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1. The chromatin remodeller ATRX facilitates diverse nuclear processes, in a stochastic manner, in both heterochromatin and euchromatin

Author

Truch, J, Downes, DJ, Scott, C, Gür, ER, Telenius, JM, Repapi, E, Schwessinger, R, Gosden, M, Brown, JM, Taylor, S, Cheong, PL, Hughes, JR, Higgs, DR, and Gibbons, RJ

Subjects
Histone variants, Clinical epigenetics, X-linked Nuclear Protein, Multidisciplinary, DNA Helicases, Nuclear Proteins, General Physics and Astronomy, Chromatin remodelling, General Chemistry, Chromatin, General Biochemistry, Genetics and Molecular Biology, Euchromatin, Histones, alpha-Thalassemia, Heterochromatin, Mental Retardation, X-Linked
Abstract

The chromatin remodeller ATRX interacts with the histone chaperone DAXX to deposit the histone variant H3.3 at sites of nucleosome turnover. ATRX is known to bind repetitive, heterochromatic regions of the genome including telomeres, ribosomal DNA and pericentric repeats, many of which are putative G-quadruplex forming sequences (PQS). At these sites ATRX plays an ancillary role in a wide range of nuclear processes facilitating replication, chromatin modification and transcription. Here, using an improved protocol for chromatin immunoprecipitation, we show that ATRX also binds active regulatory elements in euchromatin. Mutations in ATRX lead to perturbation of gene expression associated with a reduction in chromatin accessibility, histone modification, transcription factor binding and deposition of H3.3 at the sequences to which it normally binds. In erythroid cells where downregulation of α-globin expression is a hallmark of ATR-X syndrome, perturbation of chromatin accessibility and gene expression occurs in only a subset of cells. The stochastic nature of this process suggests that ATRX acts as a general facilitator of cell specific transcriptional and epigenetic programmes, both in heterochromatin and euchromatin.

Published
2022

2. Abstracts of original contributions ASNC 2004 9th annual scientific session September 3-–October 3, 2004 New York, New York

