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2. Effect of alirocumab on lipoprotein(a) and cardiovascular risk after acute coronary syndrome

Author

Bittner, V. A. (Vera A.), Szarek, M. (Michael), Aylward, P. E. (Philip E.), Bhatt, D. L. (Deepak L.), Diaz, R. (Rafael), Edelberg, J. M. (Jay M.), Fras, Z. (Zlatko), Goodman, S. G. (Shaun G.), Halvorsen, S. (Sigrun), Hanotin, C. (Corinne), Harrington, R. A. (Robert A.), Jukema, W. (Wouter), Loizeau, V. (Virginie), Moriarty, P. M. (Patrick M.), Moryusef, A. (Angèle), Pordy, R. (Robert), Roe, M. T. (Matthew T.), Sinnaeve, P. (Peter), Tsimikas, S. (Sotirios), Vogel, R. (Robert), White, H. D. (Harvey D.), Zahger, D. (Doron), Zeiher, A. M. (Andreas M.), Steg, G. (Gabriel), Schwartz, G. G. (Gregory G.), and Huikuri, H. (Heikki)

Subjects
low-density lipoprotein cholesterol, proprotein convertase subtilisin/kexin type 9 inhibition, lipids (amino acids, peptides, and proteins), acute coronary syndromes, alirocumab, cardiovascular diseases, major adverse cardiovascular events
Abstract

Background: Lipoprotein(a) concentration is associated with cardiovascular events. Alirocumab, a proprotein convertase subtilisin/kexin type 9 inhibitor, lowers lipoprotein(a) and low-density lipoprotein cholesterol (LDL-C). Objectives: A pre-specified analysis of the placebo-controlled ODYSSEY Outcomes trial in patients with recent acute coronary syndrome (ACS) determined whether alirocumab-induced changes in lipoprotein(a) and LDL-C independently predicted major adverse cardiovascular events (MACE). Methods: One to 12 months after ACS, 18,924 patients on high-intensity statin therapy were randomized to alirocumab or placebo and followed for 2.8 years (median). Lipoprotein(a) was measured at randomization and 4 and 12 months thereafter. The primary MACE outcome was coronary heart disease death, nonfatal myocardial infarction, ischemic stroke, or hospitalization for unstable angina. Results: Baseline lipoprotein(a) levels (median: 21.2 mg/dl; interquartile range [IQR]: 6.7 to 59.6 mg/dl) and LDL-C [corrected for cholesterol content in lipoprotein(a)] predicted MACE. Alirocumab reduced lipoprotein(a) by 5.0 mg/dl (IQR: 0 to 13.5 mg/dl), corrected LDL-C by 51.1 mg/dl (IQR: 33.7 to 67.2 mg/dl), and reduced the risk of MACE (hazard ratio [HR]: 0.85; 95% confidence interval [CI]: 0.78 to 0.93). Alirocumab-induced reductions of lipoprotein(a) and corrected LDL-C independently predicted lower risk of MACE, after adjustment for baseline concentrations of both lipoproteins and demographic and clinical characteristics. A 1-mg/dl reduction in lipoprotein(a) with alirocumab was associated with a HR of 0.994 (95% CI: 0.990 to 0.999; p = 0.0081). Conclusions: Baseline lipoprotein(a) and corrected LDL-C levels and their reductions by alirocumab predicted the risk of MACE after recent ACS. Lipoprotein(a) lowering by alirocumab is an independent contributor to MACE reduction, which suggests that lipoprotein(a) should be an independent treatment target after ACS. (ODYSSEY Outcomes: Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab; NCT01663402)

