115 results on '"Staszewsky L."'
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2. Anthracycline-induced cardiotoxicity: A multicenter randomised trial comparing two strategies for guiding prevention with enalapril: The International CardioOncology Society-one trial
- Author
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Cipolla, C.M., Cardinale, D., Ciceri, F., Latini, R., Sandri, M.T., Maggioni, A.P., Labianca, R., Tettamanti, M., Senni, M., Finzi, A., Grosso, F., Vago, T., Civelli, M., Gramenzi, S., Masson, S., Balconi, G., Bernasconi, R., Salvatici, M., Nicolis, E., Barlera, S., Magnoli, M., Buratti, M.G., Ojeda Fernandez, M.L., Franzosi, M.G., Staszewsky, L., Vasamì, A., Malossi, A., Sicuro, M., Thiebat, B., Barè, C., Corzani, A., Coccolo, F., Colecchia, S., Pellegrini, C., Bregni, M., Appio, L., Caico, I., G.Rossetti, Mesenzani, O., Campana, C., Giordano, M., Gilardoni, M., Scognamiglio, G., Corrado, G., Battagin, D., De Rosa, F., Carpino, C., Palazzo, S., Monopoli, A., Milandri, C., Giannessi, P.G., Zipoli, G., Ghisoni, F., Rizzo, A., Pastori, P., Callegari, S., Sesenna, C., Colombo, A., G.Curigliano, Fodor, C., Mangiavacchi, M., Cavina, R., Guiducci, D., Mazza, R., Turazza, F.M., Vallerio, P., Marbello, L., Sala, E., Fragasso, G., Trinca, S., Aquilina, M., Rocca, A., Farolfi, A., Andreis, D., Gori, S., Barbieri, E., Lanzoni, L., Marchetti, F., Falci, C., Bianchi, A., Mioranza, E., Banzato, A., Re, F., Gaibazzi, N., Gullo, M., Turina, M.C., Gervasi, E., Giaroli, F., Nassiacos, D., Verusio, C., Barco, B., Bertolini, A., Cucchi, G., Menatti, E., Sinagra, G., Aleksova, A., Guglielmi, A., Pinotti, G., Gueli, R., Mongiardi, C., Vallini, I., Cardinale, Daniela, Ciceri, Fabio, Latini, Roberto, Franzosi, Maria Grazia, Sandri, Maria Teresa, Civelli, Maurizio, Cucchi, GianFranco, Menatti, Elisabetta, Mangiavacchi, Maurizio, Cavina, Raffaele, Barbieri, Enrico, Gori, Stefania, Colombo, Alessandro, Curigliano, Giuseppe, Salvatici, Michela, Rizzo, Antonio, Ghisoni, Francesco, Bianchi, Alessandra, Falci, Cristina, Aquilina, Michele, Rocca, Andrea, Monopoli, Anna, Milandri, Carlo, Rossetti, Giuseppe, Bregni, Marco, Sicuro, Marco, Malossi, Alessandra, Nassiacos, Daniele, Verusio, Claudio, Giordano, Monica, Staszewsky, Lidia, Barlera, Simona, Nicolis, Enrico B., Magnoli, Michela, Masson, Serge, and Cipolla, Carlo M.
- Published
- 2018
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3. ESICM LIVES 2016: part three: Milan, Italy. 1–5 October 2016
- Author
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Velasquez, T., Mackey, G., Lusk, J., Kyle, U. G., Fontenot, T., Marshall, P., Shekerdemian, L. S., Coss-Bu, J. A., Nishigaki, A., Yatabe, T., Tamura, T., Yamashita, K., Yokoyama, M., Ruiz-Rodriguez, J. C., Encina, B., Belmonte, R., Troncoso, I., Tormos, P., Riveiro, M., Baena, J., Sanchez, A., Bañeras, J., Cordón, J., Duran, N., Ruiz, A., Caballero, J., Nuvials, X., Riera, J., Serra, J., Rutten, A. M. F., van Ieperen, S. N. M., Der Kinderen, E. P. H. M., Van Logten, T., Kovacikova, L., Skrak, P., Zahorec, M., Kyle, U. G., Akcan-Arikan, A., Silva, J. C., Mackey, G., Lusk, J., Goldsworthy, M., Shekerdemian, L. S., Coss-Bu, J. A., Wood, D., Harrison, D., Parslow, R., Davis, P., Pappachan, J., Goodwin, S., Ramnarayan, P., Chernyshuk, S., Yemets, H., Zhovnir, V., Pulitano’, S. M., De Rosa, S., Mancino, A., Villa, G., Tosi, F., Franchi, P., Conti, G., Patel, B., Khine, H., Shah, A., Sung, D., Singer, L., Haghbin, S., Inaloo, S., Serati, Z., Idei, M., Nomura, T., Yamamoto, N., Sakai, Y., Yoshida, T., Matsuda, Y., Yamaguchi, Y., Takaki, S., Yamaguchi, O., Goto, T., Longani, N., Medar, S., Abdel-Aal, I. R., El Adawy, A. S., Mohammed, H. M. E. H., Mohamed, A. N., Parry, S. M., Knight, L. D., Denehy, L., De Morton, N., Baldwin, C. E., Sani, D., Kayambu, G., da Silva, V. Z. M., Phongpagdi, P., Puthucheary, Z. A., Granger, C. L., Rydingsward, J. E., Horkan, C. M., Christopher, K. B., McWilliams, D., Jones, C., Reeves, E., Atkins, G., Snelson, C., Aitken, L. M., Rattray, J., Kenardy, J., Hull, A. M., Ullman, A., Le Brocque, R., Mitchell, M., Davis, C., Macfarlane, B., Azevedo, J. C., Rocha, L. L., De