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42 results on '"Ellis, S.G."'

1. Change in albuminuria and subsequent risk of end-stage kidney disease: an individual participant-level consortium meta-analysis of observational studies.

Author

Ichikawa K., Collins J.F., Drury P.L., Ellis S.G., Nadukuru R., Metzger M., Flamant M., Houillier P., Haymann J.-P., Froissart M., Kenealy T., Elley R.C., Cuddeback J.K., Ciemins E.L., Stempniewicz R., Nelson R.G., Knowler W.C., Bakker S.J., Major R.W., Medcalf J.F., Shepherd D., Barrett-Connor E., Bergstrom J., Ix J.H., Molnar M.Z., Maciulaitis R., Manley T., Smith K., Stockbridge N., Thompson A., Vetter T., Willis K., Zhang L., Coresh J., Heerspink H.J.L., Sang Y., Matsushita K., Arnlov J., Astor B.C., Black C., Brunskill N.J., Carrero J.-J., Feldman H.I., Fox C.S., Inker L.A., Ishani A., Ito S., Jassal S., Konta T., Polkinghorne K., Romundstad S., Solbu M.D., Stempniewicz N., Stengel B., Tonelli M., Umesawa M., Waikar S.S., Wen C.-P., Wetzels J.F.M., Woodward M., Grams M.E., Kovesdy C.P., Levey A.S., Gansevoort R.T., Appel L.J., Greene T., Chen T.K., Chalmers J., Arima H., Perkovic V., Levin A., Djurdjev O., Tang M., Nally J., Navaneethan S.D., Schold J.D., Weldegiorgis M., Herrington W.G., Smith M., Hsu C.Y., Hwang S.-J., Chang A.R., Kirchner H.L., Green J.A., Ho K., Marks A., Prescott G., Clark L.E., Fluck N., Shalev V., Chodick G., Blankestijn P.J., Van Zuilen A., Van den Brand J.A., Sarnak M.J., Bottinger E., Nadkarni G.N., Sumida K., de Zeeuw D., Brenner B., Qureshi A.R., Elinder C.-G., Runesson B., Evans M., Segelmark M., Stendahl M., Schon S., Naimark D.M., Tangri N., Sud M., Hirayama A., Bilo H.J., Landman G.W., Van Hateren K.J., Kleefstra N., Hallan S.I., Ballew S.H., Chen J., Kwak L., Surapaneni A., Parving H.-H., Rodby R.A., Rohde R.D., Lewis J.B., Lewis E., Perrone R.D., Abebe K.Z., Hou F.F., Xie D., Hunsicker L.G., Imai E., Kobayashi F., Makino H., Remuzzi G., Ruggenenti P., Eckardt K.-U., Gudmundsdottir H., Ichikawa K., Collins J.F., Drury P.L., Ellis S.G., Nadukuru R., Metzger M., Flamant M., Houillier P., Haymann J.-P., Froissart M., Kenealy T., Elley R.C., Cuddeback J.K., Ciemins E.L., Stempniewicz R., Nelson R.G., Knowler W.C., Bakker S.J., Major R.W., Medcalf J.F., Shepherd D., Barrett-Connor E., Bergstrom J., Ix J.H., Molnar M.Z., Maciulaitis R., Manley T., Smith K., Stockbridge N., Thompson A., Vetter T., Willis K., Zhang L., Coresh J., Heerspink H.J.L., Sang Y., Matsushita K., Arnlov J., Astor B.C., Black C., Brunskill N.J., Carrero J.-J., Feldman H.I., Fox C.S., Inker L.A., Ishani A., Ito S., Jassal S., Konta T., Polkinghorne K., Romundstad S., Solbu M.D., Stempniewicz N., Stengel B., Tonelli M., Umesawa M., Waikar S.S., Wen C.-P., Wetzels J.F.M., Woodward M., Grams M.E., Kovesdy C.P., Levey A.S., Gansevoort R.T., Appel L.J., Greene T., Chen T.K., Chalmers J., Arima H., Perkovic V., Levin A., Djurdjev O., Tang M., Nally J., Navaneethan S.D., Schold J.D., Weldegiorgis M., Herrington W.G., Smith M., Hsu C.Y., Hwang S.-J., Chang A.R., Kirchner H.L., Green J.A., Ho K., Marks A., Prescott G., Clark L.E., Fluck N., Shalev V., Chodick G., Blankestijn P.J., Van Zuilen A., Van den Brand J.A., Sarnak M.J., Bottinger E., Nadkarni G.N., Sumida K., de Zeeuw D., Brenner B., Qureshi A.R., Elinder C.-G., Runesson B., Evans M., Segelmark M., Stendahl M., Schon S., Naimark D.M., Tangri N., Sud M., Hirayama A., Bilo H.J., Landman G.W., Van Hateren K.J., Kleefstra N., Hallan S.I., Ballew S.H., Chen J., Kwak L., Surapaneni A., Parving H.-H., Rodby R.A., Rohde R.D., Lewis J.B., Lewis E., Perrone R.D., Abebe K.Z., Hou F.F., Xie D., Hunsicker L.G., Imai E., Kobayashi F., Makino H., Remuzzi G., Ruggenenti P., Eckardt K.-U., and Gudmundsdottir H.

Abstract

Background: Change in albuminuria as a surrogate endpoint for progression of chronic kidney disease is strongly supported by biological plausibility, but empirical evidence to support its validity in epidemiological studies is lacking. We aimed to assess the consistency of the association between change in albuminuria and risk of end-stage kidney disease in a large individual participant-level meta-analysis of observational studies. Method(s): In this meta-analysis, we collected individual-level data from eligible cohorts in the Chronic Kidney Disease Prognosis Consortium (CKD-PC) with data on serum creatinine and change in albuminuria and more than 50 events on outcomes of interest. Cohort data were eligible if participants were aged 18 years or older, they had a repeated measure of albuminuria during an elapsed period of 8 months to 4 years, subsequent end-stage kidney disease or mortality follow-up data, and the cohort was active during this consortium phase. We extracted participant-level data and quantified percentage change in albuminuria, measured as change in urine albumin-to-creatinine ratio (ACR) or urine protein-to-creatinine ratio (PCR), during baseline periods of 1, 2, and 3 years. Our primary outcome of interest was development of end-stage kidney disease after a baseline period of 2 years. We defined an end-stage kidney disease event as initiation of kidney replacement therapy. We quantified associations of percentage change in albuminuria with subsequent end-stage kidney disease using Cox regression in each cohort, followed by random-effects meta-analysis. We further adjusted for regression dilution to account for imprecision in the estimation of albuminuria at the participant level. We did multiple subgroup analyses, and also repeated our analyses using participant-level data from 14 clinical trials, including nine clinical trials not in CKD-PC. Finding(s): Between July, 2015, and June, 2018, we transferred and analysed data from 28 cohorts in the C

Published
2019

2. Clinical, Angiographic, and Procedural Correlates of Very Late Absorb Scaffold Thrombosis: Multistudy Registry Results

Author

Ellis, S.G., Gori, T., Serruys, P.W., Nef, H., Steffenino, G., Brugaletta, S., Munzel, T., Feliz, C., Schmidt, G, Sabate, M., Onuma, Y., Geuns, R.J.M. van, Gao, R.L., Menichelli, M., Kereiakes, D.J., Stone, G.W., Testa, L., Kimura, T., and Abizaid, A.

Subjects
Vascular damage Radboud Institute for Health Sciences [Radboudumc 16]
Abstract

Item does not contain fulltext OBJECTIVES: The aim of this study was to identify independent correlates of very late scaffold thrombosis (VLST) from an analysis of consecutively treated patients from 15 multicenter studies. BACKGROUND: Recent analyses suggest an increased risk for VLST with the Absorb Bioresorbable Vascular Scaffold compared with drug-eluting stents, but insights as to correlates of risk are limited. METHODS: A total of 55 patients were identified with scaffold thrombosis. They were matched 2:1 with control subjects selected randomly from patients without thrombosis from the same study. Quantitative coronary angiography was available for 96.4% of patients. Multiple logistic and Cox regression analysis were used to identify significant independent outcome correlates from 6 pre-specified characteristics. RESULTS: Patients had scaffold thrombosis at a median of 20 months (interquartile range: 17 to 27 months). Control subjects were followed for 36 months (interquartile range: 24 to 38 months). For the combined groups, reference vessel diameter (RVD) was 2.84 +/- 0.50 mm, scaffold length was 26 +/- 16 mm, and post-dilatation was performed in 56%. Univariate correlates of thrombosis were smaller nominal scaffold/RVD ratio (linear p = 0.001; ratio 2.72 mm; odds ratio: 3.4; p = 0.001). Post-dilatation at >/=16 atm, post-dilatation balloon/scaffold ratio, final percentage stenosis, and dual antiplatelet therapy were not correlated with VLST. Only scaffold/RVD ratio remained a significant independent correlate of VLST (p = 0.001), as smaller ratio was correlated with RVD (p < 0.001). Post hoc analysis of 8 other potential covariates revealed no other correlates of outcome. CONCLUSIONS: In the present analysis, the largest to date of its type, relative scaffold undersizing was the strongest determinant of VLST. Given current understanding of "scaffold dismantling," this finding likely has ramifications for all bioresorbable scaffolds.

Published
2018

3. Clinical, Angiographic, and Procedural Correlates of Acute, Subacute, and Late Absorb Scaffold Thrombosis

Author

Ellis, S.G., Steffenino, G., Kereiakes, D.J., Stone, G.W., Geuns, R.J.M. van, Abizaid, A., Nef, H., Cortese, B., Testa, L., Menichelli, M., Tamburino, C., Gori, T., Kimura, T., Serruys, P.W., Brugaletta, S., Sabate, M., Gao, R.L., Ellis, S.G., Steffenino, G., Kereiakes, D.J., Stone, G.W., Geuns, R.J.M. van, Abizaid, A., Nef, H., Cortese, B., Testa, L., Menichelli, M., Tamburino, C., Gori, T., Kimura, T., Serruys, P.W., Brugaletta, S., Sabate, M., and Gao, R.L.