Published
2020

5. Alirocumab and Cardiovascular Outcomes after Acute Coronary Syndrome

Author

Schwartz, G. G., Steg, P. G., Szarek, M., Bhatt, D. L., Bittner, V. A., Diaz, R., Edelberg, J. M., Goodman, S. G., Hanotin, C., Harrington, R. A., Jukema, J. W., Lecorps, G., Mahaffey, K. W., Moryusef, A., Pordy, R., Quintero, K., Roe, M. T., Sasiela, W. J., Tamby, J. -F., Tricoci, P., White, H. D., Zeiher, A. M., Aylward, Philip E., Drexel, Heinz, Sinnaeve, Peter, Dilic, Mirza, Lopes, Renato D., Gotcheva, Nina N., Goodman, Shaun G., Prieto, Juan-Carlos, Yong, Huo, Lopez-Jaramillo, Patricio, Pecin, Ivan, Reiner, Zeljko, Ostadal, Petr, Poulsen, Steen Hvitfeldt, Viigimaa, Margus, Nieminen, Markku S., Danchin, Nicolas, Chumburidze, Vakhtang, Marx, Nikolaus, Liberopoulos, Evangelos, Montenegro Valdovinos, Pablo Carlos, Tse, Hung-Fat, Kiss, Robert Gabor, Xavier, Denis, Zahger, Doron, Valgimigli, Marco, Kimura, Takeshi, Kim, Hyo Soo, Kim, Sang-Hyun, Erglis, Andrejs, Laucevicius, Aleksandras, Kedev, Sasko, Yusoff, Khalid, Ramos Lopez, Gabriel Arturo, Alings, Marco, Halvorsen, Sigrun, Correa Flores, Roger M., Sy, Rody G., Budaj, Andrzej, Morais, Joao, Dorobantu, Maria, Karpov, Yuri, Ristic, Arsen D., Chua, Terrance, Murin, Jan, Fras, Zlatko, Dalby, Anthony J., Tunon, Jose, de Silva, H. Asita, Hagstrom, Emil, Muller, Christian, Chiang, Chern-En, Sritara, Piyamitr, Guneri, Sema, Parkhomenko, Alexander, Ray, Kausik K., Moriarty, Patrick M., Vogel, Robert, Chaitman, Bernard, Kelsey, Sheryl F., Olsson, Anders G., Rouleau, Jean-Lucien, Simoons, Maarten L., Alexander, Karen, Meloni, Chiara, Rosenson, Robert, Sijbrands, Eric J. G., Alexander, John H., Armaganijan, Luciana, Bagai, Akshay, Bahit, Maria Cecilia, Brennan, J. Matthew, Clifton, Shaun, DeVore, Adam D., Deloatch, Shalonda, Dickey, Sheila, Dombrowski, Keith, Ducrocq, Gregory, Eapen, Zubin, Endsley, Patricia, Eppinger, Arleen, Hess, Connie Ng, Hlatky, Mark A., Jordan, Joseph Dedrick, Knowles, Joshua W., Kolls, Bradley J., Kong, David F., Leonardi, Sergio, Lillis, Linda, Maron, David J., Marcus, Jill, Mathews, Robin, Mehta, Rajendra H., Mentz, Robert J., Moreira, Humberto Graner, Patel, Chetan B., Pereira, Sabrina Bernardez, Perkins, Lynn, Povsic, Thomas J., Puymirat, Etienne, Jones, William Schuyler, Shah, Bimal R., Sherwood, Matthew W., Stringfellow, Kenya, Sujjavanich, Darin, Toma, Mustafa, Trotter, Charlene, van Diepen, Sean F. P., Wilson, Matthew D., Yan, Andrew Tze-Kay, Schiavi, Lilia B., Garrido, Marcelo, Alvarisqueta, Andres F., Sassone, Sonia A., Bordonava, Anselmo P., Alves De Lima, Alberto E., Schmidberg, Jorge M., Duronto, Ernesto A., Caruso, Orlando C., Novaretto, Leonardo P., Angel Hominal, Miguel, Montana, Oscar R., Caccavo, Alberto, Gomez Vilamajo, Oscar A., Lorenzatti, Alberto J., Cartasegna, Luis R., Paterlini, Gustavo A., Mackinnon, Ignacio J., Caime, Guillermo D., Amuchastegui, Marcos, Codutti, Oscar R., Jure, Horacio O., Bono, Julio O. E., Hrabar, Adrian D., Vallejos, Julio A., Ahuad Guerrero, Rodolfo A., Novoa, Federico, Patocchi, Cristian A., Zaidman, Cesar J., Giuliano, Maria E., Dran, Ricardo D., Vico, Marisa L., Carnero, Gabriela S., Guzman, Pablo N., Medrano Allende, Juan C., Garcia Brasca, Daniela F., Bustamante Labarta, Miguel H., Nani, Sebastian, Blumberg, Eduardo D. S., Colombo, Hugo R., Liberman, Alberto, Luciardi, Hector L., Waisman, Gabriel D., Berli, Mario A., Garcia Duran, Ruben O., Cestari, Horacio G., Luquez, Hugo A., Giordano, Jorge A., Saavedra, Silvia S., Waites, Jonathon H., Collins, Nicholas, Soward, Allan, Hii, Chris L. S., Shaw, James, Arstall, Margaret A., Horowitz, John, Rogers, James F., Colquhoun, David, Flores, Romulo E. Oqueli, Roberts-Thomson, Philip, Raffel, Owen, Lehman, Sam J., Coverdale, Steven G. M., Garrahy, Paul J., Starmer, Gregory, Sader, Mark, Carroll, Patrick A., Zweiker, Robert, Hoppe, Uta, Huber, Kurt, Berger, Rudolf, Weidinger, Franz, Faes, Dirk, Hermans, Kurt, Pirenne, Bruno, Leone, Attilio, Hoffer, Etienne, Vrolix, Mathias C. M., De Wolf, Luc, Wollaert, Bart, Castadot, Marc, Dujardin, Karl, Beauloye, Christophe, Vervoort, Geert, Striekwold, Harry, Convens, Carl, Roosen, John, Barbato, Emanuele, Claeys, Marc J., Cools, Frank, Terzic, Ibrahim, Barakovic, Fahir, Midzic, Zlatko, Pojskic, Belma, Fazlibegovic, Emir, Durak-Nalbantic, Azra, Vulic, Dusko, Muslibegovic, Adis, Reis, Gilmar, Sousa, Luciano, Nicolau, Jose C., Giorgeto, Flavio E., Silva, Ricardo P., Maia, Lilia Nigro, Rech, Rafael, Rossi, Paulo R. F., Cerqueira, Maria Jose A. G., Duda, Norberto, Kalil, Renato, Kormann, Adrian, Abrantes, Jose Antonio M., Pimentel Filho, Pedro, Soggia, Ana Priscila, de Santos, Mayler O. N., Neuenschwander, Fernando, Bodanese, Luiz C., Michalaros, Yorghos L., Eliaschewitz, Freddy G., Vidotti, Maria H., Leaes, Paulo E., Botelho, Roberto V., Kaiser, Sergio, Fernandes Manenti, Euler Roberto F., Precoma, Dalton B., Moura Jorge, Jose C., de Silva, Pedro G. M. B., Silveira, Jose A., Saporito, Wladimir, Marin Neto, Jose A., Feitosa, Gilson S., Ritt, Luiz Eduardo F., de Souza, Juliana A., Costa, Fernando, Souza, Weimar K. S. B., Reis, Helder J. L., Machado, Leandro, Aidar Ayoub, Jose Carlos, Todorov, Georgi V., Nikolov, Fedya P., Velcheva, Elena S., Tzekova, Maria L., Benov, Haralambi O., Petranov, Stanislav L., Tumbev, Haralin S., Shehova-Yankova, Nina S., Markov, Dimitar T., Raev, Dimitar H., Mollov, Mihail N., Kichukov, Kostadin N., Ilieva-Pandeva, Katya A., Ivanova, Raya, Mincheva, Valentina M., Lazov, Petar V., Dimov, Bojidar I., Senaratne, Manohara, Stone, James, Kornder, Jan, Pearce, Stephen, Dion, Danielle, Savard, Daniel, Pesant, Yves, Pandey, Amritanshu, Robinson, Simon, Gosselin, Gilbert, Vizel, Saul, Hoag, Gordon, Bourgeois, Ronald, Morisset, Anne, Sabbah, Eric, Sussex, Bruce, Kouz, Simon, MacDonald, Paul, Diaz, Ariel, Michaud, Nicolas, Fell, David, Leung, Raymond, Vuurmans, Tycho, Lai, Christopher, Nigro, Frank, Davies, Richard, Nogareda, Gustavo, Vijayaraghavan, Ram, Ducas, John, Lepage, Serge, Mehta, Shamir, Cha, James, Dupuis, Robert, Fong, Peter, Rodes-Cabau, Josep, Fadlallah, Hussein, Cleveland, David, Huynh, Thao, Bata, Iqbal, Hameed, Adnan, Pincetti, Cristian, Potthoff, Sergio, Acevedo, Monica, Aguirre, Arnoldo, Vejar, Margarita, Yanez, Mario, Araneda, Guillermo, Fernandez, Mauricio, Perez, Luis, Varleta, Paola, Florenzano, Fernando, Huidobro, Laura, Raffo, Carlos A., Olivares, Claudia, Chen, Jiyan, Dong, Yugang, Huang, Weijian, Wang, Jianzhong, Huang, Shi'An, Yao, Zhuhua, Cui, Lan, Lin, Wenhua, Sun, Yuemin, Wang, Jingfeng, Li, Jianping, Zhang, Xuelian, Zhu, Hong, Chen, Dandan, Huang, Lan, Dong, Shaohong, Su, Guohai, Xu, Biao, Su, Xi, Cheng, Xiaoshu, Lin, Jinxiu, Zong, Wenxia, Li, Huanming, Feng, Yi, Xu, Dingli, Yang, Xinchun, Ke, Yuannan, Lin, Xuefeng, Zhang, Zheng, Zheng, Zeqi, Luo, Zhurong, Chen, Yundai, Ding, Chunhua, Zheng, Yang, Li, Xiaodong, Peng, Daoquan, Li, Ying, Wei, Meng, Liu, Shaowen, Yu, Yihua, Qu, Baiming, Jiang, Weihong, Zhou, Yujie, Zhao, Xingsheng, Yuan, Zuyi, Guo, Ying, Xu, Xiping, Shi, Xubo, Ge, Junbo, Fu, Guosheng, Bai, Feng, Fang, Weiyi, Shou, Xiling, Yang, Xiangjun, Wang, Jian'An, Jaramillo, Nicolas, Vallejo, Gregorio Sanchez, Botia, Diana C. Luna, Lopez, Rodrigo Botero, De Salazar, Dora I. Molina, Bonfanti, Alberto J. Cadena, Higuera, Juan Diego, Silva, Sandra I. Barrera, Lozada, Henry J. Garcia, Arroyo, Julian A. Coronel, Mendoza, Jose L. Accini, Ruiz, Ricardo L. Fernandez, Fernandez, Angela M., Jatin, Fernando G. Manzur, Herazo, Aristides Sotomayor, Parada, Jeffrey Castellanos, Triana, Miguel A. Urina, Spinar, Jindrich, Horak, David, Stasek, Josef, Alan, David, Machova, Vilma, Linhart, Ales, Novotny, Vojtech, Kaucak, Vladimir, Rokyta, Richard, Naplava, Robert, Coufal, Zdenek, Adamkova, Vera, Podpera, Ivo, Zizka, Jiri, Motovska, Zuzana, Marusincova, Ivana, Svab, Premysl, Heinc, Petr, Kuchar, Jiri, Povolny, Petr, Raungaard, Bent, Clemmensen, Peter, Bang, Lia E., May, Ole, Bottcher, Morten, Hove, Jens D., Frost, Lars, Gislason, Gunnar, Larsen, John, Johansen, Peter Betton, Hald, Flemming, Jeppesen, Jorgen, Nielsen, Tonny, Kristensen, Kjeld S., Walichiewicz, Piotr Maria, Lomholdt, Jens D., Klausen, Ib C., Nielsen, Peter Kaiser, Davidsen, Flemming, Videbaek, Lars, Soots, Mai, Vahula, Veiko, Hedman, Anu, Soopold, sllar, Martsin, Kaja, Taskinen, Marja-Riitta, Porthan, Kimmo, Airaksinen, Juhani K., Juonala, Markus, Kiviniemi, Tuomas, Vikman, Saila, Posio, Pirjo, Taurio, Jyrki, Huikuri, Heikki, Kaikkonen, Kari, Coste, Pierre, Ferrari, Emile, Morel, Olivier, Montalescot, Gilles, Barone-Rochette, Gilles, Mansourati, Jacques, Cottin, Yves, Steg, Philippe