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8. Psychotropic medication use and risk of adverse cardiovascular events in women with suspected coronary artery disease: outcomes from the Women's Ischemia Syndrome and Evaluation (WISE) study

Author

Krantz, D.S., Whittaker, K.S., Francis, J.L., Rutledge, T., Johnson, B.D., Barrow, G., McClure, C., Sheps, D.S., York, K., Cornell, C., Bittner, V., Vaccarino, V., Eteiba, W., Parashar, S., Vido, D.A., and Bairey Merz, C.N.

Subjects
Antidepressants -- Complications and side effects, Antidepressants -- Research, Antianxiety agents -- Dosage and administration, Antianxiety agents -- Research, Coronary heart disease -- Risk factors, Coronary heart disease -- Research, Health
Published
2009

11. Gender in cardiovascular medicine: chest pain and coronary artery disease

Author

Mehta, P.K., Bess, C., Elias-Smale, S.E., Vaccarino, V., Quyyumi, A., Pepine, C.J., Merz, C.N. Bairey, Mehta, P.K., Bess, C., Elias-Smale, S.E., Vaccarino, V., Quyyumi, A., Pepine, C.J., and Merz, C.N. Bairey

Abstract

Contains fulltext : 215443.pdf (Publisher’s version ) (Closed access), Ischaemic heart disease (IHD) remains the leading cause of morbidity and mortality among women and men yet women are more often underdiagnosed, have a delay in diagnosis, and/or receive suboptimal treatment. An implicit gender-bias with regard to lack of recognition of sex-related differences in presentation of IHD may, in part, explain these differences in women compared with men. Indeed, existing knowledge demonstrates that angina does not commonly relate to obstructive coronary artery disease (CAD). Emerging knowledge supports an inclusive approach to chest pain symptoms in women, as well as a more thoughtful consideration of percutaneous coronary intervention for angina in stable obstructive CAD, to avoid chasing our tails. Emerging knowledge regarding the cardiac autonomic nervous system and visceral pain pathways in patients with and without obstructive CAD offers explanatory mechanisms for angina. Interdisciplinary investigation approaches that involve cardiologists, biobehavioural specialists, and anaesthesia/pain specialists to improve angina treatment should be pursued.

Published
2019

13. P5479Educational attainment is an independent predictor of adverse outcomes in patients with coronary artery disease

Author

Ghazzal, B Z, primary, Kelli, H M, additional, Mehta, A, additional, Tahhan, A S, additional, Kim, J H, additional, Dong, T A, additional, Dhindsa, D S, additional, Sandesara, P B, additional, Hayek, S S, additional, Alkhoder, A A, additional, Liu, C, additional, Ko, Y, additional, Vaccarino, V, additional, Sperling, L S, additional, and Quyyumi, A A, additional

Published
2019
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14. Non-invasive Vagal Nerve Stimulation Paired with Stress Exposure in Posttraumatic Stress Disorder (PTSD)

Author

Bremner, J., primary, Gurel, N., additional, Wittbrodt, M., additional, Nye, J., additional, Alam, Z., additional, Herring, I., additional, Ladd, S., additional, Shallenberger, L., additional, Haffer, A., additional, Levantsevych, O., additional, Murrah, N., additional, Huang, M., additional, Ko, Y., additional, Pearce, B., additional, Shandhi, M., additional, Shah, A., additional, Vaccarino, V., additional, and Inan, O., additional

Published
2019
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15. 0705 Short Sleep Duration is Associated with Lower Stress-Induced Blood Pressure Reactivity in Young Women with Early-Onset Myocardial Infarction, But Not Men

Author

Bromfield, S G, primary, Hardy, S, additional, Sullivan, S, additional, Hammadah, M, additional, Shah, A, additional, Levantsevych, O, additional, Kaseer, B, additional, Elon, L, additional, Li, L, additional, Bremner, J D, additional, Quyyumi, A, additional, Vaccarino, V, additional, and Lewis, T T, additional

Published
2018
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16. Sex differences in cardiovascular disease : Impact on care and outcomes

Author

Humphries, K. H., Izadnegandar, M., Sedlak, T., Saw, J., Johnston, Nina, Schenck-Gustafsson, K., Shah, R. U., Regitz-Zagrosek, V., Grewal, J., Vaccarino, V., Wei, J., Merz, C. N. Bairey, Humphries, K. H., Izadnegandar, M., Sedlak, T., Saw, J., Johnston, Nina, Schenck-Gustafsson, K., Shah, R. U., Regitz-Zagrosek, V., Grewal, J., Vaccarino, V., Wei, J., and Merz, C. N. Bairey

Published
2017
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19. Association between the chromosome 9p21 locus and angiographic coronary artery disease burden: A collaborative meta-analysis

Author

Chan, K, Patel, R, Newcombe, P, Nelson, C, Qasim, A, Epstein, SE, Burnett, S, Vaccarino, V, Zafari, A, Shah, S, Anderson, J, Carlquist, J, Hartiala, J, Allayee, H, Hinohara, K, Lee, B, Erl, A, Ellis, K, Goel, A, Schaefer, A, El Mokhtari, N, Goldstein, B, Hlatky, M, Go, A, and Shen, G