Author

Abidov, A, Hachamovitch, R, Friedman, JD, Hayes, SW, Kang, X, Cohen, I, Germano, G, Berman, DS, Kjaer, A, Cortsen, A, Federspiel, M, Hesse, B, Holm, S, O’Connor, M, Dhalla, AK, Wong, M-Y, Wang, W-Q, Belardinelli, L, Therapeutics, CV, Epps, A, Dave, S, Brewer, K, Chiaramida, S, Gordon, L, Hendrix, GH, Feng, B, Pretorius, PH, Bruyant, PP, Boening, G, Beach, RD, Gifford, HC, King, MA, Fessler, JA, Hsu, B-L, Case, JA, Gegen, LL, Hertenstein, GK, Cullom, SJ, Bateman, TM, Akincioglu, C, Abidov, A, Nishina, H, Kavanagh, P, Kang, X, Aboul-Enein, F, Yang, L, Hayes, S, Friedman, J, Berman, D, Germano, G, Santana, CA, Rivero, A, Folks, RD, Grossman, GB, Cooke, CD, Hunsche, A, Faber, TL, Halkar, R, Garcia, EV, Hansen, CL, Silver, S, Kaplan, A, Rasalingam, R, Awar, M, Shirato, S, Reist, K, Htay, T, Mehta, D, Cho, J-H, Heo, J, Dubovsky, E, Calnon, DA, Grewal, KS, George, PB, Richards, DR, Hsi, DH, Singh, N, Meszaros, Z, Thomas, JL, Reyes, E, Loong, CY, Latus, K, Anagnostopoulos, C, Underwood, SR, Kostacos, EJ, Araujo, LI, Kostacos, EJ, Araujo, LI, Lewin, HC, Hyun, MC, DePuey, EG, Tanaka, H, Chikamori, T, Igarashi, Y, Harafuji, K, Usui, Y, Yanagisawa, H, Hida, S, Yamashina, A, Nasr, HA, Mahmoud, SA, Dalipaj, MM, Golanowski, LN, Kemp, RA de, Chow, BJ, Beanlands, RS, Ruddy, TD, Michelena, HI, Mikolich, BM, McNelis, P, Decker, WA Van, Stathopoulos, I, Duncan, S- A, Isasi, C, Travin, MI, Kritzman, JN, Ficaro, EP, Corbett, JR, Allison, JS, Weinsaft, JW, Wong, FJ, Szulc, M, Okin, PM, Kligfield, P, Harafuji, K, Chikamori, T, Igarashi, Y, Tanaka, H, Usui, Y, Yanagisawa, H, Hida, S, Ishimaru, S, Yamashima, A, Giedd, KN, Bergmann, SR, Shah, S, Emmett, L, Allman, KC, Magee, M, Van Gaal, W, Kritharides, L, Freedman, B, Abidov, A, Gerlach, J, Akincioglu, C, Friedman, J, Kavanagh, P, Miranda, R, Germano, G, Berman, DS, Hayes, SW, Damera, N, Lone, B, Singh, R, Shah, A, Yeturi, S, Prasad, Y, Blum, S, Heller, EN, Bhalodkar, NC, Koutelou, M, Kollaros, N, Theodorakos, A, Manginas, A, Leontiadis, E, Kouzoumi, A, Cokkinos, D, Mazzanti, M, Marini, M, Cianci, G, Perna, GP, Pai, M, Greenberg, MD, Liu, F, Frankenberger, O, Kokkinos, P, Hanumara, D, Goheen, E, Wu, C, Panagiotakos, D, Fletcher, R, Greenberg, MD, Liu, F, Frankenberger, O, Kokkinos, P, Hanumara, D, Goheen, E, Rodriguez, OJ, Iyer, VN, Lue, M, Hickey, KT, Blood, DK, Bergmann, SR, Bokhari, S, Chareonthaitawee, P, Christensen, SD, Allen, JL, Kemp, BJ, Hodge, DO, Ritman, EL, Gibbons, RJ, Smanio, P, Riva, G, Rodriquez, F, Tricoti, A, Nakhlawi, A, Thom, A, Pretorius, PH, King, MA, Dahlberg, S, Leppo, J, Slomka, PJ, Nishina, H, Berman, DS, Akincioglu, C, Abidov, A, Friedman, JD, Hayes, SW, Germano, G, Petrovici, R, Husain, M, Lee, DS, Nanthakumar, K, Iwanochko, RM, Brunken, RC, DiFilippo, F, Neumann, DR, Bybel, B, Herrington, B, Bruckbauer, T, Howe, C, Lohmann, K, Hayden, C, Chatterjee, C, Lathrop, B, Brunken, RC, Chen, MS, Lohmann, KA, Howe, WC, Bruckbauer, T, Kaczur, T, Bybel, B, DiFilippo, FP, Druz, RS, Akinboboye, OA, Grimson, R, Nichols, KJ, Reichek, N, Ngai, K, Dim, R, Ho, K- T, Pary, S, Ahmed, SU, Ahlberg, A, Cyr, G, Vitols, PJ, Mann, A, Alexander, L, Rosenblatt, J, Mieres, J, Heller, GV, Ahmed, SU, Ahlberg, AW, Cyr, G, Navare, S, O’Sullivan, D, Heller, GV, Chiadika, S, Lue, M, Blood, DK, Bergmann, SR, Bokhari, S, Heston, TF, Heller, GV, Cerqueira, MD, Jones, PG, Bryngelson, JR, Moutray, KL, Gegen, LL, Hertenstein, GK, Moser, K, Case, JA, Zellweger, MJ, Burger, PC, Pfisterer, ME, Mueller-Brand, J, Kang, WJ, Lee, BI, Lee, DS, Paeng, JC, Lee, JS, Chung, J-K, Lee, MC, To, BN, O’Connell, WJ, Botvinick, EH, Duvall, WL, Croft, LB, Einstein, AJ, Fisher, JE, Haynes, PS, Rose, RK, Henzlova, MJ, Prasad, Y, Vashist, A, Blum, S, Sagar, P, Heller, EN, Kuwabara, Y, Nakayama, K, Tsuru, Y, Nakaya, J, Shindo, S, Hasegawa, M, Komuro, I, Liu, Y-H, Wackers, F, Natale, D, DePuey, G, Taillefer, R, Araujo, L, Kostacos, E, Allen, S, Delbeke, D, Anstett, F, Kansal, P, Calvin, JE, Hendel, RC, Gulati, M, Pratap, P, Takalkar, A, Kostacos, E, Alavi, A, Araujo, L, Melduni, RM, Duncan, S-A, Travin, MI, Isasi CR, Rivero, A, Santana, C, Esiashvili, S, Grossman, G, Halkar, R, Folks, RD, Garcia, EV, Su, H, Dobrucki, LW, Chow, C, Hu, X, Bourke, BN, Cavaliere, P, Hua, J, Sinusas, AJ, Spinale, FG, Sweterlitsch, S, Azure, M, Edwards, DS, Sudhakar, S, Chyun, DA, Young, LH, Inzucchi, SE, Davey, JA, Wackers, FJ, Noble, GL, Navare, SM, Calvert, J, Hussain, SA, Ahlberg, AM, Katten, DM, Boden, WE, Heller, GV, Shaw, LJ, Yang, Y, Antunes, A, Botelho, MF, Gomes, C, de Lima, JJP, Silva, ML, Moreira, JN, Simões, S, GonÇalves, L, Providência, LA, Elhendy, A, Bax, JJ, Schinkel, AF, Valkema, R, van Domburg, RT, Poldermans, D, Arrighi, J, Lampert, R, Burg, M, Soufer, R, Veress, AI, Weiss, JA, Huesman, RH, Gullberg, GT, Moser, K, Case, JA, Loong, CY, Prvulovich, EM, Reyes, E, Aswegen, A van, Anagnostopoulos, C, Underwood, SR, Htay, T, Mehta, D, Sun, L, Lacy, J, Heo, J, Brunken, RC, Kaczur, T, Jaber, W, Ramakrishna, G, Miller, TD, O’connor, MK, Gibbons, RJ, Bural, GG, Mavi, A, Kumar, R, El-Haddad, G, Srinivas, SM, A Alavi, El-Haddad, G, Alavi, A, Araujo, L, Thomas, GS, Johnson, CM, Miyamoto, MI, Thomas, JJ, Majmundar, H, Ryals, LA, Ip, ZTK, Shaw, LJ, Bishop, HA, Carmody, JP, Greathouse, WG, Yanagisawa, H, Chikamori, T, Tanaka, H, Usui, Y, Igarashi, U, Hida, S, Morishima, T, Tanaka, N, Takazawa, K, Yamashina, A, Diedrichs, H, Weber, M, Koulousakis, A, Voth, E, Schwinger, RHG, Mohan, HK, Livieratos, L, Gallagher, S, Bailey, DL, Chambers, J, Fogelman, I, Sobol, I, Barst, RJ, Nichols, K, Widlitz, A, Horn, E, Bergmann, SR, Chen, J, Galt, JR, Durbin, MK, Ye, J, Shao, L, Garcia, EV, Mahenthiran, J, Elliott, JC, Jacob, S, Stricker, S, Kalaria, VG, Sawada, S, Scott, JA, Aziz, K, Yasuda, T, Gewirtz, H, Hsu, BL, Moutray, K, Udelson, JE, Barrett, RJ, Johnson, JR, Menenghetti, C., Taillefer, R, Ruddy, T, Hachamovitch, R, Jenkins, SA, Massaro, J, Haught, H, Lim, CS, Underwood, R, Rosman, J, Hanon, S, Shapiro, M, Schweitzer, P, VanTosh, A, Jones, S, Harafuji, K, Giedd, K N, Johnson, N P, Berliner, J I, Sciacca, R R, Chou, R L, Hickey, K T, Bokhari, S S, Rodriguez, O, Bokhari, S, Moser, KW, Moutray, KL, Koutelou, M, Theodorakos, A, Kollaros, N, Manginas, A, Leontiadis, E, Cokkinos, D, Mazzanti, M, Marini, M, Cianci, G, Perna, GP, Nanasato, M, Fujita, H, Toba, M, Nishimura, T, Nikpour, M, Urowitz, M, Gladman, D, Ibanez, D, Harvey, P, Floras, J, Rouleau, J, Iwanochko, R, Pai, M, Guglin, ME, Ginsberg, FL, Reinig, M, Parrillo, JE, Cha, R, Merhige, ME, Watson, GM, Oliverio, JG, Shelton, V, Frank, SN, Perna, AF, Ferreira, MJ, Ferrer-Antunes, AI, Rodrigues, V, Santos, F, Lima, J, Cerqueira, MD, Magram, MY, Lodge, MA, Babich, JW, Dilsizian, V, Line, BR, Bhalodkar, NC, Lone, B, Singh, R, Prasad, Y, Yeturi, S, Blum, S, Heller, EN, Rodriguez, OJ, Skerrett, D, Charles, C, Shuster, MD, Itescu, S, Wang, TS, Bruyant, PP, Pretorius, PH, Dahlberg, S, King, MA, Petrovici, R, Iwanochko, RM, Lee, DS, Emmett, L, Husain, M, Hosokawa, R, Ohba, M, Kambara, N, Tadamura, E, Kubo, S, Nohara, R, Kita, T, Thompson, RC, McGhie, AI, O’Keefe, JH, Christenson, SD, Chareonthaitawee, P, Kemp, BJ, Jerome, S, Russell, TJ, Lowry, DR, Coombs, VJ, Moses, A, Gottlieb, SO, Heiba, SI, Yee, G, Coppola, J, Elmquist, T, Braff, R, Youssef, I, Ambrose, JA, Abdel-Dayem, HM, Canto, J, Dubovsky, E, Scott, J, Terndrup, TE, Faber, TL, Folks, RD, Dim, UR, Mclaughlin, J, Pollepalle, D, Schapiro, W, Wang, Y, Akinboboye, O, Ngai, K, Druz, RS, Polepalle, D, Phippen-Nater, B, Leonardis, J, and Druz, R