Gabriel, Leclercq, Florence, Belhassane, Abdelkader, Delarche, Nicolas, Boccara, Franck, Paganelli, Franck, Clerc, Jerome, Schiele, Francois, Aboyans, Victor, Probst, Vincent, Berland, Jacques, Lefevre, Thierry, Khintibidze, Irakli, Shaburishvili, Tamaz, Pagava, Zurab, Ghlonti, Ramaz, Lominadze, Zaza, Khabeishvili, George, Hemetsberger, Rayyan, Rauch-Kroehnert, Ursula, Stratmann, Matthias, Appel, Karl-Friedrich, Schmidt, Ekkehard, Omran, Heyder, Stellbrink, Christoph, Dorsel, Thomas, Lianopoulos, Emmanouil, Marx, Roger, Zirlik, Andreas, Schellenberg, Detlev, Heitzer, Thomas, Laufs, Ulrich, Gielen, Stephan, Winkelmann, Bernhard, Behrens, Steffen, Sydow, Karsten, Simonis, Gregor, Muenzel, Thomas, Werner, Nikos, Leggewie, Stefan, Boecker, Dirk, Braun-Dullaeus, Ruediger, Toursarkissian, Nicole, Jeserich, Michael, Weissbrodt, Matthias, Schaeufele, Tim, Weil, Joachim, Voeller, Heinz, Waltenberger, Johannes, Natour, Mohammed, Steiner, Stephan, Heidenreich, Lothar, Gremmler, Uwe, Killat, Holger, Patsilinakos, Sotiris, Kartalis, Athanasios, Manolis, Athanassios, Sionis, Dimitrios, Skoumas, Ioannis, Athyros, Vasilios, Parthenakis, P. I. Frangkiskos, Hahalis, P. I. Georgios, Lekakis, John, Xatzitolios, Apostolos, Fausto Ovando, Sergio R., Arango Benecke, Juan L., Rodriguez De Leon, Edgar R., Yan, Bryan P. Y., Siu, David C. W., Turi, Tibor, Merkely, Bela, Ungi, Imre, Lupkovics, Geza, Nagy, Lajos, Katona, Andras, Edes, Istvan, Muller, Gabor, Horvath, Ivan, Kapin, Tibor, Falukozy, Jozsef, Kumbla, Mukund, Sandhu, Manjinder, Annam, Sharath, Proddutur, Naveen Reddy, Premchand, Rajendra K., Mahajan, Ajaykumar, Abhyanakar, Atul D., Kerkar, Prafulla, Govinda, Ravishankar A., Oomman, Abraham, Sinha, Dhurjati, Patil, Sachin N., Kahali, Dhiman, Sawhney, Jitendra, Joshi, Abhijeet B., Chaudhary, Sanjeev, Harkut, Pankaj, Guha, Santanu, Porwal, Sanjay, Jujjuru, Srimannarayana, Pothineni, Ramesh B., Monteiro, Minguel R., Khan, Aziz, Iyengar, Shamanna S., Grewal, Jasprakash Singh, Chopda, Manoj, Fulwani, Mahesh C., Patange, Aparna, Chopra, Vijay K., Goyal, Naresh K., Shinde, Rituparna, Manakshe, Gajendra V., Patki, Nitin, Sethi, Sumeet, Munusamy, Vengatesh, Karna, Sunil, Adhyapak, Srilakshmi, Pandurangi, Ulhas, Mathur, Rishabh, Kalashetti, Suhas, Bhagwat, Ajit, Raghuraman, Bagirath, Yerra, Shiv Kumar, Bhansali, Prasant, Borse, Rohidas, Das, Srihari, Abdullakutty, Jabir, Saathe, Shireesh, Palimkar, Priya, Atar, Shaul, Shechter, Michael, Mosseri, Morris, Arbel, Yaron, Lotan, Chaim, Rosenschein, Uri, Katz, Amos, Henkin, Yaakov, Francis, Adi, Klutstein, Marc, Nikolsky, Eugenia, Turgeman, Yoav, Halabi, Majdi, Kornowski, Ran, Jonas, Michael, Amir, Offer, Rozenman, Yoseph, Fuchs, Shmuel, Hussein, Osamah, Gavish, Dov, Vered, Zvi, Caraco, Yoseph, Elias, Mazen, Tov, Naveh, Piovaccari, Giancarlo, De Pellegrin, Annamaria, Guardigli, Gabriele, Licciardello, Giovanni, Auguadro, Carla, Cuccia, Claudio, Salvioni, Alessandro, Musumeci, Giuseppe, Calabro, Paolo, Novo, Salvatore, Faggiano, Pompilio, De Cesare, Nicoletta B., Berti, Sergio, Cavallini, Claudio, Puccioni, Enrico, Galvani, Marcello, Tespili, Maurizio, Piatti, Piermarco, Palvarini, Michela, De Luca, Giuseppe, Violini, Roberto, De Leo, Alessandro, Filardi, Pasquale Perrone, Ferratini, Maurizio, Dai, Kazuoki, Kamiya, Haruo, Ando, Kenji, Takeda, Yoshihiro, Morino, Yoshihiro, Hata, Yoshiki, Kimura, Kazuo, Kishi, Koichi, Michishita, Ichiro, Uehara, Hiroki, Higashikata, Toshinori, Hirayama, Atsushi, Hirooka, Keiji, Sakagami, Satoru, Taguchi, Shuichi, Koike, Akihiro, Fujinaga, Hiroyuki, Koba, Shinji, Kozuma, Ken, Kawasaki, Tomohiro, Ono, Yujiro, Shimizu, Masatoshi, Katsuda, Yousuke, Wada, Atsuyuki, Shinke, Toshiro, Ako, Junya, Fujii, Kenshi, Takahashi, Toshiyuki, Sakamoto, Tomohiro, Furukawa, Yutaka, Sugino, Hiroshi, Mano, Toshiaki, Utsu, Noriaki, Ito, Kashima, Haraguchi, Takuya, Ueda, Yasunori, Nishibe, Akira, Fujimoto, Kazuteru, Yoon, Jung Han, Park, Hun Sik, Chae, In-Ho, Kim, Moo Hyun, Jeong, Myung Ho, Rha, Seungwoon, Kim, Chongjin, Hong, Taekjong, Busmane, Arija, Pontaga, Natalija, Strelnieks, Aldis, Mintale, Iveta, Sime, Iveta, Petrulioniene, Zaneta, Kavaliauskiene, Roma, Jurgaitiene, Ruta, Sakalyte, Gintare, Slapikas, Rimvydas, Norkiene, Sigute, Misonis, Nerijus, Kibarskis, Aleksandras, Kubilius, Raimondas, Bojovski, Stojko, Lozance, Nensi, Kjovkaroski, Aleksandar, Doncovska, Snezana, Ong, Tiong Kiam, Kasim, Sazzli, Maskon, Oteh, Kandasamy, Balachandran, Liew, Houng B., Mohamed, Wan Mohd Izani Wan, Garcia Castillo, Armando, Carrillo Calvillo, Jorge, Fajardo Campos, Pedro, Nunez Fragoso, Juan Carlos, Bayram Llamas, Edmundo Alfredo, Alcocer Gamba, Marco Antonio, Carranza Madrigal, Jaime, Gonzalez Salas, Luis Gerardo, Lopez Rosas, Enrique, Gonzalez Diaz, Belinda, Salcido Vazquez, Eduardo, Nacoud Ackar, Alfredo, Llamas Esperon, Guillermo Antonio, Martinez Sanchez, Carlos Rodolfo, Guerrero De Leon, Maria, Suarez Otero, Rodrigo, Fanghanel Salmon, Guillermo, Perez Rios, Jesus Antonio, Garza Ruiz, Jose Angel, Breedveld, Robert W., Hoogslag, Pieter A. M., Suryapranata, Harry, Oomen, Antonius, Wiersma, Jacobijne J., Van Der Wal, Ruud M. A., Van Huysduynen-Monraats, Pascalle S. Hooft, Karalis, Ioannis, Verdel, Gerardus J. E., Brueren, Bart R. G., Troquay, Roland P. Th, Viergever, Eric P., Al-Windy, Nadea Y. Y., Bartels, Gerard L., Cornel, Jan H., Hermans, Walter R. M., Herrman, Johannes P. R., Bos, Robert J., Groutars, Reginald G. E. J., Van Der Zwaan, Coenraad C., Kaplan, Refik, Ronner, Eelko, Groenemeijer, Bjorn E., Bronzwaer, Patrick N. A., Liem, Anho A. H., Rensing, Bernard J. W. M., Bokern, Marcel J. J. A., Nijmeijer, Remco, Hersbach, Ferry M. R. J., Willems, Frank F., Gosselink, Antonius T. M., Elliott, John, Wilkins, Gerard, Fisher, Raewyn, Scott, Douglas, Hart, Hamish, Stewart, Ralph, Harding, Scott, Ternouth, Ian, Fisher, Nicholas, Aitken, Denise, Anscombe, Russell, Tomala, Tadeusz, Nygard, Ottar, Sparby, Jon Arne, Andersen, Kjell, Gullestad, Lars, Jortveit, Jarle, Munk, Peter S., Hurtig, Ulf, Ticona, Jorge R. Calderon, Velasquez, Julio R. Durand, Miguel, Sandra A. Negron, Perez, Enrique S. Sanabria, Chambilla, Jesus M. Carrion, Ayala, Carlos A. Chavez, Leon, Reynaldo P. Castillo, Gonzales, Rolando J. Vargas, Zuniga, Jose D. Hernandez, Cosavalente, Luis A. Camacho, Mannucci, Jorge E. Bravo, Navarro, Nassip C. Llerena, Concha, Yudy M. Roldan, Chavez, Victor E. Rodriguez, Hernandez, Henry A. Anchante, Nunez, Carlos A. Zea, Ferrolino, Arthur, Sy, Rosa Allyn G., Tirador, Louie, Matiga, Generoso, Coching, Raul Martin, Bernan, Alisa, Rogelio, Gregorio, Morales, Dante D., Tan, Edgar, Wlodarczak, Adrian, Jaworska, Krystyna, Skonieczny, Grzegorz, Pawlowicz, Lidia, Wojewoda, Pawel, Busz-Papiez, Benita, Bednarski, Janusz, Goch, Aleksander, Staneta, Pawel, Dulak, Elzbieta, Saminski, Krzysztof, Krasowski, Wlodzimierz, Sudnik, Wanda, Zurakowski, Aleksander, Skorski, Marcin, Lysek, Roman, Miklaszewicz, Beata, Kubica, Jacek, Lipko, Jan Andrzej, Kostarska-Srokosz, Edyta, Piepiorka, Marek, Drzewiecka, Anna, Sciborski, Ryszard, Stasiewski, Arkadiusz, Blicharski, Tomasz, Bystryk, Leszek, Szpajer, Michal, Korol, Marek, Czerski, Tomasz, Mirek-Bryniarska, Ewa, Gniot, Jacek, Lubinski, Andrzej, Gorny, Jerzy, Franek, Edward, Monteiro, Pedro, Bastos, Jose Mesquita, Pereira, Helder H., Martins, Dinis, Seixo, Filipe, Mendonca, Carlos, Botelho, Ana, Minescu, Bogdan, Istratoaie, Octavian, Tesloianu, Dan N., Cristian, Gabriel, Podoleanu, Cristian G. C., Constantinescu, Mircea C. A., Bengus, Cristina M., Militaru, Constantin, Rosu, Doina, Parepa, Irinel R., Matei, Adrian V., Alexandru, Tom M., Shvarts, Yury, Orlikova, Olga, Kobalava, Zhanna, Barbarash, Olga L., Markov, Valentin, Lyamina, Nadezhda, Gordienko, Alexander, Zrazhevsky, Konstantin, Vishnevsky, Alexander Y., Gurevich, Victor, Stryuk, Raisa, Lomakin, Nikita V., Bokarev, Igor, Shalaev, Sergey, Khaisheva, Larisa, Chizhov, Petr, Viktorova, Inna, Osokina, Natalya, Akatova, Evgenia, Chumakova, Galina, Libov, Igor, Voevoda, Mikhail I., Tretyakova, Tatyana V., Baranov, Evgeny, Shustov, Sergey, Yakushin, Sergey, Gordeev, Ivan, Khasanov, Niiaz, Reshetko, Olga, Sotnikova, Tatiana, Molchanova, Olga, Nikolaev, Konstantin, Gapon, Liudmila, Baranova, Elena, Shogenov, Zaur, Kosmachova, Elena, Karpov, Yuriy, Povzun, Anton, Egorova, Liudmila, Tyrenko, Vadim V., Ivanov, Igor G., Simic, Dragan, Ivanovic, Nikola, Davidovic, Goran, Tasic, Nebojsa, Asanin, Milika