Abstract

Objectives: This study sought to ascertain the relationship of 9p21 locus with: 1) angiographic coronary artery disease (CAD) burden; and 2) myocardial infarction (MI) in individuals with underlying CAD. Background: Chromosome 9p21 variants have been robustly associated with coronary heart disease, but questions remain on the mechanism of risk, specifically whether the locus contributes to coronary atheroma burden or plaque instability. Methods: We established a collaboration of 21 studies consisting of 33,673 subjects with information on both CAD (clinical or angiographic) and MI status along with 9p21 genotype. Tabular data are provided for each cohort on the presence and burden of angiographic CAD, MI cases with underlying CAD, and the diabetic status of all subjects. Results: We first confirmed an association between 9p21 and CAD with angiographically defined cases and control subjects (pooled odds ratio [OR]: 1.31, 95% confidence interval [CI]: 1.20 to 1.43). Among subjects with angiographic CAD (n = 20,987), random-effects model identified an association with multivessel CAD, compared with those with single-vessel disease (OR: 1.10, 95% CI: 1.04 to 1.17)/copy of risk allele). Genotypic models showed an OR of 1.15, 95% CI: 1.04 to 1.26 for heterozygous carrier and OR: 1.23, 95% CI: 1.08 to 1.39 for homozygous carrier. Finally, there was no significant association between 9p21 and prevalent MI when both cases (n = 17,791) and control subjects (n = 15,882) had underlying CAD (OR: 0.99, 95% CI: 0.95 to 1.03)/risk allele. Conclusions: The 9p21 locus shows convincing association with greater burden of CAD but not with MI in the presence of underlying CAD. This adds further weight to the hypothesis that 9p21 locus primarily mediates an atherosclerotic phenotype. © 2013 American College of Cardiology Foundation.

Published
2016

20. Sex differences in cardiovascular disease – Impact on care and outcomes

Author

Humphries, K.H., primary, Izadnegahdar, M., additional, Sedlak, T., additional, Saw, J., additional, Johnston, N., additional, Schenck-Gustafsson, K., additional, Shah, R.U., additional, Regitz-Zagrosek, V., additional, Grewal, J., additional, Vaccarino, V., additional, Wei, J., additional, and Bairey Merz, C.N., additional

Published
2017
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22. Identification of ADAMTS7 as a novel locus for coronary atherosclerosis and association of ABO with myocardial infarction in the presence of coronary atherosclerosis: two genome-wide association studies