Published
2004
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3. Refining the Primrose syndrome phenotype: A study of five patients with ZBTB20 de novo variants and a review of the literature

Author

Cleaver, RJ, Berg, J, Craft, E, Foster, A, Gibbons, RJ, Hobson, E, Lachlan, K, Naik, S, Sampson, JR, Sharif, S, Smithson, S, Study, Deciphering Developmental Disorders, Parker, MJ, and Tatton-Brown, K

Subjects
Male, medicine.medical_specialty, Genotype, Nerve Tissue Proteins, Corpus callosum, Intellectual Disability, Intellectual disability, Genetics, Humans, Medicine, Missense mutation, Abnormalities, Multiple, Genetic Predisposition to Disease, Child, Ear Diseases, Genetic Association Studies, Genetics (clinical), Exome sequencing, business.industry, Macrocephaly, Calcinosis, Facies, Genetic Variation, Primrose syndrome, medicine.disease, Magnetic Resonance Imaging, Dermatology, Hypotonia, Muscular Atrophy, Phenotype, Genetic Loci, Child, Preschool, Mutation, Female, Sensorineural hearing loss, medicine.symptom, business, Transcription Factors
Abstract

Primrose syndrome is a rare autosomal dominant condition caused by heterozygous missense variants within ZBTB20. Through an exome sequencing approach (as part of the Deciphering Developmental Disorders [DDD] study) we have identified five unrelated individuals with previously unreported, de novo ZBTB20 pathogenic missense variants. All five missense variants targeted the C2H2 zinc finger domains. This genotype-up approach has allowed further refinement of the Primrose syndrome phenotype. Major characteristics (>90% individuals) include an intellectual disability (most frequently in the moderate range), a recognizable facial appearance and brain MRI abnormalities, particularly abnormalities of the corpus callosum. Other frequent clinical associations (in 50-90% individuals) include sensorineural hearing loss (83%), hypotonia (78%), cryptorchidism in males (75%), macrocephaly (72%), behavioral issues (56%), and dysplastic/hypoplastic nails (57%). Based upon these clinical data we discuss our current management of patients with Primrose syndrome.

Published
2019

4. Third universal definition of myocardial infarction

Author

Thygesen, K, Alpert, Js, Jaffe, As, Simoons, Ml, Chaitman, Br, White, Hd, the Writing Group on behalf of the Joint ESC/ACCF/AHA/WHF Task Force for the Universal Definition of Myocardial Infarction, Authors/Task Force Members Chairpersons, Biomarker, Subcommittee, Katus, Ha, Apple, Fs, Lindahl, B, Morrow, Da, Ecg, Subcommittee, Clemmensen, Pm, Johanson, P, Hod, H, Imaging, Subcommittee, Underwood, R, Bax, Jj, Bonow, Ro, Pinto, F, Gibbons, Rj, Classification, Subcommittee, Fox, Ka, Atar, D, Newby, Lk, Galvani, M, Hamm, Cw, Intervention, Subcommittee, Uretsky, Bf, Gabriel Steg, P, Wijns, W, Bassand, Jp, Menasché, P, Ravkilde, J, Trials, Registries, Subcommittee, Ohman, Em, Antman, Em, Wallentin, Lc, Armstrong, Pw, Heart Failure Subcommittee, Januzzi, Jl, Nieminen, Ms, Gheorghiade, M, Filippatos, G, Epidemiology, Subcommittee, Luepker, Rv, Fortmann, Sp, Rosamond, Wd, Levy, D, Wood, D, Global Perspective Subcommittee, Smith, Sc, Hu, D, Lopez Sendon JL, Robertson, Rm, Weaver, D, Tendera, M, Bove, Aa, Parkhomenko, An, Vasilieva, Ej, Mendis, S, ESC Committee for Practice Guidelines, Baumgartner, H, Ceconi, Claudio, Dean, V, Deaton, C, Fagard, R, Funck Brentano, C, Hasdai, D, Hoes, A, Kirchhof, P, Knuuti, J, Kolh, P, Mcdonagh, T, Moulin, C, Popescu, Ba, Reiner, Z, Sechtem, U, Sirnes, Pa, Torbicki, A, Vahanian, A, Windecker, S, Document, Reviewers, Morais, J, Aguiar, C, Almahmeed, W, Arnar, Do, Barili, F, Bloch, Kd, Bolger, Af, Bøtker, He, Bozkurt, B, Bugiardini, R, Cannon, C, de Lemos, J, Eberli, Fr, Escobar, E, Hlatky, M, James, S, Kern, Kb, Moliterno, Dj, Mueller, C, Neskovic, An, Pieske, Bm, Schulman, Sp, Storey, Rf, Taubert, Ka, Vranckx, P, Wagner, D. R., Thygesen K, Alpert JS, Jaffe AS, Simoons ML, Chaitman BR, White HD, Lindahl B, Morrow DA, Clemmensen PM, Johanson P, Hod H, Underwood R, Bax JJ, Bonow JJ, Pinto F, Gibbons RJ, Fox KA, Atar D, Newby LK, Galvani M, Hamm CW, Uretsky BF, Steg PG, Wijns W, Bassand JP, Menasche P, Ravkilde J, Ohman EM, Antman EM, Wallentin LC, Armstrong PW, Januzzi JL, Nieminen MS, Gheorghiade M, Filippatos G, Luepker RV, Fortmann SP, Rosamond WD, Levy D, Wood D, Smith SC, Hu D, Lopez-Sendon JL, Robertson RM, Weaver D, Tendera M, Bove AA, Parkhomenko AN, Vasilieva EJ, Mendis S, Baumgartner H, Ceconi C, Dean V, Deaton C, Fagard R, Funck-Brentano C, Hasdai D, Hoes A, Kirchhof P, Knuuti J, Kolh P, McDonagh T, Moulin C, Popescu BA, Reiner Z, Sechtem U, Sirnes PA, Torbicki A, Vahanian A, Windecker S, Morais J, Aguiar C, Almahmeed W, Arnar DO, Barili F, Bloch KD, Bolger AF, Botker HE, Bozkurt B, Bugiardini R, Cannon C, de Lemos J, Eberli FR, Escobar E, Hlatky M, James S, Kern KB, Moliterno DJ, Mueller C, Neskovic AN, Pieske BM, Schulman SP, Storey RF, Taubert KA, Vranckx P, Wagner DR., Cardiology, lLindahl B, K. Thygesen, J. S. Alpert, A. S. Jaffe, M. L. Simoon, B. R. Chaitman, H. D. White, H. A. Katu, F. S. Apple, B. Lindahl, D. A. Morrow, P. M. Clemmensen, P. Johanson, H. Hod, R. Underwood, J. J. Bax, R. O. Bonow, F. Pinto, R. J. Gibbon, K. A. Fox, D. Atar, L. K. Newby, M. Galvani, C. W. Hamm, B. F. Uretsky, P. Gabriel Steg, W. Wijn, J.-P. Bassand, P. Menasche, J. Ravkilde, E. M. Ohman, E. M. Antman, L. C. Wallentin, P. W. Armstrong, J. L. Januzzi, M. S. Nieminen, M. Gheorghiade, G. Filippato, R. V. Luepker, S. P. Fortmann, W. D. Rosamond, D. Levy, D. Wood, S. C. Smith, D. Hu, J.-L. Lopez-Sendon, R. M. Robertson, D. Weaver, M. Tendera, A. A. Bove, A. N. Parkhomenko, E. J. Vasilieva, S. Mendi, H. Baumgartner, C. Ceconi, V. Dean, C. Deaton, R. Fagard, C. Funck-Brentano, D. Hasdai, A. Hoe, P. Kirchhof, J. Knuuti, P. Kolh, T. McDonagh, C. Moulin, B. A. Popescu, Z. Reiner, U. Sechtem, P. A. Sirne, A. Torbicki, A. Vahanian, S. Windecker, J. Morai, C. Aguiar, W. Almahmeed, D. O. Arnar, F. Barili, K. D. Bloch, A. F. Bolger, H. E. Botker, B. Bozkurt, R. Bugiardini, C. Cannon, J. de Lemo, F. R. Eberli, E. Escobar, M. Hlatky, S. Jame, K. B. Kern, D. J. Moliterno, C. Mueller, A. N. Neskovic, B. M. Pieske, S. P. Schulman, R. F. Storey, K. A. Taubert, P. Vranckx, D. R. Wagner, Thygesen, K, Alpert, J, Jaffe, A, Simoons, Ml, Chaitman, Br, White, Hd, Katus, Ha, Apple, F, Lindahl, B, Morrow, Da, Clemmensen, Pm, Johanson, P, Hod, H, Underwood, R, Bax, Jj, Bonow, Jj, Pinto, F, Gibbons, Rj, Fox, Ka, Atar, D, Newby, Lk, Galvani, M, Hamm, Cw, Uretsky, Bf, Steg, Pg, Wijns, W, Bassand, Jp, Menasche, P, Ravkilde, J, Ohman, Em, Antman, Em, Wallentin, Lc, Armstrong, Pw, Januzzi, Jl, Nieminen, M, Gheorghiade, M, Filippatos, G, Luepker, Rv, Fortmann, Sp, Rosamond, Wd, Levy, D, Wood, D, Smith, Sc, Hu, D, Lopez-Sendon, Jl, Robertson, Rm, Weaver, D, Tendera, M, Bove, Aa, Parkhomenko, An, Vasilieva, Ej, Mendis, S, Baumgartner, H, Ceconi, C, Dean, V, Deaton, C, Fagard, R, Funck-Brentano, C, Hasdai, D, Hoes, A, Kirchhof, P, Knuuti, J, Kolh, P, Mcdonagh, T, Moulin, C, Popescu, Ba, Reiner, Z, Sechtem, U, Sirnes, Pa, Torbicki, A, Vahanian, A, Windecker, S, Morais, J, Aguiar, C, Almahmeed, W, Arnar, Do, Barili, F, Bloch, Kd, Bolger, Af, Botker, He, Bozkurt, B, Bugiardini, R, Cannon, C, de Lemos, J, Eberli, Fr, Escobar, E, Hlatky, M, James, S, Kern, Kb, Moliterno, Dj, Mueller, C, Neskovic, An, Pieske, Bm, Schulman, Sp, Storey, Rf, Taubert, Ka, Vranckx, P, and Wagner, Dr