R., Stojic, Stevo, Apostolovic, Svetlana R., Ilic, Stevan, Putnikovic, Biljana, Stankovic, Aleksandar, Arandjelovic, Aleksandra, Radovanovic, Slavica, Balinovac, Jovan, Dincic, Dragan V., Seferovic, Petar, Dodic, Slobodan, Dimkovic, Sinisa, Poh, Kian-Keong, Ong, Hean Yee, Micko, Karol, Nociar, Jan, Pella, Daniel, Fulop, Peter, Hranai, Marian, Palka, Juraj, Mazur, Juraj, Majercak, Ivan, Dzupina, Andrej, Fazekas, Frantisek, Gonsorcik, Jozef, Bugan, Viliam, Selecky, Juraj, Kamensky, Gabriel, Strbova, Jaroslava, Smik, Rudolf, Dukat, Andrej, Zuran, Ivan, Oklukar, Janez, Suligoj, Natasa Cernic, Cevc, Matija, Lipar, Luka, Cyster, Henry P., Ranjith, Naresh, Corbett, Clive, Bayat, Junaid, Makotoko, Ellen Makoali, Kapp, Ilse E., de Basson, Matthys M. V., Lottering, Hanlie, Van Zyl, Louis J., Sebastian, Peter J., Pillay, Thayabran, Saaiman, Jan A., Commerford, Patrick J., Cassimjee, Soraya, Ebrahim, Iftikhar O., Sarvan, Mahomed, Mynhardt, Joseph H., Reuter, Helmuth, Moodley, Rajendran, Vida, Manuel, Cequier Fillat, Angel R., Bodi Peris, Vicente, Fuentes Jimenez, Francisco, Marin, Francisco, Cruz Fernandez, Jose M., Gil-Extremera, Blas, Worner Diz, Fernando, Garcia-Dorado, David, Iniguez, Andres, Tunon Fernandez, Jose, Gonzalez-Juanatey, Jose R., Fernandez Portales, Javier, Civeira Murillo, Fernando, Matas Pericas, Laia, Luis Zamorano, Jose, De Mora Martin, Manuel, Bruguera Cortada, Jordi, Alonso Martin, Joaquin J., De Berrazueta Fernandez, Jose R., Diaz Fernandez, Jose Francisco, Garcia Lledo, Jose Alberto, Cosin Sales, Juan, Botas Rodriguez, Javier, Gusi Tragant, Gabriel, Benedicto, Amparo, Gonzalez-Juanatey, Carlos, Camprubi Potau, Mercedes, Plaza Perez, Ignacio, Moris De La Tassa, Cesar, Loma-Osorio Rincon, Pablo, Balaguer Recena, Javier, M Escudier, Juan, Constantine, Godwin, Haniffa, Ruvaiz, Tissera, Nirmali, Amarasekera, Stanley, Fernando, Nimali, Jayawardena, Jayanthimala, Santharaj, Wijeyasingam, Ekanayaka, Ruvan, Mendis, Sepalika, Senaratne, Vajira, Mayurathan, Gnanamoorthy, Sirisena, Thilak, Rajapaksha, Ajantha, Herath, Jagath I., Amarasena, Naomali, Berglund, Stefan, Rasmanis, Gundars, Witt, Nils, Mourtzinis, Georgios, Nicol, Peter, Hansen, Ole, Romeo, Stefano, Jensen, Steen Agergaard, Torstensson, Ingemar, Ahremark, Ulf, Sundelin, Torbjorn, Moccetti, Tiziano, Mueller, Christian, Mach, Francois, Binder, Ronald, Tsai, Wei-Chuan, Ueng, Kwo-Chang, Lai, Wen-Ter, Liu, Ming-En, Hwang, Juey-Jen, Yin, Wei-Hsian, Hsieh, I-Chang, Lin, Wei Hsiang, Kuo, Jen-Yuan, Huang, Tsuei-Yuan, Fang, Chih-Yuan, Kaewsuwanna, Pinij, Soonfuang, Wasant, Jintapakorn, Woravut, Sukonthasarn, Apichard, Wongpraparut, Nattawut, Sastravaha, Krisada, Sansanayudh, Nakarin, Kehasukcharoen, Wirash, Piyayotai, Dilok, Camsari, Ahmet, Kultursay, Hakan, Mutlu, Bulent, Ersanli, Murat, Demirtas, Mustafa, Kirma, Cevat, Ural, Ertan, Koldas, Lale, Karpenko, Oleksandr, Prokhorov, Alexander, Vakaluyk, Ihor, Myshanych, Halyna, Reshotko, Dmytro, Batushkin, Valeriy, Rudenko, Leonid, Kovalskyi, Ihor, Kushnir, Mykola, Tseluyko, Vira, Mostovoy, Yuriy, Stanislavchuk, Mykola, Kyiak, Yulian, Karpenko, Yuriy, Malynovsky, Yaroslav, Klantsa, Andriy, Kutniy, Oles, Amosova, Ekaterina, Tashchuk, Viktor, Leshchuk, Oleh, Rishko, Mykola, Kopytsya, Mykola, Yagensky, Andriy, Vatutin, Mykola, Bagriy, Andriy, Barna, Olga M., Ushakov, Olexiy, Dzyak, Georgiy, Goloborodko, Borys, Rudenko, Anatolii, Trevelyan, Jasper, Zaman, Azfar, Lee, Kaeng, Moriarty, Andrew, Aggarwal, Rajesh K., Clifford, Piers, Wong, Yuk-Ki, Iqbal, Syed M. R., Subkovas, Eduardas, Braganza, Denise, Sarkar, David, Storey, Robert, Griffiths, Huw, Mcclure, Sam, Muthusamy, Rangasamy, Kurian, John, Levy, Terry, Barr, Craig, Kadr, Honer, Gerber, Robert, Simaitis, Audrius, Soran, Handrean, Mathur, Anthony, Brodison, Adrian, Oliver, Richard, Mudawi, Telal, Reynolds, Timothy, Sharman, David, Butler, Rob, Wilkinson, Peter, Lip, Gregory Y. H., Halcox, Julian, Vardi, Gil, Baldari, Duccio, Brabham, David, Treasure, Charles, II, Dahl, Charles, Palmer, Bruce, Wiseman, Alan, Khan, Abul, Puri, Sanjeev, Mohart, Ann Elizabeth, Ince, Carlos, Flores, Enrique, Wright, Scott, Cheng, Shi-Chi, Rosenberg, Michael, Rogers, William, Jr., Kosinski, Edward, Forgosh, Les, Waltman, Jonathan, Khan, Misal, Shoukfeh, Mohammad, Dagher, Georges, Lieber, Ira, Kumar, Priya, East, Cara, Krichmar, Perry, White, Lindsey, Knickelbine, Thomas, Haldis, Thomas, Gillespie, Eve, Suh, David, Arif, Imran, Akhter, Faiq, Carlson, Eric, D'Urso, Michael, El-Ahdab, Fadi, Nelson, William, Harris, Barry, Cohen, Steven, Carter, Luther, Sabatino, Kenneth, Haddad, Tariq, Malik, Amir, Rao, Sunder, Mulkay, Angel, Jovin, Ion, Klancke, Kim, Malhotra, Vinay, Devarapalli, Sai K., Koren, Michael, Chandna, Harish, Dodds, George, III, Janik, Matthew, Moran, Joseph, Sumner, Andrew, Kobayashi, John, Davis, William, Yazdani, Shahram, Pasquini, John, Thakkar, Maitreya, Vedere, Amarnath, Leimbach, Wayne, Rider, James, Singh, Narendra, Shah, Anil V., Janosik, Denise, Pepine, Carl, Berman, Brett, Gelormini, Joseph, Daniels, Christopher, Keating, Friederike, Kondo, Nicholas I., Shetty, Sanjay, Waider, Winfried, Takata, Theodore, Abu-Fadel, Mazen, Shah, Vipul, Aggarwal, Rahul, Izzo, Mark, Kumar, Anil, Hattler, Brack, Link, Chad, Bortnick, Anna, Kinzfogl, George, III, Ghitis, Arnold, Larry, John, Teufel, Edward, Kuhlman, Peter, Mclaurin, Brent, Zhang, Wenwu, Thew, Stephen, Abbas, Jalal, White, Matthew, Ranadive, Nandkishore, Gring, Christian, Henderson, David, Schuchard, Timothy, Farhat, Naim, Kline, Geoffrey, Mahal, Sharan, Whitaker, Jack, Speirs, Shawn, Andersen, Rolf, Daboul, Nizar, Horwitz, Phillip, Jafar, Zubair, Mcgarvey, Joseph, Jr., Panchal, Vipul, Voyce, Stephen, Blok, Thomas, Sheldon, William, Azizad, Masoud M., Schmalfuss, Carsten, Picone, Mark, Herzog, William, Jr., Lindsey, Jason, Nowins, Rosemary, Lepor, Norman, El Shahawy, Mahfouz, Weintraub, Howard, Irimpen, Anand, May, Wade, Galski, Thomas, Chu, Alan, Mody, Freny, Hodes, Zachary, Fairlamb, James, Lambert, Charles, Jr., Raisinghani, Ajit, Abbate, Antonio, King, Marilyn, Carey, Charles, Gerber, Jaime, Younis, Liwa, Park, Hyeun (Tom), Vidovich, Mladen, Knutson, Thomas, Friedman, Dennis, Chaleff, Fred, Loussararian, Arthur, Kimmelstiel, Carey, Silver, Kevin, Foster, Malcolm, Tonnessen, Glen, Amlani, Mohamadali, Wali, Andreas, Malozzi, Christopher, Wattanakit, Keattiyoat, O'Donnell, Philip J., Singal, Dinesh, Jaffrani, Naseem, Banuru, Sridhar, Fisher, Daniel, Xenakis, Mark, Perlmutter, Neal, Bhagwat, Ravi, Strader, James, Jr., Akyea-Djamson, Ayim, Labroo, Ajay, Lee, Kwan, Marais, H. John, Claxton, Edmund, Jr., Berk, Martin, Rossi, Peter, Joshi, Parag, Khaira, Ajit S., Kumkumian, Greg, Lupovitch, Steven, Purow, Joshua, Welka, Stephen, Hoffman, David, Fischer, Stuart, Soroka, Eugene, Eagerton, Donald, Pancholy, Samir, Ray, Michael, Farrar, Michael, Pollock, Stewart, French, William J., Diamantis, Steve, Gimple, Lawrence, Schwartz, Steven, Pereira, Edward, Spriggs, Douglas, Strain, Janet, Vo, Anthony, Chane, Majed, Hall, Jason, Vijay, Nampalli, Lotun, Kapildeo, Lester, F. Martin, Nahhas, Ahed, Pope, Theodore, Nager, Paul, Vohra, Rakesh, Bashir, Riyaz, Ahmed, Hinan, Berlowitz, Michael, Fishberg, Robert, Barrucco, Robert, Yang, Eric, Radin, Michael, Sporn, Daniel, Eisenberg, Steven, Landzberg, Joel, Mcgough, Martin, Turk, Samir, Schwartz, Michael, Sundram, P. Sandy, Jain, Diwakar, Zainea, Mark, Bayron, Carlos, Karlsberg, Ronald, Lui, Henry, Keen, William, Westerhausen, Donald, Jr., Khurana, Sandeep, Agarwal, Himanshu, Birchem, Jessica, Penny, William, Jr., Chang, Mark, Gilbert, John M., Chalavarya, Gopal, Eaton, Charles, Schmedtje, John F., Jr., Christenson, Stuart, Denham, Douglas, Macdonell, Alexander, Gibson, Paul, Rahman, Aref, Al Joundi, Tammam, Conrad, Gary, Kotha, Purushotham, Love, Michael, Giesler, Gregory, Rubenstein, Howard, Akright, Laura, Schifferdecker, Branislav, Krawczyk, Justine, Wells, Terry, Welker, James, Foster, Robert, Gilmore, Richard, Anderson, Jay, Jacoby, Douglas, Harris, Bill, Gardner, Geraldine, Dandillaya, Ramprasad, Vora, Kishor, Kostis, John, Hunter, John, Laxson, David, Ball, Eric, Internal Medicine, ODYSSEY OUTCOMES Comm Inv, VA Boston Healthcare System, Department of General Surgery. Surgical Oncology Unit, Reina Sofía University Hospital, Metacohorts Consortium, Sanofi [Vitry-sur-Seine], SANOFI Recherche, CIC Brest, Université de Brest (UBO)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Hôpital de la Cavale Blanche, University of Zurich, and Schwartz, Gregory G

Subjects
Adult, Male, medicine.medical_specialty, Acute coronary syndrome, Evinacumab, [SDV]Life Sciences [q-bio], Vascular damage Radboud Institute for Health Sciences [Radboudumc 16], Hypercholesterolemia, 610 Medicine & health, 2700 General Medicine, 030204 cardiovascular system & hematology, Antibodies, Monoclonal, Humanized, Placebo, 11171 Cardiocentro Ticino, 03 medical and health sciences, 0302 clinical medicine, Double-Blind Method, [SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, Internal medicine, Humans, Medicine, 03.02. Klinikai orvostan, 030212 general & internal medicine, Myocardial infarction, Acute Coronary Syndrome, ComputingMilieux_MISCELLANEOUS, Aged, Alirocumab, business.industry, Unstable angina, Anticholesteremic Agents, PCSK9, PCSK9 Inhibitors, Hazard ratio, Antibodies, Monoclonal, Cholesterol, LDL, General Medicine, Middle Aged, ta3121, medicine.disease, 3. Good health, Cardiovascular Diseases, Cardiology, Female, Human medicine, business, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, Follow-Up Studies
Abstract

PubMed: 30403574, 2-s2.0-85057337718, BACKGROUND Patients who have had an acute coronary syndrome are at high risk for recurrent ischemic cardiovascular events. We sought to determine whether alirocumab, a human monoclonal antibody to proprotein convertase subtilisin-kexin type 9 (PCSK9), would improve cardiovascular outcomes after an acute coronary syndrome in patients receiving high-intensity statin therapy. METHODS We conducted a multicenter, randomized, double-blind, placebo-controlled trial involving 18,924 patients who had an acute coronary syndrome 1 to 12 months earlier, had a low-density lipoprotein (LDL) cholesterol level of at least 70 mg per deciliter (1.8 mmol per liter), a non-highdensity lipoprotein cholesterol level of at least 100 mg per deciliter (2.6 mmol per liter), or an apolipoprotein B level of at least 80 mg per deciliter, and were receiving statin therapy at a high-intensity dose or at the maximum tolerated dose. Patients were randomly assigned to receive alirocumab subcutaneously at a dose of 75 mg (9462 patients) or matching placebo (9462 patients) every 2 weeks. The dose of alirocumab was adjusted under blinded conditions to target an LDL cholesterol level of 25 to 50 mg per deciliter (0.6 to 1.3 mmol per liter). The primary end point was a composite of death from coronary heart disease, nonfatal myocardial infarction, fatal or nonfatal ischemic stroke, or unstable angina requiring hospitalization. RESULTS The median duration of follow-up was 2.8 years. A composite primary end-point event occurred in 903 patients (9.5%) in the alirocumab group and in 1052 patients (11.1%) in the placebo group (hazard ratio, 0.85; 95% confidence interval [CI], 0.78 to 0.93; P

Published
2018

6. Ticagrelor versus clopidogrel in patients with acute coronary syndromes intended for non-invasive management: substudy from prospective randomised PLATelet inhibition and patient Outcomes (PLATO) trial

Author

James, S. K., Roe, M. T., Cannon, C. P., Cornel, J. H., Horrow, J., Husted, S., Katus, H., Morais, J., Steg, P. G., Storey, R. F., Stevens, S., Wallentin, L., and Harrington, R. A.

Abstract

Objective To evaluate efficacy and safety outcomes in patients in the\ud PLATelet inhibition and patient Outcomes (PLATO) trial who at\ud randomisation were planned for a non-invasive treatment strategy.\ud Design Pre-specified analysis of pre-randomisation defined subgroup\ud of prospective randomised clinical trial.\ud Setting 862 centres in 43 countries.\ud Participants 5216 (28%) of 18 624 patients admitted to hospital for\ud acute coronary syndrome who were specified as planned for non-invasive\ud management.\ud Interventions Randomised treatment with ticagrelor (n=2601) versus\ud clopidogrel (2615).\ud Main outcome measurements Primary composite end point of\ud cardiovascular death, myocardial infarction, and stroke; their individual\ud components; and PLATO defined major bleeding during one year.\ud Results 2183 (41.9%) patients had coronary angiography during their\ud initial hospital admission, 1065 (20.4%) had percutaneous coronary\ud intervention, and 208 (4.0%) had coronary artery bypass surgery.\ud Cumulatively, 3143 (60.3%) patients had been managed non-invasively\ud by the end of follow-up. The incidence of the primary end point was lower\ud with ticagrelor than with clopidogrel (12.0% (n=295) v 14.3% (346);\ud hazard ratio 0.85, 95% confidence interval 0.73 to 1.00; P=0.04). Overall\ud mortality was also lower (6.1% (147) v 8.2% (195); 0.75, 0.61 to 0.93;\ud P=0.01). The incidence of total major bleeding (11.9% (272) v 10.3%\ud (238); 1.17, 0.98 to 1.39; P=0.08) and non-coronary artery bypass\ud grafting related major bleeding (4.0% (90) v 3.1% (71); 1.30, 0.95 to\ud 1.77; P=0.10) was numerically higher with ticagrelor than with clopidogrel.\ud Conclusions In patients with acute coronary syndrome initially intended\ud for non-invasive management, the benefits of ticagrelor over clopidogrel\ud were consistent with those from the overall PLATO results, indicating\ud the broad benefits of P2Y12 inhibition with ticagrelor regardless of\ud intended management strategy.\ud Trial registration Clinical trials NCT00391872.

Published
2011

15. Creatine kinase-MB elevation after coronary artery bypass grafting surgery in patients with non-ST-segment elevation acute coronary syndromes predict worse outcomes: results from four large clinical trials

Author

Mahaffey, K. W., primary, Roe, M. T., additional, Kilaru, R., additional, Alexander, J. H., additional, Van de Werf, F., additional, Califf, R. M., additional, Simoons, M. L., additional, Topol, E. J., additional, and Harrington, R. A., additional

Published
2007
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21. National treatment guidelines reduce hospital deaths.

Author

Peterson, E. D., Roe, M. T., and Mulgund, J.

Subjects
MEDICAL care, CORONARY heart disease treatment, PATIENTS, HOSPITALS, DEATH rate
Abstract

Claims that receiving care at a hospital with higher adherence to guidelines for treatment of patients with acute coronary syndromes (ACS) is associated with a decreased likelihood of in-hospital death, according to the April 26, 2006 "Journal of the American Medical Association." Results of the research.

Published
2006

22. Comparison of benefits and complications of hirudin versus heparin for patients with acute coronary syndromes undergoing early percutaneous coronary intervention.

Author

Roe, Matthew T., Granger, Christopher B., Puma, Joseph A., Hellkamp, Anne S., Hochman, Judith S., Ohman, E. Magnus, White, Harvey D., Van de Werf, Frans, Armstrong, Paul W., Ellis, Stephen G., Califf, Robert M., Topol, Eric J., Roe, M T, Granger, C B, Puma, J A, Hellkamp, A S, Hochman, J S, Ohman, E M, White, H D, and Van de Werf, F

Subjects
*ANTICOAGULANTS, *CORONARY heart disease treatment
Abstract

Evaluates the potential benefits of pretreatment with hirudin compared with heparin among patients with acute coronary syndrome (ACS) who undergo early percutaneous coronary intervention (PCI). Association of hirudin with a significant reduction in infarction and a trend for a reduced risk of death or reinfarction; Complementary therapeutic strategies for patients with ACS.

Published
2001
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23. Initial experience with multivessel percutaneous coronary intervention during mechanical reperfusion for acute myocardial infarction.

Author

Roe, Matthew T., Cura, Fernando A., Joski, Peter S., Garcia, Eulogio, Guetta, Victor, Kereiakes, Dean J., Zijlstra, Felix, Brodie, Bruce R., Grines, Cindy L., Ellis, Stephen G., Roe, M T, Cura, F A, Joski, P S, Garcia, E, Guetta, V, Kereiakes, D J, Zijlstra, F, Brodie, B R, Grines, C L, and Ellis, S G

Subjects
*MYOCARDIAL infarction, *ANGIOGRAPHY, *FIBRINOLYSIS
Abstract

The feasibility and safety of simultaneous multivessel percutaneous coronary intervention during mechanical reperfusion for acute myocardial infarction was analyzed in a retrospective, case-controlled study. Patients who underwent multivessel coronary intervention had a higher risk of adverse clinical outcomes through 6 months compared with matched controls in whom coronary intervention was limited to the infarct-related artery. [ABSTRACT FROM AUTHOR]

Published
2001
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24. Prognostic importance of concomitant heparin with eptifibatide in acute coronary syndromes. PURSUIT Investigators. Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy.