Abstract

Item does not contain fulltext, OBJECTIVES: The authors sought to identify and verify independent correlates of device thrombosis from an analysis of multicenter trials and registries. BACKGROUND: Recent analyses suggest an increased risk of device thrombosis with Absorb bioresorbable vascular scaffold (Abbott Vascular, Santa Clara, California) implantation compared with metallic drug-eluting stents, and data from moderate size studies suggest a risk relationship to vessel size and technique. METHODS: From 8,771 consecutively treated patients, 105 patients (1.2%) were identified with scaffold thrombosis within 1 year of implantation. They were matched 2:1 with controls selected randomly from nonthrombosis patients. Data-restricted multiple logistic analysis was used to identify significant independent covariates of the outcome. RESULTS: Early (within 1 month) scaffold thrombosis occurred in 69 patients and late (1 to 12 months) thrombosis occurred in 36 patients. Modelling found significant correlations of thrombosis to be final minimal lumen diameter <1.85 mm (odds ratio [OR]: 3.1; p = 0.004), off dual antiplatelet therapy (DAPT) status (OR: 3.1 to 3.5; p = 0.006 to 0.053), no post-dilatation with >1.1:1 balloon/scaffold ratio (OR: 2.3; p = 0.022), and reference vessel diameter <2.40 mm (OR: 2.1; p = 0.036). CONCLUSIONS: Suboptimal vessel sizing, procedural technique, angiographic outcomes, and dual antiplatelet therapy discontinuation appear to be the principal determinants of Absorb scaffold thrombosis risk through 12 months after implantation.

Published
2017

5. Large-scale association analysis identifies 13 new susceptibility loci for coronary artery disease

Author

Schunkert, H. König, I.R. Kathiresan, S. Reilly, M.P. Assimes, T.L. Holm, H. Preuss, M. Stewart, A.F.R. Barbalic, M. Gieger, C. Absher, D. Aherrahrou, Z. Allayee, H. Altshuler, D. Anand, S.S. Andersen, K. Anderson, J.L. Ardissino, D. Ball, S.G. Balmforth, A.J. Barnes, T.A. Becker, D.M. Becker, L.C. Berger, K. Bis, J.C. Boekholdt, S.M. Boerwinkle, E. Braund, P.S. Brown, M.J. Burnett, M.S. Buysschaert, I. Carlquist, J.F. Chen, L. Cichon, S. Codd, V. Davies, R.W. Dedoussis, G. Dehghan, A. Demissie, S. Devaney, J.M. Diemert, P. Do, R. Doering, A. Eifert, S. Mokhtari, N.E.E. Ellis, S.G. Elosua, R. Engert, J.C. Epstein, S.E. De Faire, U. Fischer, M. Folsom, A.R. Freyer, J. Gigante, B. Girelli, D. Gretarsdottir, S. Gudnason, V. Gulcher, J.R. Halperin, E. Hammond, N. Hazen, S.L. Hofman, A. Horne, B.D. Illig, T. Iribarren, C. Jones, G.T. Jukema, J.W. Kaiser, M.A. Kaplan, L.M. Kastelein, J.J.P. Khaw, K.-T. Knowles, J.W. Kolovou, G. Kong, A. Laaksonen, R. Lambrechts, D. Leander, K. Lettre, G. Li, M. Lieb, W. Loley, C. Lotery, A.J. Mannucci, P.M. Maouche, S. Martinelli, N. McKeown, P.P. Meisinger, C. Meitinger, T. Melander, O. Merlini, P.A. Mooser, V. Morgan, T. Mühleisen, T.W. Muhlestein, J.B. Münzel, T. Musunuru, K. Nahrstaedt, J. Nelson, C.P. Nöthen, M.M. Olivieri, O. Patel, R.S. Patterson, C.C. Peters, A. Peyvandi, F. Qu, L. Quyyumi, A.A. Rader, D.J. Rallidis, L.S. Rice, C. Rosendaal, F.R. Rubin, D. Salomaa, V. Sampietro, M.L. Sandhu, M.S. Schadt, E. Scḧsignfer, A. Schillert, A. Schreiber, S. Schrezenmeir, J. Schwartz, S.M. Siscovick, D.S. Sivananthan, M. Sivapalaratnam, S. Smith, A. Smith, T.B. Snoep, J.D. Soranzo, N. Spertus, J.A. Stark, K. Stirrups, K. Stoll, M. Tang, W.H.W. Tennstedt, S. Thorgeirsson, G. Thorleifsson, G. Tomaszewski, M. Uitterlinden, A.G. Van Rij, A.M. Voight, B.F. Wareham, N.J. Wells, G.A. Wichmann, H.-E. Wild, P.S. Willenborg, C. Witteman, J.C.M. Wright, B.J. Ye, S. Zeller, T. Ziegler, A. Cambien, F. Goodall, A.H. Cupples, L.A. Quertermous, T. Mäsignrz, W. Hengstenberg, C. Blankenberg, S. Ouwehand, W.H. Hall, A.S. Deloukas, P. Thompson, J.R. Stefansson, K. Roberts, R. Thorsteinsdottir, U. O'Donnell, C.J. McPherson, R. Erdmann, J. Samani, N.J.

Subjects
cardiovascular diseases
Abstract

We performed a meta-analysis of 14 genome-wide association studies of coronary artery disease (CAD) comprising 22,233 individuals with CAD (cases) and 64,762 controls of European descent followed by genotyping of top association signals in 56,682 additional individuals. This analysis identified 13 loci newly associated with CAD at P < 5 - 10'8 and confirmed the association of 10 of 12 previously reported CAD loci. The 13 new loci showed risk allele frequencies ranging from 0.13 to 0.91 and were associated with a 6% to 17% increase in the risk of CAD per allele. Notably, only three of the new loci showed significant association with traditional CAD risk factors and the majority lie in gene regions not previously implicated in the pathogenesis of CAD. Finally, five of the new CAD risk loci appear to have pleiotropic effects, showing strong association with various other human diseases or traits. © 2011 Nature America, Inc. All rights reserved.

Published
2011

6. Genome-wide association identifies nine common variants associated with fasting proinsulin levels and provides new insights into the pathophysiology of type 2 diabetes