Subjects
High-sensitivity troponin, Ticagrelor, Chest pain unit, Quality Assurance, Health Care, Epidemiology, medicine.medical_treatment, Myocardial Infarction, Myocardial ischaemia, Global Health, Early invasive strategy, Electrocardiography, Stent, Myocardial Revascularization, Myocardial infarction, Coronary Artery Bypass, Intraoperative Complications, Left bundle branch block, Health Policy, Electrocardiography in myocardial infarction, Cangrelor, Stents, Acute coronary syndrome, Cardiology and Cardiovascular Medicine, Prasugrel, Diagnostic Imaging, medicine.medical_specialty, Public Policy, Risk Assessment, Vorapaxar, Percutaneous Coronary Intervention, Physiology (medical), Terminology as Topic, Humans, Enoxaparin, Bypass surgery, Community and Home Care, Heart Failure, Rhythm monitoring, Aspirin, Unstable angina, Angioplasty, Recommendation, ta3121, medicine.disease, Myocardial infarction diagnosis, Bivalirudin, Biomarkers, Time Factors, Platelet inhibition, Consensus Development Conferences as Topic, Diagnostic Techniques, Cardiovascular, Myocardial Ischemia, Guideline, Diabete, Nitrate, Left ventricular hypertrophy, Coronary artery disease, Rivaroxaban, Recurrence, Apixaban, Clinical Trials as Topic, Graft Occlusion, Vascular, Atherothrombosi, Acute cardiac care, Right bundle branch block, Clopidogrel, Dabigatran, Prosthesis Failure, AHA Scientific Statements, Practice Guidelines as Topic, Cardiology, Biological Markers, Radiology, Critical Care, Glycoprotein IIb/IIIa inhibitor, European Society of Cardiology, Diagnosis, Differential, Anticoagulation, Internal medicine, medicine, Beta-blocker, cardiovascular diseases, Heparin, business.industry, Revascularization, Cardiovascular Surgical Procedures, MYOCARDIAL INFARCTION, Statin, Percutaneous coronary intervention, Arrhythmias, Cardiac, Cardiac Imaging Techniques, Fondaparinux, Heart failure, Non-ST-elevation myocardial infarction, business
Abstract

ACCF : American College of Cardiology Foundation ACS : acute coronary syndrome AHA : American Heart Association CAD : coronary artery disease CABG : coronary artery bypass grafting CKMB : creatine kinase MB isoform cTn : cardiac troponin CT : computed tomography CV : coefficient of variation ECG : electrocardiogram ESC : European Society of Cardiology FDG : fluorodeoxyglucose h : hour(s) HF : heart failure LBBB : left bundle branch block LV : left ventricle LVH : left ventricular hypertrophy MI : myocardial infarction mIBG : meta-iodo-benzylguanidine min : minute(s) MONICA : Multinational MONItoring of trends and determinants in CArdiovascular disease) MPS : myocardial perfusion scintigraphy MRI : magnetic resonance imaging mV : millivolt(s) ng/L : nanogram(s) per litre Non-Q MI : non-Q wave myocardial infarction NSTEMI : non-ST-elevation myocardial infarction PCI : percutaneous coronary intervention PET : positron emission tomography pg/mL : pictogram(s) per millilitre Q wave MI : Q wave myocardial infarction RBBB : right bundle branch block sec : second(s) SPECT : single photon emission computed tomography STEMI : ST elevation myocardial infarction ST–T : ST-segment –T wave URL : upper reference limit WHF : World Heart Federation WHO : World Health Organization Myocardial infarction (MI) can be recognised by clinical features, including electrocardiographic (ECG) findings, elevated values of biochemical markers (biomarkers) of myocardial necrosis, and by imaging, or may be defined by pathology. It is a major cause of death and disability worldwide. MI may be the first manifestation of coronary artery disease (CAD) or it may occur, repeatedly, in patients with established disease. Information on MI rates can provide useful information regarding the burden of CAD within and across populations, especially if standardized data are collected in a manner that …