Author

Reilly MP, Li M, He J, Ferguson JF, Stylianou IM, Mehta NN, Burnett MS, Devaney JM, Knouff CW, Thompson JR, Horne BD, Stewart AF, Assimes TL, Wild PS, Allayee H, Nitschke PL, Patel RS, Myocardial Infarction Genetics Consortium, Wellcome Trust Case Control Consortium, Martinelli N, Girelli D, Quyyumi AA, Anderson JL, Erdmann J, Hall AS, Schunkert H, Quertermous T, Blankenberg S, Hazen SL, Roberts R, Kathiresan S, Samani NJ, Epstein SE, Rader DJ, Qasim AN, DerOhannessian SL, Qu L, Cappola TP, Chen Z, Matthai W, Hakonarson HH, Wilensky R, Kent KM, Lindsay JM, Pichard AD, Satler L, Waksman R, Knoupf CW, Walker MC, Waterworth DM, Mosser V, Braund PS, Wright B, Balmforth AJ, Ball SG, Chen L, Wells GA, McPherson R, Lackner K, Munzel TF, Schillert A, Schnabel R, Zeller T, Ziegler A, Absher D, Hlatky MA, Iribaren C, Knowles JW, Linsel Nitschke P, König IR, Hengstenberg C, Nahrstaedt J, Peters A, Schreiber S, Wichmann E, Willenborg C, Su S, Bouzyk M, Vaccarino V, Zafari AM, Carlquist JF, Muhlestein JB, Olivieri O, Barnard J, Hartiala J, Tang WH, Burton PR, Clayton DG, Cardon LR, Craddock N, Deloukas P, Duncanson A, Kwiatkowski DP, McCarthy MI, Ouwehand WH, Todd JA, Donnelly P, Barrett JC, Davison D, Easton D, Evans DM, Leung HT, Marchini JL, Morris AP, Spencer CC, Tobin MD, Attwood AP, Boorman JP, Cant B, Everson U, Hussey JM, Jolley JD, Knight AS, Koch K, Meech E, Nutland S, Prowse CV, Stevens HE, Taylor NC, Walters GR, Walker NM, Watkins NA, Winzer T, Jones RW, McArdle WL, Ring SM, Strachan DP, Pembrey M, Breen G, St Clair D, Caesar S, Gordon Smith K, Jones L, Fraser C, Green EK, Grozeva D, Hamshere ML, Holmans PA, Jones IR, Kirov G, Moskvina V, Nikolov I, O'Donovan MC, Owen MJ, Collier DA, Elkin A, Farmer A, Williamson R, McGuffin P, Young AH, Ferrier IN, Barrett JH, Bishop DT, Iles MM, Maqbool A, Yuldasheva N, Dixon RJ, Mangino M, Stevens S, Bredin F, Tremelling M, Parkes M, Drummond H, Lees CW, Nimmo ER, Satsangi J, Fisher SA, Forbes A, Lewis CM, Onnie CM, Prescott NJ, Sanderson J, Mathew CG, Barbour J, Mohiuddin MK, Todhunter CE, Mansfield JC, Ahmad T, Cummings FR, Jewell DP, Webster J, Brown MJ, Lathrop M, Connell J, Dominiczak A, Marcano CA, Burke B, Dobson R, Gungadoo J, Lee KL, Munroe PB, Newhouse SJ, Onipinla A, Wallace C, Xue M, Caulfield M, Farrall M, Barton A, Bruce IN, Donovan H, Eyre S, Gilbert PD, Hider SL, Hinks AM, John SL, Potter C, Silman AJ, Symmons DP, Thomson W, Worthington J, Dunger DB, Widmer B, Frayling TM, Freathy RM, Lango H, Perry JR, Shields BM, Weedon MN, Hattersley AT, Hitman GA, Walker M, Elliott KS, Groves CJ, Lindgren CM, Rayner NW, Timpson NJ, Zeggini E, Newport M, Sirugo G, Lyons E, Vannberg F, Hill AV, Bradbury LA, Farrar C, Pointon JJ, Wordsworth P, Brown MA, Franklyn JA, Heward JM, Simmonds MJ, Gough SC, Seal S, Stratton MR, Rahman N, Ban M, Goris A, Sawcer SJ, Compston A, Conway D, Jallow M, Rockett KA, Bumpstead SJ, Chaney A, Downes K, Ghori MJ, Gwilliam R, Hunt SE, Inouye M, Keniry A, King E, McGinnis R, Potter S, Ravindrarajah R, Whittaker P, Widden C, Withers D, Cardin NJ, Ferreira T, Pereira Gale J, Hallgrimsdóttir IB, Bowie BN, Su Z, Teo YY, Vukcevic D, Bentley D, Meigs JB, Williams G, Nathan DM, MacRae CA, O'Donnell CJ, Ardissino D, Merlini PA, Berzuini C, Bernardinelli L, Peyvandi F, Tubaro M, Celli P, Ferrario M, Fetiveau R, Marziliano N, Galli M, Ribichini F, Rossi M, Bernardi F, Zonzin P, Piazza A, Mannucci PM, Schwartz SM, Siscovick DS, Yee J, Friedlander Y, Elosua R, Marrugat J, Lucas G, Subirana I, Sala J, Ramos R, Salomaa V, Havulinna AS, Peltonen L, Melander O, Berglund G, Voight BF, Hirschhorn JN, Asselta R, Duga S, Spreafico M, Musunuru K, Daly MJ, Purcell S, Surti A, Guiducci C, Gianniny L, Mirel D, Parkin M, Burtt N, Gabriel SB, CASARI , GIORGIO NEVIO, Reilly, Mp, Li, M, He, J, Ferguson, Jf, Stylianou, Im, Mehta, Nn, Burnett, M, Devaney, Jm, Knouff, Cw, Thompson, Jr, Horne, Bd, Stewart, Af, Assimes, Tl, Wild, P, Allayee, H, Nitschke, Pl, Patel, R, Myocardial Infarction Genetics, Consortium, Wellcome Trust Case Control, Consortium, Martinelli, N, Girelli, D, Quyyumi, Aa, Anderson, Jl, Erdmann, J, Hall, A, Schunkert, H, Quertermous, T, Blankenberg, S, Hazen, Sl, Roberts, R, Kathiresan, S, Samani, Nj, Epstein, Se, Rader, Dj, Qasim, An, Derohannessian, Sl, Qu, L, Cappola, Tp, Chen, Z, Matthai, W, Hakonarson, Hh, Wilensky, R, Kent, Km, Lindsay, Jm, Pichard, Ad, Satler, L, Waksman, R, Knoupf, Cw, Walker, Mc, Waterworth, Dm, Mosser, V, Braund, P, Wright, B, Balmforth, Aj, Ball, Sg, Chen, L, Wells, Ga, Mcpherson, R, Lackner, K, Munzel, Tf, Schillert, A, Schnabel, R, Zeller, T, Ziegler, A, Absher, D, Hlatky, Ma, Iribaren, C, Knowles, Jw, Linsel Nitschke, P, König, Ir, Hengstenberg, C, Nahrstaedt, J, Peters, A, Schreiber, S, Wichmann, E, Willenborg, C, Su, S, Bouzyk, M, Vaccarino, V, Zafari, Am, Carlquist, Jf, Muhlestein, Jb, Olivieri, O, Barnard, J, Hartiala, J, Tang, Wh, Burton, Pr, Clayton, Dg, Cardon, Lr, Craddock, N, Deloukas, P, Duncanson, A, Kwiatkowski, Dp, Mccarthy, Mi, Ouwehand, Wh, Todd, Ja, Donnelly, P, Barrett, Jc, Davison, D, Easton, D, Evans, Dm, Leung, Ht, Marchini, Jl, Morris, Ap, Spencer, Cc, Tobin, Md, Attwood, Ap, Boorman, Jp, Cant, B, Everson, U, Hussey, Jm, Jolley, Jd, Knight, A, Koch, K, Meech, E, Nutland, S, Prowse, Cv, Stevens, He, Taylor, Nc, Walters, Gr, Walker, Nm, Watkins, Na, Winzer, T, Jones, Rw, Mcardle, Wl, Ring, Sm, Strachan, Dp, Pembrey, M, Breen, G, St Clair, D, Caesar, S, Gordon Smith, K, Jones, L, Fraser, C, Green, Ek, Grozeva, D, Hamshere, Ml, Holmans, Pa, Jones, Ir, Kirov, G, Moskvina, V, Nikolov, I, O'Donovan, Mc, Owen, Mj, Collier, Da, Elkin, A, Farmer, A, Williamson, R, Mcguffin, P, Young, Ah, Ferrier, In, Barrett, Jh, Bishop, Dt, Iles, Mm, Maqbool, A, Yuldasheva, N, Dixon, Rj, Mangino, M, Stevens, S, Bredin, F, Tremelling, M, Parkes, M, Drummond, H, Lees, Cw, Nimmo, Er, Satsangi, J, Fisher, Sa, Forbes, A, Lewis, Cm, Onnie, Cm, Prescott, Nj, Sanderson, J, Mathew, Cg, Barbour, J, Mohiuddin, Mk, Todhunter, Ce, Mansfield, Jc, Ahmad, T, Cummings, Fr, Jewell, Dp, Webster, J, Brown, Mj, Lathrop, M, Connell, J, Dominiczak, A, Marcano, Ca, Burke, B, Dobson, R, Gungadoo, J, Lee, Kl, Munroe, Pb, Newhouse, Sj, Onipinla, A, Wallace, C, Xue, M, Caulfield, M, Farrall, M, Barton, A, Bruce, In, Donovan, H, Eyre, S, Gilbert, Pd, Hider, Sl, Hinks, Am, John, Sl, Potter, C, Silman, Aj, Symmons, Dp, Thomson, W, Worthington, J, Dunger, Db, Widmer, B, Frayling, Tm, Freathy, Rm, Lango, H, Perry, Jr, Shields, Bm, Weedon, Mn, Hattersley, At, Hitman, Ga, Walker, M, Elliott, K, Groves, Cj, Lindgren, Cm, Rayner, Nw, Timpson, Nj, Zeggini, E, Newport, M, Sirugo, G, Lyons, E, Vannberg, F, Hill, Av, Bradbury, La, Farrar, C, Pointon, Jj, Wordsworth, P, Brown, Ma, Franklyn, Ja, Heward, Jm, Simmonds, Mj, Gough, Sc, Seal, S, Stratton, Mr, Rahman, N, Ban, M, Goris, A, Sawcer, Sj, Compston, A, Conway, D, Jallow, M, Rockett, Ka, Bumpstead, Sj, Chaney, A, Downes, K, Ghori, Mj, Gwilliam, R, Hunt, Se, Inouye, M, Keniry, A, King, E, Mcginnis, R, Potter, S, Ravindrarajah, R, Whittaker, P, Widden, C, Withers, D, Cardin, Nj, Ferreira, T, Pereira Gale, J, Hallgrimsdóttir, Ib, Bowie, Bn, Su, Z, Teo, Yy, Vukcevic, D, Bentley, D, Meigs, Jb, Williams, G, Nathan, Dm, Macrae, Ca, O'Donnell, Cj, Ardissino, D, Merlini, Pa, Berzuini, C, Bernardinelli, L, Peyvandi, F, Tubaro, M, Celli, P, Ferrario, M, Fetiveau, R, Marziliano, N, Casari, GIORGIO NEVIO, Galli, M, Ribichini, F, Rossi, M, Bernardi, F, Zonzin, P, Piazza, A, Mannucci, Pm, Schwartz, Sm, Siscovick, D, Yee, J, Friedlander, Y, Elosua, R, Marrugat, J, Lucas, G, Subirana, I, Sala, J, Ramos, R, Salomaa, V, Havulinna, A, Peltonen, L, Melander, O, Berglund, G, Voight, Bf, Hirschhorn, Jn, Asselta, R, Duga, S, Spreafico, M, Musunuru, K, Daly, Mj, Purcell, S, Surti, A, Guiducci, C, Gianniny, L, Mirel, D, Parkin, M, Burtt, N, and Gabriel, Sb