Author

Peterson, John G., Topol, Eric J., Roe, Matthew T., Sapp, Shelley K., Lincoff, A. Michael, Decker, Jaap W., Blackstone, Eugene H., Harrington, Robert A., Califf, Robert M., Lauer, Michael S., Peterson, J G, Topol, E J, Roe, M T, Sapp, S K, Lincoff, A M, Deckers, J W, Blackstone, E H, Harrington, R A, Califf, R M, and Lauer, M S

Subjects
*HEPARIN, *CORONARY disease
Abstract

Platelet glycoprotein IIb/IIIa inhibitors have been extensively studied in the treatment of patients with ischemic heart disease. Data regarding the use of these agents in the absence of concomitant intravenous heparin have been conflicting. We sought to determine, using propensity analysis, whether the benefit of eptifibatide, a IIb/IIIa inhibitor, in the treatment of acute coronary syndromes is affected by the concurrent administration of heparin. By trial design, patients were randomized to either eptifibatide or placebo, whereas use of intravenous heparin was left to the discretion of treating physicians. The effect of eptifibatide on the 30-day composite end point of death or myocardial infarction was studied in patients who received heparin and those who did not. Propensity analysis methods were used to control for confounding and presumed selection biases. Among 5,576 patients who were receiving heparin when the bolus dose of the study drug was administered, eptifibatide was associated with a reduced composite end point rate (13%) compared with that of placebo (14.5% vs 16.6%, p = 0.03). In contrast, among 1,441 patients who were not receiving heparin, there was no difference in 30-day event rates with eptifibatide compared with placebo (13.7% vs 13.1%, p > 0.7). After a propensity score for use of heparin was developed, however, use of heparin did not affect the reduced risk associated with eptifibatide (adjusted relative risk [RR] for heparin-eptifibatide interaction term 0.90, 95% confidence interval [CI] 0.61 to 1.32, p > 0.5), but the propensity for heparin use was a strong predictor of events (adjusted RR 1.76, 95% CI 1.42 to 2.17, p < 0.001). The use of eptifibatide independently predicted a lower risk of events (adjusted RR 0.31, 95% CI 0.10 to 0.93, p = 0.04). Thus, the apparent positive impact of heparin on the benefits of eptifibatide therapy was largely due to confounding and bias. [ABSTRACT FROM AUTHOR]

Published
2001
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25. Direct myocardial revascularization and angiogenesis--how many patients might be eligible?

Author

Mukherjee, Debabrata, Bhatt, Deepak L., Mukherjee, D, Bhatt, D L, Roe, M T, Patel, V, and Ellis, S G

Subjects
*CORONARY heart disease treatment, *MYOCARDIAL revascularization
Abstract

This study examines the proportion of patients with ischemic heart disease who may be candidates for the newer modalities of revascularization. A significant proportion (approximately 5%) of patients who undergo coronary angiography at tertiary referral centers may be eligible for newer methods of therapy. [ABSTRACT FROM AUTHOR]

Published
1999
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26. Trends in use of anti-thrombotic agents and outcomes in patients with non-ST-segment elevation myocardial infarction (NSTEMI) managed with an invasive strategy.

Author

Wayangankar SA, Roe MT, Chen AY, Gupta RS, Giugliano RP, Newby LK, de Lemos JA, Alexander KP, Sanborn TA, and Saucedo JF

Subjects
Antithrombins administration & dosage, Dose-Response Relationship, Drug, Electrocardiography, Female, Follow-Up Studies, Hemorrhage chemically induced, Hemorrhage epidemiology, Hospital Mortality trends, Humans, Incidence, Male, Middle Aged, Non-ST Elevated Myocardial Infarction diagnosis, Non-ST Elevated Myocardial Infarction mortality, Recombinant Proteins administration & dosage, Retrospective Studies, Time Factors, United States epidemiology, Angioplasty, Balloon, Coronary methods, Fibrinolytic Agents administration & dosage, Heparin, Low-Molecular-Weight administration & dosage, Hirudins administration & dosage, Non-ST Elevated Myocardial Infarction drug therapy, Peptide Fragments administration & dosage, Registries
Abstract

Objective: To analyze trends in utilization of anti-thrombotic agents (ATA) and in-hospital clinical outcomes in non-ST-elevation myocardial infarction (NSTEMI) patients managed with an invasive strategy from 2007 to 2010., Methods & Results: Using ACTION Registry(®)-GWTG™ data, we analyzed trends in use of ATA and in-hospital clinical outcomes among 64,199 NSTEMI patients managed invasively between 2007 and 2010. ATA included unfractionated heparin (UFH), low molecular weight heparin (LMWH), glycoprotein IIb/IIIa inhibitors (GPI) and bivalirudin. Although the proportion of NSTEMI patients treated with PCI within 48h of hospital arrival was similar in 2007 and 2010, percentage use of bivalirudin (13.4-27.3%; p<0.01) and UFH increased (60.0-67.5%, p<0.01), and that of GPI (62.3-41.0%; p<0.01) and LMWH (41.5-36.8%; p<0.01) declined. Excess dosing of UFH (75.9-59.3%, p<0.01), LMWH (9.6-5.2%; p<0.01) and GPI (8.9-5.9%, p<0.01) was also significantly lower in 2010 compared with 2007. Though in-hospital mortality rates were similar in 2007 and 2010 (2.3-1.9%, p=0.08), the rates of in-hospital major bleeding (8.7-6.6%, p<0.01) and non-CABG related RBC transfusion (6.3-4.6%, p<0.01) were significantly lower in 2010 compared with 2007., Conclusion: Compared with 2007, patients with NSTEMI, who were managed invasively in 2010 received GPI and LMWH less often and bivalirudin and UFH more frequently. There were sizeable reductions in the rates of excess dosing of UFH (though still occurred in 67% of patients), GPI and LMWH. In-hospital major bleeding complications and post-procedural RBC transfusion were lower in 2010 compared with 2007., (Copyright © 2015 Cardiological Society of India. Published by Elsevier B.V. All rights reserved.)

Published
2016
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27. Explaining the unexpected: insights from the PLATelet inhibition and clinical Outcomes (PLATO) trial comparing ticagrelor and clopidogrel. Editorial on Serebruany "Viewpoint: Paradoxical excess mortality in the PLATO trial should be independently verified" (Thromb Haemost 2011; 105.5).

Author

Ohman EM and Roe MT

Subjects
Adenosine therapeutic use, Clinical Trials as Topic, Clopidogrel, Epidemiologic Research Design, Europe, Humans, Patient Selection, Practice Guidelines as Topic, Statistics as Topic, Survival Analysis, Survival Rate, Ticagrelor, Ticlopidine therapeutic use, Treatment Outcome, United States, Acute Coronary Syndrome drug therapy, Acute Coronary Syndrome epidemiology, Acute Coronary Syndrome mortality, Adenosine analogs & derivatives, Ticlopidine analogs & derivatives
Published
2011
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28. Creatine kinase-MB elevation after percutaneous coronary intervention predicts adverse outcomes in patients with acute coronary syndromes.

Author

Roe MT, Mahaffey KW, Kilaru R, Alexander JH, Akkerhuis KM, Simoons ML, Harrington RA, Tardiff BE, Granger CB, Ohman EM, Moliterno DJ, Lincoff AM, Armstrong PW, Van de Werf F, Califf RM, and Topol EJ

Subjects
Acute Disease, Aged, Biomarkers blood, Coronary Disease mortality, Coronary Disease therapy, Creatine Kinase, MB Form, Female, Hospital Mortality, Humans, Male, Middle Aged, Multivariate Analysis, Patient Selection, Treatment Outcome, Coronary Disease enzymology, Creatine Kinase metabolism, Isoenzymes metabolism
Abstract

Aim: To study the relationship between outcomes and peak creatine kinase (CK)-MB levels after percutaneous coronary intervention (PCI) in patients with non-ST-segment elevation acute coronary syndromes (NSTE ACS)., Methods and Results: Peak CK-MB ratios (peak CK-MB level/upper limit of normal [ULN]) after PCI were analysed in 6164 patients with NSTE ACS from four randomized trials who underwent in-hospital PCI. We excluded 696 patients with elevated CK or CK-MB levels <24h before PCI; the primary analysis included 2384 of the remaining 5468 patients (43.6%) with CK-MB levels measured <==24h after PCI. The incidence of in-hospital heart failure (0.1%, 0.8%, 3.4%, 4.1%, and 6.1%; P<0.001), arrhythmias (0.8%, 1.9%, 6.9%, 4.1%, and 7.9%; P<0.001), cardiogenic shock (0.1%, 1.3%, 2.0%, 2.3%, and 2.6%; P=0.004), and mortality through 6 months (2.1%, 2.4%, 4.9%, 4.1%, and 5.7%, P=0.005) was increased with peak CK-MB ratios of 0-1, 1-3, 3-5, 5-10, and >10xULN, respectively. The continuous peak CK-MB ratio after PCI significantly predicted adjusted 6-month mortality (risk ratio, 1.06 per unit increase above ULN; 95% confidence interval, 1.01-1.11; P=0.017)., Conclusions: Greater CK-MB elevation after PCI is independently associated with adverse outcomes in NSTE ACS. These results underscore the adverse implications of elevated CK-MB levels after PCI in this high-risk population.

Published
2004
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29. Monitoring and identifying antibiotic resistance mechanisms in bacteria.

Author

Roe MT and Pillai SD

Subjects
Animal Husbandry methods, Animals, Chickens, Drug Resistance, Bacterial genetics, Drug Resistance, Bacterial physiology, Ecosystem, Humans, Microbial Sensitivity Tests, Poultry Products microbiology, Public Health, Bacteria drug effects, Bacteria genetics, Integrons physiology
Abstract

Sub-therapeutic administration of antibiotics to animals is under intense scrutiny because they contribute to the dissemination of antibiotic-resistant bacteria into the food chain. Studies suggest that there is a link between the agricultural use of antibiotics and antibiotic-resistant human infections. Antibiotic-resistant organisms from animal and human wastes reenter the human and animal populations through a number of pathways including natural waters, irrigation water, drinking water, and vegetables and foods. Antibiotic usage in the United States for animal production (disease prevention and growth promotion) is estimated to be 18 million pounds annually. As much as 25 to 75% of the antibiotics administered to feedlot animals are excreted unaltered in feces. Because about 180 million dry tons of livestock and poultry waste is generated annually in the United States, it is not surprising that animal-derived antibiotic-resistant organisms are found contaminating groundwater, surface water, and food crops. It is extremely important to clearly understand the molecular mechanisms that could potentially cause lateral or horizontal gene transfer of antibiotic resistance genes among bacteria. Once the mechanisms and magnitude of resistance gene transfer are clearly understood and quantified, strategies can be instituted to reduce the potential for dissemination of these genes.

Published
2003
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30. Clinical outcome of a cohort of patients eligible for therapeutic angiogenesis or transmyocardial revascularization.