Published
2012

5. Risk in special population oral abstract session

Author

Rouzet, F. Francois, Lim, P., Sarda-Mantel, L., Bleichner-Pérez, S., Lasalmonie, D., Slama, M., Cohen-Solal, A., Guludec, D. Le, Acampa, W., Spinelli, L., Petretta, M., Lauro, F. De, Ibello, F., Cuocolo, A. Alberto, Wong, R. C. C., Wong, H. C., Azizi, F., Wong, S. K., Ho, K. T. Kheng-Thye, Ramakrishna, G. Gautam, Miller, T. D., Breen, J. F., Araoz, P. A., Hodge, D. O., Gibbons, RJ., Navare, S. Sachin, Noble, G., Katten, D., Ahlberg, A., Platt, M., Heller, G., and Kudes, M. Mark

Published
2005
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6. A nonsense mutation of the ATRX gene causing mild mental retardation and epilepsy

Author

Renzo Guerrini, Shanahan, Jl, Carrozzo, R., Bonanni, P., Higgs, Dr, and Gibbons, Rj

Abstract

Mutations in the X-encoded gene ATRX are known to give rise to profound syndromal mental retardation (MR). Here, we describe a pedigree, including 4 affected family members with a 324C-->T nonsense mutation in the ATRX gene. Although 2 patients have moderate to profound MR and the typical facial features of ATR-X syndrome, the other 2 patients presented with mild MR and epilepsy but without the characteristic facial dysmorphism. Mutations in the ATRX gene should be considered as a cause of mild MR in male patients lacking specific diagnostic features.

Published
2016

11. Understanding α-globin gene regulation and implications for the treatment of β-thalassemia

Author

Mettananda, S, Gibbons, RJ, and Higgs, DR

Subjects
hemic and lymphatic diseases
Abstract

Over the past three decades, a vast amount of new information has been uncovered describing how the globin genes are regulated. This knowledge has provided significant insights into the general understanding of the regulation of human genes. It is now known that molecular defects within and around the α- and β-globin genes, as well as in the distant regulatory elements, can cause thalassemia. Unbalanced production of globin chains owing to defective synthesis of one, and the continued unopposed synthesis of another, is the central causative factor in the cellular pathology and pathophysiology of thalassemia. A large body of clinical, genetic, and experimental evidence suggests that altering globin chain imbalance by reducing the production of α-globin synthesis ameliorates the disease severity in patients with β-thalassemia. With the development of new genetic-based therapeutic tools that have a potential to decrease the expression of a selected gene in a tissue-specific manner, the possibility of decreasing expression of the α-globin gene to improve the clinical severity of β-thalassemia could become a reality.

Published
2016

12. Variant ATRX syndrome with dysfunction of ATRX and MAGT1 genes

Author

Wolf Minotti, Federica, Qiao, Y, Mondal, K, Trapani, Valentina, Wen, J, Carpenter, G, Wildin, R, Price, Em, Gibbons, Rj, Eichmeyer, J, Jiang, R, Dupont, B, Martell, S, Lewis, Sm, Robinson, Wp, O'Driscoll, M, Wolf, Fi, Zwick, Me, and Rajcan Separovic, E.

Subjects
Male, X-linked Nuclear Protein, Biology, medicine.disease_cause, Settore MED/03 - GENETICA MEDICA, DNA, Ribosomal, Exon, Genes, Duplicate, Gene duplication, Genetics, medicine, x-linked intellectual disability, Humans, Point Mutation, Exome, Cation Transport Proteins, Genetics (clinical), X chromosome, Exome sequencing, ATRX, Cytokinesis, Oligonucleotide Array Sequence Analysis, Mutation, Chromosomes, Human, X, X LINKED DISEASE, magnesium channels, Point mutation, Pruritus, DNA Helicases, Nuclear Proteins, Sequence Analysis, DNA, Syndrome, DNA Methylation, Introns, Pedigree, Phenotype, MAGNESIUM, Cancer research, Mental Retardation, X-Linked, Female
Abstract

A 0.8 kb intronic duplication in MAGT1 and a single base pair deletion in the last exon of ATRX were identified using a chromosome X-specific microarray and exome sequencing in a family with five males demonstrating intellectual disability (ID) and unusual skin findings (e.g., generalized pruritus). MAGT1 is an Mg²⁺ transporter previously associated with primary immunodeficiency and ID, whereas mutations in ATRX cause ATRX-ID syndrome. In patient cells, the function of ATRX was demonstrated to be abnormal based on altered RNA/protein expression, hypomethylation of rDNA, and abnormal cytokinesis. Dysfunction of MAGT1 was reflected in reduced RNA/protein expression and Mg²⁺ influx. The mutation in ATRX most likely explains the ID, whereas MAGT1 disruption could be linked to abnormal skin findings, as normal magnesium homeostasis is necessary for skin health. This work supports observations that multiple mutations collectively contribute to the phenotypic variability of syndromic ID, and emphasizes the importance of correlating clinical phenotype with genomic and cell function analyses.

Published
2014

13. An alternative method for rapid preparation of 99Tcm-sestamibi

Author

Joseph C. Hung, Wilson Me, and Gibbons Rj

Subjects
Technetium Tc 99m Sestamibi, Alternative methods, Materials science, business.industry, Microwave oven, Combined use, Analytical chemistry, General Medicine, Natural rubber, Breakage, Microwave heating, visual_art, Boiling, Methods, visual_art.visual_art_medium, Humans, Radiology, Nuclear Medicine and imaging, Power setting, Nuclear medicine, business
Abstract

The availability of 99Tcm-sestamibi is limited, especially in emergency cases due to the time-consuming preparation procedure that requires a 10-min boiling water bath and a 30-min radiochemical purity (RCP) analysis. These two restrictions have been surmounted by the combined use of a microwave oven heating method and a minipaper chromatography system. However, use of the microwave oven heating method presents some potential problems: (1) technical error in setting the microwave oven heating time and power setting; (2) ejection of the rubber septum if the vial is not evacuated; (3) breakage of the vial during the microwave heating process; (4) inconsistent and inhomogeneous microwave heating; (5) reevaluation process required for use of a different type of microwave oven. Although a 1-min boiling water bath time is sufficient to provide an acceptable RCP for 99Tcm-sestamibi, additional time is required to heat the water to a boiling state. An instant hot water machine was evaluated for possible replacement of the microwave heating method. Three millilitres of 5500 MBq (150 mCi) 99Tcm was added to a Cardiolite kit and then placed in a 150-ml insulated beaker filled with hot water (86.2 +/- 1.9 degrees C, n = 45) from an instant hot water machine. A minipaper chromatography system was used to determine the RCP of samples after 1, 1.5, 2, 3, 4 and 5 min incubation periods. Our results show that 2 min was the shortest incubation time that yielded an acceptable RCP of 94.7 +/- 0.4% (n = 60) over the 24 h evaluation time. The use of an instant hot water machine not only avoids those problems associated with the microwave heating method, but also provides a rapid, efficient and relatively simple option for preparation of 99Tcm-sestamibi.