Subjects
Adult, Male, medicine.medical_specialty, Linkage disequilibrium, ABO, ADAMTS7 Protein, ADAMTS7, Genome-wide association study, Coronary Angiography, Polymorphism, Single Nucleotide, Linkage Disequilibrium, ABO Blood-Group System, Coronary artery disease, Gene Frequency, ABO blood group system, Internal medicine, medicine, Genetic predisposition, Humans, Genetic Predisposition to Disease, cardiovascular diseases, Myocardial infarction, Genetic risk factor, genetic locus, Coronary atherosclerosis, Aged, business.industry, coronary atherosclerosis, General Medicine, Middle Aged, medicine.disease, ADAM Proteins, myocardial infarction, Genetic Loci, Cardiology, Myocardial infarction complications, Female, business, coronary artery disease, Genome-Wide Association Study
Abstract

BACKGROUND: We tested whether genetic factors distinctly contribute to either development of coronary atherosclerosis or, specifically, to myocardial infarction in existing coronary atherosclerosis. METHODS: We did two genome-wide association studies (GWAS) with coronary angiographic phenotyping in participants of European ancestry. To identify loci that predispose to angiographic coronary artery disease (CAD), we compared individuals who had this disorder (n=12,393) with those who did not (controls, n=7383). To identify loci that predispose to myocardial infarction, we compared patients who had angiographic CAD and myocardial infarction (n=5783) with those who had angiographic CAD but no myocardial infarction (n=3644). FINDINGS: In the comparison of patients with angiographic CAD versus controls, we identified a novel locus, ADAMTS7 (p=4·98×10(-13)). In the comparison of patients with angiographic CAD who had myocardial infarction versus those with angiographic CAD but no myocardial infarction, we identified a novel association at the ABO locus (p=7·62×10(-9)). The ABO association was attributable to the glycotransferase-deficient enzyme that encodes the ABO blood group O phenotype previously proposed to protect against myocardial infarction. INTERPRETATION: Our findings indicate that specific genetic predispositions promote the development of coronary atherosclerosis whereas others lead to myocardial infarction in the presence of coronary atherosclerosis. The relation to specific CAD phenotypes might modify how novel loci are applied in personalised risk assessment and used in the development of novel therapies for CAD. FUNDING: The PennCath and MedStar studies were supported by the Cardiovascular Institute of the University of Pennsylvania, by the MedStar Health Research Institute at Washington Hospital Center and by a research grant from GlaxoSmithKline. The funding and support for the other cohorts contributing to the paper are described in the webappendix.

Published
2011

23. Ischaemic heart disease in women: are there sex differences in pathophysiology and risk factors? Position paper from the working group on coronary pathophysiology and microcirculation of the European Society of Cardiology

Author

Vaccarino V, Badimon L, Corti R, De Wit C, Dorobantu M, Hall A, Koller A, Marzilli M, Pries A, Working Group on Coronary Pathophysiology, Microcirculation, BUGIARDINI, RAFFAELE, Vaccarino V, Badimon L, Corti R, De Wit C, Dorobantu M, Hall A, Koller A, Marzilli M, Pries A, Bugiardini R, and Working Group on Coronary Pathophysiology and Microcirculation.

Subjects
Male, ACUTE MYOCARDIAL-INFARCTION, medicine.medical_specialty, NATIONAL-HEART, HORMONE-THERAPY, Physiology, Myocardial Ischemia, Reviews, BLOOD-PRESSURE, Disease, Risk Assessment, ESTROGEN PLUS PROGESTIN, Sex Factors, Risk Factors, Physiology (medical), Coronary Circulation, Epidemiology, medicine, Humans, cardiovascular diseases, Risk factor, Intensive care medicine, Coronary atherosclerosis, Societies, Medical, Cause of death, GENDER-DIFFERENCES, Evidence-Based Medicine, business.industry, CARDIOVASCULAR RISK, Microcirculation, Health Status Disparities, C-REACTIVE PROTEIN, Surgery, Europe, POSTMENOPAUSAL WOMEN, DEPRESSIVE SYMPTOMS, Etiology, Female, Cardiology and Cardiovascular Medicine, business, Risk assessment, Sex characteristics
Abstract