Author

Mukherjee D, Comella K, Bhatt DL, Roe MT, Patel V, and Ellis SG

Subjects
Aged, Angiogenesis Inhibitors therapeutic use, Cohort Studies, Coronary Angiography, Female, Humans, Logistic Models, Male, Middle Aged, Patient Selection, Treatment Outcome, Coronary Disease therapy, Myocardial Revascularization methods
Abstract

Background: Newer methods of coronary revascularization are being investigated in patients who are not candidates for coronary artery bypass grafting or percutaneous intervention. Our objective was to determine the proportion of patients eligible for newer methods of revascularization and determine their 1-year clinical outcome., Methods: Five hundred consecutive charts and angiograms from patients undergoing diagnostic angiography for coronary artery disease from January to May of 1998 were reviewed to assess the suitability for revascularization. Patients ineligible for conventional revascularization were followed up for 1 year., Results: Fifty-nine patients of the 500 studied were identified who had refractory ischemia but were not candidates for traditional revascularization. The 59 patients ineligible for traditional methods of revascularization had a rehospitalization rate of 128% (76 total hospitalizations), a 25.5% rate of myocardial infarction (15 of 59), and a mortality rate of 16.9% (10 of 59)., Conclusions: The prognosis of many patients eligible for newer methods of revascularization on maximal medical therapy is poor.

Published
2001
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31. Effect of lipid-lowering therapy on early mortality after acute coronary syndromes: an observational study.

Author

Aronow HD, Topol EJ, Roe MT, Houghtaling PL, Wolski KE, Lincoff AM, Harrington RA, Califf RM, Ohman EM, Kleiman NS, Keltai M, Wilcox RG, Vahanian A, Armstrong PW, and Lauer MS

Subjects
Acute Disease, Aged, Angina, Unstable complications, Angina, Unstable drug therapy, Female, Humans, Hyperlipidemias complications, Logistic Models, Male, Middle Aged, Myocardial Infarction complications, Myocardial Infarction drug therapy, Randomized Controlled Trials as Topic, Survival Rate, Thrombolytic Therapy, Angina, Unstable mortality, Hypolipidemic Agents therapeutic use, Myocardial Infarction mortality
Abstract

Background: Lipid-lowering agents are known to reduce long-term mortality in patients with stable coronary disease or significant risk factors. However, the effect of lipid-lowering therapy on short-term mortality immediately after an acute coronary syndrome has not been determined. We did an observational study using data from two randomised trials to investigate this issue., Methods: We used data from the GUSTO IIb and PURSUIT trials to compare all-cause mortality among patients with acute coronary syndromes who were discharged on lipid-lowering agents (n=3653) with those who were not (n=17,156). A propensity analysis was done to adjust for presumed selection biases in the prescription of lipid-lowering agents., Findings: Lipid-lowering therapy was associated with a smaller proportion of deaths at 30 days (17 [0.5%] vs 179 [1.0%], hazard ratio 0.44 [95% CI 0.27-0.73], p=0.001) and at 6 months (63 [1.7%] vs 605 [3.5%], 0.48 [0.37-0.63], p<0.0001). After adjustment for the propensity to be prescribed lipid-lowering agents and other potential confounders, prescription of a lipid-lowering agent at discharge remained associated with a reduced risk of death at 6 months (0.67 [0.48-0.95], p=0.023)., Interpretation: Prescription of a lipid-lowering drug at hospital discharge was independently associated with reduced short-term mortality among patients after an acute coronary syndrome.

Published
2001
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32. Determination of the falloff constant (k(f)) from modeling biochemical marker release: a new variable for discriminating therapies.

Author

Christenson RH, Duh SH, Roe MT, and Ohman EM

Subjects
Algorithms, Biomarkers, Cardiovascular Agents therapeutic use, Clinical Trials as Topic, Coronary Disease blood, Coronary Disease psychology, Creatine Kinase, MB Form, Endpoint Determination, Humans, Models, Biological, Platelet Glycoprotein GPIIb-IIIa Complex antagonists & inhibitors, Prognosis, Treatment Outcome, Coronary Disease diagnosis, Creatine Kinase blood, Data Interpretation, Statistical, Isoenzymes blood
Abstract

A new variable termed the falloff constant (k(f)) was derived from the curve fitting of serial CK-MB measurements. k(f) represents the rate constant of maximal decline in serum CK-MB and is determined from the slope of the lognormal curve at the inflection point. Physiologically, kf's magnitude reflects the balance between CK-MB's rate of release from tissue and the rate of elimination. We examined k(f) in two myocardial infarction (MI) patient sets. The first set was homogeneous and taken from the TAMI 7 study (n = 147) and included 111 patients having TIMI 2-3 flow after thrombolytic therapy and 36 patients who initially had TIMI 0-1 flow. The TIMI 0-1 patients were opened to TIMI 3 by angioplasty within 3 h. The second set consisted of 196 patients enrolled in the IMPACT-AMI study that demonstrated the efficacy of the glycoprotein (GP) IIb/IIIa antagonist eptifibatide. This second set consisted of 93 patients in the GP IIb/IIIa treatment group and 103 in the placebo group. Log-normal curve-fitting parameters including peak maximum and curve area were also compared to k(f) in the GP IIb/IIIa versus placebo set. The Wilcoxon test showed no difference between the two groups of TAMI 7 patients (p = 0.22). However, there was a highly significant difference in kf between the GP IIb/IIIa treatment group versus the placebo group (p = 0.0014). Both k(f) and peak maximum from curve fitting showed significant differences between the GP IIb/IIIa treatment group and the placebo group; however, k(f) showed a substantially lower p-value (p = 0.0014 and p = 0.023, respectively). As expected, k(f) showed no difference between the TAMI 7 groups because this was a homogeneous patient set in that they all had TIMI 3 patency status within 3 h of treatment. However, in the patient set having very different treatments, GP IIb/IIIa versus placebo, there was a highly significant difference in the kf variable. These data suggest that differences in reperfusion are reflected by kf and that this variable may represent a valuable new nonmortality end point derived from curve fitting analysis.

Published
2001
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33. Shifting the open-artery hypothesis downstream: the quest for optimal reperfusion.

Author

Roe MT, Ohman EM, Maas AC, Christenson RH, Mahaffey KW, Granger CB, Harrington RA, Califf RM, and Krucoff MW

Subjects
Animals, Diagnostic Imaging, Humans, Microcirculation physiopathology, Myocardial Infarction physiopathology, Myocardial Reperfusion Injury physiopathology, Treatment Outcome, Coronary Circulation physiology, Myocardial Infarction therapy, Myocardial Reperfusion Injury prevention & control, Myocardial Revascularization
Abstract

Successful reperfusion after acute myocardial infarction (MI) has traditionally been considered to be restoration of epicardial patency, but increasing evidence suggests that disordered microvascular function and inadequate myocardial tissue perfusion are often present despite infarct vessel patency. Thus, optimal reperfusion is being redefined to include intact microvascular flow and restored myocardial perfusion, as well as sustained epicardial patency. Coronary angiography has been used as the gold standard to define failed reperfusion, according to the Thrombolysis In Myocardial Infarction (TIMI) flow grades. However, new angiographic techniques, including the corrected TIMI frame count and myocardial blush grade, have been used to show that epicardial TIMI flow grade 3 may be an incomplete measure of reperfusion success. Furthermore, evolving noninvasive diagnostic techniques, including measurement of infarct size with cardiac marker release patterns or technetium-99m-sestamibi single-photon emission computed tomographic imaging and analysis of ST segment resolution appear to be useful complements to angiography for the assessment of myocardial tissue reperfusion. Promising adjunctive therapies that target microvascular dysfunction, including platelet glycoprotein IIb/IIIa inhibitors, and agents designed to improve tissue perfusion and attenuate reperfusion injury are being evaluated to further improve clinical outcomes after acute MI. To accelerate development of these new reperfusion regimens, an integrated approach to phase II clinical trials that incorporates multiple efficacy variables, including angiography and noninvasive biomarkers of microvascular dysfunction, should be considered. Thus, as the reperfusion era moves into the next millennium, the open-artery hypothesis is expected to shift downstream and guide efforts to further improve myocardial salvage and clinical outcomes after acute MI.

Published
2001
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34. Enhanced efficacy of eptifibatide administration in patients with acute coronary syndrome requiring in-hospital coronary artery bypass grafting. PURSUIT Investigators.

Author

Marso SP, Bhatt DL, Roe MT, Houghtaling PL, Labinaz M, Kleiman NS, Dyke C, Simmoons ML, Califf RM, Harrington RA, and Topol EJ

Subjects
Acute Disease, Aged, Bleeding Time, Coronary Disease mortality, Coronary Disease surgery, Double-Blind Method, Eptifibatide, Female, Humans, Male, Middle Aged, Platelet Glycoprotein GPIIb-IIIa Complex antagonists & inhibitors, Survival Analysis, Time Factors, Treatment Outcome, Coronary Artery Bypass, Coronary Disease drug therapy, Peptides therapeutic use, Platelet Aggregation Inhibitors therapeutic use
Abstract

Background: Patients with a recent episode of non-ST-segment elevation acute coronary syndrome before CABG have higher rates of operative morbidity and mortality than patients with stable coronary syndromes. The efficacy of administering eptifibatide to these patients undergoing in-hospital CABG is unknown., Methods and Results: The Platelet Glycoprotein IIb-IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) trial randomized 10 948 patients to receive either eptifibatide or placebo. There were 1558 study participants who underwent in-hospital CABG: 692 received placebo, and 866 received eptifibatide. The main substudy analysis end point was death or myocardial infarction (MI) rates at the 6-month follow-up. The 30-day death or MI rates were 30. 8% and 26.1% for the placebo and eptifibatide groups, respectively (P:=0.041). The benefit of eptifibatide administration persisted through 6-months of follow-up (32.7% versus 27.6% for placebo versus eptifibatide, respectively; P:=0.029). There was a greater reduction in the 6-month death or MI rate for patients who received eptifibatide within 72 hours of CABG (33.6% versus 23.8%; P:=0.002) compared with the >72-hour group (31.6% versus 32%; P:=1.0). The incidence of major bleeding was 56.6% for placebo-treated patients versus 58.2% for eptifibatide-treated patients (P:=0.7)., Conclusions: Eptifibatide administration in patients undergoing in-hospital CABG with a recent episode of a non-ST-segment elevation acute coronary syndrome results in a significant reduction in death or MI that is evident at 7 days and persists through the 6-month follow-up without a significant increase in perioperative bleeding rates.