Published
1993

14. Variant ATRX syndrome with dysfunction of ATRX and MAGT1 genes

Author

Qiao, Y, Mondal, K, Trapani, Valentina, Wen, J, Carpenter, G, Wildin, R, Price, Em, Gibbons, Rj, Eichmeyer, J, Jiang, R, Dupont, B, Martell, S, Lewis, Sm, Robinson, Wp, O'Driscoll, M, Wolf Minotti, Federica, Zwick, Me, Rajcan Separovic, E., Trapani, Valentina (ORCID:0000-0002-0259-6624), Wolf, Federica (ORCID:0000-0003-1361-1049), Qiao, Y, Mondal, K, Trapani, Valentina, Wen, J, Carpenter, G, Wildin, R, Price, Em, Gibbons, Rj, Eichmeyer, J, Jiang, R, Dupont, B, Martell, S, Lewis, Sm, Robinson, Wp, O'Driscoll, M, Wolf Minotti, Federica, Zwick, Me, Rajcan Separovic, E., Trapani, Valentina (ORCID:0000-0002-0259-6624), and Wolf, Federica (ORCID:0000-0003-1361-1049)

Abstract

A 0.8kb intronic duplication in MAGT1 and a single base pair deletion in the last exon of ATRX were identified using a chromosome X-specific microarray and exome sequencing in a family with five males demonstrating intellectual disability (ID) and unusual skin findings (e.g., generalized pruritus). MAGT1 is an Mg2+ transporter previously associated with primary immunodeficiency and ID, whereas mutations in ATRX cause ATRX-ID syndrome. In patient cells, the function of ATRX was demonstrated to be abnormal based on altered RNA/protein expression, hypomethylation of rDNA, and abnormal cytokinesis. Dysfunction of MAGT1 was reflected in reduced RNA/protein expression and Mg2+ influx. The mutation in ATRX most likely explains the ID, whereas MAGT1 disruption could be linked to abnormal skin findings, as normal magnesium homeostasis is necessary for skin health. This work supports observations that multiple mutations collectively contribute to the phenotypic variability of syndromic ID, and emphasizes the importance of correlating clinical phenotype with genomic and cell function analyses.

Published
2014

15. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias--executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology

Author

Blomström-Lundqvist, C, Scheinman, MM, Aliot, EM, Alpert, JS, Calkins, H, Camm, AJ, Campbell, WB, Haines, DE, Kuck, K-H, Lerman, BB, Miller, DD, Shaeffer, CW, Stevenson, WG, Tomaselli, GF, Antman, EM, Smith, SC, Faxon, DP, Fuster, V, Gibbons, RJ, Gregoratos, G, Hiratzka, LF, Hunt, SA, Jacobs, AK, Russell, RO, Priori, SG, le Blanc, J-J, Budaj, A, Burgos, EF, Cowie, M, Deckers, Jaap, Garcia, MAA, Klein, WW, Lekakis, J, Lindahl, B, Mazzotta, G, Morais, CA, Smiseth, O, Trappe, HJ, and Cardiology

Published
2003

22. Comparative effectiveness of exercise electrocardiography with or without myocardial perfusion single photon emission computed tomography in women with suspected coronary artery disease: results from the What Is the Optimal Method for Ischemia Evaluation in Women (WOMEN) trial.

Author

Shaw LJ, Mieres JH, Hendel RH, Boden WE, Gulati M, Veledar E, Hachamovitch R, Arrighi JA, Merz CN, Gibbons RJ, Wenger NK, Heller GV, WOMEN Trial Investigators, Shaw, Leslee J, Mieres, Jennifer H, Hendel, Robert H, Boden, William E, Gulati, Martha, Veledar, Emir, and Hachamovitch, Rory

Published
2011
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25. Evaluation of coronary CTA Appropriateness Criteria in an academic medical center.

Author

Miller JA, Raichlin E, Williamson EE, McCully RB, Pellikka PA, Hodge DO, Miller TD, Gibbons RJ, Araoz PA, Miller, John A, Raichlin, Eugenia, Williamson, Eric E, McCully, Robert B, Pellikka, Patricia A, Hodge, David O, Miller, Todd D, Gibbons, Raymond J, and Araoz, Philip A

Abstract

Background: The aim of this study was to evaluate published appropriateness criteria for CT angiography (CTA) at the authors' academic medical center. Methods: Two observers independently reviewed the medical records of 251 patients who had undergone dual-source coronary CTA from June 1 to December 31, 2007. Patients were assigned to indications from 1 of 7 tables from the American College of Cardiology Foundation and ACR Appropriateness Criteria. Agreement between the two observers was assessed using kappa statistics. Disagreements were resolved by consensus panel. The final numbers of appropriate, uncertain, inappropriate, and not classifiable indications were recorded. Results: Indications for testing were classified as appropriate in 69 patients (27%), inappropriate in 42 patients (17%), and uncertain in 25 patients (10%). One hundred fifteen indications for coronary CTA (46%) were not classifiable. Analysis of interobserver variability for overall appropriateness yielded a kappa value of 0.31, which was considered to indicate fair agreement. Conclusion: The results of this study suggest that a significant proportion (46%) of the coronary CTA studies performed at the authors' institution are for indications that are not covered by the published appropriateness criteria. Modifications to these criteria could help decrease the number of studies that are not classifiable. Physician education could decrease the number of inappropriate studies. [ABSTRACT FROM AUTHOR]

Published
2010
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27. Perioperative cardiovascular assessment of patients undergoing noncardiac surgery.

Author

Freeman WK, Gibbons RJ, Freeman, William K, and Gibbons, Raymond J

Abstract

Preoperative assessment of the cardiac patient before noncardiac surgery is common in the clinical practice of the medical consultant, anesthesiologist, and surgeon. Currently, most noncardiac surgical procedures are performed for patients of advanced age, and the number of such surgeries is likely to increase with the aging of the population. These same patients have an increased prevalence of cardiovascular disease, especially ischemic heart disease, which is the primary cause of perioperative morbidity and mortality associated with noncardiac surgery. Since 1996, 3 American College of Cardiology/American Heart Association guideline documents have been published, each reflecting the available literature, with recommendations for the preoperative cardiovascular evaluation and treatment of the patient undergoing noncardiac surgery. Our review describes the 2007 American College of Cardiology/American Heart Association guidelines, the most recent revision, focusing on a newly recommended 5-step algorithmic approach to managing this clinical problem, particularly for the patient with known or suspected coronary heart disease. Continued emphasis should be given to preoperative clinical risk stratification, with noninvasive testing reserved for those patients in whom a substantial change in medical management would be anticipated based on results of testing. Pharmacologic therapy holds more promise than coronary revascularization for the reduction of major adverse perioperative cardiac events that might complicate noncardiac surgery. [ABSTRACT FROM AUTHOR]

Published
2009
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33. Quantitation of regional ejection fractions using gated tomographic imaging with 99mTc-sestamibi.