Cardiovascular disease (CVD) is the leading cause of death in women, and knowledge of the clinical consequences of atherosclerosis and CVD in women has grown tremendously over the past 20 years. Research efforts have increased and many reports on various aspects of ischaemic heart disease (IHD) in women have been published highlighting sex differences in pathophysiology, presentation, and treatment of IHD. Data, however, remain limited. A description of the state of the science, with recognition of the shortcomings of current data, is necessary to guide future research and move the field forward. In this report, we identify gaps in existing literature and make recommendations for future research. Women largely share similar cardiovascular risk factors for IHD with men; however, women with suspected or confirmed IHD have less coronary atherosclerosis than men, even though they are older and have more cardiovascular risk factors than men. Coronary endothelial dysfunction and microvascular disease have been proposed as important determinants in the aetiology and prognosis of IHD in women, but research is limited on whether sex differences in these mechanisms truly exist. Differences in the epidemiology of IHD between women and men remain largely unexplained, as we are still unable to explain why women are protected towards IHD until older age compared with men. Eventually, a better understanding of these processes and mechanisms may improve the prevention and the clinical management of IHD in women.

Published
2011

25. Presentation, management, and outcomes of ischaemic heart disease in women

Author

Vaccarino, V, Badimon, L, Corti, R, de Wit, C, Dorobantu, M, Manfrini, O, Koller, A, Pries, A, Cenko, E, and Bugiardini, R

Abstract

Scientific interest in ischaemic heart disease (IHD) in women has grown considerably over the past 2 decades. A substantial amount of the literature on this subject is centred on sex differences in clinical aspects of IHD. Many reports have documented sex-related differences in presentation, risk profiles, and outcomes among patients with IHD, particularly acute myocardial infarction. Such differences have often been attributed to inequalities between men and women in the referral and treatment of IHD, but data are insufficient to support this assessment. The determinants of sex differences in presentation are unclear, and few clues are available as to why young, premenopausal women paradoxically have a greater incidence of adverse outcomes after acute myocardial infarction than men, despite having less-severe coronary artery disease. Although differential treatment on the basis of patient sex continues to be described, the extent to which such inequalities persist and whether they reflect true disparity is unclear. Additionally, much uncertainty surrounds possible sex-related differences in response to cardiovascular therapies, partly because of a persistent lack of female-specific data from cardiovascular clinical trials. In this Review, we assess the evidence for sex-related differences in the clinical presentation, treatment, and outcome of IHD, and identify gaps in the literature that need to be addressed in future research efforts.

Published
2013

26. One more consequence of depression: heart failure

Author

Abramson, J, Berger, A, Krumholz, HM, and Vaccarino, V

Subjects
Heart failure -- Psychological aspects, Depression, Mental -- Physiological aspects, Geriatrics -- Research, Health, Seniors
Abstract

Depression, which is associated with an increased risk of coronary heart disease in general and MI in particular, also is associated with an increased risk of heart failure in older [...]

Published
2001

27. Ischemic heart disease in women: are there sex differences in pathophysiology and risk factors?: position paper from the Working Group on Coronary Pathophysiology & Microcirculation of the European Society of Cardiology

Author

Vaccarino, V, Badimon, L, Corti, R, de Wit, C, Dorobantu, M, Hall, A, Koller, A, Marzilli, M, Pries, A, Bugiardini, R, University of Zurich, and Bugiardini, R

Subjects
2737 Physiology (medical), 10209 Clinic for Cardiology, 610 Medicine & health, 1314 Physiology, 2705 Cardiology and Cardiovascular Medicine
Published
2011

28. Ischaemic heart disease in women: are there sex differences in pathophysiology and risk factors? Position Paper from the Working Group on Coronary Pathophysiology and Microcirculation of the European Society of Cardiology

Author

Vaccarino, V, Badimon, L, Corti, R, de Wit, C, Dorobantu, M, Hall, A, Koller, A, Marzilli, M, Pries, A, and Bugiardini, R

Subjects
Risk factors, Epidemiology, Microcirculation, Gender, Ischaemia
Abstract

Cardiovascular disease (CVD) is the leading cause of death in women, and knowledge of the clinical consequences of atherosclerosis and CVD in women has grown tremendously over the past 20 years. Research efforts have increased and many reports on various aspects of ischaemic heart disease (IHD) in women have been published highlighting sex differences in pathophysiology, presentation, and treatment of IHD. Data, however, remain limited. A description of the state of the science, with recognition of the shortcomings of current data, is necessary to guide future research and move the field forward. In this report, we identify gaps in existing literature and make recommendations for future research. Women largely share similar cardiovascular risk factors for IHD with men; however, women with suspected or confirmed IHD have less coronary atherosclerosis than men, even though they are older and have more cardiovascular risk factors than men. Coronary endothelial dysfunction and microvascular disease have been proposed as important determinants in the aetiology and prognosis of IHD in women, but research is limited on whether sex differences in these mechanisms truly exist. Differences in the epidemiology of IHD between women and men remain largely unexplained, as we are still unable to explain why women are protected towards IHD until older age compared with men. Eventually, a better understanding of these processes and mechanisms may improve the prevention and the clinical management of IHD in women.

