mohler; Claudia S. Moy; Michael E. Mussolino

Author(s): Go, Alan S; Mozaffarian, Dariush; Roger, Veronique L; Benjamin, Emelia J; Berry, Jarett D; Borden, William B; Bravata, Dawn M; Dai, Shifan; Ford, Earl S; Fox, Caroline S; Franco, Sheila; Fullerton, Heather J; Gillespie, Cathleen; Hailpern, Susan M; Heit, John A; Howard, Virginia J; Huffman, Mark D; Kissela, Brett M; Kittner, Steven J; Lackland, Daniel T; Lichtman, Judith H; Lisabeth, Lynda D; Magid, David; Marcus, Gregory M; Marelli, Ariane; Matchar, David B; McGuire, Darren K; Mohler, Emile R; Moy, Claudia S; Mussolino, Michael E; Nichol, Graham; Paynter, Nina P; Schreiner, Pamela J; Sorlie, Paul D; Stein, Joel; Turan, Tanya N; Virani, Salim S; Wong, Nathan D; Woo, Daniel; Turner, Melanie B; American Heart Association Statistics Committee and Stroke Statistics Subcommittee


Circulation | 2007

Soft Drink Consumption and Risk of Developing Cardiometabolic Risk Factors and the Metabolic Syndrome in Middle-Aged Adults in the Community

Ravi Dhingra; Lisa M. Sullivan; Paul F. Jacques; Thomas J. Wang; Caroline S. Fox; James B. Meigs; Ralph B. D’Agostino; J. Michael Gaziano

Background— Consumption of soft drinks has been linked to obesity in children and adolescents, but it is unclear whether it increases metabolic risk in middle-aged individuals. Methods and Results— We related the incidence of metabolic syndrome and its components to soft drink consumption in participants in the Framingham Heart Study (6039 person-observations, 3470 in women; mean age 52.9 years) who were free of baseline metabolic syndrome. Metabolic syndrome was defined as the presence of ≥3 of the following: waist circumference ≥35 inches (women) or ≥40 inches (men); fasting blood glucose ≥100 mg/dL; serum triglycerides ≥150 mg/dL; blood pressure ≥135/85 mm Hg; and high-density lipoprotein cholesterol <40 mg/dL (men) or <50 mg/dL (women). Multivariable models included adjustments for age, sex, physical activity, smoking, dietary intake of saturated fat, trans fat, fiber, magnesium, total calories, and glycemic index. Cross-sectionally, individuals consuming ≥1 soft drink per day had a higher prevalence of metabolic syndrome (odds ratio [OR], 1.48; 95% CI, 1.30 to 1.69) than those consuming <1 drink per day. On follow-up (mean of 4 years), new-onset metabolic syndrome developed in 765 (18.7%) of 4095 participants consuming <1 drink per day and in 474 (22.6%) of 2059 persons consuming ≥1 soft drink per day. Consumption of ≥1 soft drink per day was associated with increased odds of developing metabolic syndrome (OR, 1.44; 95% CI, 1.20 to 1.74), obesity (OR, 1.31; 95% CI, 1.02 to 1.68), increased waist circumference (OR, 1.30; 95% CI, 1.09 to 1.56), impaired fasting glucose (OR, 1.25; 95% CI, 1.05 to 1.48), higher blood pressure (OR, 1.18; 95% CI, 0.96 to 1.44), hypertriglyceridemia (OR, 1.25; 95% CI, 1.04 to 1.51), and low high-density lipoprotein cholesterol (OR, 1.32; 95% CI 1.06 to 1.64). Conclusions— In middle-aged adults, soft drink consumption is associated with a higher prevalence and incidence of multiple metabolic risk factors.

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Shih-Jen Hwang

National Institutes of Health

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Joanne M. Murabito

National Institutes of Health

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