Author

Lapeyre AC III, Klodas E, Rogers PJ, Sinak LJ, Hammell TC, O'Connor MK, Gibbons RJ, Lapeyre, André C 3rd, Klodas, Elizabeth, Rogers, Paul J, Sinak, Lawrence J, Hammell, Thomas C, O'Connor, Michael K, and Gibbons, Raymond J

Abstract

Background: Gated single photon emission CT (SPECT) sestamibi imaging allows the simultaneous assessment of myocardial perfusion and left ventricular function. Objective: The purpose of this study was to evaluate a technique for quantitative regional wall motion assessment using gated SPECT (99m)Tc-sestamibi imaging. Patients and Interventions: Fourteen subjects without cardiac pathology and 25 patients who had experienced myocardial infarction (MI) were studied. After tomographic reconstruction of gated short-axis slices, the identification of endocardial borders was made using a standard edge-detection program in systole and diastole in each of five selected slices. Regional ejection fraction (EF) and myocardial perfusion were determined for five regions within each slice. Ten patients underwent echocardiographic regional wall-motion analysis, the results of which were compared to corresponding regional EF results. Results: High interobserver reproducibility in the assessment of regional EFs was found, with r values ranging from 0.94 to 0.98. In patients with anterior and inferior MIs, the regional EFs were abnormal in the anterior and septal regions, and the inferior and lateral regions, respectively. The regional EFs correlated significantly with regional perfusion in the anterior walls (r = 0.71; p = 0.0001), the lateral walls (r = 0.66; p = 0.0001), and inferior walls (r = 0.54; p = 0.0004). There was a significant association between the regional EFs and the echocardiographic regional wall motion assessment at the base (p < 0.0001), mid-ventricle (p = 0.0004), and apex (p = 0.0003). Conclusions: Gated SPECT images obtained (99m)Tc-sestamibi can provide reproducible quantitative, segmental regional EFs for multiple left ventricular slices that are significantly associated with subjective regional wall motion assessment by echocardiography. [ABSTRACT FROM AUTHOR]

Published
2005
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34. Clinical guidelines. Primary care management of chronic stable angina and asymptomatic suspected or known coronary artery disease: a clinical practice guideline from the American College of Physicians [corrected] [published erratum appears in ANN INTERN MED 2005 Jan 4;142(1):79].

Author

Snow V, Barry P, Fihn SD, Gibbons RJ, Owens DK, Williams SV, Mottur-Pilson C, Weiss KB, American College of Physicians/American College of Cardiology Chronic Stable Angina Panel, Snow, Vincenza, Barry, Patricia, Fihn, Stephan D, Gibbons, Raymond J, Owens, Douglas K, Williams, Sankey V, Mottur-Pilson, Christel, Weiss, Kevin B, American College of Physicians, and American College of Cardiology Chronic Stable Angina Panel

Abstract

In 1999, the American College of Physicians (ACP), then the American College of Physicians-American Society of Internal Medicine, and the American College of Cardiology/American Heart Association (ACC/AHA) developed joint guidelines on the management of patients with chronic stable angina. The ACC/AHA then published an updated guideline in 2002, which ACP recognized as a scientifically valid review of the evidence and background paper. This ACP guideline summarizes the recommendations of the 2002 ACC/AHA updated guideline and underscores the recommendations most likely to be important to physicians seeing patients in the primary care setting. This guideline is the second of 2 that provide guidance on the management of patients with chronic stable angina. This document covers treatment and follow-up of symptomatic patients who have not had an acute myocardial infarction or revascularization procedure in the previous 6 months. Sections addressing asymptomatic patients are also included. Asymptomatic refers to patients with known or suspected coronary disease based on a history or electrocardiographic evidence of previous myocardial infarction, coronary angiography, or abnormal results on noninvasive tests. A previous guideline covered diagnosis and risk stratification for symptomatic patients who have not had an acute myocardial infarction or revascularization procedure in the previous 6 months and asymptomatic patients with known or suspected coronary disease based on a history or electrocardiographic evidence of previous myocardial infarction, coronary angiography, or abnormal results on noninvasive tests. [ABSTRACT FROM AUTHOR]

Published
2004
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35. Evaluation of primary care patients with chronic stable angina: guidelines from the American College of Physicians.

Author

Snow V, Barry P, Fihn SD, Gibbons RJ, Owens DK, Williams SV, Weiss KB, Mottur-Pilson C, ACP/ACC Chronic Stable Angina Panel, Snow, Vincenza, Barry, Patricia, Fihn, Stephan D, Gibbons, Raymond J, Owens, Douglas K, Williams, Sankey V, Weiss, Kevin B, Mottur-Pilson, Christel, ACP, and ACC Chronic Stable Angina Panel

Abstract

In 1999, the American College of Physicians (ACP), then the American College of Physicians-American Society of Internal Medicine, and the American College of Cardiology/American Heart Association (ACC/AHA) developed joint guidelines on the management of patients with chronic stable angina. The ACC/AHA then published an updated guideline in 2002, which the ACP recognized as a scientifically valid review of the evidence and background paper. This ACP guideline summarizes the recommendations of the 2002 ACC/AHA updated guideline and underscores the recommendations most likely to be important to physicians seeing patients in the primary care setting. This guideline is the first of 2 that will provide guidance on the management of patients with chronic stable angina. This document will cover diagnosis and risk stratification for symptomatic patients who have not had an acute myocardial infarction or revascularization procedure in the previous 6 months. Sections addressing asymptomatic patients are also included. Asymptomatic refers to patients with known or suspected coronary disease based on history or on electrocardiographic evidence of previous myocardial infarction, coronary angiography, or abnormal results on noninvasive tests. A future guideline will cover pharmacologic therapy and follow-up. [ABSTRACT FROM AUTHOR]

Published
2004
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38. ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult: Executive Summary A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1995 Guidelines for the Evaluation and Management of Heart Failure): Developed in Collaboration With the International Society for Heart and Lung Transplantation; Endorsed by the Heart Failure Society of America.