Author

Strawbridge, R.J. Dupuis, J. Prokopenko, I. Barker, A. Ahlqvist, E. Rybin, D. Petrie, J.R. Travers, M.E. Bouatia-Naji, N. Dimas, A.S. Nica, A.C. Wheeler, E. Chen, H. Voight, B.F. Taneera, J. Kanoni, S. Peden, J.F. Turrini, F. Gustafsson, S. Zabena, C. Almgren, P. Barker, D.J.P. Barnes, D. Dennison, E.M. Eriksson, J.G. Eriksson, P. Eury, E. Folkersen, L. Fox, C.S. Frayling, T.M. Goel, A. Gu, H.F. Horikoshi, M. Isomaa, B. Jackson, A.U. Jameson, K.A. Kajantie, E. Kerr-Conte, J. Kuulasmaa, T. Kuusisto, J. Loos, R.J.F. Luan, J. Makrilakis, K. Manning, A.K. Martínez-Larrad, M.T. Narisu, N. Mannila, M.N. Öhrvik, J. Osmond, C. Pascoe, L. Payne, F. Sayer, A.A. Sennblad, B. Silveira, A. Stančcáková, A. Stirrups, K. Swift, A.J. Syvänen, A.-C. Tuomi, T. Van't Hooft, F.M. Walker, M. Weedon, M.N. Xie, W. Zethelius, B. Scott, L.J. Steinthorsdottir, V. Morris, A.P. Dina, C. Welch, R.P. Zeggini, E. Huth, C. Aulchenko, Y.S. Thorleifsson, G. Mcculloch, L.J. Ferreira, T. Grallert, H. Amin, N. Wu, G. Willer, C.J. Raychaudhuri, S. McCarroll, S.A. Hofmann, O.M. Qi, L. Segre, A.V. Van Hoek, M. Navarro, P. Ardlie, K. Balkau, B. Benediktsson, R. Bennett, A.J. Blagieva, R. Boerwinkle, E. Bonnycastle, L.L. Bostrom, K.B. Bravenboer, B. Bumpstead, S. Burtt, N.P. Charpentier, G. Chines, P.S. Cornelis, M. Couper, D.J. Crawford, G. Doney, A.S.F. Elliott, K.S. Elliott, A.L. Erdos, M.R. Franklin, C.S. Ganser, M. Gieger, C. Grarup, N. Green, T. Griffin, S. Groves, C.J. Guiducci, C. Hadjadj, S. Hassanali, N. Herder, C. Johnson, P.R.V. Jorgensen, T. Kao, W.H.L. Klopp, N. Kong, A. Kraft, P. Lauritzen, T. Li, M. Lieverse, A. Lindgren, C.M. Lyssenko, V. Marre, M. Meitinger, T. Midthjell, K. Morken, M.A. Nilsson, P. Owen, K.R. Perry, J.R.B. Petersen, A.-K. Platou, C. Proenca, C. Rathmann, W. Rayner, N.W. Robertson, N.R. Rocheleau, G. Roden, M. Sampson, M.J. Saxena, R. Shields, B.M. Shrader, P. Sigurdsson, G. Sparso, T. Strassburger, K. Stringham, H.M. Sun, Q. Thorand, B. Tichet, J. Van Dam, R.M. Van Haeften, T.W. Van Herpt, T. Van Vliet-Ostaptchouk, J.V. Walters, G.B. Wijmenga, C. Witteman, J.C.M. Bergman, R.N. Cauchi, S. Collins, F.S. Gloyn, A.L. Gyllensten, U. Hansen, T. Hide, W.A. Hitman, G.A. Hofman, A. Hunter, D.J. Hveem, K. Laakso, M. Mohlke, K.L. Morris, A.D. Palmer, C.N.A. Pramstaller, P.P. Rudan, I. Sijbrands, E. Stein, L.D. Tuomilehto, J. Uitterlinden, A.G. Wareham, N.J. Watanabe, R.M. Abecasis, G.R. Boehm, B.O. Campbell, H. Daly, M.J. Hattersley, A.T. Hu, F.B. Meigs, J.B. Pankow, J.S. Pedersen, O. Wichmann, H.-E. Barroso, I. Groop, L. Sladek, R. Thorsteinsdottir, U. Wilson, J.F. Illig, T. Froguel, P. Van Duijn, C.M. Stefansson, K. Altshuler, D. Boehnke, M. McCarthy, M.I. Speliotes, E.K. Berndt, S.I. Monda, K.L. Allen, H.L. Magi, R. Randall, J.C. Vedantam, S. Winkler, T.W. Workalemahu, T. Heid, I.M. Wood, A.R. Weyant, R.J. Estrada, K. Liang, L. Nemesh, J. Park, J.-H. Kilpelainen, T.O. Yang, J. Esko, T. Feitosa, M.F. Kutalik, Z. Mangino, M. Scherag, A. Smith, A.V. Zhao, J.H. Aben, K.K. Absher, D.M. Dixon, A.L. Fisher, E. Glazer, N.L. Goddard, M.E. Heard-Costa, N.L. Hoesel, V. Hottenga, J.-J. Johansson, A. Johnson, T. Ketkar, S. Lamina, C. Li, S. Moffatt, M.F. Myers, R.H. Peters, M.J. Preuss, M. Ripatti, S. Rivadeneira, F. Sandholt, C. Timpson, N.J. Tyrer, J.P. Van Wingerden, S. White, C.C. Wiklund, F. Barlassina, C. Chasman, D.I. Cooper, M.N. Jansson, J.-O. Lawrence, R.W. Pellikka, N. Shi, J. Thiering, E. Alavere, H. Alibrandi, M.T.S. Arnold, A.M. Aspelund, T. Atwood, L.D. Balmforth, A.J. Ben-Shlomo, Y. Bergmann, S. Biebermann, H. Blakemore, A.I.F. Boes, T. Bornstein, S.R. Brown, M.J. Buchanan, T.A. Busonero, F. Cappuccio, F.P. Cavalcanti-Proenca, C. Chen, Y.-D.I. Chen, C.-M. Clarke, R. Coin, L. Connell, J. Day, I.N.M. Den Heijer, M. Duan, J. Ebrahim, S. Elliott, P. Elosua, R. Eiriksdottir, G. Facheris, M.F. Felix, S.B. Fischer-Posovszky, P. Folsom, A.R. Friedrich, N. Freimer, N.B. Fu, M. Gaget, S. Gejman, P.V. Geus, E.J.C. Gjesing, A.P. Goyette, P. Grasler, J. Greenawalt, D.M. Gudnason, V. Hartikainen, A.-L. Hall, A.S. Havulinna, A.S. Hayward, C. Heath, A.C. Hengstenberg, C. Hicks, A.A. Hinney, A. Homuth, G. Hui, J. Igl, W. Iribarren, C. Jacobs, K.B. Jarick, I. Jewell, E. John, U. Jousilahti, P. Jula, A. Kaakinen, M. Kaplan, L.M. Kathiresan, S. Kettunen, J. Kinnunen, L. Knowles, J.W. Kolcic, I. König, I.R. Koskinen, S. Kovacs, P. Kvaloy, K. Laitinen, J. Lantieri, O. Lanzani, C. Launer, L.J. Lecoeur, C. Lehtimaki, T. Lettre, G. Liu, J. Lokki, M.-L. Lorentzon, M. Luben, R.N. Ludwig, B. Manunta, P. Marek, D. Martin, N.G. McArdle, W.L. McCarthy, A. McKnight, B. Melander, O. Meyre, D. Montgomery, G.W. Mulic, R. Ngwa, J.S. Nelis, M. Neville, M.J. Nyholt, D.R. O'Donnell, C.J. O'Rahilly, S. Ong, K.K. Oostra, B. Pare, G. Parker, A.N. Perola, M. Pichler, I. Pietilainen, K.H. Platou, C.G.P. Polasek, O. Pouta, A. Rafelt, S. Raitakari, O. Rayner, N.W. Ridderstrale, M. Rief, W. Ruokonen, A. Rzehak, P. Salomaa, V. Sanders, A.R. Sandhu, M.S. Sanna, S. Saramies, J. Savolainen, M.J. Scherag, S. Schipf, S. Schreiber, S. Schunkert, H. Silander, K. Sinisalo, J. Siscovick, D.S. Smit, J.H. Soranzo, N. Sovio, U. Stephens, J. Surakka, I. Tammesoo, M.-L. Tardif, J.-C. Teder-Laving, M. Teslovich, T.M. Thompson, J.R. Thomson, B. Tonjes, A. Van Meurs, J.B.J. Van Ommen, G.-J. Vatin, V. Viikari, J. Visvikis-Siest, S. Vitart, V. Vogel, C.I.G. Waite, L.L. Wallaschofski, H. Widen, E. Wiegand, S. Wild, S.H. Willemsen, G. Witte, D.R. Xu, J. Zhang, Q. Zgaga, L. Ziegler, A. Zitting, P. Beilby, J.P. Farooqi, I.S. Hebebrand, J. Huikuri, H.V. James, A.L. Kahonen, M. Levinson, D.F. Macciardi, F. Nieminen, M.S. Ohlsson, C. Palmer, L.J. Ridker, P.M. Stumvoll, M. Beckmann, J.S. Boeing, H. Boomsma, D.I. Caulfield, M.J. Chanock, S.J. Cupples, L.A. Smith, G.D. Erdmann, J. Gronberg, H. Hall, P. Harris, T.B. Hayes, R.B. Heinrich, J. Jarvelin, M.-R. Kaprio, J. Karpe, F. Khaw, K.-T. Kiemeney, L.A. Krude, H. Lawlor, D.A. Metspalu, A. Munroe, P.B. Ouwehand, W.H. Penninx, B.W. Peters, A. Quertermous, T. Reinehr, T. Rissanen, A. Samani, N.J. Schwarz, P.E.H. Shuldiner, A.R. Spector, T.D. Uda, M. Valle, T.T. Wabitsch, M. Waeber, G. Watkins, H. Wright, A.F. Zillikens, M.C. Chatterjee, N. Purcell, S. Schadt, E.E. Visscher, P.M. Assimes, T.L. Borecki, I.B. Deloukas, P. Haritunians, T. Kaplan, R.C. O'Connell, J.R. Peltonen, L. Schlessinger, D. Strachan, D.P. North, K.E. Hirschhorn, J.N. Ingelsson, E. Parts, L. Glass, D. Nisbet, J. Barrett, A. Sekowska, M. Potter, S. Grundberg, E. Small, K. Hedman, A.K. Bataille, V. Bell, J.T. Surdulescu, G. Ingle, C. Nestle, F.O. Di Meglio, P. Min, J.L. Wilk, A. Hammond, C.J. Yang, T.-P. Montgomery, S.B. Zondervan, K.T. Durbin, R. Ahmadi, K. Dermitzakis, E.T. Reilly, M.P. Holm, H. Stewart, A.F.R. Barbalic, M. Aherrahrou, Z. Allayee, H. Anand, S.S. Andersen, K. Anderson, J.L. Ardissino, D. Ball, S.G. Barnes, T.A. Becker, D.M. Becker, L.C. Berger, K. Bis, J.C. Boekholdt, S.M. Braund, P.S. Burnett, M.S. Buysschaert, I. Carlquist, J.F. Chen, L. Codd, V. Davies, R.W. Cichon, S. Dedoussis, G.V. Demissie, S. Dehghan, A. Devaney, J.M. Diemert, P. Do, R. Doering, A. Eifert, S. El Mokhtari, N.E. Ellis, S.G. Engert, J.C. Epstein, S.E. De Faire, U. Fischer, M. Freyer, J. Gigante, B. Girelli, D. Gretarsdottir, S. Gulcher, J.R. Halperin, E. Hammond, N. Hazen, S.L. Horne, B.D. Jones, G.T. Jukema, J.W. Kaiser, M.A. Kastelein, J.J.P. Kolovou, G. Laaksonen, R. Lambrechts, D. Leander, K. Li, M. Lieb, W. Loley, C. Lotery, A.J. Mannucci, P.M. Maouche, S. Martinelli, N. McKeown, P.P. Meisinger, C. Merlini, P.A. Mooser, V. Morgan, T. Mühleisen, T.W. Muhlestein, J.B. Münzel, T. Musunuru, K. Nahrstaedt, J. Nelson, C.P. Nöthen, M.M. Olivieri, O. Patel, R.S. Patterson, C.C. Peyvandi, F. Qu, L. Quyyumi, A.A. Rader, D.J. Rallidis, L.S. Rice, C. Rosendaal, F.R. Rubin, D. Sampietro, M.L. Sandhu, M.S. Schadt, E. Schäfer, A. Schillert, A. Schrezenmeir, J. Schwartz, S.M. Sivananthan, M. Sivapalaratnam, S. Smith, T.B. Snoep, J.D. Spertus, J.A. Stark, K. Stoll, M. Wilson Tang, W.H. Tennstedt, S. Thorgeirsson, G. Tomaszewski, M. Van Rij, A.M. Wells, G.A. Wild, P.S. Willenborg, C. Wright, B.J. Ye, S. Zeller, T. Cambien, F. Goodall, A.H. Marz, W. Blankenberg, S. Roberts, R. McPherson, R. Hopewell, J.C. Parish, S. Offer, A. Bowman, L. Sleight, P. Armitage, J. Peto, R. Collins, R. Chambers, J.C. Ahmed, N. Donnelly, P. Kooner, A.S. Scott, J. Sehmi, J. Zhang, W. Kooner, J. Sabater-Lleal, M. Mälarstig, A. Hellénius, M.-L. Olsson, G. Rust, S. Assmann, G. Seedorf, U. Barlera, S. Tognoni, G. Franzosi, M.G. Linksted, P. Ongen, H. Kyriakou, T. Green, F. Farrall, M. Saleheen, D. Rasheed, A. Zaidi, M. Shah, N. Samuel, M. Mallick, N. Azhar, M. Zaman, K. Samad, A. Ishaq, M. Gardezi, A. Memon, F.-U.-R. Frossard, P. Danesh, J. Östenson, C.-G. Lind, L. Cooper, C.C. Serrano-Ríos, M. Ferrannini, E. Forsen, T.J. Pattou, F. Langenberg, C. Hamsten, A. Florez, J.C.

Subjects
endocrine system, endocrine system diseases, nutritional and metabolic diseases
Abstract

OBJECTIVE - Proinsulin is a precursor of mature insulin and C-peptide. Higher circulating proinsulin levels are associated with impaired b-cell function, raised glucose levels, insulin resistance, and type 2 diabetes (T2D). Studies of the insulin processing pathway could provide new insights about T2D pathophysiology. RESEARCH DESIGN AND METHODS - We have conducted a meta-analysis of genome-wide association tests of ;2.5 million genotyped or imputed single nucleotide polymorphisms (SNPs) and fasting proinsulin levels in 10,701 nondiabetic adults of European ancestry, with follow-up of 23 loci in up to 16,378 individuals, using additive genetic models adjusted for age, sex, fasting insulin, and study-specific covariates. RESULTS - Nine SNPs at eight loci were associated with proinsulin levels (P < 5 × 10-8). Two loci (LARP6 and SGSM2) have not been previously related to metabolic traits, one (MADD) has been associated with fasting glucose, one (PCSK1) has been implicated in obesity, and four (TCF7L2, SLC30A8, VPS13C/ C2CD4A/B, and ARAP1, formerly CENTD2) increase T2D risk. The proinsulin-raising allele of ARAP1 was associated with a lower fasting glucose (P = 1.7 3 10-4), improved b-cell function (P = 1.1 × 10-5), and lower risk of T2D (odds ratio 0.88; P = 7.8 × 10-6). Notably, PCSK1 encodes the protein prohormone convertase 1/3, the first enzyme in the insulin processing pathway. A genotype score composed of the nine proinsulin-raising alleles was not associated with coronary disease in two large case-control datasets. CONCLUSIONS - We have identified nine genetic variants associated with fasting proinsulin. Our findings illuminate the biology underlying glucose homeostasis and T2D development in humans and argue against a direct role of proinsulin in coronary artery disease pathogenesis. © 2011 by the American Diabetes Association.

Published
2011

7. Large-scale gene-centric analysis identifies novel variants for coronary artery disease

Author

Butterworth, A.S., Braund, P.S., Hardwick, R.J., Saleheen, D., Peden, J.F., Soranzo, N., Chambers, J.C., Kleber, M.E., Keating, B., Qasim, A., Klopp, N., Erdmann, J., Basart, H., Baumert, J.H., Bezzina, C.R., Boehm, B.O., Brocheton, J., Bugert, P., Cambien, F., Collins, R., Couper, D., Jong, J.S. de, Diemert, P., Ejebe, K., Elbers, C.C., Elliott, P., Fornage, M., Frossard, P., Garner, S., Hunt, S.E., Kastelein, J.J., Klungel, O.H., Kluter, H., Koch, K., Konig, I.R., Kooner, A.S., Liu, K., McPherson, R., Musameh, M.D., Musani, S., Papanicolaou, G., Peters, A., Peters, B.J., Potter, S., Psaty, B.M., Rasheed, A., Scott, J., Seedorf, U., Sehmi, J.S., Sotoodehnia, N., Stark, K., Stephens, J., Schoot, C.E. van der, Schouw, Y.T. van der, Harst, P. van der, Vasan, R.S., Wilde, A.A., Willenborg, C., Winkelmann, B.R., Zaidi, M., Zhang, W., Ziegler, A., Koenig, W., Matz, W., Trip, M.D., Reilly, M.P., Kathiresan, S., Schunkert, H., Hamsten, A., Hall, A.S., Kooner, J.S., Thompson, S.G., Thompson, J.R., Watkins, H., Danesh, J., Barnes, T., Rafelt, S., Codd, V., Bruinsma, N., Dekker, L.R., Henriques, J.P., Koch, K.T., Winter, R.J. de, Alings, M., Allaart, C.F., Gorgels, A.P., Verheugt, F.W.A., Mueller, M., Meisinger, C., DerOhannessian, S., Mehta, N.N., Ferguson, J., Hakonarson, H., Matthai, W., Wilensky, R., Hopewell, J.C., Parish, S., Linksted, P., Notman, J., Gonzalez, H., Young, A., Ostley, T., Munday, A., Goodwin, N., Verdon, V., Shah, S., Edwards, C., Mathews, C., Gunter, R., Benham, J., Davies, C., Cobb, M., Cobb, L., Crowther, J., Richards, A., Silver, M., Tochlin, S., Mozley, S., Clark, S., Radley, M., Kourellias, K., Olsson, P., Barlera, S., Tognoni, G., Rust, S., Assmann, G., Heath, S., Zelenika, D., Gut, I., Green, F., Farrall, M., Goel, A., Ongen, H., Franzosi, M.G., Lathrop, M., Clarke, R., Aly, A., Anner, K., Bjorklund, K., Blomgren, G., Cederschiold, B., Danell-Toverud, K., Eriksson, P., Grundstedt, U., Heinonen, M., Hellenius, M.L., Hooft, F. van 't, Husman, K., Lagercrantz, J., Larsson, A., Larsson, M., Mossfeldt, M., Malarstig, A., Olsson, G., Sabater-Lleal, M., Sennblad, B., Silveira, A., Strawbridge, R., Soderholm, B., Ohrvik, J., Zaman, K.S., Mallick, N.H., Azhar, M., Samad, A., Ishaq, M., Shah, N., Samuel, M., Kathiresan, S.C., Assimes, T.L., Holm, H., Preuss, M., Stewart, A.F., Barbalic, M., Gieger, C., Absher, D., Aherrahrou, Z., Allayee, H., Altshuler, D., Anand, S., Andersen, K., Anderson, J.L., Ardissino, D., Ball, S.G., Balmforth, A.J., Barnes, T.A., Becker, L.C., Becker, D.M., Berger, K., Bis, J.C., Boekholdt, S.M., Boerwinkle, E., Brown, M.J., Burnett, M.S., Buysschaert, I., Carlquist, J.F., Chen, L., Davies, R.W., Dedoussis, G., Dehghan, A., Demissie, S., Devaney, J., Do, R., Doering, A., El Mokhtari, N.E., Ellis, S.G., Elosua, R., Engert, J.C., Epstein, S., Faire, U. de, Fischer, M., Folsom, A.R., Freyer, J., Gigante, B., Girelli, D., Gretarsdottir, S., Gudnason, V., Gulcher, J.R., Tennstedt, S., Halperin, E., Hammond, N., Hazen, S.L., Hofman, A., Horne, B.D., Illig, T., Iribarren, C., Jones, G.T., Jukema, J.W., Kaiser, M.A., Kaplan, L.M., Khaw, K.T., Knowles, J.W., Kolovou, G., Kong, A., Laaksonen, R., Lambrechts, D., Leander, K., Li, M., Lieb, W., Lettre, G., Loley, C., Lotery, A.J., Mannucci, P.M., Martinelli, N., McKeown, P.P., Meitinger, T., Melander, O., Merlini, P.A., Mooser, V., Morgan, T., Muhleisen T.W., ., Muhlestein, J.B., Musunuru, K., Nahrstaedt, J., Nothen, Markus, Olivieri, O., Peyvandi, F., Patel, R.S., Patterson, C.C., Qu, L., Quyyumi, A.A., Rader, D.J., Rallidis, L.S., Rice, C., Roosendaal, F.R., Rubin, D., Salomaa, V., Sampietro, M.L., Sandhu, M.S., Schadt, E., Schafer, A., Schillert, A., Schreiber, S., Schrezenmeir, J., Schwartz, S.M., Siscovick, D.S., Sivananthan, M., Sivapalaratnam, S., Smith, A.V., Smith, T.B., Snoep, J.D., Spertus, J.A., Stefansson, K., Stirrups, K., Stoll, M., Tang, W.H., Thorgeirsson, G., Thorleifsson, G., Tomaszewski, M., Uitterlinden, A.G., Rij, A.M. van, Voight, B.F., Wareham, N.J., AWells, G., Wichmann, H.E., Witteman, J.C., Wright, B.J., Ye, S., Cupples, L.A., Quertermous, T., Marz, W., Blankenberg, S., Thorsteinsdottir, U., Roberts, R., O'Donnell, C.J., Onland-Moret, N.C., Setten, J. van, Bakker, P.I. de, Verschuren, W.M., Boer, J.M., Wijmenga, C., Hofker, M.H., Maitland-van der Zee, A.H., Boer, A. de, Grobbee, D.E., Attwood, T., Belz, S., Cooper, J., Crisp-Hihn, A., Deloukas, P., Foad, N., Goodall, A.H., Gracey, J., Gray, E., Gwilliams, R., Heimerl, S., Hengstenberg, C., Jolley, J., Krishnan, U., Lloyd-Jones, H., Lugauer, I., Lundmark, P., Maouche, S., Moore, J.S., Muir, D., Murray, E., Nelson, C.P., Neudert, J., Niblett, D., O'Leary, K., Ouwehand, W.H., Pollard, H., Rankin, A., Rice, C.M., Sager, H., Samani, N.J., Sambrook, J., Schmitz, G., Scholz, M., Schroeder, L., Syvannen, A.C., Wallace, C., Butterworth, A.S., Braund, P.S., Hardwick, R.J., Saleheen, D., Peden, J.F., Soranzo, N., Chambers, J.C., Kleber, M.E., Keating, B., Qasim, A., Klopp, N., Erdmann, J., Basart, H., Baumert, J.H., Bezzina, C.R., Boehm, B.O., Brocheton, J., Bugert, P., Cambien, F., Collins, R., Couper, D., Jong, J.S. de, Diemert, P., Ejebe, K., Elbers, C.C., Elliott, P., Fornage, M., Frossard, P., Garner, S., Hunt, S.E., Kastelein, J.J., Klungel, O.H., Kluter, H., Koch, K., Konig, I.R., Kooner, A.S., Liu, K., McPherson, R., Musameh, M.D., Musani, S., Papanicolaou, G., Peters, A., Peters, B.J., Potter, S., Psaty, B.M., Rasheed, A., Scott, J., Seedorf, U., Sehmi, J.S., Sotoodehnia, N., Stark, K., Stephens, J., Schoot, C.E. van der, Schouw, Y.T. van der, Harst, P. van der, Vasan, R.S., Wilde, A.A., Willenborg, C., Winkelmann, B.R., Zaidi, M., Zhang, W., Ziegler, A., Koenig, W., Matz, W., Trip, M.D., Reilly, M.P., Kathiresan, S., Schunkert, H., Hamsten, A., Hall, A.S., Kooner, J.S., Thompson, S.G., Thompson, J.R., Watkins, H., Danesh, J., Barnes, T., Rafelt, S., Codd, V., Bruinsma, N., Dekker, L.R., Henriques, J.P., Koch, K.T., Winter, R.J. de, Alings, M., Allaart, C.F., Gorgels, A.P., Verheugt, F.W.A., Mueller, M., Meisinger, C., DerOhannessian, S., Mehta, N.N., Ferguson, J., Hakonarson, H., Matthai, W., Wilensky, R., Hopewell, J.C., Parish, S., Linksted, P., Notman, J., Gonzalez, H., Young, A., Ostley, T., Munday, A., Goodwin, N., Verdon, V., Shah, S., Edwards, C., Mathews, C., Gunter, R., Benham, J., Davies, C., Cobb, M., Cobb, L., Crowther, J., Richards, A., Silver, M., Tochlin, S., Mozley, S., Clark, S., Radley, M., Kourellias, K., Olsson, P., Barlera, S., Tognoni, G., Rust, S., Assmann, G., Heath, S., Zelenika, D., Gut, I., Green, F., Farrall, M., Goel, A., Ongen, H., Franzosi, M.G., Lathrop, M., Clarke, R., Aly, A., Anner, K., Bjorklund, K., Blomgren, G., Cederschiold, B., Danell-Toverud, K., Eriksson, P., Grundstedt, U., Heinonen, M., Hellenius, M.L., Hooft, F. van 't, Husman, K., Lagercrantz, J., Larsson, A., Larsson, M., Mossfeldt, M., Malarstig, A., Olsson, G., Sabater-Lleal, M., Sennblad, B., Silveira, A., Strawbridge, R., Soderholm, B., Ohrvik, J., Zaman, K.S., Mallick, N.H., Azhar, M., Samad, A., Ishaq, M., Shah, N., Samuel, M., Kathiresan, S.C., Assimes, T.L., Holm, H., Preuss, M., Stewart, A.F., Barbalic, M., Gieger, C., Absher, D., Aherrahrou, Z., Allayee, H., Altshuler, D., Anand, S., Andersen, K., Anderson, J.L., Ardissino, D., Ball, S.G., Balmforth, A.J., Barnes, T.A., Becker, L.C., Becker, D.M., Berger, K., Bis, J.C., Boekholdt, S.M., Boerwinkle, E., Brown, M.J., Burnett, M.S., Buysschaert, I., Carlquist, J.F., Chen, L., Davies, R.W., Dedoussis, G., Dehghan, A., Demissie, S., Devaney, J., Do, R., Doering, A., El Mokhtari, N.E., Ellis, S.G., Elosua, R., Engert, J.C., Epstein, S., Faire, U. de, Fischer, M., Folsom, A.R., Freyer, J., Gigante, B., Girelli, D., Gretarsdottir, S., Gudnason, V., Gulcher, J.R., Tennstedt, S., Halperin, E., Hammond, N., Hazen, S.L., Hofman, A., Horne, B.D., Illig, T., Iribarren, C., Jones, G.T., Jukema, J.W., Kaiser, M.A., Kaplan, L.M., Khaw, K.T., Knowles, J.W., Kolovou, G., Kong, A., Laaksonen, R., Lambrechts, D., Leander, K., Li, M., Lieb, W., Lettre, G., Loley, C., Lotery, A.J., Mannucci, P.M., Martinelli, N., McKeown, P.P., Meitinger, T., Melander, O., Merlini, P.A., Mooser, V., Morgan, T., Muhleisen T.W., ., Muhlestein, J.B., Musunuru, K., Nahrstaedt, J., Nothen, Markus, Olivieri, O., Peyvandi, F., Patel, R.S., Patterson, C.C., Qu, L., Quyyumi, A.A., Rader, D.J., Rallidis, L.S., Rice, C., Roosendaal, F.R., Rubin, D., Salomaa, V., Sampietro, M.L., Sandhu, M.S., Schadt, E., Schafer, A., Schillert, A., Schreiber, S., Schrezenmeir, J., Schwartz, S.M., Siscovick, D.S., Sivananthan, M., Sivapalaratnam, S., Smith, A.V., Smith, T.B., Snoep, J.D., Spertus, J.A., Stefansson, K., Stirrups, K., Stoll, M., Tang, W.H., Thorgeirsson, G., Thorleifsson, G., Tomaszewski, M., Uitterlinden, A.G., Rij, A.M. van, Voight, B.F., Wareham, N.J., AWells, G., Wichmann, H.E., Witteman, J.C., Wright, B.J., Ye, S., Cupples, L.A., Quertermous, T., Marz, W., Blankenberg, S., Thorsteinsdottir, U., Roberts, R., O'Donnell, C.J., Onland-Moret, N.C., Setten, J. van, Bakker, P.I. de, Verschuren, W.M., Boer, J.M., Wijmenga, C., Hofker, M.H., Maitland-van der Zee, A.H., Boer, A. de, Grobbee, D.E., Attwood, T., Belz, S., Cooper, J., Crisp-Hihn, A., Deloukas, P., Foad, N., Goodall, A.H., Gracey, J., Gray, E., Gwilliams, R., Heimerl, S., Hengstenberg, C., Jolley, J., Krishnan, U., Lloyd-Jones, H., Lugauer, I., Lundmark, P., Maouche, S., Moore, J.S., Muir, D., Murray, E., Nelson, C.P., Neudert, J., Niblett, D., O'Leary, K., Ouwehand, W.H., Pollard, H., Rankin, A., Rice, C.M., Sager, H., Samani, N.J., Sambrook, J., Schmitz, G., Scholz, M., Schroeder, L., Syvannen, A.C., and Wallace, C.