Published
2011

30. Genome-wide association study identifies a sequence variant within the DAB2IP gene conferring susceptibility to abdominal aortic aneurysm

Author

Gretarsdottir, S, Baas, AF, Thorleifsson, G, Holm, H, den Heijer, M, de Vries, JPPM, Kranendonk, SE, Zeebregts, CJAM, van Sterkenburg, SM, Geelkerken, RH, van Rij, AM, Williams, MJA, Boll, APM, Kostic, JP, Jonasdottir, A, Walters, GB, Masson, G, Sulem, P, Saemundsdottir, J, Mouy, M, Magnusson, KP, Tromp, G, Elmore, JR, Sakalihasan, N, Limet, R, Defraigne, JO, Ferrell, RE, Ronkainen, A, Ruigrok, YM, Wijmenga, C, Grobbee, DE, Shah, SH, Granger, CB, Quyyumi, AA, Vaccarino, V, Patel, RS, Zafari, AM, Levey, AI, Austin, H, Girelli, D, Pignatti, PF, Olivieri, O, Martinelli, N, Malerba, G, Trabetti, E, Becker, LC, Becker, DM, Reilly, MP, Rader, DJ, Mueller, T, Dieplinger, B, Haltmayer, M, Urbonavicius, S, Lindblad, B, Gottsater, A, Gaetani, E, Pola, R, Wells, P, Rodger, M, Forgie, M, Langlois, N, Corral, J, Vicente, V, Fontcuberta, J, Espana, F, Grarup, N, Jorgensen, T, Witte, DR, Hansen, T, Pedersen, O, Aben, KK, de Graaf, J, Holewijn, S, Folkersen, L, Franco-Cereceda, A, Eriksson, P, Collier, DA, Stefansson, H, Steinthorsdottir, V, Rafnar, T, Valdimarsson, EM, Magnadottir, HB, Sveinbjornsdottir, S, Olafsson, I, Magnusson, MK, Palmason, R, Haraldsdottir, V, Andersen, K, Onundarson, PT, Thorgeirsson, G, Kiemeney, LA, Powell, JT, Carey, DJ, Kuivaniemi, H, Lindholt, JS, Jones, GT, Kong, A, Blankensteijn, JD, Matthiasson, SE, Thorsteinsdottir, U, and Stefansson, K

Abstract

We performed a genome-wide association study on 1,292 individuals with abdominal aortic aneurysms (AAAs) and 30,503 controls from Iceland and The Netherlands, with a follow-up of top markers in up to 3,267 individuals with AAAs and 7,451 controls. The A allele of rs7025486 on 9q33 was found to associate with AAA, with an odds ratio (OR) of 1.21 and P = 4.6 x 10(-10). In tests for association with other vascular diseases, we found that rs7025486[A] is associated with early onset myocardial infarction (OR = 1.18, P = 3.1 x 10(-5)), peripheral arterial disease (OR = 1.14, P = 3.9 x 10(-5)) and pulmonary embolism (OR = 1.20, P = 0.00030), but not with intracranial aneurysm or ischemic stroke. No association was observed between rs7025486[A] and common risk factors for arterial and venous diseases-that is, smoking, lipid levels, obesity, type 2 diabetes and hypertension. Rs7025486 is located within DAB2IP, which encodes an inhibitor of cell growth and survival.

Published
2010

35. Genome-wide association study identifies a sequence variant within the DAB2IP gene conferring susceptibility to abdominal aortic aneurysm.

Author

Gretarsdottir, S., Baas, A.F., Thorleifsson, G., Holm, H., Heijer, M. den, Vries, J.P. de, Kranendonk, S.E., Zeebregts, C.J.A., Sterkenburg, S.M. van, Geelkerken, R.H., Rij, A.M. van, Williams, M.J., Boll, A.P.M., Kostic, J., Jonasdottir, A., Walters, G.B., Masson, G., Sulem, P., Saemundsdottir, J., Mouy, M., Magnusson, K.P., Tromp, G., Elmore, J.B., Sakalihasan, N., Limet, R., Defraigne, J.O., Ferrell, R.E., Ronkainen, A., Ruigrok, Y.M., Wijmenga, C., Grobbee, D.E., Shah, S.H., Granger, C.B., Quyyumi, A.A., Vaccarino, V., Patel, R., Zafari, A.M., Levey, A.I., Austin, H., Girelli, D., Pignatti, P.F., Olivieri, O., Martinelli, N., Malerba, G., Trabetti, E., Becker, L.C., Becker, D.M., Reilly, M.P., Rader, D.J., Mueller, T., Dieplinger, B., Haltmayer, M., Urbonavicius, S., Lindblad, B., Gottsäter, A., Gaetani, E., Pola, R., Wells, P., Rodger, M., Forgie, M., Langlois, N., Corral, J., Vicente, V., Fontcuberta, J., España, F., Grarup, N., Jørgensen, T., Witte, D.R., Hansen, T., Pedersen, O., Aben, K.K.H., Graaf, J. de, Holewijn, S., Folkersen, L., Franco-Cereceda, A., Eriksson, P., Collier, D.A., Stefansson, H., Steinthorsdottir, V., Rafnar, T., Valdimarsson, E.M., Magnadottir, H.B., Sveinbjornsdottir, S., Olafsson, I., Magnusson, M.K., Palmason, R., Haraldsdottir, V., Andersen, K., Onundarson, P.T., Thorgeirsson, G., Kiemeney, L.A.L.M., Powell, J.T., Carey, D.J., Kuivaniemi, H., Lindholt, J.S., Jones, G.T., Blankensteijn, J.D., Gretarsdottir, S., Baas, A.F., Thorleifsson, G., Holm, H., Heijer, M. den, Vries, J.P. de, Kranendonk, S.E., Zeebregts, C.J.A., Sterkenburg, S.M. van, Geelkerken, R.H., Rij, A.M. van, Williams, M.J., Boll, A.P.M., Kostic, J., Jonasdottir, A., Walters, G.B., Masson, G., Sulem, P., Saemundsdottir, J., Mouy, M., Magnusson, K.P., Tromp, G., Elmore, J.B., Sakalihasan, N., Limet, R., Defraigne, J.O., Ferrell, R.E., Ronkainen, A., Ruigrok, Y.M., Wijmenga, C., Grobbee, D.E., Shah, S.H., Granger, C.B., Quyyumi, A.A., Vaccarino, V., Patel, R., Zafari, A.M., Levey, A.I., Austin, H., Girelli, D., Pignatti, P.F., Olivieri, O., Martinelli, N., Malerba, G., Trabetti, E., Becker, L.C., Becker, D.M., Reilly, M.P., Rader, D.J., Mueller, T., Dieplinger, B., Haltmayer, M., Urbonavicius, S., Lindblad, B., Gottsäter, A., Gaetani, E., Pola, R., Wells, P., Rodger, M., Forgie, M., Langlois, N., Corral, J., Vicente, V., Fontcuberta, J., España, F., Grarup, N., Jørgensen, T., Witte, D.R., Hansen, T., Pedersen, O., Aben, K.K.H., Graaf, J. de, Holewijn, S., Folkersen, L., Franco-Cereceda, A., Eriksson, P., Collier, D.A., Stefansson, H., Steinthorsdottir, V., Rafnar, T., Valdimarsson, E.M., Magnadottir, H.B., Sveinbjornsdottir, S., Olafsson, I., Magnusson, M.K., Palmason, R., Haraldsdottir, V., Andersen, K., Onundarson, P.T., Thorgeirsson, G., Kiemeney, L.A.L.M., Powell, J.T., Carey, D.J., Kuivaniemi, H., Lindholt, J.S., Jones, G.T., and Blankensteijn, J.D.

Abstract

Contains fulltext : 88507.pdf (publisher's version ) (Closed access)

Published
2010

37. The same sequence variant on 9p21 associates with myocardial infarction, abdominal aortic aneurysm and intracranial aneurysm.

Author

Helgadottir, A., Thorleifsson, G., Magnusson, K.P., Gretarsdottir, S., Steinthorsdottir, V., Manolescu, A., Jones, G.T., Rinkel, G.J., Blankensteijn, J.D., Ronkainen, A., Jaaskelainen, J.E., Kyo, Y., Lenk, G.M., Sakalihasan, N., Kostulas, K., Gottsater, A., Flex, A., Stefansson, H., Hansen, T., Andersen, G., Weinsheimer, S., Borch-Johnsen, K., Jorgensen, T., Shah, S.H., Quyyumi, A.A., Granger, C.B., Reilly, M.P., Austin, H., Levey, A.I., Vaccarino, V., Palsdottir, E., Walters, G.B., Jonsdottir, T., Snorradottir, S., Magnusdottir, D., Gudmundsson, G., Ferrell, R.E., Sveinbjornsdottir, S., Hernesniemi, J., Niemela, M., Limet, R., Andersen, K., Sigurdsson, G., Benediktsson, R., Verhoeven, E.L., Teijink, J.A., Grobbee, D.E., Rader, D.J., Collier, D.A., Pedersen, O., Pola, R., Hillert, J., Lindblad, B., Valdimarsson, E.M., Magnadottir, H.B., Wijmenga, C., Tromp, G., Baas, A.F., Ruigrok, Y.M., Rij, A.M. van, Kuivaniemi, H., Powell, J.T., Matthiasson, S.E., Gulcher, J.R., Thorgeirsson, G., Kong, A., Thorsteinsdottir, U., Stefansson, K., Helgadottir, A., Thorleifsson, G., Magnusson, K.P., Gretarsdottir, S., Steinthorsdottir, V., Manolescu, A., Jones, G.T., Rinkel, G.J., Blankensteijn, J.D., Ronkainen, A., Jaaskelainen, J.E., Kyo, Y., Lenk, G.M., Sakalihasan, N., Kostulas, K., Gottsater, A., Flex, A., Stefansson, H., Hansen, T., Andersen, G., Weinsheimer, S., Borch-Johnsen, K., Jorgensen, T., Shah, S.H., Quyyumi, A.A., Granger, C.B., Reilly, M.P., Austin, H., Levey, A.I., Vaccarino, V., Palsdottir, E., Walters, G.B., Jonsdottir, T., Snorradottir, S., Magnusdottir, D., Gudmundsson, G., Ferrell, R.E., Sveinbjornsdottir, S., Hernesniemi, J., Niemela, M., Limet, R., Andersen, K., Sigurdsson, G., Benediktsson, R., Verhoeven, E.L., Teijink, J.A., Grobbee, D.E., Rader, D.J., Collier, D.A., Pedersen, O., Pola, R., Hillert, J., Lindblad, B., Valdimarsson, E.M., Magnadottir, H.B., Wijmenga, C., Tromp, G., Baas, A.F., Ruigrok, Y.M., Rij, A.M. van, Kuivaniemi, H., Powell, J.T., Matthiasson, S.E., Gulcher, J.R., Thorgeirsson, G., Kong, A., Thorsteinsdottir, U., and Stefansson, K.

Abstract

Contains fulltext : 70663.pdf (publisher's version ) (Closed access), Recently, two common sequence variants on 9p21, tagged by rs10757278-G and rs10811661-T, were reported to be associated with coronary artery disease (CAD) and type 2 diabetes (T2D), respectively. We proceeded to further investigate the contributions of these variants to arterial diseases and T2D. Here we report that rs10757278-G is associated with, in addition to CAD, abdominal aortic aneurysm (AAA; odds ratio (OR) = 1.31, P = 1.2 x 10(-12)) and intracranial aneurysm (OR = 1.29, P = 2.5 x 10(-6)), but not with T2D. This variant is the first to be described that affects the risk of AAA and intracranial aneurysm in many populations. The association of rs10811661-T to T2D replicates in our samples, but the variant does not associate with any of the five arterial diseases examined. These findings extend our insight into the role of the sequence variant tagged by rs10757278-G and show that it is not confined to atherosclerotic diseases.

Published
2008

38. 126 CHROMOSOME 9P21 LOCUS AND ANGIOGRAPHIC CORONARY ARTERY DISEASE BURDEN: A COLLABORATIVE META-ANALYSIS

Author

Chan, K, primary, Patel, R S, additional, Newcombe, P, additional, Nelson, C P, additional, Qasim, A, additional, Epstein, S E, additional, Burnett, S, additional, Vaccarino, V L, additional, Zafari, A M, additional, Shah, S H, additional, Anderson, J L, additional, Carlquist, J F, additional, Hartiala, J, additional, Allayee, H, additional, Hinohara, K, additional, Lee, B S, additional, Erl, A, additional, Ellis, K L, additional, Goel, A, additional, Schaefer, A S, additional, Mokhtari, N E, additional, Goldstein, B A, additional, Hlatky, M A, additional, Go, A S, additional, Shen, G Q, additional, Gong, Y, additional, Pepine, C, additional, Laxton, R C, additional, Wittaker, J C, additional, Tang, W H W, additional, Johnson, J A, additional, Wang, Q K, additional, Assimes, T L, additional, Nöthlings, U, additional, Farrall, M, additional, Watkins, H, additional, Richards, A M, additional, Cameron, V A, additional, Muendlein, A, additional, Drexel, H, additional, Koch, W, additional, Park, J E, additional, Kimura, A, additional, Shen, W F, additional, Simpson, I A, additional, Hazen, S L, additional, Horne, B D, additional, Hauser, E R, additional, Quyyumi, A A, additional, Reilly, M P, additional, Samani, N J, additional, and Ye, S, additional

Published
2013
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39. A propensity-matched study of the effect of diabetes on the natural history of heart failure: variations by sex and age

Author

Ahmed, A, Aban, Ib, Vaccarino, V, Lloyd Jones, Dm, Goff, Dc, Zhao, J, Love, Te, Ritchie, C, Ovalle, F, Gambassi, Giovanni, Dell'Italia, Lj, Gambassi, Giovanni (ORCID:0000-0002-7030-9359), Ahmed, A, Aban, Ib, Vaccarino, V, Lloyd Jones, Dm, Goff, Dc, Zhao, J, Love, Te, Ritchie, C, Ovalle, F, Gambassi, Giovanni, Dell'Italia, Lj, and Gambassi, Giovanni (ORCID:0000-0002-7030-9359)

Abstract

Poor prognosis in heart failure (HF) patients with diabetes is often attributed to increased co-morbidity and advanced disease. Further, this effect may be worse in women.

Published
2007

41. Sex differences in cardiac catheterization: the role of physician gender.

Author

Rathore SS, Chen J, Wang Y, Radford MJ, Vaccarino V, Krumholz HM, Lauer MS, Rathore, S S, Chen, J, Wang, Y, Radford, M J, Vaccarino, V, and Krumholz, H M

Abstract

Context: Many studies indicate that women are less likely than men to undergo cardiac procedures after an acute myocardial infarction (AMI), raising concerns of sexual bias in clinical care. However, no data exist regarding the relationship between patient sex, physician sex, and use of cardiac procedures.Objective: To determine whether sex differences in cardiac catheterization after AMI were greater when patients were treated by male attending physicians compared with female attending physicians.Design, Setting, and Patients: Analysis of data from the Cooperative Cardiovascular Project, a retrospective medical record review. A total of 104 >231 Medicare fee-for-service beneficiaries who were hospitalized in US acute care hospitals for an AMI between January 1994 and February 1995.Main Outcome Measure: Use of cardiac catheterization within 60 days of admission, compared between the 4 groups of patient sex-physician sex combinations.Results: Women underwent fewer cardiac catheterizations than men when treated by either male physicians (38.6% vs 50.8%; P =.001) or female physicians (34.8% vs 45.8%; P =.001). Sex differences in procedure use were not greater when a patient and physician were of different sexes (P for interaction =.85). After potential confounders in multivariable analysis were accounted for, women were less likely to undergo cardiac catheterization (risk ratio, 0.90 [95% confidence interval (CI), 0.88-0.92]), regardless of the treating physician's sex. Patients treated by male physicians were more likely to undergo cardiac catheterization (risk ratio, 1.06 [95%CI, 1.02-1.10]) than those treated by female physicians, regardless of patient sex.Conclusions: Women who have had an AMI undergo a cardiac catheterization less often than men, whether treated by a male or female physician. These results suggest that factors other than sexual bias by male physicians toward women account for sex differences in cardiac procedure use. [ABSTRACT FROM AUTHOR]

Published
2001
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42. Pulse pressure and risk of cardiovascular events in the systolic hypertension in the elderly program.

Author

Vaccarino V, Berger AK, Abramson J, Black HR, Setaro JF, Davey JA, Krumholz HM, Vaccarino, V, Berger, A K, Abramson, J, Black, H R, Setaro, J F, Davey, J A, and Krumholz, H M

Abstract

Pulse pressure has been related to higher risk of cardiovascular events in older persons. Isolated systolic hypertension is common among the elderly and is accompanied by elevated pulse pressure. Treatment of isolated systolic hypertension may further increase pulse pressure if diastolic pressure is lowered to a greater extent than systolic pressure. Little is known regarding pulse pressure as a predictor of cardiovascular outcomes in elderly persons with isolated systolic hypertension, and the influence of treatment on the pulse pressure effect. We assessed the relation between pulse pressure, measured throughout the follow-up period, and the incidence of coronary heart disease (CHD), heart failure (HF), and stroke in 4,632 participants in the Systolic Hypertension in the Elderly Program, a 5-year randomized, placebo-controlled clinical trial of treatment of isolated systolic hypertension in older adults. In the treatment group, a 10-mm Hg increase in pulse pressure was associated with a statistically significant 32% increase in risk of HF and a 24% increase in risk of stroke after controlling for systolic blood pressure and other known risk factors, as well as with a 23% increase in risk of HF and a 19% increase in risk of stroke after controlling for diastolic blood pressure and other risk factors. Pulse pressure was not significantly associated with HF or stroke in the placebo group, nor with incidence of CHD in either the placebo or treatment group. These results suggest that pulse pressure is a useful marker of risk for HF and stroke among older adults being treated for isolated systolic hypertension. [ABSTRACT FROM AUTHOR]

Published
2001
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45. The chromosome 9p21 risk locus is associated with angiographic severity and progression of coronary artery disease

Author

Patel, R. S., primary, Su, S., additional, Neeland, I. J., additional, Ahuja, A., additional, Veledar, E., additional, Zhao, J., additional, Helgadottir, A., additional, Holm, H., additional, Gulcher, J. R., additional, Stefansson, K., additional, Waddy, S., additional, Vaccarino, V., additional, Zafari, A. M., additional, and Quyyumi, A. A., additional

Published
2010
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