Published
2000
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35. Treatment strategies for microvascular dysfunction following acute myocardial infarction.

Author

Roe MT

Subjects
Coronary Angiography, Humans, Microcirculation, Myocardium metabolism, Platelet Aggregation Inhibitors therapeutic use, Vascular Patency drug effects, Vasodilator Agents therapeutic use, Myocardial Infarction drug therapy, Myocardial Infarction physiopathology, Myocardial Reperfusion
Abstract

Successful reperfusion following acute myocardial infarction is considered to be restoration of epicardial infarct vessel patency, but recent studies suggest that disrupted microvascular function and inadequate myocardial tissue perfusion are often present despite epicardial patency. New angiographic techniques, including the corrected Thrombolysis in Myocardial Infarction (TIMI) frame count and myocardial blush grade, have been used to demonstrate that restoration of downstream coronary flow and tissue perfusion may be the key links to improved clinical outcomes. Additionally, other diagnostic techniques, including infarct size measurement with cardiac marker release patterns, or (99m) Tc-sestamibi single photon emission computed tomography imaging, and analysis of ST-segment resolution have also been used to assess microvascular function and tissue perfusion. Promising adjunctive therapies that target microvascular dysfunction, including platelet glycoprotein IIb/IIIa inhibitors, anti-inflammatory agents, vasodilators, glucose-insulin-potassium, and embolization protection devices, may ameliorate microvascular dysfunction following epicardial reperfusion. However, these therapies have not yet been shown to improve clinical outcomes and are thus currently being studied together with fibrinolytics and primary angioplasty in clinical trials. Therefore, shifting the focus of reperfusion therapy to the microcirculation offers the potential to further improve myocardial salvage and clinical outcomes following acute myocardial infarction.

Published
2000
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36. Clinical information determines the impact of transesophageal echocardiography on the diagnosis of infective endocarditis by the duke criteria.

Author

Roe MT, Abramson MA, Li J, Heinle SK, Kisslo J, Corey GR, and Sexton DJ

Subjects
Diagnosis, Differential, Endocarditis, Bacterial classification, Endocarditis, Bacterial pathology, Female, Humans, Male, Middle Aged, Observer Variation, Predictive Value of Tests, Retrospective Studies, Echocardiography, Transesophageal, Endocarditis, Bacterial diagnostic imaging, Severity of Illness Index
Abstract

Background: Although transesophageal echocardiography (TEE) is more sensitive than transthoracic echocardiography (TTE) in detecting echocardiographic evidence of infective endocarditis (IE), the impact of TEE on the clinical diagnosis of IE has not been clearly delineated., Methods and Results: We studied 112 patients with 114 suspected episodes of IE over a 6-year period who underwent both TTE and TEE during their diagnostic evaluation. Using the results of these studies along with clinical and microbiologic data, we attempted to determine the incremental value of TEE to the Duke Endocarditis Diagnostic Criteria. Patients were initially classified into a diagnostic category of the Duke criteria with TTE data, and then the diagnostic classification was reconsidered with TEE data. A diagnostic category reassignment occurred in 25 of 114 episodes of IE evaluated when TEE results were incorporated into the evaluation with the Duke criteria (22 patients were reclassified from possible IE to definite IE whereas 3 patients were reclassified from rejected to possible IE). Diagnostic reclassification occurred in 9 (11%) of the 80 episodes of suspected IE with native cardiac valves and 13 (34%) of 34 episodes with prosthetic cardiac valves. Most patients reclassified from possible IE to definite IE with TEE data (19 of 22) had an intermediate clinical likelihood of IE, whereas 92% of patients had negative TTE results. Pathologic examination of valvular tissue in 22 of the 114 episodes of suspected IE revealed that the positive predictive value of the Duke criteria with TEE data for diagnosis of IE was 85% in patients with native valves and 89% in patients with prosthetic valves., Conclusions: When clinical evidence of IE is present, TEE improves the sensitivity of the Duke criteria to diagnose definite IE. TEE data appears to be especially useful for the diagnostic evaluation of patients with suspected IE who have prosthetic valves.

Published
2000
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37. Glycoprotein IIb/IIIa inhibitors in acute coronary syndromes.

Author

Roe MT, Sapp SK, and Lincoff AM

Subjects
Abciximab, Antibodies, Monoclonal therapeutic use, Drug Therapy, Combination, Eptifibatide, Fibrinolytic Agents administration & dosage, Heparin therapeutic use, Humans, Immunoglobulin Fab Fragments therapeutic use, Peptides therapeutic use, Platelet Aggregation Inhibitors administration & dosage, Tirofiban, Tyrosine analogs & derivatives, Tyrosine therapeutic use, Angina, Unstable drug therapy, Fibrinolytic Agents therapeutic use, Myocardial Infarction drug therapy, Platelet Aggregation Inhibitors therapeutic use, Platelet Glycoprotein GPIIb-IIIa Complex antagonists & inhibitors
Abstract

Glycoprotein (GP) IIb/IIIa inhibitors are potent antiplatelet agents and represent an exciting breakthrough in the treatment of acute coronary syndromes. However, their safety and cost-effectiveness require further investigation, and more information on risk stratification is needed to clarify which patients benefit the most from empiric use of these agents.

Published
2000
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38. Emerging treatment of acute coronary syndromes with platelet glycoprotein IIB/IIIA inhibitors.

Author

Roe MT and Moliterno DJ

Subjects
Abciximab, Acute Disease, Administration, Oral, Angina, Unstable drug therapy, Angioplasty, Balloon, Coronary, Antibodies, Monoclonal therapeutic use, Blood Platelets physiology, Clinical Trials as Topic, Clinical Trials, Phase III as Topic, Combined Modality Therapy, Coronary Disease therapy, Cost-Benefit Analysis, Drug Costs, Electrocardiography, Humans, Immunoglobulin Fab Fragments therapeutic use, Injections, Intravenous, Myocardial Infarction drug therapy, Myocardial Infarction therapy, Platelet Aggregation drug effects, Platelet Aggregation Inhibitors economics, Treatment Outcome, Coronary Disease drug therapy, Platelet Aggregation Inhibitors therapeutic use, Platelet Glycoprotein GPIIb-IIIa Complex antagonists & inhibitors
Published
1999
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40. Management of non-Q-wave myocardial infarction.

Author

Roe MT, Bowen TE, and Topol EJ

Subjects
Coronary Angiography, Humans, Myocardial Infarction mortality, Survival Analysis, Myocardial Infarction therapy, Myocardial Revascularization, Platelet Glycoprotein GPIIb-IIIa Complex antagonists & inhibitors
Published
1998

41. Calcified cardiac lesion.

Author

Gopal AK and Roe MT

Subjects
Aged, Humans, Male, Tomography, X-Ray Computed, Calcinosis diagnostic imaging, Cardiomyopathies diagnostic imaging, Heart Aneurysm diagnostic imaging
Published
1996
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42. Microglia are not exclusively associated with plaque-rich regions of the dentate gyrus in Alzheimer's disease.

Author

Roe MT, Dawson DV, Hulette CM, Einstein G, and Crain BJ

Subjects
Aged, Cell Count, Humans, Immunohistochemistry, tau Proteins analysis, Alzheimer Disease pathology, Dentate Gyrus pathology, Microglia metabolism
Abstract

The functional significance of microglia found in neuritic plaques in Alzheimer's disease (AD) remains a source of controversy. In the present study, we explored the anatomic relationships between microglia and neuritic plaques in order to determine the potential role of microglia in plaque formation. We chose to study the molecular layer of the hippocampal dentate gyrus, a brain region where plaques have a strong tendency to line up parallel to the adjacent granule cell layer. We found that ferritin-labeled microglia were indeed most numerous in the same distinct band as plaques, but that microglia were relatively more common in the outer molecular layer. The distribution of microglia was more variable than that of plaques. Overall, microglial cell distribution was a relatively poor predictor of plaque distribution, particularly when cases were considered individually. Thus, there must be multiple triggers for microglial cell activation and accumulation in the AD brain, triggers which do not all necessarily lead to neuritic plaque formation.

Published
1996
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43. The hormonogenic sites of turtle thyroglobulin and their homology with those of mammals.

Author

Roe MT, Anderson PC, Dunn AD, and Dunn JT

Subjects
Alkylation, Amino Acid Sequence, Animals, Binding Sites, Cattle, Chromatography, High Pressure Liquid, Guinea Pigs, Humans, Iodine Radioisotopes, Male, Molecular Sequence Data, Peptide Fragments isolation & purification, Rabbits, Rats, Sequence Homology, Nucleic Acid, Thyroxine metabolism, Triiodothyronine metabolism, Trypsin metabolism, Thyroglobulin analysis, Thyroglobulin metabolism, Turtles metabolism
Abstract

Thyroglobulin (Tg) from turtles previously injected with 125I was reduced, alkylated, and digested with trypsin. We purified the resultant peptides on HPLC columns, determined their amino acid sequences and the locations of [125I]T4 and [125I]T3 residues, and compared them with established sequences from humans, cows, rabbits, rats, and guinea pigs. We found five major T4 peptides, three of which were homologous with the major hormonogenic sites A, B, and D of mammalian Tg. Site A, the highly conserved major T4 site in mammals, had substitutions in three residues near the T4 residue and had much less of Tg's newly synthesized T4 than is found in mammalian Tg (25% in turtle vs. 44% in rabbit). Site B contained correspondingly more of Tg's new T4 (42% vs. 24% in rabbit). Turtle Tg contained little [125I]T3, and we did not find site C (Ser-T3/T4-Ser, the major T3 site in guinea pig and rabbit) in turtles, but did find Val-T4, a possible homolog. Site D was quantitatively less important than in mammals. The fifth turtle hormonogenic site, containing 12% of Tg's newly formed T4, had a tyrosyl residue substituted for the phenylalanine at residue 632 in the human sequence. We conclude that Tg's major hormonogenic sites are generally conserved across a considerable evolutionary distance, but that differences in primary structure occur and may contribute to changes in priority of hormone synthesis among these sites.

Published
1989
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