Abstract

Contains fulltext : 98050.pdf (publisher's version ) (Open Access), Coronary artery disease (CAD) has a significant genetic contribution that is incompletely characterized. To complement genome-wide association (GWA) studies, we conducted a large and systematic candidate gene study of CAD susceptibility, including analysis of many uncommon and functional variants. We examined 49,094 genetic variants in approximately 2,100 genes of cardiovascular relevance, using a customised gene array in 15,596 CAD cases and 34,992 controls (11,202 cases and 30,733 controls of European descent; 4,394 cases and 4,259 controls of South Asian origin). We attempted to replicate putative novel associations in an additional 17,121 CAD cases and 40,473 controls. Potential mechanisms through which the novel variants could affect CAD risk were explored through association tests with vascular risk factors and gene expression. We confirmed associations of several previously known CAD susceptibility loci (eg, 9p21.3:p<10(-33); LPA:p<10(-19); 1p13.3:p<10(-17)) as well as three recently discovered loci (COL4A1/COL4A2, ZC3HC1, CYP17A1:p<5x10(-7)). However, we found essentially null results for most previously suggested CAD candidate genes. In our replication study of 24 promising common variants, we identified novel associations of variants in or near LIPA, IL5, TRIB1, and ABCG5/ABCG8, with per-allele odds ratios for CAD risk with each of the novel variants ranging from 1.06-1.09. Associations with variants at LIPA, TRIB1, and ABCG5/ABCG8 were supported by gene expression data or effects on lipid levels. Apart from the previously reported variants in LPA, none of the other approximately 4,500 low frequency and functional variants showed a strong effect. Associations in South Asians did not differ appreciably from those in Europeans, except for 9p21.3 (per-allele odds ratio: 1.14 versus 1.27 respectively; P for heterogeneity = 0.003). This large-scale gene-centric analysis has identified several novel genes for CAD that relate to diverse biochemical and cellular f