Freitas, F. F. M., Cavalheiro, A. M., Lucinio, N. M., Lobato, M. S., Ebeling, G., Kraegpoeth, A., Laerkner, E., De Brito-Ashurst, I., White, C., Gregory, S., Forni, L. G., Flowers, E., Curtis, A., Wood, C. A., Siu, K., Venkatesan, K., Muhammad, J. B. H., Ng, L., Seet, E., Baptista, N., Escoval, A., Tomas, E., Agrawal, R., Mathew, R., Varma, A., Dima, E., Charitidou, E., Perivolioti, E., Pratikaki, M., Vrettou, C., Giannopoulos, A., Zakynthinos, S., Routsi, C., Atchade, E., Houzé, S., Jean-Baptiste, S., Thabut, G., Genève, C., Tanaka, S., Lortat-Jacob, B., Augustin, P., Desmard, M., Montravers, P., de Molina, F. J. González, Barbadillo, S., Alejandro, R., Álvarez-Lerma, F., Vallés, J., Catalán, R. M., Palencia, E., Jareño, A., Granada, R. M., Ignacio, M. L., Cui, N., Liu, D., Wang, H., Su, L., Qiu, H., Li, R., Jaffal, K., Rouzé, A., Poissy, J., Sendid, B., Nseir, S., Paramythiotou, E., Rizos, M., Frantzeskaki, F., Antoniadou, A., Vourli, S., Zerva, L., Armaganidis, A., Riera, J., Gottlieb, J., Greer, M., Wiesner, O., Martínez, M., Acuña, M., Rello, J., Welte, T., Atchade, E., Mignot, T., Houzé, S., Jean-Baptiste, S., Thabut, G., Lortat-Jacob, B., Tanaka, S., Augustin, P., Desmard, M., Montravers, P., Soussi, S., Dudoignon, E., Ferry, A., Chaussard, M., Benyamina, M., Alanio, A., Touratier, S., Chaouat, M., Lafaurie, M., Mimoun, M., Mebazaa, A., Legrand, M., Sheils, M. A., Patel, C., Mohankumar, L., Akhtar, N., Noriega, S. K. Pacheco, Aldana, N. Navarrete, León, J. L. Ávila, Baquero, J. Durand, Bernal, F. Fernández, Ahmadnia, E., Hadley, J. S., Millar, M., Hall, D., Hewitt, H., Yasuda, H., Sanui, M., Komuro, T., Kawano, S., Andoh, K., Yamamoto, H., Noda, E., Hatakeyama, J., Saitou, N., Okamoto, H., Kobayashi, A., Takei, T., Matsukubo, S., Rotzel, H. B., Lázaro, A. Serrano, Prada, D. Aguillón, Gimillo, M. Rodriguez, Barinas, O. Diaz, Cortes, M. L. Blasco, Franco, J. Ferreres, Roca, J. M. Segura, Carratalá, A., Gonçalves, B., Turon, R., Mendes, A., Miranda, F., Mata, P. J., Cavalcanti, D., Melo, N., Lacerda, P., Kurtz, P., Righy, C., Rosario, L. E. de la Cruz, Lesmes, S. P. Gómez, Romero, J. C. García, Herrera, A. N. García, Pertuz, E. D. Díaz, Sánchez, M. J. Gómez, Sanz, E. Regidor, Hualde, J. Barado, Hernández, A. Ansotegui, Irazabal, J. M. Guergué, Spatenkova, V., Bradac, O., Suchomel, P., Urli, T., Lazzeri, E. Heusch, Aspide, R., Zanello, M., Perez-Borrero, L., Garcia-Alvarez, J. M., Arias-Verdu, M. D., Aguilar-Alonso, E., Rivera-Fernandez, R., Mora-Ordoñez, J., De La Fuente-Martos, C., Castillo-Lorente, E., Guerrero-Lopez, F., Lesmes, S. P. Gómez, Rosario, L. E. De la Cruz, Pertuz, E. D. Díaz, Hernández, A. Ansotegui, Romero, J. C. García, Sánchez, M. J. Gómez, Herrera, A. N. García, Ramírez, J. Roldán, Sanz, E. Regidor, Hualde, J. Barado, León, J. P. Tirapu, Navarro-Guillamón, L., Cordovilla-Guardia, S., Iglesias-Santiago, A., Guerrero-López, F., Fernández-Mondéjar, E., Vidal, A., Perez, M., Juez, A., Arias, N., Colino, L., Perez, J. L., Pérez, H., Calpe, P., Alcala, M. A., Robaglia, D., Perez, C., Lan, S. K., Cunha, M. M., Moreira, T., Santos, F., Lafuente, E., Fernandes, M. J., Silva, J. G., Rosario, L. E. de la Cruz, Lesmes, S. P. Gómez, Herrera, A. N. García, Romero, J. C. García, Pertuz, E. D. Díaz, Sánchez, M. J. Gómez, Sanz, E. Regidor, Echeverría, J. G. Armando, Hernández, A. Ansotegui, Hualde, J. Barado, Podlepich, V., Sokolova, E., Alexandrova, E., Lapteva, K., Kurtz, P., Shuinotsuka, C., Rabello, L., Vianna, G., Reis, A., Cairus, C., Salluh, J., Bozza, F., Torres, J. C. Barrios, Araujo, N. J. Fernández, García-Olivares, P., Keough, E., Dalorzo, M., Tang, L. K., De Sousa, I., Díaz, M., Marcos-Zambrano, L. J., Guerrero, J. E., Gomez, S. E. Zamora, Lopez, G. D. Hernandez, Cuellar, A. I. Vazquez, Nieto, O. R. Perez, Gonzalez, J. A. Castanon, Bhasin, D., Rai, S., Singh, H., Gupta, O., Bhattal, M. K., Sampley, S., Sekhri, K., Nandha, R., Aliaga, F. A., Olivares, F., Appiani, F., Farias, P., Alberto, F., Hernández, A., Pons, S., Sonneville, R., Bouadma, L., Neuville, M., Mariotte, E., Radjou, A., Lebut, J., Chemam, S., Voiriot, G., Dilly, M. P., Mourvillier, B., Dorent, R., Nataf, P., Wolff, M., Timsit, J. F., Ediboglu, O., Ataman, S., Ozkarakas, H., Kirakli, C., Vakalos, A., Avramidis, V., Obukhova, O., Kurmukov, I. A., Kashiya, S., Golovnya, E., Baikova, V. N., Ageeva, T., Haritydi, T., Kulaga, E. V., Rios-Toro, J. J., Perez-Borrero, L., Aguilar-Alonso, E., Arias-Verdu, M. D., Garcia-Alvarez, J. M., Lopez-Caler, C., De La Fuente-Martos, C., Rodriguez-Fernandez, S., Sanchez-Orézzoli, M. Gomez, Martin-Gallardo, F., Nikhilesh, J., Joshi, V., Villarreal, E., Ruiz, J., Gordon, M., Quinza, A., Gimenez, J., Piñol, M., Castellanos, A., Ramirez, P., Jeon, Y. D., Jeong, W. Y., Kim, M. H., Jeong, I. Y., Ahn, M. Y., Ahn, J. Y., Han, S. H., Choi, J. Y., Song, Y. G., Kim, J. M., Ku, N. S., Shah, H., Kellner, F., Rezai, F., Mistry, N., Yodice, P., Ovnanian, V., Fless, K., Handler, E., Alejos, R. Martínez, Romeu, J. D. Martí, Antón, D. González, Quinart, A., Martí, A. Torres, Llaurado-Serra, M., Lobo-Civico, A., Ventura-Rosado, A., Piñol-Tena, A., Pi-Guerrero, M., Paños-Espinosa, C., Peralvo-Bernat, M., Marine-Vidal, J., Gonzalez-Engroba, R., Montesinos-Cerro, N., Treso-Geira, M., Valeiras-Valero, A., Martinez-Reyes, L., Sandiumenge, A., Jimenez-Herrera, M. F., Helyar, S., Riozzi, P., Noon, A., Hallows, G., Cotton, H., Keep, J., Hopkins, P. A., Taggu, A., Renuka, S., Sampath, S., Rood, P. J. T., Frenzel, T., Verhage, R., Bonn, M., Pickkers, P., van der Hoeven, J. G., van den Boogaard, M., Corradi, F., Melnyk, L., Moggia, F., Pienovi, R., Adriano, G., Brusasco, C., Mariotti, L., Lattuada, M., Bloomer, M. J., Coombs, M., Ranse, K., Endacott, R., Maertens, B., Blot, K., Blot, S., Amerongen, M. P. van Nieuw, van der Heiden, E. S., Twisk, J. W. R., Girbes, A. R. J., Spijkstra, J. J., Riozzi, P., Helyar, S., Cotton, H., Hallows, G., Noon, A., Bell, C., Peters, K., Feehan, A., Keep, J., Hopkins, P. A., Churchill, K., Hawkins, K., Brook, R., Paver, N., Endacott, R., Maistry, N., van Wijk, A., Rouw, N., van Galen, T., Evelein-Brugman, S., Taggu, A., Krishna, B., Sampath, S., Putzu, A., Fang, M., Berto, M. Boscolo, Belletti, A., Cassina, T., Cabrini, L., Mistry, M., Alhamdi, Y., Welters, I., Abrams, S. T., Toh, C. H., Han, H. S., Gil, E. M., Lee, D. S., Park, C. M., Winder-Rhodes, S., Lotay, R., Doyle, J., Ke, M. W., Huang, W. C., Chiang, C. H., Hung, W. T., Cheng, C. C., Lin, K. C., Lin, S. C., Chiou, K. R., Wann, S. R., Shu, C. W., Kang, P. L., Mar, G. Y., Liu, C. P., Dubó, S., Aquevedo, A., Jibaja, M., Berrutti, D., Labra, C., Lagos, R., García, M. F., Ramirez, V., Tobar, M., Picoita, F., Peláez, C., Carpio, D., Alegría, L., Hidalgo, C., Godoy, K., Bakker, J., Hernández, G., Sadamoto, Y., Katabami, K., Wada, T., Ono, Y., Maekawa, K., Hayakawa, M., Sawamura, A., Gando, S., Marin-Mateos, H., Perez-Vela, J. L., Garcia-Gigorro, R., Peiretti, M. A. Corres, Lopez-Gude, M. J., Chacon-Alves, S., Renes-Carreño, E., Montejo-González, J. C., Parlevliet, K. L., Touw, H. R. W., Beerepoot, M., Boer, C., Elbers, P. W. G., Tuinman, P. R., Abdelmonem, S. A., Helmy, T. A., El Sayed, I., Ghazal, S., Akhlagh, S. H., Masjedi, M., Hozhabri, K., Kamali, E., Zýková, I., Paldusová, B., Sedlák, P., Morman, D., Youn, A. M., Ohta, Y., Sakuma, M., Bates, D., Morimoto, T., Su, P. L., Chang, W. Y., Lin, W. C., Chen, C. W., Facchin, F., Zarantonello, F., Panciera, G., De Cassai, A., Venrdramin, A., Ballin, A., Tonetti, T., Persona, P., Ori, C., Del Sorbo, L., Rossi, S., Vergani, G., Cressoni, M., Chiumello, D., Chiurazzi, C., Brioni, M., Algieri, I., Tonetti, T., Guanziroli, M., Colombo, A., Tomic, I., Colombo, A., Crimella, F., Carlesso, E., Gasparovic, V., Gattinoni, L., Neto, A. Serpa, Schmidt, M., Pham, T., Combes, A., de Abreu, M. Gama, Pelosi, P., Schultz, M. J., Katira, B. H., Engelberts, D., Giesinger, R. E., Ackerley, C., Yoshida, T., Zabini, D., Otulakowski, G., Post, M., Kuebler, W. M., McNamara, P. J., Kavanagh, B. P., Pirracchio, R., Rigon, M. Resche, Carone, M., Chevret, S., Annane, D., Eladawy, S., El-Hamamsy, M., Bazan, N., Elgendy, M., De Pascale, G., Vallecoccia, M. S., Cutuli, S. L., Di Gravio, V., Pennisi, M. A., Conti, G., Antonelli, M., Andreis, D. T., Khaliq, W., Singer, M., Hartmann, J., Harm, S., Carmona, S. Alcantara, Almudevar, P. Matia, Abellán, A. Naharro, Ramos, J. Veganzones, Pérez, L. Pérez, Valbuena, B. Lobo, Sanz, N. Martínez, Simón, I. Fernández, Arrigo, M., Feliot, E., Deye, N., Cariou, A., Guidet, B., Jaber, S., Leone, M., Resche-Rigon, M., Baron, A. Vieillard, Legrand, M., Gayat, E., Mebazaa, A., Balik, M., Kolnikova, I., Maly, M., Waldauf, P., Tavazzi, G., Kristof, J., Herpain, A., Su, F., Post, E., Taccone, F., Vincent, J. L., Creteur, J., Lee, C., Hatib, F., Jian, Z., Buddi, S., Cannesson, M., Fileković, S., Turel, M., Knafelj, R., Gorjup, V., Stanić, R., Gradišek, P., Cerović, O., Mirković, T., Noč, M., Tirkkonen, J., Hellevuo, H., Olkkola, K. T., Hoppu, S., Lin, K. C., Hung, W. T., Chiang, C. C., Huang, W. C., Juan, W. C., Lin, S. C., Cheng, C. C., Lin, P. H., Fong, K. Y., Hou, D. S., Kang, P. L., Wann, S. R., Chen, Y. S., Mar, G. Y., Liu, C. P., Paul, M., Bougouin, W., Geri, G., Dumas, F., Champigneulle, B., Legriel, S., Charpentier, J., Mira, J. P., Sandroni, C., Cariou, A., Zimmerman, J., Sullivan, E., Noursadeghi, M., Fox, B., Sampson, D., McHugh, L., Yager, T., Cermelli, S., Seldon, T., Bhide, S., Brandon, R. A., Brandon, R. B., Zwaag, J., Beunders, R., Pickkers, P., Kox, M., Gul, F., Arslantas, M. K., Genc, D., Zibandah, N., Topcu, L., Akkoc, T., Cinel, I., Greco, E., Lauretta, M. P., Andreis, D. T., Singer, M., Garcia, I. Palacios, Cordero, M., Martin, A. Diaz, Pallás, T. Aldabó, Montero, J. Garnacho, Rey, J. Revuelto, Malo, L. Roman, Montoya, A. A. Tanaka, Martinez, A. D. C. Amador, Ayala, L. Y. Delgado, Zepeda, E. Monares, Granillo, J. Franco, Sanchez, J. Aguirre, Alejo, G. Camarena, Cabrera, A. Rugerio, Montenegro, A. Pedraza, Pham, T., Beduneau, G., Schortgen, F., Piquilloud, L., Zogheib, E., Jonas, M., Grelon, F., Runge, I., Terzi, N., Grangé, S., Barberet, G., Guitard, P. G., Frat, J. P., Constan, A., Chrétien, J. M., Mancebo, J., Mercat, A., Richard, J. C. M., Brochard, L., Soilemezi, E., Koco, E., Savvidou, S., Nouris, C., Matamis, D., Di Mussi, R., Spadaro, S., Volta, C. A., Mariani, M., Colaprico, A., Antonio, C., Bruno, F., Grasso, S., Rodriguez, A., Martín-Loeches, I., Díaz, E., Masclans, J. R., Gordo, F., Solé-Violán, J., Bodí, M., Avilés-Jurado, F. X., Trefler, S., Magret, M., Reyes, L. F., Marín-Corral, J., Yebenes, J. C., Esteban, A., Anzueto, A., Aliberti, S., Restrepo, M. I., Larsson, J. Skytte, Redfors, B., Ricksten, S. E., Haines, R., Powell-Tuck, J., Leonard, H., Ostermann, M., Berthelsen, R. E., Itenov, T. S., Perner, A., Jensen, J. U., Ibsen, M., Jensen, A. E. K., Bestle, M. H., Bucknall, T., Dixon, J., Boa, F., MacPhee, I., Philips, B. J., Doyle, J., Saadat, F., Samuels, T., Huddart, S., McCormick, B., DeBrunnar, R., Preece, J., Swart, M., Peden, C., Richardson, S., Forni, L., Kalfon, P., Baumstarck, K., Estagnasie, P., Geantot, M. A., Berric, A., Simon, G., Floccard, B., Signouret, T., Boucekine, M., Fromentin, M., Nyunga, M., Sossou, A., Venot, M., Robert, R., Follin, A., Renault, A., Garrouste, M., Collange, O., Levrat, Q., Villard, I., Thévenin, D., Pottecher, J., Patrigeon, R. G., Revel, N., Vigne, C., Mimoz, O., Auquier, P., Pawar, S., Jacques, T., Deshpande, K., Pusapati, R., Wood, B., Pulham, R. A., Wray, J., Brown, K., Pierce, C., Nadel, S., Ramnarayan, P., Azevedo, J. R., Montenegro, W. S., Rodrigues, D. P., Sousa, S. C., Araujo, V. F., Leitao, A. L., Prazeres, P. H., Mendonca, A. V., Paula, M. P., Das Neves, A., Loudet, C. I., Busico, M., Vazquez, D., Villalba, D., Lischinsky, A., Veronesi, M., Emmerich, M., Descotte, E., Juliarena, A., Bisso, M. Carboni, Grando, M., Tapia, A., Camargo, M., Ulla, D. Villani, Corzo, L., dos Santos, H. Placido, Ramos, A., Doglia, J. A., Estenssoro, E., Carbonara, M., Magnoni, S., Donald, C. L. Mac, Shimony, J. S., Conte, V., Triulzi, F., Stretti, F., Macrì, M., Snyder, A. Z., Stocchetti, N., Brody, D. L., Podlepich, V., Shimanskiy, V., Savin, I., Lapteva, K., Chumaev, A., Tjepkema-Cloostermans, M. C., Hofmeijer, J., Beishuizen, A., Hom, H., Blans, M. J., van Putten, M. J. A. M., Longhi, L., Frigeni, B., Curinga, M., Mingone, D., Beretta, S., Patruno, A., Gandini, L., Vargiolu, A., Ferri, F., Ceriani, R., Rottoli, M. R., Lorini, L., Citerio, G., Pifferi, S., Battistini, M., Cordolcini, V., Agarossi, A., Di Rosso, R., Ortolano, F., Stocchetti, N., Lourido, C. Mora, Cabrera, J. L. Santana, Santana, J. D. Martín, Alzola, L. Melián, del Rosario, C. García, Pérez, H. Rodríguez, Torrent, R. Lorenzo, Eslami, S., Dalhuisen, A., Fiks, T., Schultz, M. J., Hanna, A. Abu, Spronk, P. E., Wood, M., Maslove, D., Muscedere, J., Scott, S. H., Saha, T., Hamilton, A., Petsikas, D., Payne, D., Boyd, J. G., Puthucheary, Z. A., McNelly, A. S., Rawal, J., Connolly, B., McPhail, M. J., Sidhu, P., Rowlerson, A., Moxham, J., Harridge, S. D., Hart, N., Montgomery, H. E., Jovaisa, T., Thomas, B., Gupta, D., Wijayatilake, D. S., Shum, H. P., King, H. S., Chan, K. C., Tang, K. B., Yan, W. W., Arias, C. Castro, Latorre, J., De La Rica, A. Suárez, Garrido, E. Maseda, Feijoo, A. Montero, Gancedo, C. Hernández, Tofiño, A. López, Rodríguez, F. Gilsanz, Gemmell, L. K., Campbell, R., Doherty, P., MacKay, A., Singh, N., Vitaller, S., Nagib, H., Prieto, J., Del Arco, A., Zayas, B., Gomez, C., Tirumala, S., Pasha, S. A., Kumari, B. K., Martinez-Lopez, P., Puerto-Morlán, A., Nuevo-Ortega, P., Pujol, L. Martinez, Dolset, R. 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J., Gonzalez, C. A., Pinto, J. L., Orozco, V., Patiño, J. A., Garcia, P. K., Contreras, K. M., Rodriguez, P., Echeverri, J. E., GETGAG Working Group, JSEPTIC (Japanese Society of Education for Physicians and Trainees in Intensive Care) Clinical Trial Group, CAPCRI Study, for the ReVA Research Network and the PROVE Network Investigators, from the FROG ICU Investigators, The WIND study group, Plug Working Group, GETGAG/SEMICYUC, AKI Research Group, St George’s University of London, IPREA Study Group, FINNRESUSCI Study Group, PICS- HCPA: Programa Intrahospitalar de Combate à Sepse do Hospital de Clínicas de Porto Alegre, ENVIN-HELICS Study Group, ARIAM registry of adult cardiac surgery, The Rapid Diagnosis of Infections in the Critically Ill Team, Tokyo Womens Medical University, PLUG working group, PLUG Working Group, On behalf of Okayama Research Investigation Organizing Network (ORION)investigators, PS-ICU Group, Japan Septic Disseminated Intravascular Coagulation (JSEPTIC DIC) study group, Student Research Committee - Shiraz University of Medical Sciences, ARIAM-ANDALUCIA, The WIND study group, PLUG Working Group, The WIND study group, PLUG Working Group, and Plug working group
- Published
- 2016
- Full Text
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4. Treatment with insulin increases mortality in diabetic patients with chronic heart failure: data from the GISSI-HF Trial.: 676
- Author
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Cosmi, D, Barlera, S, Masson, S, Staszewsky, L, Aldo Pietro Maggioni, A P, Tavazzi, L, Tognoni, G, Cosmi, F, and Latini, R
- Published
- 2016
5. Murine models of myocardial and limb ischemia: Diagnostic end-points and relevance to clinical problems
- Author
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Madeddu, P., Emanueli, C., Spillmann, F., Meloni, M., Bouby, N., Richer, C., Alhenc-Gelas, F., Van Weel, V., Eefting, D., Quax, P.H.A., Hu, Y., Xu, Q., Hemdahl, A.L., van Golde, J., Huijberts, M., de Lussanet, Q., Boudier, H. Struijker, Couffinhal, T., Duplaa, C., Chimenti, S., Staszewsky, L., Latini, R., Baumans, V., and Levy, B.I.
- Published
- 2006
- Full Text
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6. Ex vivo expanded bone marrow CD34+ for acute myocardial infarction treatment: in vitro and in vivo studies: P1002
- Author
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Gunetti, M., Ferrero, I., Noghero, A., Staszewsky, L., De Angelis, N., Soldo, A., Russo, I., Errichiello, E., Rustichelli, D., Berger, M., Marra, S., Bussolino, F., Latini, R., and Fagioli, F.
- Published
- 2011
7. Circulating cardiovascular biomarkers in recurrent atrial fibrillation: data from the GISSI-Atrial Fibrillation Trial
- Author
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Latini, R., Masson, S., Pirelli, S., Barlera, S., Pulitano, G., Carbonieri, E., Gulizia, M., Vago, T., Favero, C., Zdunek, D., Struck, J., Staszewsky, L., Maggioni, A. P., Franzosi, M. G., and Disertori, M.
- Published
- 2011
- Full Text
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8. Valsartan for prevention of recurrent atrial fibrillation
- Author
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GISSI AF Investigators, Disertori M, Latini R, Barlera S, Franzosi MG, Staszewsky L, Maggioni AP, Lucci D, Di Pasquale G, Tognoni G, Delise P, Bertocchi F, Maiocchi G, Geraci E, Correale E, Lombardi F, Mugelli A, Urso R, Scardi S, Fabbri G, Bartolomei B, Barbato G, Carbonieri E, Ciricugno S, Cosmi F, Pratola C, Rossi MG, Sciarra L, Zeni P, Ceseri M, Atzori A, Bambi F, Baviera M, Bianchini F, Fenicia E, Gianfriddo M, Lonardo G, Luise A, Nota R, Orlando ME, Petrolo R, Pierattini C, Pierota V, Ragno A, Serio C, Tafi A, Tellaroli E, Masson S, Vago T, Gramenzi S, Orso F, Suliman I, Nicolis E, Casola C, Dall'Osso D, Gorini M, Bianchini E, Cabiddu S, Cangioli I, Carnaghi A, Cipressa ML, Cipressa L, Galbiati L, Lorimer A, Priami P, Moccetti T, Vaghi F, Capello AF, Rossetti G, Viada E, Morena L, Delucchi M, Reynaud SG, Allemano P, Massobrio N, Gavazzi A, Taddei F, Mor DA, Bortolini F, Lorini M, Inama G, Durin O, Pirelli S, Spotti A, Procopio R, Cuzzucrea D, Gentile G, Margonato A, Bassanelli G, Tavazzi L, Buzzi MP, Rordorf R, Gualco A, Opasich C, Gronda E, Genovese L, Mattioli R, Donatelli F, Uriarte JA, Rauhe W, Bertagnolli C, Canestrini S, Stefenelli C, Cioffi G, Giovanelli C, Rigatelli G, Boni S, Pasini A, Sitta N, Sacchetta A, Borgese L, Sciascia R, Targa L, Raviele A, Madalosso M, Bertaglia E, Zoppo FC, Capanna M, Fiorencis R, Baracca E, Rossi R, Rossi I, Trappolin R, Morgera T, Barducci E, Baldin MG, Gobbo G, Zardo F, Hrovatin E, Mos L, Vriz O, Sinagra G, Aleksova A, Mazzone C, Fresco C, Rubartelli P, Moroni LA, Camerieri A, Piana M, Mureddu R, Bertoli D, Petacchi R, Pancaldi LG, Gabrieli L, Urbinati S, Pedone C, Di Niro M, Brunelli A, Bosi S, Censi S, Moruzzi P, Pastori P, Modena MG, Malavasi V, Mezzetti M, Melandri F, Zuppiroli A, Fazi A, Testa R, Venturini E, Mazzinghi F, Cosmi D, Santoro GM, Minneci C, Galli M, Paperini L, Bovenzi FM, Cortigiani L, Cocchieri M, Severini D, Arcuri GM, Bagliani G, Bernardinangeli M, Proietti G, Bocconcelli P, Pierantozzi A, Monti F, Giamundo L, Tancredi P, Rossini E, Bianchi C, Bettiol F, Giovannini E, Fera MS, Santini M, Bianconi L, Boccanelli A, Morosetti P, Volpe M, Facciolo C, Vacri A, Romanazzi F, Napoletano C, Piccioni LL, Candelmo F, De Marco G, Arnese MR, Vetrano A, Prinzi D, De Rosa P, Capuano V, Torre S, D'Onofrio A, Ammendola E, Battista R, De Fusco A, Molero U, Iervoglini A, Stefanelli S, Fattore L, Bosco B, Liguori A, Padula G, De Luca I, Sorino M, Colonna P, D'Agostino C, Pierfelice O, Pettinati G, Muscella A, De Lorenzi E, Falco M, Giannattasio C, Baldi N, Clemente MA, D'Alessandro B, Truncellito L, Arabia F, Ciconte VA, Perticone F, Ruberto C, Buffon A, Tomaselli C, De Rosa F, Mazza S, Zampaglione G, Pirozzi AM, Butera A, Levato M, Musacchio D, Polimeni RM, Lacquaniti V, Pulitanò G, Ruggeri A, Provenzano A, Cuccurullo O, Musolino M, Marrari A, Anastasio L, Schiavello M, Comito MG, Gulizia MM, Francese GM, Vasquez L, Coppolino C, Casale A, D'Urso G, Oliva G, Giordano U, Andolina S, Sanfilippo N, Ingrillì F, Accardo S, Grasso S, Buffa L, Serra E., CHIARIELLO, MASSIMO, PERRONE FILARDI, PASQUALE, Delise, P., Bertocchi, F., Maiocchi, G., Geraci, E., Correale, E., Lombardi, F., Mugelli, A., Urso, R., Scardi, S., Fabbri, G., Bartolomei, B., Barbato, G., Carbonieri, E., Ciricugno, S., Cosmi, F., Pratola, C., Rossi, M. G., Sciarra, L., Zeni, P., Ceseri, M., Atzori, A., Bambi, F., Baviera, M., Bianchini, F., Fenicia, E., Gianfriddo, M., Lonardo, G., Luise, A., Nota, R., Orlando, M. E., Petrolo, R., Pierattini, C., Pierota, V., Ragno, A., Serio, C., Tafi, A., Tellaroli, E., Masson, S., Vago, T., Gramenzi, S., Orso, F., Suliman, I., Nicolis, E., Casola, C., Dall'Osso, D., Gorini, M., Bianchini, E., Cabiddu, S., Cangioli, I., Carnaghi, A., Cipressa, M. L., Cipressa, L., Galbiati, L., Lorimer, A., Priami, P., Moccetti, T., Vaghi, F., Capello, A. F., Rossetti, G., Viada, E., Morena, L., Delucchi, M., Reynaud, S. G., Allemano, P., Massobrio, N., Gavazzi, A., Taddei, F., Mor, D. A., Bortolini, F., Lorini, M., Inama, G., Durin, O., Pirelli, S., Spotti, A., Procopio, R., Cuzzucrea, D., Gentile, G., Margonato, A., Bassanelli, G., Tavazzi, L., Buzzi, M. P., Rordorf, R., Gualco, A., Opasich, C., Gronda, E., Genovese, L., Mattioli, R., Donatelli, F., Uriarte, J. A., Rauhe, W., Bertagnolli, C., Canestrini, S., Stefenelli, C., Cioffi, G., Giovanelli, C., Rigatelli, G., Boni, S., Pasini, A., Sitta, N., Sacchetta, A., Borgese, L., Sciascia, R., Targa, L., Raviele, A., Madalosso, M., Bertaglia, E., Zoppo, F. C., Capanna, M., Fiorencis, R., Baracca, E., Rossi, R., Rossi, I., Trappolin, R., Morgera, T., Barducci, E., Baldin, M. G., Gobbo, G., Zardo, F., Hrovatin, E., Mos, L., Vriz, O., Sinagra, G., Aleksova, A., Mazzone, C., Fresco, C., Rubartelli, P., Moroni, L. A., Camerieri, A., Piana, M., Mureddu, R., Bertoli, D., Petacchi, R., Pancaldi, L. G., Gabrieli, L., Urbinati, S., Pedone, C., Di Niro, M., Brunelli, A., Bosi, S., Censi, S., Moruzzi, P., Pastori, P., Modena, M. G., Malavasi, V., Mezzetti, M., Melandri, F., Zuppiroli, A., Fazi, A., Testa, R., Venturini, E., Mazzinghi, F., Cosmi, D., Santoro, G. M., Minneci, C., Galli, M., Paperini, L., Bovenzi, F. M., Cortigiani, L., Cocchieri, M., Severini, D., Arcuri, G. M., Bagliani, G., Bernardinangeli, M., Proietti, G., Bocconcelli, P., Pierantozzi, A., Monti, F., Giamundo, L., Tancredi, P., Rossini, E., Bianchi, C., Bettiol, F., Giovannini, E., Fera, M. S., Santini, M., Bianconi, L., Boccanelli, A., Morosetti, P., Volpe, M., Facciolo, C., Vacri, A., Romanazzi, F., Napoletano, C., Piccioni, L. L., Candelmo, F., De Marco, G., Arnese, M. R., Vetrano, A., Prinzi, D., De Rosa, P., Capuano, V., Torre, S., D'Onofrio, A., Ammendola, E., Chiariello, M., Filardi, Pp., Battista, R., De Fusco, A., Molero, U., Iervoglini, A., Stefanelli, S., Fattore, L., Bosco, B., Liguori, A., Padula, G., De Luca, I., Sorino, M., Colonna, P., D'Agostino, C., Pierfelice, O., Pettinati, G., Muscella, A., De Lorenzi, E., Falco, M., Giannattasio, C., Baldi, N., Clemente, M. A., D'Alessandro, B., Truncellito, L., Arabia, F., Ciconte, V. A., Perticone, F., Ruberto, C., Buffon, A., Tomaselli, C., De Rosa, F., Mazza, S., Zampaglione, G., Pirozzi, A. M., Butera, A., Levato, M., Musacchio, D., Polimeni, R. M., Lacquaniti, V., Pulitano, G., Ruggeri, A., Provenzano, A., Cuccurullo, O., Musolino, M., Marrari, A., Anastasio, L., Schiavello, M., Comito, M. G., Gulizia, M. M., Francese, G. M., Vasquez, L., Coppolino, C., Casale, A., D'Urso, G., Oliva, G., Giordano, U., Andolina, S., Sanfilippo, N., Ingrilli, F., Accardo, S., Grasso, S., Buffa, L., Serra, E., Disertori, Marcello, Latini, Roberto, Barlera, Simona, Franzosi, Maria Grazia, Staszewsky, Lidia, Maggioni, Aldo Pietro, Lucci, Donata, Di Pasquale, Giuseppe, Tognoni, Gianni, GISSI AF, Investigator, Disertori, M, Latini, R, Barlera, S, Franzosi, Mg, Staszewsky, L, Maggioni, Ap, Lucci, D, Di Pasquale, G, Tognoni, G, Delise, P, Bertocchi, F, Maiocchi, G, Geraci, E, Correale, E, Lombardi, F, Mugelli, A, Urso, R, Scardi, S, Fabbri, G, Bartolomei, B, Barbato, G, Carbonieri, E, Ciricugno, S, Cosmi, F, Pratola, C, Rossi, Mg, Sciarra, L, Zeni, P, Ceseri, M, Atzori, A, Bambi, F, Baviera, M, Bianchini, F, Fenicia, E, Gianfriddo, M, Lonardo, G, Luise, A, Nota, R, Orlando, Me, Petrolo, R, Pierattini, C, Pierota, V, Ragno, A, Serio, C, Tafi, A, Tellaroli, E, Masson, S, Vago, T, Gramenzi, S, Orso, F, Suliman, I, Nicolis, E, Casola, C, Dall'Osso, D, Gorini, M, Bianchini, E, Cabiddu, S, Cangioli, I, Carnaghi, A, Cipressa, Ml, Cipressa, L, Galbiati, L, Lorimer, A, Priami, P, Moccetti, T, Vaghi, F, Capello, Af, Rossetti, G, Viada, E, Morena, L, Delucchi, M, Reynaud, Sg, Allemano, P, Massobrio, N, Gavazzi, A, Taddei, F, Mor, Da, Bortolini, F, Lorini, M, Inama, G, Durin, O, Pirelli, S, Spotti, A, Procopio, R, Cuzzucrea, D, Gentile, G, Margonato, A, Bassanelli, G, Tavazzi, L, Buzzi, Mp, Rordorf, R, Gualco, A, Opasich, C, Gronda, E, Genovese, L, Mattioli, R, Donatelli, F, Uriarte, Ja, Rauhe, W, Bertagnolli, C, Canestrini, S, Stefenelli, C, Cioffi, G, Giovanelli, C, Rigatelli, G, Boni, S, Pasini, A, Sitta, N, Sacchetta, A, Borgese, L, Sciascia, R, Targa, L, Raviele, A, Madalosso, M, Bertaglia, E, Zoppo, Fc, Capanna, M, Fiorencis, R, Baracca, E, Rossi, R, Rossi, I, Trappolin, R, Morgera, T, Barducci, E, Baldin, Mg, Gobbo, G, Zardo, F, Hrovatin, E, Mos, L, Vriz, O, Sinagra, G, Aleksova, A, Mazzone, C, Fresco, C, Rubartelli, P, Moroni, La, Camerieri, A, Piana, M, Mureddu, R, Bertoli, D, Petacchi, R, Pancaldi, Lg, Gabrieli, L, Urbinati, S, Pedone, C, Di Niro, M, Brunelli, A, Bosi, S, Censi, S, Moruzzi, P, Pastori, P, Modena, Mg, Malavasi, V, Mezzetti, M, Melandri, F, Zuppiroli, A, Fazi, A, Testa, R, Venturini, E, Mazzinghi, F, Cosmi, D, Santoro, Gm, Minneci, C, Galli, M, Paperini, L, Bovenzi, Fm, Cortigiani, L, Cocchieri, M, Severini, D, Arcuri, Gm, Bagliani, G, Bernardinangeli, M, Proietti, G, Bocconcelli, P, Pierantozzi, A, Monti, F, Giamundo, L, Tancredi, P, Rossini, E, Bianchi, C, Bettiol, F, Giovannini, E, Fera, M, Santini, M, Bianconi, L, Boccanelli, A, Morosetti, P, Volpe, M, Facciolo, C, Vacri, A, Romanazzi, F, Napoletano, C, Piccioni, Ll, Candelmo, F, De Marco, G, Arnese, Mr, Vetrano, A, Prinzi, D, De Rosa, P, Capuano, V, Torre, S, D'Onofrio, A, Ammendola, E, Chiariello, Massimo, PERRONE FILARDI, Pasquale, Battista, R, De Fusco, A, Molero, U, Iervoglini, A, Stefanelli, S, Fattore, L, Bosco, B, Liguori, A, Padula, G, De Luca, I, Sorino, M, Colonna, P, D'Agostino, C, Pierfelice, O, Pettinati, G, Muscella, A, De Lorenzi, E, Falco, M, Giannattasio, C, Baldi, N, Clemente, Ma, D'Alessandro, B, Truncellito, L, Arabia, F, Ciconte, Va, Perticone, F, Ruberto, C, Buffon, A, Tomaselli, C, De Rosa, F, Mazza, S, Zampaglione, G, Pirozzi, Am, Butera, A, Levato, M, Musacchio, D, Polimeni, Rm, Lacquaniti, V, Pulitanò, G, Ruggeri, A, Provenzano, A, Cuccurullo, O, Musolino, M, Marrari, A, Anastasio, L, Schiavello, M, Comito, Mg, Gulizia, Mm, Francese, Gm, Vasquez, L, Coppolino, C, Casale, A, D'Urso, G, Oliva, G, Giordano, U, Andolina, S, Sanfilippo, N, Ingrillì, F, Accardo, S, Grasso, S, and Buffa, L
- Subjects
Male ,medicine.medical_specialty ,medicine.medical_treatment ,Tetrazoles ,Cardiomegaly ,Comorbidity ,Placebo ,Cardioversion ,Double-Blind Method ,Recurrence ,Multicenter trial ,Internal medicine ,Angiotensin II Type 1 Receptor Blocker ,Cardiovascular Disease ,Atrial Fibrillation ,medicine ,Left atrial enlargement ,Diabetes Mellitus ,Humans ,Sinus rhythm ,cardiovascular diseases ,Prospective Studies ,Tetrazole ,Proportional Hazards Models ,Aged ,business.industry ,Medicine (all) ,Hazard ratio ,Atrial fibrillation ,Diabetes Mellitu ,Valine ,General Medicine ,Middle Aged ,medicine.disease ,valsartan ,atrial fibrillation ,Prospective Studie ,Valsartan ,Cardiovascular Diseases ,cardiovascular system ,Cardiology ,Proportional Hazards Model ,Female ,business ,Angiotensin II Type 1 Receptor Blockers ,medicine.drug ,Human - Abstract
BACKGROUND: Atrial fibrillation is the most common cardiac arrhythmia, and no current therapy is ideal for control of this condition. Experimental studies suggest that angiotensin II-receptor blockers (ARBs) can influence atrial remodeling, and some clinical studies suggest that they may prevent atrial fibrillation. METHODS: We conducted a large, randomized, prospective, placebo-controlled, multicenter trial to test whether the ARB valsartan could reduce the recurrence of atrial fibrillation. We enrolled patients who were in sinus rhythm but had had either two or more documented episodes of atrial fibrillation in the previous 6 months or successful cardioversion for atrial fibrillation in the previous 2 weeks. To be eligible, patients also had to have underlying cardiovascular disease, diabetes, or left atrial enlargement. Patients were randomly assigned to receive valsartan or placebo. The two primary end points were the time to a first recurrence of atrial fibrillation and the proportion of patients who had more than one recurrence of atrial fibrillation over the course of 1 year. RESULTS: A total of 1442 patients were enrolled in the study. Atrial fibrillation recurred in 371 of the 722 patients (51.4%) in the valsartan group, as compared with 375 of 720 (52.1%) in the placebo group (adjusted hazard ratio, 0.97; 96% confidence interval [CI], 0.83 to 1.14; P = 0.73). More than one episode of atrial fibrillation occurred in 194 of 722 patients (26.9%) in the valsartan group and in 201 of 720 (27.9%) in the placebo group (adjusted odds ratio, 0.89; 99% CI, 0.64 to 1.23; P = 0.34). The results were similar in all predefined subgroups of patients, including those who were not receiving angiotensin-converting-enzyme inhibitors. CONCLUSIONS: Treatment with valsartan was not associated with a reduction in the incidence of recurrent atrial fibrillation. (ClinicalTrials.gov number, NCT00376272.) Copyright © 2009 Massachusetts Medical Society.
- Published
- 2009
9. A porcine model of severe hemorrhagic shock with fluid and blood resuscitation to evaluate plasma peptidomic modifications
- Author
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Babini, G., Maffioli, E., Grassi Scalvini, F., Luciani, A., De Giorgio, D., Staszewsky, L., Baselli, G., Tedeschi, G., and Ristagno, G.
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- 2017
- Full Text
- View/download PDF
10. Valsartan for prevention of recurrent atrial fibrillation (New England Journal of Medicine (2009) 360, (1606-1617))
- Author
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Delise, P., Bertocchi, F., Maiocchi, G., Geraci, E., Correale, E., Lombardi, F., Mugelli, A., Urso, R., Scardi, S., Fabbri, G., Bartolomei, B., Barbato, G., Carbonieri, E., Ciricugno, S., Cosmi, F., Pratola, C., Rossi, M. G., Sciarra, L., Zeni, P., Ceseri, M., