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1. Radiomics-Derived Brain Age Predicts Functional Outcome After Acute Ischemic Stroke.

Author

Bretzner, Martin, Bonkhoff, Anna K., Schirmer, Markus D., Hong, Sungmin, Dalca, Adrian, Donahue, Kathleen, Giese, Anne-Katrin, Etherton, Mark R., Rist, Pamela M., Nardin, Marco, Regenhardt, Robert W., Leclerc, Xavier, Lopes, Renaud, Gautherot, Morgan, Wang, Clinton, Benavente, Oscar R., Cole, John W., Donatti, Amanda, Griessenauer, Christoph, and Heitsch, Laura

Published
2023
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2. Radiomics-Derived Brain Age Predicts Functional Outcome After Acute Ischemic Stroke

Author

Bretzner, Martin, Bonkhoff, Anna K., Schirmer, Markus D., Hong, Sungmin, Dalca, Adrian, Donahue, Kathleen, Giese, Anne-Katrin, Etherton, Mark R., Rist, Pamela M., Nardin, Marco, Regenhardt, Robert W., Leclerc, Xavier, Lopes, Renaud, Gautherot, Morgan, Wang, Clinton, Benavente, Oscar R., Cole, John W., Donatti, Amanda, Griessenauer, Christoph, Heitsch, Laura, Holmegaard, Lukas, Jood, Katarina, Jimenez-Conde, Jordi, Kittner, Steven J., Lemmens, Robin, Levi, Christopher R., McArdle, Patrick F., McDonough, Caitrin W., Meschia, James F., Phuah, Chia-Ling, Rolfs, Arndt, Ropele, Stefan, Rosand, Jonathan, Roquer, Jaume, Rundek, Tatjana, Sacco, Ralph L., Schmidt, Reinhold, Sharma, Pankaj, Slowik, Agnieszka, Sousa, Alessandro, Stanne, Tara M., Strbian, Daniel, Tatlisumak, Turgut, Thijs, Vincent, Vagal, Achala, Wasselius, Johan, Woo, Daniel, Wu, Ona, Zand, Ramin, Worrall, Bradford B., Maguire, Jane, Lindgren, Arne G., Jern, Christina, Golland, Polina, Kuchcinski, Grégory, and Rost, Natalia S.

Published
2023
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3. Contribution of Common Genetic Variants to Risk of Early-Onset Ischemic Stroke

Author

Jaworek, Thomas, Xu, Huichun, Gaynor, Brady J., Cole, John W., Rannikmae, Kristiina, Stanne, Tara M., Tomppo, Liisa, Abedi, Vida, Amouyel, Philippe, Armstrong, Nicole D., Attia, John, Bell, Steven, Benavente, Oscar R., Boncoraglio, Giorgio B., Butterworth, Adam, Carcel-Marquez, Jara, Chen, Zhengming, Chong, Michael, Cruchaga, Carlos, Cushman, Mary, Danesh, John, Debette, Stéphanie, Duggan, David J., Durda, Jon Peter, Engstrom, Gunnar, Enzinger, Chris, Faul, Jessica D., Fecteau, Natalie S., Fernandez-Cadenas, Israel, Gieger, Christian, Giese, Anne-Katrin, Grewal, Raji P., Grittner, Ulrike, Havulinna, Aki S., Heitsch, Laura, Hochberg, Marc C., Holliday, Elizabeth, Hu, Jie, Ilinca, Andreea, Irvin, Marguerite R., Jackson, Rebecca D., Jacob, Mina A., Rabionet, Raquel, Jimenez-Conde, Jordi, Johnson, Julie A., Kamatani, Yoichiro, Kardia, Sharon L.R., Koido, Masaru, Kubo, Michiaki, Lange, Leslie, Lee, Jin-Moo, Lemmens, Robin, Levi, Christopher R., Li, Jiang, Li, Liming, Lin, Kuang, Lopez, Haley, Luke, Sothear, Maguire, Jane, McArdle, Patrick F., McDonough, Caitrin W., Meschia, James F., Metso, Tiina, Müller-Nurasyid, Martina, O'Connor, Timothy D., O'Donnell, Martin, Peddareddygari, Leema R., Pera, Joanna, Perry, James A., Peters, Annette, Putaala, Jukka, Ray, Debashree, Rexrode, Kathryn, Ribases, Marta, Rosand, Jonathan, Rothwell, Peter M., Rundek, Tatjana, Ryan, Kathleen A., Sacco, Ralph L., Salomaa, Veikko, Sanchez-Mora, Cristina, Schmidt, Reinhold, Sharma, Pankaj, Slowik, Agnieszka, Smith, Jennifer A., Smith, Nicholas L., Wassertheil-Smoller, Sylvia, Söderholm, Martin, Stine, O. Colin, Strbian, Daniel, Sudlow, Cathie L.M., Tatlisumak, Turgut, Terao, Chikashi, Thijs, Vincent, Torres-Aguila, Nuria P., Trégouët, David-Alexandre, Tuladhar, Anil M., Veldink, Jan H., Walters, Robin G., Weir, David R., Woo, Daniel, Worrall, Bradford B., Hong, Charles C., Ross, Owen A., Zand, Ramin, Leeuw, Frank-Erik de, Lindgren, Arne G., Pare, Guillaume, Anderson, Christopher D., Markus, Hugh S., Jern, Christina, Malik, Rainer, Dichgans, Martin, Mitchell, Braxton D., and Kittner, Steven J.

Published
2022
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4. Multi‐phenotype analyses of hemostatic traits with cardiovascular events reveal novel genetic associations

Author

Temprano‐Sagrera, Gerard, Sitlani, Colleen M., Bone, William P., Martin‐Bornez, Miguel, Voight, Benjamin F., Morrison, Alanna C., Damrauer, Scott M., de Vries, Paul S., Smith, Nicholas L., Sabater‐Lleal, Maria, Dehghan, Abbas, Heath, Adam S, Morrison, Alanna C, Reiner, Alex P, Johnson, Andrew, Richmond, Anne, Peters, Annette, van Hylckama Vlieg, Astrid, McKnight, Barbara, Psaty, Bruce M, Hayward, Caroline, Ward‐Caviness, Cavin, O’Donnell, Christopher, Chasman, Daniel, Strachan, David P, Tregouet, David A, Mook‐Kanamori, Dennis, Gill, Dipender, Thibord, Florian, Asselbergs, Folkert W, Leebeek, Frank W.G., Rosendaal, Frits R, Davies, Gail, Homuth, Georg, Temprano, Gerard, Campbell, Harry, Taylor, Herman A, Bressler, Jan, Huffman, Jennifer E, Rotter, Jerome I, Yao, Jie, Wilson, James F, Bis, Joshua C, Hahn, Julie M, Desch, Karl C, Wiggins, Kerri L, Raffield, Laura M, Bielak, Lawrence F, Yanek, Lisa R, Kleber, Marcus E, Sabater‐Lleal, Maria, Mueller, Martina, Kavousi, Maryam, Mangino, Massimo, Liu, Melissa, Brown, Michael R, Conomos, Matthew P, Jhun, Min‐A, Chen, Ming‐Huei, de Maat, Moniek P.M., Pankratz, Nathan, Smith, Nicholas L, Peyser, Patricia A, Elliot, Paul, de Vries, Paul S, Wei, Peng, Wild, Philipp S, Morange, Pierre E, van der Harst, Pim, Yang, Qiong, Le, Ngoc‐Quynh, Marioni, Riccardo, Li, Ruifang, Damrauer, Scott M, Cox, Simon R, Trompet, Stella, Felix, Stephan B, Völker, Uwe, Tang, Weihong, Koenig, Wolfgang, Jukema, J. Wouter, Guo, Xiuqing, Lindstrom, Sara, Wang, Lu, Smith, Erin N, Gordon, William, van Hylckama Vlieg, Astrid, de Andrade, Mariza, Brody, Jennifer A, Pattee, Jack W, Haessler, Jeffrey, Brumpton, Ben M, Chasman, Daniel I, Suchon, Pierre, Chen, Ming‐Huei, Turman, Constance, Germain, Marine, Wiggins, Kerri L, MacDonald, James, Braekkan, Sigrid K, Armasu, Sebastian M, Pankratz, Nathan, Jackson, Rabecca D, Nielsen, Jonas B, Giulianini, Franco, Puurunen, Marja K, Ibrahim, Manal, Heckbert, Susan R, Bammler, Theo K, Frazer, Kelly A, McCauley, Bryan M, Taylor, Kent, Pankow, James S, Reiner, Alexander P, Gabrielsen, Maiken E, Deleuze, Jean‐François, O’Donnell, Chris J, Kim, Jihye, McKnight, Barbara, Kraft, Peter, Hansen, John‐Bjarne, Rosendaal, Frits R, Heit, John A, Psaty, Bruce M, Tang, Weihong, Kooperberg, Charles, Hveem, Kristian, Ridker, Paul M, Morange, Pierre‐Emmanuel, Johnson, Andrew D, Kabrhel, Christopher, Trégouët, David‐Alexandre, Smith, Nicholas L, Malik, Rainer, Chauhan, Ganesh, Traylor, Matthew, Sargurupremraj, Muralidharan, Okada, Yukinori, Mishra, Aniket, Rutten‐Jacobs, Loes, Giese, Anne‐Katrin, van der Laan, Sander W, Gretarsdottir, Solveig, Anderson, Christopher D, Chong, Michael, Adams, Hieab HH, Ago, Tetsuro, Almgren, Peter, Amouyel, Philippe, Ay, Hakan, Bartz, Traci M, Benavente, Oscar R, Bevan, Steve, Boncoraglio, Giorgio B, Brown, Robert D, Butterworth, Adam S, Carrera, Caty, Carty, Cara L, Chasman, Daniel I, Chen, Wei‐Min, Cole, John W, Correa, Adolfo, Cotlarciuc, Ioana, Cruchaga, Carlos, Danesh, John, de Bakker, Paul IW, DeStefano, Anita L, den Hoed, Marcel, Duan, Qing, Engelter, Stefan T, Falcone, Guido J, Gottesman, Rebecca F, Grewal, Raji P, Gudnason, Vilmundur, Gustafsson, Stefan, Haessler, Jeffrey, Harris, Tamara B, Hassan, Ahamad, Havulinna, Aki S, Heckbert, Susan R, Holliday, Elizabeth G, Howard, George, Hsu, Fang‐Chi, Hyacinth, Hyacinth I, Arfan Ikram, M, Ingelsson, Erik, Irvin, Marguerite R, Jian, Xueqiu, Jiménez‐Conde, Jordi, Johnson, Julie A, Jukema, J Wouter, Kanai, Masahiro, Keene, Keith L, Kissela, Brett M, Kleindorfer, Dawn O, Kooperberg, Charles, Kubo, Michiaki, Lange, Leslie A, Langefeld, Carl D, Langenberg, Claudia, Launer, Lenore J, Lee, Jin‐Moo, Lemmens, Robin, Leys, Didier, Lewis, Cathryn M, Lin, Wei‐Yu, Lindgren, Arne G, Lorentzen, Erik, Magnusson, Patrik K, Maguire, Jane, Manichaikul, Ani, McArdle, Patrick F, Meschia, James F, Mitchell, Braxton D, Mosley, Thomas H, Nalls, Michael A, Ninomiya, Toshiharu, O’Donnell, Martin J, Psaty, Bruce M, Pulit, Sara L, Rannikmäe, Kristiina, Reiner, Alexander P, Rexrode, Kathryn M, Rice, Kenneth, Rich, Stephen S, Ridker, Paul M, Rost, Natalia S, Rothwell, Peter M, Rotter, Jerome I, Rundek, Tatjana, Sacco, Ralph L, Sakaue, Saori, Sale, Michele M, Salomaa, Veikko, Sapkota, Bishwa R, Schmidt, Reinhold, Schmidt, Carsten O, Schminke, Ulf, Sharma, Pankaj, Slowik, Agnieszka, Sudlow, Cathie LM, Tanislav, Christian, Tatlisumak, Turgut, Taylor, Kent D, Thijs, Vincent NS, Thorleifsson, Gudmar, Thorsteinsdottir, Unnur, Tiedt, Steffen, Trompet, Stella, Tzourio, Christophe, van Duijn, Cornelia M, Walters, Matthew, Wareham, Nicholas J, Wassertheil‐Smoller, Sylvia, Wilson, James G, Wiggins, Kerri L, Yang, Qiong, Yusuf, Salim, Amin, Najaf, Aparicio, Hugo S, Arnett, Donna K, Attia, John, Beiser, Alexa S, Berr, Claudine, Buring, Julie E, Bustamante, Mariana, Caso, Valeria, Cheng, Yu‐Ching, Hoan Choi, Seung, Chowhan, Ayesha, Cullell, Natalia, Dartigues, Jean‐François, Delavaran, Hossein, Delgado, Pilar, Dörr, Marcus, Engström, Gunnar, Ford, Ian, Gurpreet, Wander S, Hamsten, Anders, Heitsch, Laura, Hozawa, Atsushi, Ibanez, Laura, Ilinca, Andreea, Ingelsson, Martin, Iwasaki, Motoki, Jackson, Rebecca D, Jood, Katarina, Jousilahti, Pekka, Kaffashian, Sara, Kalra, Lalit, Kamouchi, Masahiro, Kitazono, Takanari, Kjartansson, Olafur, Kloss, Manja, Koudstaal, Peter J, Krupinski, Jerzy, Labovitz, Daniel L, Laurie, Cathy C, Levi, Christopher R, Li, Linxin, Lind, Lars, Lindgren, Cecilia M, Lioutas, Vasileios, Mei Liu, Yong, Lopez, Oscar L, Makoto, Hirata, Martinez‐Majander, Nicolas, Matsuda, Koichi, Minegishi, Naoko, Montaner, Joan, Morris, Andrew P, Muiño, Elena, Müller‐Nurasyid, Martina, Norrving, Bo, Ogishima, Soichi, Parati, Eugenio A, Reddy Peddareddygari, Leema, Pedersen, Nancy L, Pera, Joanna, Perola, Markus, Pezzini, Alessandro, Pileggi, Silvana, Rabionet, Raquel, Riba‐Llena, Iolanda, Ribasés, Marta, Romero, Jose R, Roquer, Jaume, Rudd, Anthony G, Sarin, Antti‐Pekka, Sarju, Ralhan, Sarnowski, Chloe, Sasaki, Makoto, Satizabal, Claudia L, Satoh, Mamoru, Sattar, Naveed, Sawada, Norie, Sibolt, Gerli, Sigurdsson, Ásgeir, Smith, Albert, Sobue, Kenji, Soriano‐Tárraga, Carolina, Stanne, Tara, Colin Stine, O, Stott, David J, Strauch, Konstantin, Takai, Takako, Tanaka, Hideo, Tanno, Kozo, Teumer, Alexander, Tomppo, Liisa, Torres‐Aguila, Nuria P, Touze, Emmanuel, Tsugane, Shoichiro, Uitterlinden, Andre G, Valdimarsson, Einar M, van der Lee, Sven J, Völzke, Henry, Wakai, Kenji, Weir, David, Williams, Stephen R, Wolfe, Charles DA, Wong, Quenna, Xu, Huichun, Yamaji, Taiki, Sanghera, Dharambir K, Melander, Olle, Jern, Christina, Strbian, Daniel, Fernandez‐Cadenas, Israel, Longstreth, W T, Rolfs, Arndt, Hata, Jun, Woo, Daniel, Rosand, Jonathan, Pare, Guillaume, Hopewell, Jemma C, Saleheen, Danish, Stefansson, Kari, Worrall, Bradford B, Kittner, Steven J, Seshadri, Sudha, Fornage, Myriam, Markus, Hugh S, Howson, Joanna MM, Kamatani, Yoichiro, Debette, Stephanie, and Dichgans, Martin

Abstract

Multi‐phenotype analysis of genetically correlated phenotypes can increase the statistical power to detect loci associated with multiple traits, leading to the discovery of novel loci. This is the first study to date to comprehensively analyze the shared genetic effects within different hemostatic traits, and between these and their associated disease outcomes.

Published
2022
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5. Multi‐phenotype analyses of hemostatic traits with cardiovascular events reveal novel genetic associations

Author

Temprano‐Sagrera, Gerard, Sitlani, Colleen M., Bone, William P., Martin‐Bornez, Miguel, Voight, Benjamin F., Morrison, Alanna C., Damrauer, Scott M., de Vries, Paul S., Smith, Nicholas L., Sabater‐Lleal, Maria, Dehghan, Abbas, Heath, Adam S, Morrison, Alanna C, Reiner, Alex P, Johnson, Andrew, Richmond, Anne, Peters, Annette, van Hylckama Vlieg, Astrid, McKnight, Barbara, Psaty, Bruce M, Hayward, Caroline, Ward‐Caviness, Cavin, O’Donnell, Christopher, Chasman, Daniel, Strachan, David P, Tregouet, David A, Mook‐Kanamori, Dennis, Gill, Dipender, Thibord, Florian, Asselbergs, Folkert W, Leebeek, Frank W.G., Rosendaal, Frits R, Davies, Gail, Homuth, Georg, Temprano, Gerard, Campbell, Harry, Taylor, Herman A, Bressler, Jan, Huffman, Jennifer E, Rotter, Jerome I, Yao, Jie, Wilson, James F, Bis, Joshua C, Hahn, Julie M, Desch, Karl C, Wiggins, Kerri L, Raffield, Laura M, Bielak, Lawrence F, Yanek, Lisa R, Kleber, Marcus E, Sabater‐Lleal, Maria, Mueller, Martina, Kavousi, Maryam, Mangino, Massimo, Liu, Melissa, Brown, Michael R, Conomos, Matthew P, Jhun, Min‐A, Chen, Ming‐Huei, de Maat, Moniek P.M., Pankratz, Nathan, Smith, Nicholas L, Peyser, Patricia A, Elliot, Paul, de Vries, Paul S, Wei, Peng, Wild, Philipp S, Morange, Pierre E, van der Harst, Pim, Yang, Qiong, Le, Ngoc‐Quynh, Marioni, Riccardo, Li, Ruifang, Damrauer, Scott M, Cox, Simon R, Trompet, Stella, Felix, Stephan B, Völker, Uwe, Tang, Weihong, Koenig, Wolfgang, Jukema, J. Wouter, Guo, Xiuqing, Lindstrom, Sara, Wang, Lu, Smith, Erin N, Gordon, William, van Hylckama Vlieg, Astrid, de Andrade, Mariza, Brody, Jennifer A, Pattee, Jack W, Haessler, Jeffrey, Brumpton, Ben M, Chasman, Daniel I, Suchon, Pierre, Chen, Ming‐Huei, Turman, Constance, Germain, Marine, Wiggins, Kerri L, MacDonald, James, Braekkan, Sigrid K, Armasu, Sebastian M, Pankratz, Nathan, Jackson, Rabecca D, Nielsen, Jonas B, Giulianini, Franco, Puurunen, Marja K, Ibrahim, Manal, Heckbert, Susan R, Bammler, Theo K, Frazer, Kelly A, McCauley, Bryan M, Taylor, Kent, Pankow, James S, Reiner, Alexander P, Gabrielsen, Maiken E, Deleuze, Jean‐François, O’Donnell, Chris J, Kim, Jihye, McKnight, Barbara, Kraft, Peter, Hansen, John‐Bjarne, Rosendaal, Frits R, Heit, John A, Psaty, Bruce M, Tang, Weihong, Kooperberg, Charles, Hveem, Kristian, Ridker, Paul M, Morange, Pierre‐Emmanuel, Johnson, Andrew D, Kabrhel, Christopher, Trégouët, David‐Alexandre, Smith, Nicholas L, Malik, Rainer, Chauhan, Ganesh, Traylor, Matthew, Sargurupremraj, Muralidharan, Okada, Yukinori, Mishra, Aniket, Rutten‐Jacobs, Loes, Giese, Anne‐Katrin, van der Laan, Sander W, Gretarsdottir, Solveig, Anderson, Christopher D, Chong, Michael, Adams, Hieab HH, Ago, Tetsuro, Almgren, Peter, Amouyel, Philippe, Ay, Hakan, Bartz, Traci M, Benavente, Oscar R, Bevan, Steve, Boncoraglio, Giorgio B, Brown, Robert D, Butterworth, Adam S, Carrera, Caty, Carty, Cara L, Chasman, Daniel I, Chen, Wei‐Min, Cole, John W, Correa, Adolfo, Cotlarciuc, Ioana, Cruchaga, Carlos, Danesh, John, de Bakker, Paul IW, DeStefano, Anita L, den Hoed, Marcel, Duan, Qing, Engelter, Stefan T, Falcone, Guido J, Gottesman, Rebecca F, Grewal, Raji P, Gudnason, Vilmundur, Gustafsson, Stefan, Haessler, Jeffrey, Harris, Tamara B, Hassan, Ahamad, Havulinna, Aki S, Heckbert, Susan R, Holliday, Elizabeth G, Howard, George, Hsu, Fang‐Chi, Hyacinth, Hyacinth I, Arfan Ikram, M, Ingelsson, Erik, Irvin, Marguerite R, Jian, Xueqiu, Jiménez‐Conde, Jordi, Johnson, Julie A, Jukema, J Wouter, Kanai, Masahiro, Keene, Keith L, Kissela, Brett M, Kleindorfer, Dawn O, Kooperberg, Charles, Kubo, Michiaki, Lange, Leslie A, Langefeld, Carl D, Langenberg, Claudia, Launer, Lenore J, Lee, Jin‐Moo, Lemmens, Robin, Leys, Didier, Lewis, Cathryn M, Lin, Wei‐Yu, Lindgren, Arne G, Lorentzen, Erik, Magnusson, Patrik K, Maguire, Jane, Manichaikul, Ani, McArdle, Patrick F, Meschia, James F, Mitchell, Braxton D, Mosley, Thomas H, Nalls, Michael A, Ninomiya, Toshiharu, O’Donnell, Martin J, Psaty, Bruce M, Pulit, Sara L, Rannikmäe, Kristiina, Reiner, Alexander P, Rexrode, Kathryn M, Rice, Kenneth, Rich, Stephen S, Ridker, Paul M, Rost, Natalia S, Rothwell, Peter M, Rotter, Jerome I, Rundek, Tatjana, Sacco, Ralph L, Sakaue, Saori, Sale, Michele M, Salomaa, Veikko, Sapkota, Bishwa R, Schmidt, Reinhold, Schmidt, Carsten O, Schminke, Ulf, Sharma, Pankaj, Slowik, Agnieszka, Sudlow, Cathie LM, Tanislav, Christian, Tatlisumak, Turgut, Taylor, Kent D, Thijs, Vincent NS, Thorleifsson, Gudmar, Thorsteinsdottir, Unnur, Tiedt, Steffen, Trompet, Stella, Tzourio, Christophe, van Duijn, Cornelia M, Walters, Matthew, Wareham, Nicholas J, Wassertheil‐Smoller, Sylvia, Wilson, James G, Wiggins, Kerri L, Yang, Qiong, Yusuf, Salim, Amin, Najaf, Aparicio, Hugo S, Arnett, Donna K, Attia, John, Beiser, Alexa S, Berr, Claudine, Buring, Julie E, Bustamante, Mariana, Caso, Valeria, Cheng, Yu‐Ching, Hoan Choi, Seung, Chowhan, Ayesha, Cullell, Natalia, Dartigues, Jean‐François, Delavaran, Hossein, Delgado, Pilar, Dörr, Marcus, Engström, Gunnar, Ford, Ian, Gurpreet, Wander S, Hamsten, Anders, Heitsch, Laura, Hozawa, Atsushi, Ibanez, Laura, Ilinca, Andreea, Ingelsson, Martin, Iwasaki, Motoki, Jackson, Rebecca D, Jood, Katarina, Jousilahti, Pekka, Kaffashian, Sara, Kalra, Lalit, Kamouchi, Masahiro, Kitazono, Takanari, Kjartansson, Olafur, Kloss, Manja, Koudstaal, Peter J, Krupinski, Jerzy, Labovitz, Daniel L, Laurie, Cathy C, Levi, Christopher R, Li, Linxin, Lind, Lars, Lindgren, Cecilia M, Lioutas, Vasileios, Mei Liu, Yong, Lopez, Oscar L, Makoto, Hirata, Martinez‐Majander, Nicolas, Matsuda, Koichi, Minegishi, Naoko, Montaner, Joan, Morris, Andrew P, Muiño, Elena, Müller‐Nurasyid, Martina, Norrving, Bo, Ogishima, Soichi, Parati, Eugenio A, Reddy Peddareddygari, Leema, Pedersen, Nancy L, Pera, Joanna, Perola, Markus, Pezzini, Alessandro, Pileggi, Silvana, Rabionet, Raquel, Riba‐Llena, Iolanda, Ribasés, Marta, Romero, Jose R, Roquer, Jaume, Rudd, Anthony G, Sarin, Antti‐Pekka, Sarju, Ralhan, Sarnowski, Chloe, Sasaki, Makoto, Satizabal, Claudia L, Satoh, Mamoru, Sattar, Naveed, Sawada, Norie, Sibolt, Gerli, Sigurdsson, Ásgeir, Smith, Albert, Sobue, Kenji, Soriano‐Tárraga, Carolina, Stanne, Tara, Colin Stine, O, Stott, David J, Strauch, Konstantin, Takai, Takako, Tanaka, Hideo, Tanno, Kozo, Teumer, Alexander, Tomppo, Liisa, Torres‐Aguila, Nuria P, Touze, Emmanuel, Tsugane, Shoichiro, Uitterlinden, Andre G, Valdimarsson, Einar M, van der Lee, Sven J, Völzke, Henry, Wakai, Kenji, Weir, David, Williams, Stephen R, Wolfe, Charles DA, Wong, Quenna, Xu, Huichun, Yamaji, Taiki, Sanghera, Dharambir K, Melander, Olle, Jern, Christina, Strbian, Daniel, Fernandez‐Cadenas, Israel, Longstreth, W T, Rolfs, Arndt, Hata, Jun, Woo, Daniel, Rosand, Jonathan, Pare, Guillaume, Hopewell, Jemma C, Saleheen, Danish, Stefansson, Kari, Worrall, Bradford B, Kittner, Steven J, Seshadri, Sudha, Fornage, Myriam, Markus, Hugh S, Howson, Joanna MM, Kamatani, Yoichiro, Debette, Stephanie, and Dichgans, Martin

Abstract

Multi‐phenotype analysis of genetically correlated phenotypes can increase the statistical power to detect loci associated with multiple traits, leading to the discovery of novel loci. This is the first study to date to comprehensively analyze the shared genetic effects within different hemostatic traits, and between these and their associated disease outcomes. To discover novel genetic associations by combining summary data of correlated hemostatic traits and disease events. Summary statistics from genome wide‐association studies (GWAS) from seven hemostatic traits (factor VII [FVII], factor VIII [FVIII], von Willebrand factor [VWF] factor XI [FXI], fibrinogen, tissue plasminogen activator [tPA], plasminogen activator inhibitor 1 [PAI‐1]) and three major cardiovascular (CV) events (venous thromboembolism [VTE], coronary artery disease [CAD], ischemic stroke [IS]), were combined in 27 multi‐trait combinations using metaUSAT. Genetic correlations between phenotypes were calculated using Linkage Disequilibrium Score Regression (LDSC). Newly associated loci were investigated for colocalization. We considered a significance threshold of 1.85 × 10−9obtained after applying Bonferroni correction for the number of multi‐trait combinations performed (n= 27). Across the 27 multi‐trait analyses, we found 4 novel pleiotropic loci (XXYLT1, KNG1, SUGP1/MAU2, TBL2/MLXIPL) that were not significant in the original individual datasets, were not described in previous GWAS for the individual traits, and that presented a common associated variant between the studied phenotypes. The discovery of four novel loci contributes to the understanding of the relationship between hemostasis and CV events and elucidate common genetic factors between these traits.

Published
2022
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7. Genome-Wide Association Study Meta-Analysis of Stroke in 22 000 Individuals of African Descent Identifies Novel Associations With Stroke

Author

Keene, Keith L., Hyacinth, Hyacinth I., Bis, Joshua C., Kittner, Steven J., Mitchell, Braxton D., Cheng, Yu-Ching, Pare, Guillaume, Chong, Michael, O’Donnell, Martin, Meschia, James F., Chen, Wei-Min, Sale, Michèle M., Rich, Stephen S., Nalls, Mike A., Zonderman, Alan B., Evans, Michele K., Wilson, James G., Correa, Adolfo, Markus, Hugh S., Traylor, Matthew, Lewis, Cathryn M., Carty, Cara L., Reiner, Alexander, Haessler, Jeff, Langefeld, Carl D., Gottesman, Rebecca, Mosley, Thomas H., Woo, Daniel, Yaffe, Kristine, Liu, YongMei, Longstreth, William T., Psaty, Bruce M., Kooperberg, Charles, Lange, Leslie A., Sacco, Ralph, Rundek, Tatjana, Lee, Jin-Moo, Cruchaga, Carlos, Furie, Karen L., Arnett, Donna K., Benavente, Oscar R., Grewal, Raji P., Peddareddygari, Leema Reddy, Dichgans, Martin, Malik, Rainer, Worrall, Bradford B., and Fornage, Myriam

Abstract

Supplemental Digital Content is available in the text.

Published
2020
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8. Dabigatran Treatment of Acute Noncardioembolic Ischemic Stroke

Author

Butcher, Ken S., Ng, Kelvin, Sheridan, Patrick, Field, Thalia S., Coutts, Shelagh B., Siddiqui, Muzzafar, Gioia, Laura C., Buck, Brian, Hill, Michael D., Miller, Jodi, Klahr, Ana C., Sivakumar, Leka, Benavente, Oscar R., Hart, Robert G., and Sharma, Mike

Abstract

Supplemental Digital Content is available in the text.

Published
2020
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9. Effect of Postural Hypotension on Recurrent Stroke: Secondary Prevention of Small Subcortical Strokes (SPS3) Study.

Author

Mehta, Tapan, McClure, Leslie A., White, Carole L., Taylor, Addison, Benavente, Oscar R., and Lakshminarayan, Kamakshi

Abstract

Background: Orthostatic hypotension (OH) has been independently associated with increased risk of stroke and other cardiovascular events. We sought to investigate the relationship between OH at follow-up and recurrent stroke risk in SPS3 (Secondary Prevention of Small Subcortical Strokes) trial patient cohort. This is a retrospective cohort analysis.Methods: We included all SPS3 trial participants with blood pressure measurements in both sitting and standing position per protocol at baseline, with at least 1 follow-up visit to establish the relationship between OH at follow-up and recurrent stroke risk (primary outcome). Secondary outcomes included major vascular events, myocardial infarction, all-cause mortality, and, ischemic and hemorrhagic stroke subtypes. Participants were classified as having OH at baseline and at each follow-up visit based on a systolic BP decline ≥20 mm Hg or a diastolic BP decline ≥10 mm Hg on position change from sitting to standing. We used Cox proportional hazards regression modeling to compare the risk of outcomes among those with and without OH.Results: A total of 2275 patients were included with a mean follow up time 3.2 years (standard deviation = 1.6 years). 39% (881/2275) had OH at some point during their follow-up. Of these, 41% (366/881) had orthostatic symptoms accompanying the BP drop. In a fully adjusted model, those with OH had a 1.8 times higher risk of recurrent stroke than those without OH (95% confidence interval: 1.1-3.0). The risk of ischemic stroke, major vascular events, and all-cause mortality was similarly elevated among the OH group.Conclusion: OH was associated with increased recurrent stroke risk, vascular events, and all-cause death in this large cohort of lacunar stroke patients. Whether minimizing OH in the management of poststroke hypertension in patients with lacunar stroke reduces recurrent stroke risk deserves further study. [ABSTRACT FROM AUTHOR]

Published
2019
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10. Impact of Clopidogrel Therapy on Mortality and Cancer in Patients With Cardiovascular and Cerebrovascular Disease: A Patient-Level Meta-Analysis.

Author

Elmariah, Sammy, Doros, Gheorghe, Benavente, Oscar R., Bhatt, Deepak L., Connolly, Stuart J., Yusuf, Salim, Steinhubl, Steven R., Yuyin Liu, Wen-Hua Hsieh, Yeh, Robert W., and Mauri, Laura

Abstract

Background--Clinical trial data associate extended clopidogrel therapy with increased mortality and cancer. We sought to determine the impact of continued clopidogrel use on mortality and cancer within a patient-level meta-analysis of randomized clinical trials. Methods and Results--Meta-analytic clinical event rates for all-cause, cardiovascular, noncardiovascular, and cancerrelated mortality; cancer; myocardial infarction; stroke; and fatal and major nonfatal bleeding were generated using patient-level data from 6 randomized trials comparing prolonged versus no or short-duration clopidogrel on a background of aspirin in patients with cardiovascular and cerebrovascular disease. Among 48 817 randomized patients (median follow-up 546 days), there was no difference in all-cause (7.23% versus 7.26%; P=0.97), cardiovascular (5.25% versus 5.22%; P=0.86), noncardiovascular (1.98% versus 2.03%; P=0.73), and cancer-related (0.93% versus 0.99%; P=0.59) mortality or in new cancer diagnoses (2.97% versus 2.96%; P>0.99). Rates of myocardial infarction (3.21% versus 4.05%; P<0.0001) and stroke (3.04% versus 3.75%; P<0.0001) were significantly lower in patients receiving continued clopidogrel. Fatal bleeding was more common with continued clopidogrel use (0.39% versus 0.27%; P=0.03), as were major nonfatal bleeding (4.06% versus 2.68%; P<0.0001) and intracranial hemorrhage (0.43% versus 0.30%; P=0.02). Conclusions--Across trials of cardiovascular and cerebrovascular disease, extended-duration clopidogrel on a background of aspirin has no overall effect on mortality or cancer but does reduce rates of myocardial infarction and stroke and increase rates of bleeding. These findings emphasize the need for selective use of extended clopidogrel therapy in patients in whom the risks of ischemia are not fully counterbalanced by the risks of bleeding. [ABSTRACT FROM AUTHOR]

Published
2018
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11. Genome-wide association analysis of common genetic variants of resistant hypertension

Author

El Rouby, Nihal, McDonough, Caitrin W., Gong, Yan, McClure, Leslie A., Mitchell, Braxton D., Horenstein, Richard B., Talbert, Robert L., Crawford, Dana C., Gitzendanner, Matthew A., Takahashi, Atsushi, Tanaka, Toshihiro, Kubo, Michiaki, Pepine, Carl J., Cooper-DeHoff, Rhonda M., Benavente, Oscar R., Shuldiner, Alan R., and Johnson, Julie A.

Abstract

Resistant hypertension (RHTN), defined as uncontrolled blood pressure (BP) ≥ 140/90 using three or more drugs or controlled BP (<140/90) using four or more drugs, is associated with adverse outcomes, including decline in kidney function. We conducted a genome-wide association analysis in 1194 White and Hispanic participants with hypertension and coronary artery disease from the INternational VErapamil-SR Trandolapril STudy—GENEtic Substudy (INVEST-GENES). Top variants associated with RHTN at p< 10−4were tested for replication in 585 White and Hispanic participants with hypertension and subcortical strokes from the Secondary Prevention of Subcortical Strokes GENEtic Substudy (SPS3-GENES). A genetic risk score for RHTN was created by summing the risk alleles of replicated RHTN signals. rs11749255 in MSX2was associated with RHTN in INVEST (odds ratio (OR) (95% CI) = 1.50 (1.2–1.8), p= 7.3 × 10−5) and replicated in SPS3 (OR = 2.0 (1.4–2.8), p= 4.3 × 10−5), with genome-wide significance in meta-analysis (OR = 1.60 (1.3–1.9), p= 3.8 × 10−8). Other replicated signals were in IFLTD1and PTPRD. IFLTD1rs6487504 was associated with RHTN in INVEST (OR = 1.90 (1.4–2.5), p= 1.1 × 10−5) and SPS3 (OR = 1.70 (1.2–2.5), p= 4 × 10−3). PTPRDrs324498, a previously reported RHTN signal, was among the top signals in INVEST (OR = 1.60 (1.3–2.0), p= 3.4 × 10−5) and replicated in SPS3 (OR = 1.60 (1.1–2.4), one-sided p= 0.005). Participants with the highest number of risk alleles were at increased risk of RHTN compared to participants with a lower number (p-trend = 1.8 × 10−15). Overall, we identified and replicated associations with RHTN in the MSX2, IFLTD1, and PTPRDregions, and combined these associations to create a genetic risk score.

Published
2019
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13. Multiancestry genome-wide association study of 520,000 subjects identifies 32 loci associated with stroke and stroke subtypes

Author

Malik, Rainer, Chauhan, Ganesh, Traylor, Matthew, Sargurupremraj, Muralidharan, Okada, Yukinori, Mishra, Aniket, Rutten-Jacobs, Loes, Giese, Anne-Katrin, van der Laan, Sander W., Gretarsdottir, Solveig, Anderson, Christopher D., Chong, Michael, Adams, Hieab H. H., Ago, Tetsuro, Almgren, Peter, Amouyel, Philippe, Ay, Hakan, Bartz, Traci M., Benavente, Oscar R., Bevan, Steve, Boncoraglio, Giorgio B., Brown, Robert D., Butterworth, Adam S., Carrera, Caty, Carty, Cara L., Chasman, Daniel I., Chen, Wei-Min, Cole, John W., Correa, Adolfo, Cotlarciuc, Ioana, Cruchaga, Carlos, Danesh, John, de Bakker, Paul I. W., DeStefano, Anita L., den Hoed, Marcel, Duan, Qing, Engelter, Stefan T., Falcone, Guido J., Gottesman, Rebecca F., Grewal, Raji P., Gudnason, Vilmundur, Gustafsson, Stefan, Haessler, Jeffrey, Harris, Tamara B., Hassan, Ahamad, Havulinna, Aki S., Heckbert, Susan R., Holliday, Elizabeth G., Howard, George, Hsu, Fang-Chi, Hyacinth, Hyacinth I., Ikram, M. Arfan, Ingelsson, Erik, Irvin, Marguerite R., Jian, Xueqiu, Jiménez-Conde, Jordi, Johnson, Julie A., Jukema, J. Wouter, Kanai, Masahiro, Keene, Keith L., Kissela, Brett M., Kleindorfer, Dawn O., Kooperberg, Charles, Kubo, Michiaki, Lange, Leslie A., Langefeld, Carl D., Langenberg, Claudia, Launer, Lenore J., Lee, Jin-Moo, Lemmens, Robin, Leys, Didier, Lewis, Cathryn M., Lin, Wei-Yu, Lindgren, Arne G., Lorentzen, Erik, Magnusson, Patrik K., Maguire, Jane, Manichaikul, Ani, McArdle, Patrick F., Meschia, James F., Mitchell, Braxton D., Mosley, Thomas H., Nalls, Michael A., Ninomiya, Toshiharu, O’Donnell, Martin J., Psaty, Bruce M., Pulit, Sara L., Rannikmäe, Kristiina, Reiner, Alexander P., Rexrode, Kathryn M., Rice, Kenneth, Rich, Stephen S., Ridker, Paul M., Rost, Natalia S., Rothwell, Peter M., Rotter, Jerome I., Rundek, Tatjana, Sacco, Ralph L., Sakaue, Saori, Sale, Michele M., Salomaa, Veikko, Sapkota, Bishwa R., Schmidt, Reinhold, Schmidt, Carsten O., Schminke, Ulf, Sharma, Pankaj, Slowik, Agnieszka, Sudlow, Cathie L. M., Tanislav, Christian, Tatlisumak, Turgut, Taylor, Kent D., Thijs, Vincent N. S., Thorleifsson, Gudmar, Thorsteinsdottir, Unnur, Tiedt, Steffen, Trompet, Stella, Tzourio, Christophe, van Duijn, Cornelia M., Walters, Matthew, Wareham, Nicholas J., Wassertheil-Smoller, Sylvia, Wilson, James G., Wiggins, Kerri L., Yang, Qiong, Yusuf, Salim, Bis, Joshua C., Pastinen, Tomi, Ruusalepp, Arno, Schadt, Eric E., Koplev, Simon, Björkegren, Johan L. M., Codoni, Veronica, Civelek, Mete, Smith, Nicholas L., Trégouët, David A., Christophersen, Ingrid E., Roselli, Carolina, Lubitz, Steven A., Ellinor, Patrick T., Tai, E. Shyong, Kooner, Jaspal S., Kato, Norihiro, He, Jiang, van der Harst, Pim, Elliott, Paul, Chambers, John C., Takeuchi, Fumihiko, Johnson, Andrew D., Sanghera, Dharambir K., Melander, Olle, Jern, Christina, Strbian, Daniel, Fernandez-Cadenas, Israel, Longstreth, W. T., Rolfs, Arndt, Hata, Jun, Woo, Daniel, Rosand, Jonathan, Pare, Guillaume, Hopewell, Jemma C., Saleheen, Danish, Stefansson, Kari, Worrall, Bradford B., Kittner, Steven J., Seshadri, Sudha, Fornage, Myriam, Markus, Hugh S., Howson, Joanna M. M., Kamatani, Yoichiro, Debette, Stephanie, and Dichgans, Martin

Abstract

Stroke has multiple etiologies, but the underlying genes and pathways are largely unknown. We conducted a multiancestry genome-wide-association meta-analysis in 521,612 individuals (67,162 cases and 454,450 controls) and discovered 22 new stroke risk loci, bringing the total to 32. We further found shared genetic variation with related vascular traits, including blood pressure, cardiac traits, and venous thromboembolism, at individual loci (n= 18), and using genetic risk scores and linkage-disequilibrium-score regression. Several loci exhibited distinct association and pleiotropy patterns for etiological stroke subtypes. Eleven new susceptibility loci indicate mechanisms not previously implicated in stroke pathophysiology, with prioritization of risk variants and genes accomplished through bioinformatics analyses using extensive functional datasets. Stroke risk loci were significantly enriched in drug targets for antithrombotic therapy.

Published
2018
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14. High Prevalence of Cerebral Microbleeds in Inner City Young Stroke Patients.

Author

Shoamanesh, Ashkan, Catanese, Luciana, Romero, Jose R., Lau, Helena, Babikian, Viken L., Benavente, Oscar R., Kase, Carlos S., and Pikula, Aleksandra

Abstract

Background: Data on cerebral microbleeds (CMBs) in younger populations are lacking, particularly in young stroke patients. We sought to characterize CMBs in an inner city cohort of young adults with stroke.Methods: CMB presence, count, and topography were assessed on magnetic resonance imaging (MRI) scans of 104 young stroke patients (≤49 years) presenting to Boston Medical Center between January 2006 and February 2010. Subsequent MRIs were assessed for the occurrence of new microbleeds in 29 patients. We performed cross-sectional analysis comparing baseline characteristics between patients with and without microbleeds, and between predefined microbleed burden and topography categories. We performed additional analysis to assess the determinants of new microbleeds on repeat MRI.Results: Microbleeds were present in 17% of the sample. Male sex (odds ratio [OR] 5.7, 95% confidence interval [CI] 1.0-32.6, P = .049), hypertension (OR 6.2, 95% CI 1.2-32, P = .03), moderate-severe white matter hyperintensities on MRI (OR 5.8, 95% CI 1.6-29.0, P = .01), and intracerebral hemorrhage (ICH; OR 5.0, 95% CI 1.2-20, P = .03) were over-represented in patients with microbleeds. Patients who developed new microbleeds on repeat MRI (14%) had higher microbleed counts on baseline MRI (50% versus 0% ≥ 3 CMBs, P = .02), history of illicit drug use (75% versus 24%, P = .08), positive serum toxicology for cocaine (67% versus 13%, P = .11), ICH as their presenting stroke subtype (50% versus 8%, P = .08), and over-representation of moderate-severe white matter hyperintensities (75% versus 20%, P = .05).Conclusions: Results from this inner city cohort suggest that microbleeds are prevalent in young stroke patients and are largely associated with modifiable risk factors. [ABSTRACT FROM AUTHOR]

Published
2016
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16. Achieved Blood Pressure and Outcomes in the Secondary Prevention of Small Subcortical Strokes Trial.

Author

Odden, Michelle C., McClure, Leslie A., Sawaya, B. Peter, White, Carole L., Peralta, Carmen A., Field, Thalia S., Hart, Robert G., Benavente, Oscar R., and Pergola, Pablo E.

Abstract

Unlabelled: Studies suggest a J-shaped association between blood pressure and cardiovascular events in the setting of intensive systolic blood pressure control; whether there is a similar association with stroke remains less well established. The Secondary Prevention of Small Subcortical Strokes was a randomized trial to evaluate higher (130-149 mm Hg) versus lower (<130 mm Hg) systolic blood pressure targets in participants with recent lacunar infarcts. We evaluated the association of mean achieved blood pressure, 6 months after randomization, and recurrent stroke, major vascular events, and all-cause mortality. After a mean follow up of 3.7 years, there was a J-shaped association between achieved blood pressure and outcomes; the lowest risk was at ≈124 and 67 mm Hg systolic and diastolic blood pressure, respectively. For example, above a systolic blood pressure of 124 mm Hg, 1 standard deviation higher (11.1 mm Hg) was associated with increased mortality (adjusted hazard ratio: 1.9; 95% confidence interval: 1.4, 2.7), whereas below this level, this relationship was inverted (0.29; 0.10, 0.79), P<0.001 for interaction. Above a diastolic blood pressure of 67 mm Hg, a 1 standard deviation higher (8.2 mm Hg) was associated with an increased risk of stroke (2.2; 1.4, 3.6), whereas below this level, the association was in the opposite direction (0.34; 0.13, 0.89), P=0.02 for interaction. The lowest risk of all events occurred at a nadir of ≈120 to 128 mm Hg systolic blood pressure and 65 to 70 mm Hg diastolic blood pressure. Future studies should evaluate the impact of excessive blood pressure reduction, especially in older populations with preexisting vascular disease.Clinical Trial Registration: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00059306. [ABSTRACT FROM AUTHOR]

Published
2016
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17. Microbleeds, Cerebral Hemorrhage, and Functional Outcome After Stroke Thrombolysis

Author

Charidimou, Andreas, Turc, Guillaume, Oppenheim, Catherine, Yan, Shenqiang, Scheitz, Jan F., Erdur, Hebun, Klinger-Gratz, Pascal P., El-Koussy, Marwan, Takahashi, Wakoh, Moriya, Yusuke, Wilson, Duncan, Kidwell, Chelsea S., Saver, Jeffrey L., Sallem, Asma, Moulin, Solene, Edjlali-Goujon, Myriam, Thijs, Vincent, Fox, Zoe, Shoamanesh, Ashkan, Albers, Gregory W., Mattle, Heinrich P., Benavente, Oscar R., Jäger, H. Rolf, Ambler, Gareth, Aoki, Junya, Baron, Jean-Claude, Kimura, Kazumi, Kakuda, Wataru, Takizawa, Shunya, Jung, Simon, Nolte, Christian H., Lou, Min, Cordonnier, Charlotte, and Werring, David J.

Abstract

Supplemental Digital Content is available in the text.

Published
2017
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19. Contribution of Common Genetic Variants to Risk of Early Onset Ischemic Stroke.

Author

Jaworek, Thomas, Huichun Xu, Gaynor, Brady J., Xu, Huichun, Cole, John W, Rannikmae, Kristiina, Stanne, Tara M, Tomppo, Liisa, Abedi, Vida, Amouyel, Philippe, Armstrong, Nicole D, Attia, John, Bell, Steven, Benavente, Oscar R, Boncoraglio, Giorgio B, Butterworth, Adam, Cervical Artery Dissections and Ischemic Stroke Patients (CADSIP) Consortium, Carcel-Marquez, Jara, Chen, Zhengming, and Chong, Michael

Published
2022
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21. Left Ventricular Geometry on Transthoracic Echocardiogram and Prognosis after Lacunar Stroke: The SPS3 Trial.

Author

Field, Thalia S., Pearce, Lesly A., Asinger, Richard W., Smyth, Nathan G. Chan, De, Sabe K., Hart, Robert G., and Benavente, Oscar R.

Abstract

Background The spectrum, prevalence, and prognostic implications of abnormal left ventricular geometry (LVG) in patients with lacunar stroke are unknown. We examined the spectrum of LVG and its relationship with vascular risk factors and outcomes after lacunar stroke. Methods LVG was determined with transthoracic echocardiography for 1961 patients with magnetic resonance imaging–verified recent lacunar stroke participating in the Secondary Prevention of Small Subcortical Strokes trial. Multivariable logistic regression and Cox proportional hazards models were used to identify characteristics independently associated with LVG and to estimate risk from abnormal LVG for recurrent stroke and death. Results Abnormal LVG was present in 77%. Hispanic (odds ratio [OR], 1.4; 95% confidence interval, 1.1-1.8) or black (OR, 2.0; 1.3-2.9) race-ethnicity, diabetes (OR, 1.3; 1.0-1.7), hypertension, impaired renal function (OR, 1.8; 1.2-2.5), intracranial stenosis (OR, 1.5; 1.1-2.1), and abnormal left ventricular function (OR, 2.0; 1.4-3.0) were independently associated with abnormal LVG. Subjects with abnormal LVG also more frequently had advanced manifestations of small-vessel disease specifically previous subcortical infarcts and white matter hyperintensities. After adjusting for assigned treatments, clinical risk factors, and advanced manifestations of small-vessel disease, subjects with abnormal LVG remained at increased risk of stroke recurrence (hazard ratio, 1.5; confidence interval, 1.0-2.4). There was no interaction between LVG and assigned antiplatelet or blood pressure target. Abnormal LVG was not associated with mortality. Conclusions LVG consistent with chronic hypertensive changes was highly prevalent and correlated with neuroradiologic manifestations of small-vessel disease in lacunar stroke patients. These results support the constructs that both cerebral small-vessel disease and LVG represent end-organ consequences of chronic hypertension. [ABSTRACT FROM AUTHOR]

Published
2015
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22. Vertebrobasilar Ectasia in Patients with Lacunar Stroke: The Secondary Prevention of Small Subcortical Strokes Trial.

Author

Nakajima, Makoto, Pearce, Lesly A., Ohara, Nobuyuki, Field, Thalia S., Bazan, Carlos, Anderson, David C., Hart, Robert G., and Benavente, Oscar R.