Published
2011

8. Large-scale association analysis identifies 13 new susceptibility loci for coronary artery disease

Author

Schunkert, H. (Heribert), König, I.R. (Inke), Kathiresan, S. (Sekar), Reilly, M.P. (Muredach), Assimes, T.L. (Themistocles), Holm, H. (Hilma), Preuss, M. (Michael), Stewart, A.F.R. (Alexandre), Barbalic, M. (maja), Gieger, C. (Christian), Absher, D. (Devin), Aherrahrou, Z. (Zouhair), Allayee, H. (Hooman), Altshuler, D. (David), Anand, S.S. (Sonia), Andersen, K.K. (Karl), Anderson, J.L. (Jeffrey), Ardissino, D. (Diego), Ball, S.G. (Stephen), Balmforth, A.J. (Anthony), Barnes, T.A. (Timothy), Becker, D.M. (Diane), Berger, K. (Klaus), Bis, J.C. (Joshua), Boekholdt, S.M. (Matthijs), Boerwinkle, E.A. (Eric), Braund, P.S. (Peter), Brown, M.J. (Morris), Burnett, M.S., Buysschaert, I. (Ian), Carlquist, J.F. (John), Chen, L. (Li), Cichon, S. (Sven), Codd, V. (Veryan), Davies, R.W. (Robert), Dedoussis, G.V. (George), Dehghan, A. (Abbas), Demissie, S. (Serkalem), Devaney, J. (Joseph), Diemert, P. (Patrick), Do, R. (Ron), Doering, A. (Angela), Eifert, S. (Sandra), Mokhtari, N.E.E., Ellis, S.G. (Stephen), Elosua, R. (Roberto), Engert, J.C. (James), Epstein, S.E. (Stephen), Faire, U. (Ulf) de, Fischer, M. (Marcus), Folsom, A.R. (Aaron), Freyer, J. (Jennifer), Gigante, B. (Bruna), Girelli, D. (Domenico), Gretarsdottir, S. (Solveig), Gudnason, V. (Vilmundur), Gulcher, J.R. (Jeffrey), Halperin, E. (Eran), Hammond, N. (Naomi), Hazen, S.L. (Stanley), Hofman, A. (Albert), Horne, B.D. (Benjamin), Illig, T. (Thomas), Iribarren, C. (Carlos), Jones, G.T. (Gregory), Jukema, J.W. (Jan Wouter), Kaiser, M.A. (Michael), Kaplan, R.C. (Robert), Khaw, K-T. (Kay-Tee), Knowles, J.W. (Joshua), Kolovou, G. (Genovefa), Kong, A. (Augustine), Laaksonen, R. (Reijo), Lambrechts, D. (Diether), Leander, K. (Karin), Lettre, G. (Guillaume), Lieb, W. (Wolfgang), Loley, C. (Christina), Lotery, A.J. (Andrew), Mannucci, P.M. (Pier), Maouche, S. (Seraya), Martinelli, N. (Nicola), McKeown, P.P. (Pascal), Meisinger, C. (Christa), Meitinger, T. (Thomas), Melander, O. (Olle), Merlini, P.A., Mooser, V. (Vincent), Morgan, T. (Thomas), Mühleisen, T.W. (Thomas), Muhlestein, J.B. (Joseph), Münzel, T. (Thomas), Musunuru, K. (Kiran), Nahrstaedt, J. (Janja), Nelson, C.P. (Christopher P.), Nöthen, M.M. (Markus), Olivieri, O. (Oliviero), Patel, R.S. (Riyaz), Patterson, C.C. (Chris), Peters, A. (Annette), Peyvandi, F. (Flora), Qu, L. (Liming), Quyyumi, A.A. (Arshed), Rader, D.J. (Daniel), Rallidis, L.S. (Loukianos), Rice, C. (Catherine), Rosendaal, F.R. (Frits), Rubin, D. (Diana), Salomaa, V. (Veikko), Sampietro, M.L. (Maria Lourdes), Sandhu, M.S. (Manj), Schadt, E.E. (Eric), Schillert, A. (Arne), Schreiber, S. (Stefan), Schrezenmeir, J. (Jürgen), Schwartz, S.M. (Stephen), Siscovick, D.S. (David), Sivananthan, M. (Mohan), Sivapalaratnam, S. (Suthesh), Smith, A.V. (Albert Vernon), Snoep, J.D. (Jaapjan), Soranzo, N. (Nicole), Spertus, J.A. (John), Stark, K. (Klaus), Stirrups, K. (Kathy), Stoll, M. (Monika), Tang, W.H.W. (Wilson), Tennstedt, S. (Stephanie), Thorgeirsson, G. (Gudmundur), Thorleifsson, G. (Gudmar), Tomaszewski, M. (Maciej), Uitterlinden, A.G. (André), Rij, A.M. (Andre) van, Voight, B.F. (Benjamin), Wareham, N.J. (Nick), Wells, G.A. (George), Wichmann, H.E. (Heinz Erich), Wild, P.S. (Philipp), Willenborg, C. (Christina), Witteman, J.C.M. (Jacqueline), Wright, B.J. (Benjamin), Ye, S. (Shu), Zeller, T. (Tanja), Ziegler, A. (Andreas), Cambien, F. (François), Goodall, A.H. (Alison), Cupples, L.A. (Adrienne), Quertermous, T. (Thomas), Mäsignrz, W. (Winfried), Hengstenberg, C. (Christian), Blankenberg, S. (Stefan), Ouwehand, W.H. (Willem), Hall, A.S. (Alistair), Kastelein, J.J.P. (John), Deloukas, P. (Panagiotis), Thompson, J.R. (John), Stefansson, K. (Kari), Roberts, R. (Robert), Li, M. (Mingyao), Thorsteinsdottir, U. (Unnur), O'Donnell, C.J. (Christopher), McPherson, R. (Ruth), Erdmann, J. (Jeanette), Samani, N.J. (Nilesh), Schäffer, A. (Arne), Schunkert, H. (Heribert), König, I.R. (Inke), Kathiresan, S. (Sekar), Reilly, M.P. (Muredach), Assimes, T.L. (Themistocles), Holm, H. (Hilma), Preuss, M. (Michael), Stewart, A.F.R. (Alexandre), Barbalic, M. (maja), Gieger, C. (Christian), Absher, D. (Devin), Aherrahrou, Z. (Zouhair), Allayee, H. (Hooman), Altshuler, D. (David), Anand, S.S. (Sonia), Andersen, K.K. (Karl), Anderson, J.L. (Jeffrey), Ardissino, D. (Diego), Ball, S.G. (Stephen), Balmforth, A.J. (Anthony), Barnes, T.A. (Timothy), Becker, D.M. (Diane), Berger, K. (Klaus), Bis, J.C. (Joshua), Boekholdt, S.M. (Matthijs), Boerwinkle, E.A. (Eric), Braund, P.S. (Peter), Brown, M.J. (Morris), Burnett, M.S., Buysschaert, I. (Ian), Carlquist, J.F. (John), Chen, L. (Li), Cichon, S. (Sven), Codd, V. (Veryan), Davies, R.W. (Robert), Dedoussis, G.V. (George), Dehghan, A. (Abbas), Demissie, S. (Serkalem), Devaney, J. (Joseph), Diemert, P. (Patrick), Do, R. (Ron), Doering, A. (Angela), Eifert, S. (Sandra), Mokhtari, N.E.E., Ellis, S.G. (Stephen), Elosua, R. (Roberto), Engert, J.C. (James), Epstein, S.E. (Stephen), Faire, U. (Ulf) de, Fischer, M. (Marcus), Folsom, A.R. (Aaron), Freyer, J. (Jennifer), Gigante, B. (Bruna), Girelli, D. (Domenico), Gretarsdottir, S. (Solveig), Gudnason, V. (Vilmundur), Gulcher, J.R. (Jeffrey), Halperin, E. (Eran), Hammond, N. (Naomi), Hazen, S.L. (Stanley), Hofman, A. (Albert), Horne, B.D. (Benjamin), Illig, T. (Thomas), Iribarren, C. (Carlos), Jones, G.T. (Gregory), Jukema, J.W. (Jan Wouter), Kaiser, M.A. (Michael), Kaplan, R.C. (Robert), Khaw, K-T. (Kay-Tee), Knowles, J.W. (Joshua), Kolovou, G. (Genovefa), Kong, A. (Augustine), Laaksonen, R. (Reijo), Lambrechts, D. (Diether), Leander, K. (Karin), Lettre, G. (Guillaume), Lieb, W. (Wolfgang), Loley, C. (Christina), Lotery, A.J. (Andrew), Mannucci, P.M. (Pier), Maouche, S. (Seraya), Martinelli, N. (Nicola), McKeown, P.P. (Pascal), Meisinger, C. (Christa), Meitinger, T. (Thomas), Melander, O. (Olle), Merlini, P.A., Mooser, V. (Vincent), Morgan, T. (Thomas), Mühleisen, T.W. (Thomas), Muhlestein, J.B. (Joseph), Münzel, T. (Thomas), Musunuru, K. (Kiran), Nahrstaedt, J. (Janja), Nelson, C.P. (Christopher P.), Nöthen, M.M. (Markus), Olivieri, O. (Oliviero), Patel, R.S. (Riyaz), Patterson, C.C. (Chris), Peters, A. (Annette), Peyvandi, F. (Flora), Qu, L. (Liming), Quyyumi, A.A. (Arshed), Rader, D.J. (Daniel), Rallidis, L.S. (Loukianos), Rice, C. (Catherine), Rosendaal, F.R. (Frits), Rubin, D. (Diana), Salomaa, V. (Veikko), Sampietro, M.L. (Maria Lourdes), Sandhu, M.S. (Manj), Schadt, E.E. (Eric), Schillert, A. (Arne), Schreiber, S. (Stefan), Schrezenmeir, J. (Jürgen), Schwartz, S.M. (Stephen), Siscovick, D.S. (David), Sivananthan, M. (Mohan), Sivapalaratnam, S. (Suthesh), Smith, A.V. (Albert Vernon), Snoep, J.D. (Jaapjan), Soranzo, N. (Nicole), Spertus, J.A. (John), Stark, K. (Klaus), Stirrups, K. (Kathy), Stoll, M. (Monika), Tang, W.H.W. (Wilson), Tennstedt, S. (Stephanie), Thorgeirsson, G. (Gudmundur), Thorleifsson, G. (Gudmar), Tomaszewski, M. (Maciej), Uitterlinden, A.G. (André), Rij, A.M. (Andre) van, Voight, B.F. (Benjamin), Wareham, N.J. (Nick), Wells, G.A. (George), Wichmann, H.E. (Heinz Erich), Wild, P.S. (Philipp), Willenborg, C. (Christina), Witteman, J.C.M. (Jacqueline), Wright, B.J. (Benjamin), Ye, S. (Shu), Zeller, T. (Tanja), Ziegler, A. (Andreas), Cambien, F. (François), Goodall, A.H. (Alison), Cupples, L.A. (Adrienne), Quertermous, T. (Thomas), Mäsignrz, W. (Winfried), Hengstenberg, C. (Christian), Blankenberg, S. (Stefan), Ouwehand, W.H. (Willem), Hall, A.S. (Alistair), Kastelein, J.J.P. (John), Deloukas, P. (Panagiotis), Thompson, J.R. (John), Stefansson, K. (Kari), Roberts, R. (Robert), Li, M. (Mingyao), Thorsteinsdottir, U. (Unnur), O'Donnell, C.J. (Christopher), McPherson, R. (Ruth), Erdmann, J. (Jeanette), Samani, N.J. (Nilesh), and Schäffer, A. (Arne)

Abstract

We performed a meta-analysis of 14 genome-wide association studies of coronary artery disease (CAD) comprising 22,233 individuals with CAD (cases) and 64,762 controls of European descent followed by genotyping of top association signals in 56,682 additional individuals. This analysis identified 13 loci newly associated with CAD at P < 5 - 10'8 and confirmed the association of 10 of 12 previously reported CAD loci. The 13 new loci showed risk allele frequencies ranging from 0.13 to 0.91 and were associated with a 6% to 17% increase in the risk of CAD per allele. Notably, only three of the new loci showed significant association with traditional CAD risk factors and the majority lie in gene regions not previously implicated in the pathogenesis of CAD. Finally, five of the new CAD risk loci appear to have pleiotropic effects, showing strong association with various other human diseases or traits.

Published
2011
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9. Connective tissue activation. xxxvi. the origin, variety, distribution, and biologic fate of connective tissue activating peptide-iii isoforms: characteristics in patients with rheumatic, renal, and arterial disease

Author

Rackham Arthritis Research Unit and the Rheumatology, Cardiology, and Nephrology Divisions, Department of Internal Medicine, and the Department of Biological Chemistry, The University of Michigan Medical School, Ann Arbor. ; Department of Internal Medicine, The University of Michigan Medical Center, Room 4570 Kresge I, Box 0531, Ann Arbor, MI 48109-0531, Rackham Arthritis Research Unit and the Rheumatology, Cardiology, and Nephrology Divisions, Department of Internal Medicine, and the Department of Biological Chemistry, The University of Michigan Medical School, Ann Arbor., Castor, C. William, Andrews, Philip C., Swartz, Richard D., Ellis, S.G., Hossler, Paul A., Clark, M.R., Matteson, Eric L., Sachter, E.F., Rackham Arthritis Research Unit and the Rheumatology, Cardiology, and Nephrology Divisions, Department of Internal Medicine, and the Department of Biological Chemistry, The University of Michigan Medical School, Ann Arbor. ; Department of Internal Medicine, The University of Michigan Medical Center, Room 4570 Kresge I, Box 0531, Ann Arbor, MI 48109-0531, Rackham Arthritis Research Unit and the Rheumatology, Cardiology, and Nephrology Divisions, Department of Internal Medicine, and the Department of Biological Chemistry, The University of Michigan Medical School, Ann Arbor., Castor, C. William, Andrews, Philip C., Swartz, Richard D., Ellis, S.G., Hossler, Paul A., Clark, M.R., Matteson, Eric L., and Sachter, E.F.

Published
2006

10. American College of Cardiology key data elements and definitions for measuring the clinical management and outcomes of patients with acute coronary syndromes.

Author

Cannon, C.P., Battler, A. (Alexander), Brindis, R.G. (Ralph), Cox, J.L. (Jafna), Ellis, S.G. (Stephen), Every, N.R. (Nathan), Flaherty, J.T. (Joh), Harrington, R.A. (Robert Alex), Krimholz, H.M., Simoons, M.L. (Maarten), Werf, F.J.J. (Frans) van de, Weintraub, W.S. (William), Cannon, C.P., Battler, A. (Alexander), Brindis, R.G. (Ralph), Cox, J.L. (Jafna), Ellis, S.G. (Stephen), Every, N.R. (Nathan), Flaherty, J.T. (Joh), Harrington, R.A. (Robert Alex), Krimholz, H.M., Simoons, M.L. (Maarten), Werf, F.J.J. (Frans) van de, and Weintraub, W.S. (William)

Published
2001
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14. Contemporary percutaneous treatment of unprotected left main coronary stenoses: initial results from a multicenter registry analysis 1994-1996.

Author

Ellis, S.G. (Stephen), Tamai, H. (Hideo), Kosuga, K., Colombo, A. (Antonio), Holmes Jr, D.R. (David), Miguel, C.M. (Carlos), Grines, C.L., Whitlow, P.L. (Patrick), White, H.J., Moses, J., Teirstein, P.S. (Paul), Serruys, P.W.J.C. (Patrick), Bittl, J.A., Mooney, M.R., Shimshak, T.M., Block, P.C. (Peter), Erbel, R. (Raimund), Nobuyoshi, M. (Masakiyo), Ellis, S.G. (Stephen), Tamai, H. (Hideo), Kosuga, K., Colombo, A. (Antonio), Holmes Jr, D.R. (David), Miguel, C.M. (Carlos), Grines, C.L., Whitlow, P.L. (Patrick), White, H.J., Moses, J., Teirstein, P.S. (Paul), Serruys, P.W.J.C. (Patrick), Bittl, J.A., Mooney, M.R., Shimshak, T.M., Block, P.C. (Peter), Erbel, R. (Raimund), and Nobuyoshi, M. (Masakiyo)

Abstract

BACKGROUND: Coronary artery bypass surgery (CABG) has been considered the therapy of choice for patients with unprotected left main (ULMT) coronary stenoses. Selected single-center reports suggest that the results of percutaneous intervention may now approach those of CABG. METHODS AND RESULTS: To assess the results of percutaneous ULMT treatment from a wide variety of experienced interventional centers, we requested data on consecutive patients treated after January 1, 1994, from 25 centers. One hundred seven patients were identified who were treated either electively (n=91) or for acute myocardial infarction (n=16). Of patients treated electively, 25% were considered inoperable, and 27% were considered high risk for bypass surgery. Primary treatment included stents (50%), directional atherectomy (24%), and balloon angioplasty (20%). Follow-up was 98.8% complete at 15+/-8 months. Results varied considerably, depending on presentation and treatment. For patients

Published
1997

16. Directional atherectomy versus balloon angioplasty for coronary ostial and nonostial left anterior descending coronary artery lesions: Results from a randomized multicenter trial

Author

Boehrer, J.D. (James), Ellis, S.G. (Stephen), Pieper, K.S. (Karen), Holmes, D.R. (David), Keeler, G.P., Debowey, D. (Darrell), Chapekis, A.T. (Anthony), Leya, F., Mooney, M.R., Gottlieb, B. (Bruce), Serruys, P.W.J.C. (Patrick), Califf, R.M. (Robert), Topol, E.J. (Eric), Boehrer, J.D. (James), Ellis, S.G. (Stephen), Pieper, K.S. (Karen), Holmes, D.R. (David), Keeler, G.P., Debowey, D. (Darrell), Chapekis, A.T. (Anthony), Leya, F., Mooney, M.R., Gottlieb, B. (Bruce), Serruys, P.W.J.C. (Patrick), Califf, R.M. (Robert), and Topol, E.J. (Eric)

Abstract

Objectives. We hypothesized that atherectomy would be superior to balloon angioplasty for ostial and nonostial left anterior descending coronary artery lesions. Background. Balloon angioplasty of ostial coronary artery lesions has been associated with a lower procedural success rate and a higher rate of complications and of restenosis than angioplasty of nonostial stenoses. Directional coronary atherectomy has been proposed as an alternative therapy for ostial lesions. Methods. In the Coronary Angioplasty Versus Excisional Atherectomy Trial (CAVEAT-1), 1, 012 patients were randomized to undergo either procedure; 563 patients had proximal left anterior descending coronary artery lesions, of which 74 were ostial. We compared balloon angioplasty with directional atherect

Published
1995
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17. A comparison of directional atherectomy with coronary angioplasty in patients with coronary artery disease

Author

Topol, E.J. (Eric), Leya, F., Pinkerton, C.A., Whitlow, P.L. (Patrick), Hofling, B., Simonton, C.A., Masden, R.R., Serruys, P.W.J.C. (Patrick), Leon, M.B. (Martin), Williams, D.O. (David), King 3rd, S.B. (Spencer), Daniel, B., Mark, D.B. (Daniel), Isner, J.M., Holmes Jr, D.R. (David), Ellis, S.G. (Stephen), Lee, K.L. (Kerry), Keeler, G.P., Berdan, L.G. (Lisa), Hinohara, T., Califf, R.M. (Robert), Topol, E.J. (Eric), Leya, F., Pinkerton, C.A., Whitlow, P.L. (Patrick), Hofling, B., Simonton, C.A., Masden, R.R., Serruys, P.W.J.C. (Patrick), Leon, M.B. (Martin), Williams, D.O. (David), King 3rd, S.B. (Spencer), Daniel, B., Mark, D.B. (Daniel), Isner, J.M., Holmes Jr, D.R. (David), Ellis, S.G. (Stephen), Lee, K.L. (Kerry), Keeler, G.P., Berdan, L.G. (Lisa), Hinohara, T., and Califf, R.M. (Robert)

Abstract

BACKGROUND. Directional coronary atherectomy is a new technique of coronary revascularization by which atherosclerotic plaque is excised and retrieved from target lesions. With respect to the rate of restenosis and clinical outcomes, it is not known how this procedure compares with balloon angioplasty, which relies on dilation of the plaque and vessel wall. We compared the rate of restenosis after angioplasty with that after atherectomy. METHODS. At 35 sites in the United States and Europe, 1012 patients were randomly assigned to either atherectomy (512 patients) or angioplasty (500 patients). The patients underwent coronary

Published
1993

29. So you want to be a specialist registrar?--What to put in your CV.

Author

Ellis, P.E., Ellis, S.G. S., O'Brien, K.D., and Joshi, R.I.

Subjects
*TRAINING of dentists, *DENTAL specialties
Abstract

Dentists applying to a specialist training programme often receive conflicting advice over what to put in their curriculum vitae (CV). We conducted a survey of the Training Programme Directors of the dental specialties to determine what aspects of CV content and presentation styles are considered important. This has allowed us to construct guidelines for what to put in a CV. Recently, structured application forms have become increasingly popular and may be a more objective way to carry out the shortlisting process. The guidelines presented could also be used as a framework for medical personnel departments if structured application forms eventually replace the CV. [ABSTRACT FROM AUTHOR]

Published
2002
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30. Frequency and long-term impact of myonecrosis after coronary stenting.

Author

Brener, S.J., Ellis, S.G., Schneider, J., and Topol, E.J.

Abstract

Aims To study the frequency of creatine kinase MB elevation in stent recipients and to correlate the magnitude of myonecrosis with long-term ischaemic events.Methods and Results We evaluated the frequency and impact (major adverse ischaemic events) of creatine kinase MB elevation in 3478 patients undergoing planned coronary stenting and divided them in five strata according to peak creatine kinase MB: normal, 1–3×, 3–5×, 5–10× and >10× above upper limit of normal. Graft intervention was done in 15% and 61% received platelet glycoprotein IIb/IIIa receptor inhibitors. The average follow-up period was 15±15 (range 1–72) months. Creatine kinase MB elevation above upper limit of normal occurred in 24% and in 5·3% it was greater than 5×upper limit of normal. The unadjusted rates of actuarial mortality in the five strata were: 7·5% (198/2637), 8·0% (40/502), 11·0% (17/155), 10·8% (11/102) and 29·3% (24/82), respectively, P<0·001. Logistic regression analysis including 18 demographic and procedural variables revealed that, in addition to age, extent of coronary disease, ventricular function and coronary risk profile, creatine kinase MB elevation was associated with a significant increase in major ischaemic events at follow-up. The excess risk was concentrated mainly in the highest stratum of creatine kinase MB elevation.Conclusions Thus, in the era of stenting and aggressive adjunctive pharmacology, peri-procedural myonecrosis still remains frequent and has an important impact on long-term event-free survival. Intensive efforts to reduce creatine kinase MB elevation after revascularization are warranted and should lead to important benefits. Copyright 2001 The European Society of Cardiology. Published by Elsevier Science Ltd. All rights reserved [ABSTRACT FROM PUBLISHER]

Published
2002
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32. Corrected TIMI frame count does not predict 30-day adverse outcomes after reperfusion therapy for acute myocardial infarction

Author

Bhatt, D.L., Ellis, S.G., Ivanc, T.B., Crowe, T., Balazs, E., Debowey, D., Pangerl, A., and Chew, P.H.

Abstract

Background Thrombolysis in Myocardial Infarction (TIMI) flow grading is limited by subjectivity and imprecision. The corrected TIMI frame count (cTFC) has been proposed to obviate these problems. We sought to validate the utility of the cTFC in predicting adverse clinical outcomes after reperfusion therapy. Methods and Results We used angiographic core laboratory data from the Intravenous nPA for Treating Infarcting Myocardium Early Study (lanoteplase versus alteplase) to assess the predictive capacity of both final TIMI flow and cTFC on 30 day-composite adverse outcome (death, reinfarction, and new or worsening congestive heart failure). Only 390 angiograms of 586 were analyzable for cTFC; 33.4% of angiograms could not be analyzed for cTFC because filling of distal landmarks was not visualized for technical reasons such as inadequate panning. The interobserver correlation for determination of the cTFC was 0.99 and the intraobserver correlation was 0.97. The cTFC in the group with adverse outcomes was 49 +/- 34; in the group without adverse outcomes, it was 44 +/- 31 (P = .27). Of note, the TIMI flow correlated with adverse outcome in the overall group of patients (P = .018, area under the receiver-operator characteristic curve [c] = 0.590) as well as in the group of patients with cines analyzable for cTFC (P = .025, c = 0.600). The independent correlates of adverse outcomes were age (P < .001), heart rate (P = .001), TIMI flow grade (P = .027), and infarct location (P = .038) but not cTFC. Conclusions The cTFC did not predict adverse outcomes in this population of patients but did show excellent reproducibility within our core laboratory. (Am Heart J 1999;138:785-90.)

Published
1999
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33. Smoking status and outcome after primary coronary angioplasty for acute myocardial infarction

Author

Hasdai, D., Lerman, A., Rihal, C.S., Criger, D.A., Garratt, K.N., Betriu, A., White, H.D., Topol, E.J., Granger, C.B., Ellis, S.G., Califf, R.M., and Holmes, D.R.

Abstract

Background Because of the increased propensity of intracoronary thrombi to form in cigarette smokers, percutaneous transluminal angioplasty (PTCA) for acute myocardial infarction (AMI) may be less effective in smokers. We sought to determine the impact of smoking status on outcome after PTCA for AMI. Methods Patients enrolled in the GUSTO IIb Angioplasty Substudy were randomly assigned to receive PTCA or tissue-plasminogen activator (tPA) for AMI. The interaction of smoking status (nonsmokers = 344, former smokers = 294, current smokers = 490) and treatment strategy with the occurrence of death, nonfatal reinfarction, or nonfatal, disabling stroke at 30 days was analyzed. Procedural success (residual stenosis <50% and Thrombolysis in Myocardial Infarction [TIMI] flow grade 3) was also analyzed for patients who underwent PTCA (n = 444). Results Among patients who underwent PTCA, nonsmokers had worse percent stenosis of the culprit lesion before reperfusion (P = .03) and more often had TIMI flow grade 0 (P < .05). Procedural success was more common in smokers (65.6%) than in former smokers (53.3%) and nonsmokers (52.4%; P = .02), reflecting a higher rate of postprocedure TIMI 3 flow. PTCA was associated with a better 30-day outcome than tPA for current smokers (odds ratio [95% confidence interval] = 0.41 [0.19 to 0.88]), with a similar trend for former smokers (0.73 [0.34 to 1.58]) and nonsmokers (0.77 [0.42 to 1.40]). At 6 months, smokers randomly assigned to PTCA also had fewer deaths and reinfarction (0.58 [0.31 to 1.07]). Conclusions Although smoking status affects angiographic variables before and after PTCA for AMI, PTCA is associated with a better 30-day outcome than tPA regardless of smoking status and should be considered when readily available. (Am Heart J 1999;137:612-20.)

Published
1999
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34. A profile of candidates for repeat myocardial revascularization: Implications for selection of treatment

Author

Brener, S.J., Loop, F.D., Lytle, B.W., Ellis, S.G., Cosgrove, D.M., and Topol, E.J.

Abstract

Objectives: It is not known whether the results of randomized trials comparing coronary artery bypass grafting to percutaneous transluminal coronary angioplasty for initial revascularization apply to repeat revascularization in patients with prior bypass grafts. We studied the differences between the patients with prior bypass grafts referred for surgery or angioplasty to identify the clinical and angiographic characteristics that correlated best with either choice and to find clues that might aid in selecting one treatment over the other. Methods: Between 1992 and 1904, 870 patients underwent first isolated reoperation and 793 patients underwent first balloon angioplasty after a previous operation. A jeopardy score (0 to 8 points) was derived for each patient on the basis of the relative size of the ischemic territory. Clinical and angiographic data were analyzed for association with the revascularization strategy. Results: The following characteristics were more prevalent in the reoperation group: male sex, diabetes, hypertension, valvular disease, normocholesterolemia, and severe left ventricular systolic dysfunction; fewer functioning venous and arterial grafts; and a higher jeopardy score (p < 0.01 for all) than in the angioplasty group. A higher jeopardy score, diabetes, and a lower number of functioning arterial or venous grafts were strong, independent predictors of referral for reoperation (p < 0.01 for all). In-hospital death and Q-wave infarction (p < 0.01 for both) were more frequent in the reoperation group. Conclusions: Reoperation was the revascularization procedure of choice when larger regions of myocardium were in jeopardy. Angioplasty was more frequently chosen in the presence of a patent arterial graft to the left anterior descending coronary artery or multiple functioning bypass grafts. Reoperation was associated with a higher risk of in-hospital complications than angioplasty. J Thorac Cardiovasc Surg 1997;114:153-61

Published
1997
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35. Influence of local delivery of the protein tyrosine kinase receptor inhibitor tyrphostin-47 on smooth-muscle cell proliferation in a rat carotid balloon-injury model

Author

Gottsauner-Wolf, M., Jang, Y., Lincoff, A., Cohen, J.L., Labhasetwar, V., Poptic, E.J., Forudi, F., Guzman, L.A., DiCorleto, P.E., Levy, R.J., Topol, E.J., and Ellis, S.G.

Abstract

Smooth-muscle cell proliferation in response to arterial injury represents an important etiologic factor in restenosis after angioplasty. Tyrphostin-47, a protein tyrosine kinase inhibitor, inhibits smooth-muscle cell proliferation in vitro. In this study tyrphostin-47 was incorporated into matrixes to determine whether prolonged local delivery would result in a reduction of neointimal proliferation after arterial injury in a rat carotid balloon-injury model. A polymer matrix (polylactic polyglycolic acid copolymer and pluronic gel F-127, mean matrix weight 7.83 +/- 0.39 mg) was loaded with tyrphostin-47 (25% w/w). Release studies demonstrated delivery of 11% of the incorporated drug over a 21-day release period. In cell culture, tyrphostin-47 released from the polymer matrix produced a reduction in smooth-muscle cell proliferation ( p < 0.0007). Balloon denudation injury of the left common carotid artery of 34 animals was performed. In 12 animals, polymer matrixes containing tyrphostin-47 were wrapped around the injured arteries to provide prolonged drug delivery (estimated dosage 28 @mg/kg/24 hr); in 10 animals a polymer matrix without tyrphostin-47 was implanted; and in 12 animals only balloon injury was performed. The mean neointimal cross-sectional areas, luminal areas, and intima/media ratios were not significantly different among animals receiving local treatment with tyrphostin-47, sham polymer after injury, or balloon injury without polymer implantation. We conclude that despite inhibition of smooth-muscle cell proliferation by tyrphostin-47 in vitro, sustained local delivery of this tyrosine kinase inhibitor does not result in a reduction of neointimal proliferation in the rat carotid injury model. (Am Heart J 1997;133:329-34.)

Published
1997
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36. Stenting for ischemic heart disease

Author

Belli, G., Ellis, S.G., and Topol, E.J.

Abstract

This article examines current indications to intracoronary stenting for percutaneous cardiac revascularization. The data sources are a review of the published English literature, with focus on clinical and randomized trials of coronary artery stenting. Stents reduce the need for emergency bypass surgery in the setting of acute or threatened vessel closure after percutaneous transluminal coronary angioplasty (PTCA). In selected cases, when deployed electively in large native vessels with focal stenosis, clinical and angiographic recurrence are significantly reduced. Preliminary studies have also suggested a potential role in the treatment of saphenous vein graft lesions and restenotic lesions, and in improving on suboptimal results in lesions refractory to balloon dilatation. To prevent stent thrombosis, adjunctive antiplatelet therapy has been shown to be more efficacious than anticoagulation, and optimal stent apposition to the vessel wall appears to be critical. A recent exponential increase in the use of coronary stents has revolutionized the contemporary practice of interventional cardiology. Although technical factors and feasibility have been well refined and shown, evidence-based practice is lacking for many patient subsets.

Published
1997
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38. A New Method for the Rapid Examination of Textile Fiber Sections at High Magnification.

Author

Ellis, S.G.

Abstract

The fiber or yarn is formed into a self-supporting "tow" by embedding with a small amount of fast-acting cyanoacrylate adhesive. It is sectioned on an ultramicrotome to 0.25 μm thickness. The sections can be immediately examined at magnifications up to 1000X without a cover glass and mounting medium if an appropriately corrected objective (such as that used on metallurgical microscopes) is available. The total elapsed time from receiving the specimen to viewing the sections is typically one hour. [ABSTRACT FROM PUBLISHER]

Published
1975
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41. Facilitated percutaneous coronary intervention versus primary percutaneous coronary intervention: design and rationale of the facilitated intervention with enhanced reperfusion speed to stop events (FINESSE) trial

Author

Ellis, S.G., Armstrong, P., Betriu, A., Brodie, B., Herrmann, H., Montalescot, G., Neumann, F.J., Smith, J.J., and Topol, E.

Abstract

Background: Percutaneous coronary intervention (PCI) has emerged as the strategy of choice in reestablishing effective flow in occluded infarct-related arteries in patients with acute myocardial infarction (MI) if it can be administered in a timely fashion. Patients who enter the catheterization laboratory with Thrombolysis In Myocardial Infarction (TIMI) grade 3 blood flow in the infarct-related vessel have better clinical outcomes than patients presenting with impaired flow. We hypothesize that a strategy of early pharmacologic reperfusion therapy with abciximab alone or in conjunction with reduced-dose reteplase, followed by PCI will improve the outcome of patients eligible for primary PCI. Study design: The Facilitated Intervention with Enhanced Reperfusion Speed to Stop Events (FINESSE) study is a 3000-patient, prospective, multicenter, randomized, double-blind, placebo-controlled trial. The study is designed to compare the efficacy and safety of early administration of reduced-dose reteplase and abciximab combination therapy or abciximab alone followed by PCI with abciximab alone administered just before PCI for acute MI. Patients will be randomized to one of these 2 facilitated PCI treatments or primary PCI in a 1:1:1 fashion. The primary efficacy end point of FINESSE is the composite of all-cause mortality or post-MI complications within 90 days of randomization. The primary safety outcome assessment will be Thrombolysis In Myocardial Infarction (TIMI) major bleeding. Conclusions: The FINESSE study will answer important questions regarding the efficacy and safety of ''upstream'' medical therapy followed by planned intervention for patients with ST-elevation MI, potentially expanding the population eligible for a primary PCI approach. This study will also provide insight as to which facilitated regimen (reteplase/abciximab combination therapy or abciximab monotherapy) provides the best balance of efficacy and safety.

Published
2004
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