Author

Hunt SA, Gibbons RJ, American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1995 Guidelines for the Evaluaton and Management of Heart Failure), Hunt, S A, Baker, D W, Chin, M H, Cinquegrani, M P, Feldman, A M, Francis, G S, Ganiats, T G, Goldstein, S, Gregoratos, G, Jessup, M L, Noble, R J, Packer, M, Silver, M A, Stevenson, L W, Gibbons, R J, Antman, E M, and Alpert, J S

Published
2001

39. Guidelines for the management of patients with chronic stable angina: treatment.

Author

Fihn SD, Williams SV, Daley J, Gibbons RJ, Fihn, S D, Williams, S V, Daley, J, Gibbons, R J, American College of Cardiology, American Heart Association, and American College of Physicians-American Society of Internal Medicine

Abstract

The dual aims of treating patients with chronic stable angina are 1) to reduce morbidity and mortality and 2) to eliminate angina with minimal adverse effects and allow the patient to return to normal activities. In the absence of contraindications, beta-blockers are recommended as initial therapy. All beta-blockers seem to be equally effective. If the patient has serious contraindications to beta-blockers, unacceptable side effects, or persistent angina, calcium antagonists should be administered. Long-acting dihydropyridine and nondihydropyridine agents are generally as effective as beta-blockers in relieving angina. Long-acting nitrates are considered third-line therapy because a nitrate-free interval is required to avoid developing tolerance. All long-acting nitrates seem to be equally effective. Patients with angina should take 75 to 325 mg of aspirin daily unless they have contraindications. Such risk factors as smoking, elevated low-density lipoprotein cholesterol level, diabetes, and hypertension should be treated appropriately. Coronary revascularization has not been shown to improve survival for most patients with chronic angina but may be required to control symptoms. However, coronary artery bypass grafting (CABG) is often indicated for symptomatic patients with left-main disease, three-vessel disease, or two-vessel disease including proximal stenosis of the left anterior descending coronary artery; it improves their survival. Percutaneous transluminal coronary angioplasty is an alternative to CABG for patients with normal left ventricular function and favorable angiographic features. Coronary artery bypass grafting is initially more effective in relieving angina than medical therapy, but the two procedures yield similar results after 5 to 10 years. Eighty percent of patients who undergo CABG remain angina-free 5 years after surgery. In low-risk patients, percutaneous transluminal coronary angioplasty seems to control angina better than medical therapy, but recurrent angina and repeated procedures are more likely than with CABG. Patient education is an important component of management. Long-term follow-up should be individualized to ascertain clinical stability at regular intervals and to reassess prognosis when warranted. [ABSTRACT FROM AUTHOR]

Published
2001
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40. ACC/AHA guidelines for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction: executive summary and recommendations. A report of the American College of Cardiology/American Heart Association task force on practice guidelines (committee on the management of patients with unstable angina).

Author

Braunwald E, Antman EM, Beasley JW, Califf RM, Cheitlin MD, Hochman JS, Jones RH, Kereiakes D, Kupersmith J, Levin TN, Pepine CJ, Schaeffer JW, Smith EE III, Steward DE, Theroux P, Gibbons RJ, Alpert JS, Eagle KA, Faxon DP, and Fuster V

Published
2000

43. Prognostic value of a treadmill exercise score in symptomatic patients with nonspecific ST-T abnormalities on resting ECG.

Author

Kwok JMF, Miller TD, Christian TF, Hodge DO, Gibbons RJ, Kwok, J M, Miller, T D, Christian, T F, Hodge, D O, and Gibbons, R J

Abstract

Context: Exercise testing of patients with ST-T abnormalities on the resting electrocardiogram (ECG) is problematic because in the presence of pre-existing ST-T abnormalities, the exercise test is less specific for the diagnosis of coronary artery disease. The prognostic capability of the Duke treadmill score in patients with ST-T abnormalities vs those with normal findings on resting ECG has, to our knowledge, not been evaluated.Objective: To compare the prognostic accuracy of the Duke treadmill score in patients with nonspecific ST-T abnormalities vs those with normal results on resting ECG.Design: Inception cohort study with 7 years of follow-up.Setting: Nuclear cardiology laboratory of a US referral center.Patients: All symptomatic patients who underwent exercise thallium testing between 1989 and 1991,939 of whom had nonspecific ST-T abnormalities and 1466 of whom had normal findings on resting ECG. Exclusion criteria included congenital, valvular, or cardiomyopathic heart disease; prior coronary artery revascularization; resting ECG with secondary ST-T abnormalities; or missing data.Main Outcome Measures: Rates of overall mortality and cardiac death for subjects classified by Duke treadmill score risk group.Results: For the end point cardiac death, 7-year survival in the study population in the low-, intermediate-, and high-risk groups was 97%, 92%, and 76%, respectively (P<.001). Compared with the control group, the study group had lower 7-year survival (94% vs 98%; P<.001), fewer low-risk patients (426 [45%] vs 811 [55%]; P<.001) with worse 7-year survival (97% vs 99%; P= .008), and more high-risk patients (49 [5%] vs 34 [2%];P<.001) with a nonsignificant trend toward worse 7-year survival (76% vs 93%; P= .36).Conclusions: The Duke treadmill score can effectively risk-stratify patients with ST-T abnormalities on the resting ECG. In classified risk categories, patients with ST-T abnormalities have a worse prognosis than those with normal results on resting ECG. [ABSTRACT FROM AUTHOR]

Published
1999
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44. Incremental value of the leukocyte differential and the rapid creatine kinase-MB isoenzyme for the early diagnosis of myocardial infarction.

Author

Thomson SP, Gibbons RJ, Smars PA, Suman VJ, Pierre RV, Santrach PJ, Jiang NS, Thomson, S P, Gibbons, R J, Smars, P A, Suman, V J, Pierre, R V, Santrach, P J, and Jiang, N S

Abstract

Objective: To test whether automated measurements of cortisol-induced changes in the leukocyte differential can provide an early marker of myocardial infarction, especially when combined with the rapid creatine kinase-MB isoenzyme.Design: A prospective, blinded study of these measurements at the time of initial assessment in the emergency department.Setting: Large multispecialty clinic hospital.Patients: 511 consecutive patients presenting to the emergency department with chest pain. One hundred twenty-seven patients with infection, trauma, or metastatic cancer or receiving myelosuppressive or glucocorticoid therapy were excluded.Measurements: Automated leukocyte differentials, rapid creatine kinase-MB levels, cortisol levels, and routine clinical measurements.Results: Of 69 patients with myocardial infarction, only 39% had diagnostic electrocardiographic ST-segment elevation. ST-segment elevation had a specificity of 99% and a positive predictive value of 93%. A relative lymphocytopenia (lymphocyte decrease < 20.3%) or elevated rapid creatine kinase-MB level (> 4.7 ng/mL) was more sensitive than ST-segment elevation (sensitivities of 58% and 56%, respectively) but less specific (specificities of 91% and 93%, respectively). The presence of both a relative lymphocytopenia and an elevated rapid creatine kinase-MB level had a sensitivity of 44%, a specificity of 99.7%, and a positive predictive value of 97% (95% Cl, 80% to 99%). Both a relative lymphocytopenia and an elevated rapid creatine kinase-MB level were independent (P < 0.001) predictors of infarction in patients without ST-segment elevation. If myocardial infarction was suspected by the presence of both abnormal markers or ST-segment elevation, the sensitivity for early diagnosis increased from 39% (ST elevation alone) to 65% (Cl, 52% to 76%); the specificity was 99%; and the positive predictive value was 94% (Cl, 82% to 98%).Conclusions: The presence of both a relative lymphocytopenia and an elevated rapid creatine kinase-MB level was an accurate early marker of myocardial infarction that appeared to improve the sensitivity of early diagnosis compared with that of ST-segment elevation alone. [ABSTRACT FROM AUTHOR]

Published
1995
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