Abstract

Background The clinical implications of vertebrobasilar ectasia (VBE) in patients with cerebral small-artery disease are not well defined. We investigated whether VBE is associated with recurrent stroke, major hemorrhage, and death in a large cohort of patients with recent lacunar stroke. Methods Maximum diameters of the vertebral and basilar arteries were measured by magnetic resonance angiography and computed tomographic angiography in 2621 participants in the Secondary Prevention of Small Subcortical Strokes trial. VBE was defined a priori as basilar artery greater than 4.5 mm and/or vertebral artery greater than 4.0 mm. Patient characteristics and risks of stroke recurrence and mortality during follow-up (median, 3.5 years) were compared between patients with and without VBE. Results VBE affecting 1 or more arteries was present in 200 (7.6%) patients. Patient features independently associated with VBE were increasing age, male sex, white race ethnicity, hypertension, and higher baseline diastolic blood pressure. Baseline systolic blood pressure was inversely associated with VBE. After adjustment for other risk factors, VBE was not predictive of recurrent stroke (hazard ratio [HR], 1.3; 95% confidence interval [CI], .85-1.9) or major hemorrhage (HR, 1.5; CI, .94-2.6), but was of death (HR, 1.7; CI, 1.1-2.7). Conclusions In this large well-characterized cohort of patients with recent lacunar stroke, VBE was predictive of death but not of recurrent stroke or major hemorrhage. In these exploratory analyses, the frequency of VBE was directly related to diastolic blood pressure but inversely related to systolic blood pressure. [ABSTRACT FROM AUTHOR]

Published
2015
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34. Predictors of Stroke Recurrence in Patients with Recent Lacunar Stroke and Response to Interventions According to Risk Status: Secondary Prevention of Small Subcortical Strokes Trial.

Author

Hart, Robert G., Pearce, Lesly A., Bakheet, Majid F., Benavente, Oscar R., Conwit, Robin A., McClure, Leslie A., Talbert, Robert L., and Anderson, David C.

Abstract

Background: Among participants in the Secondary Prevention of Small Subcortical Strokes randomized trial, we sought to identify patients with high versus low rates of recurrent ischemic stroke and to assess effects of aggressive blood pressure control and dual antiplatelet therapy according to risk status. Methods: Multivariable analyses of 3020 participants with recent magnetic resonance imaging–defined lacunar strokes followed for a mean of 3.7 years with 243 recurrent ischemic strokes. Results: Prior symptomatic lacunar stroke or transient ischemic attack (TIA) (hazard ratio [HR] 2.2, 95% confidence interval [CI] 1.6, 2.9), diabetes (HR 2.0, 95% CI 1.5, 2.5), black race (HR 1.7, 95% CI 1.3, 2.3), and male sex (HR 1.5, 95% CI 1.1, 1.9) were each independently predictive of recurrent ischemic stroke. Recurrent ischemic stroke occurred at a rate of 4.3% per year (95% CI 3.4, 5.5) in patients with prior symptomatic lacunar stroke or TIA (15% of the cohort), 3.1% per year (95% CI 2.6, 3.9) in those with more than 1 of the other 3 risk factors (27% of the cohort), and 1.3% per year (95% CI 1.0, 1.7) in those with 0-1 risk factors (58% of the cohort). There were no significant interactions between treatment effects and stroke risk status. Conclusions: In this large, carefully followed cohort of patients with recent lacunar stroke and aggressive blood pressure management, prior symptomatic lacunar ischemia, diabetes, black race, and male sex independently predicted ischemic stroke recurrence. The effects of blood pressure targets and dual antiplatelet therapy were similar across the spectrum of independent risk factors and recurrence risk. [Copyright &y& Elsevier]

Published
2014
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37. ASA failure.

Author

Côté, Robert, Yu Zhang, Hart, Robert G., McClure, Leslie A., Anderson, David C., Talbert, Robert L., and Benavente, Oscar R.

Published
2014

38. Lobar distribution of white matter abnormalities in Alzheimer's, vascular and mixed dementias: Neuroimaging / differential diagnosis.

Author

Lee, Hyunwoo, Wiggermann, Vanessa, Rauscher, Alexander, Beg, Mirza Faisal, Popuri, Karteek, Tam, Roger, Lam, Kevin, Jacova, Claudia, Sossi, Vesna, Pettersen, Jacqueline, Benavente, Oscar R., and Hsiung, Ging‐Yuek Robin

Abstract

Background: Vascular dementia (VaD) is often difficult to distinguish from Alzheimer's disease (AD).[O'Brien_2015] Areas of cognitive/clinical decline due to cerebrovascular diseases depend on the frequency and location of the lesions, and may overlap with those found in AD.[Suri_2014] Moreover, AD and cerebrovascular diseases frequently occur simultaneously, leading to heterogeneous 'mixed dementia (MixD)'.[Wang_2012][Langa_2004] It is unclear whether the presence of both neurodegenerative and cerebrovascular pathologies further aggravates dementia‐related imaging abnormalities. We investigated whether the lobar distribution of white matter hyperintensities (WMHs) on MRI differed among AD, VaD and MixD. Method: N=17 participants (cross‐sectional; subtypes:7 MixD/5 Subcortical VaD/5 AD; Sex: 11M/6F; Age: 75±8yrs) were scanned on a 3T Philips Achieva. T1‐weighted MP‐RAGE images were processed with Freesurfer 6.0. Areas of WMHs were segmented on Fluid Attenuated Inversion Recovery (3D‐FLAIR) images using a combination of intensity thresholding and manual correction. Left and right frontal, temporal, occipital and parietal lobes plus basal ganglia volumes were constructed using the Freesurfer segmentation outputs. Individual WMH masks were transformed to their respective T1‐weighted spaces, and the ratios of WMH volumes to different lobar volumes were calculated. Result: Average WMH volumes were (mean±SD) AD: 5191±4693mm3, MixD: 34680±17059mm3 (sig. greater than AD), SVaD: 20896±14920mm3 (n.s. from MixD or AD). We used a linear model to predict the ratios of WMH to lobar volumes from the diagnosis subtypes, adjusting for age and sex. A significant diagnosis‐subtype effect was found in both the left and right frontal lobes. (p=0.012 and 0.045, respectively). In the left frontal lobe, the proportion of WMHs was significantly greater in the MixD subgroup compared to the AD (p=0.0045) or the VaD (p=0.026) subtypes. In the right frontal lobe, the proportion was greater in the MixD subtype compared to the AD (p=0.018) but not compared to VaD (p=0.074) subtype. AD vs. VaD were not significantly different in either sides (p=0.5). Conclusion: The MixD subtype of our pilot study cohort was characterized by a significantly greater presence of WMHs in the frontal lobar areas. Future studies are warranted to investigate the characteristics of underlying tissue abnormalities that could be specific to the diagnosis subtypes. [ABSTRACT FROM AUTHOR]

Published
2020
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39. Associations between white matter hyperintensities and cognitive dysfunction in Alzheimer's, vascular and mixed dementias: Neuroimaging / Optimal neuroimaging measures for early detection.

Author

Lee, Hyunwoo, Wiggermann, Vanessa, Rauscher, Alexander, Beg, Mirza Faisal, Popuri, Karteek, Tam, Roger, Lam, Kevin, Liu‐Ambrose, Teresa, Dao, Elizabeth, Keridy, Walid Ahmed Al, Jacova, Claudia, Sossi, Vesna, Pettersen, Jacqueline, Benavente, Oscar R., and Hsiung, Ging‐Yuek Robin

Abstract

Background: Increased burden of white‐matter hyperintensities (WMHs) on MRI is common among different types of dementia. WMHs can be caused by various underlying etiologies and are non‐specific markers of tissue abnormality. Therefore, global measures such as WMH burdens may not distinguish between degrees of cognitive impairment. We explored the associations between lobar‐specific WMH volumes and cognitive dysfunction across different dementia subtypes. Method: N=57 participants (7 Alzheimer's disease [AD]/5 subcortical vascular dementia [SVaD]/7 mixed dementia [MixD]/38 vascular cognitive impairment [VCI]; Sex:34M/23F; Age:73±8yrs; pooled from three independent studies) were scanned on 3T MRI. WMHs were segmented on 3D‐FLAIR (MixD/AD/SVaD) or dual‐echo PD/T2‐weighted (VCI) images. T1‐weighted images were processed with Freesurfer 6.0. Left and right frontal, temporal, occipital and parietal lobes plus basal ganglia volumes were constructed using the Freesurfer segmentation outputs. We calculated the proportion of WMH burden within each lobe, i.e. the ratio of lobar WMH volume over the lobar volume. The Montreal Cognitive Assessment (MoCA) was used as a measure of cognitive function. We used a general linear model to determine the association between the WMH/lobar volume ratios and the MoCA scores. Covariates included age, sex, and presence of AD‐related (yes for MixD/AD, no for rest) and vascular‐related conditions (yes for SVaD/VCI/MixD, no for AD). Additionally, we assessed the relationship between the MoCA scores and the ratio of total WMH burden over the whole‐brain parenchymal volume. Result: The model yielded a significant association between the MoCA scores and WMH/lobar ratios within the left (p=0.031) and the right (p=0.035) frontal lobes, with higher ratios predicting lower MoCA scores. The effect was not significant within the temporal, occipital, parietal lobes and the basal ganglia. The effect was insignificant at the whole‐brain level (p=0.08). Conclusion: We found a significant association between the frontal lobe WMH burden and the MoCA scores, especially sensitive to frontal executive functions. This suggests that region‐specific assessments of WMHs may provide improved imaging‐cognitive correlations over the global WMH burden. Future studies with more consistent imaging protocols and broader cognitive/clinical assessments are warranted to further characterize the relationship between WMHs and cognitive impairment. [ABSTRACT FROM AUTHOR]

Published
2020
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40. Pilot study of MRI white matter tissue properties in Alzheimer's, vascular and mixed dementias: Neuroimaging / differential diagnosis.

Author

Lee, Hyunwoo, Wiggermann, Vanessa, Rauscher, Alexander, Beg, Mirza Faisal, Popuri, Karteek, Tam, Roger, Lam, Kevin, Jacova, Claudia, Sossi, Vesna, Pettersen, Jacqueline, Benavente, Oscar R., and Hsiung, Ging‐Yuek Robin

Abstract

Background: Alzheimer's disease (AD) with cerebrovascular disease is known as 'mixed' dementia (MixD).[Wang_2012][Langa_2004] MixD can have heterogeneous clinical/imaging presentations. This makes it difficult to distinguish MixD from AD or vascular dementia (VaD) using structural markers such as atrophy or white matter hyperintensity (WMH) volumes. [Suri_2014] We explored whether WM tissue properties on MRI, represented by R2* and diffusion‐tensor (DTI) images, could distinguish MixD from AD or VaD. Method: N=17 participants (cross‐sectional; 7 MixD/5 Subcortical VaD/5 AD; Sex: 11M/6F; Age: 75±8yrs) were scanned on a 3T Philips Achieva. WMHs were segmented on 3D‐Fluid Attenuated Inversion Recovery images. T1‐weighted MP‐RAGE images were segmented into the grey/white‐matters using SPM12. These outputs were combined to construct WMH and normal‐appearing WM (NAWM) masks. DTI images were processed using FSL. R2* images were computed using in‐house software. For each participant, the average R2*, fractional anisotropy (FA) and mean diffusivity (MDf) values were calculated within the WMH and NAWM masks. Result: Average WMH volumes were (mean±SD) AD: 5191±4693mm3, MD: 34680±17059mm3 (p<.05 compared to AD), SVaD: 20896±14920mm3 (p>.05 compared to MixD or AD). A linear model was used to predict the measured R2*, FA or MDf values from the diagnosis subtypes, adjusting for age and sex. R2* results: Pairwise t‐tests revealed significantly lower R2* values within the WMHs compared to NAWM (all subtypes p<0.0005). MixD had significantly lower WMH R2* values compared to AD (p=0.01) or VaD (p=0.02) subgroups. DTI results: Pairwise t‐tests revealed significantly higher MDf values within the WMHs compared to NAWM (all subtypes p<0.009). FA values were significantly lower within the WMHs compared to NAWM for the MixD (p=0.0002) and VaD (p=0.03) but not the AD (p=0.09) subtype. Conclusion: Our MixD cohort was characterized by potentially disrupted fiber integrity (represented by decreased FA) and increased water content (represented by lower R2*) within the WMH areas. These abnormalities likely represent etiologies caused by both neurodegenerative and cerebrovascular factors. Future studies that incorporate measures of neurodegeneration or neuroinflammation, such as biofluid markers, may help to further characterize WM tissue abnormalities in MixD compared to those found in 'pure' AD or VaD. [ABSTRACT FROM AUTHOR]

Published
2020
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43. Efficacy of Antiplatelet Therapy in Secondary Prevention Following Lacunar Stroke

Author

Kwok, Chun Shing, Shoamanesh, Ashkan, Copley, Hannah Charlotte, Myint, Phyo Kyaw, Loke, Yoon K., and Benavente, Oscar R.

Abstract

Lacunar stroke accounts for 25 of ischemic stroke, but optimal antiplatelet regimen to prevent stroke recurrence remains unclear. We aimed to evaluate the efficacy of antiplatelet agents in secondary stroke prevention after a lacunar stroke.

Published
2015
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44. Long-term disability after lacunar stroke

Author

Dhamoon, Mandip S., McClure, Leslie A., White, Carole L., Lakshminarayan, Kamakshi, Benavente, Oscar R., and Elkind, Mitchell S.V.

Abstract

To determine whether vascular and demographic factors predict worsening disability up to 8 years after lacunar stroke.

Published
2015
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45. Stroke Genetics Network (SiGN) study: design and rationale for a genome-wide association study of ischemic stroke subtypes.

Author

Meschia, James F, Arnett, Donna K, Ay, Hakan, Brown Jr, Robert D, Benavente, Oscar R, Cole, John W, de Bakker, Paul I W, Dichgans, Martin, Doheny, Kimberly F, Fornage, Myriam, Grewal, Raji P, Gwinn, Katrina, Jern, Christina, Conde, Jordi Jimenez, Johnson, Julie A, Jood, Katarina, Laurie, Cathy C, Lee, Jin-Moo, Lindgren, Arne, and Markus, Hugh S

Published
2013
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46. Stroke Genetics Network (SiGN) Study.

Author

Meschia, James F., Arnett, Donna K., Ay, Hakan, Brown Jr., Robert D., Benavente, Oscar R., Cole, John W., de Bakker, Paul I.W., Dichgans, Martin, Doheny, Kimberly F., Fornage, Myriam, Grewal, Raji P., Gwinn, Katrina, Jern, Christina, Jimenez Conde, Jordi, Johnson, Julie A., Jood, Katarina, Laurie, Cathy C., Jin-Moo Lee, Lindgren, Arne, and Markus, Hugh S.

Published
2013
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47. Clinical Features and Racial/Ethnic Differences Among the 3020 Participants in the Secondary Prevention of Small Subcortical Strokes (SPS3) Trial.

Author

White, Carole L., Szychowski, Jeff M., Roldan, Ana, Benavente, Marie-France, Pretell, Edwin J., Del Brutto, Oscar H., Kase, Carlos S., Arauz, Antonio, Meyer, Brett C., Meissner, Irene, Demaerschalk, Bart M., McClure, Leslie A., Coffey, Christopher S., Pearce, Lesly A., Conwit, Robin, Irby, Lisa H., Peri, Kalyani, Pergola, Pablo E., Hart, Robert G., and Benavente, Oscar R.

Abstract

This study examined the baseline characteristics, racial/ethnic differences, and geographic differences among participants in the Secondary Prevention of Small Subcortical Strokes (SPS3) study. The SPS3 trial enrolled patients who experienced a symptomatic small subcortical stroke (lacunar stroke) within the previous 6 months and an eligible lesion on detected on magnetic resonance imaging. The patients were randomized, in a factorial design, to antiplatelet therapy (aspirin 325 mg daily plus clopidogrel 75 mg daily vs aspirin 325 mg daily plus placebo) and to one of two levels of systolic blood pressure targets (“intensive” [<130 mmHg] or “usual” [130-149 mmHg]). A total of 3020 participants were recruited from 81 clinical sites in 8 countries. In this cohort, the mean age was 63 years, 63% were men, 75% had a history of hypertension, and 37% had diabetes. The racial distribution was 51% white, 30% Hispanic, and 16% black. Compared with white subjects, black subjects were younger (mean age, 58 years vs 64 years; P <.001) and had a higher prevalence of hypertension (87% vs 70%; P <.001). The prevalence of diabetes was higher in the Hispanic and black subjects compared with the white subjects (42% and 40% vs 32%; both P <.001). Tobacco smoking at the time of qualifying stroke was much more frequent in the Spanish participants than in subjects from North America and from Latin America (32%, 22%, and 9%, respectively; P <.001). Mean systolic blood pressure at study entry was 4 mmHg lower in the Spanish subjects compared with the North American subjects (P <.01). The SPS3 cohort is the largest magnetic resonance imaging–defined series of patients with S3. Among the racially/ethnically diverse SPS3 participants, important differences in patient features and vascular risk factors could influence prognosis for recurrent stroke and response to interventions. [Copyright &y& Elsevier]

Published
2013
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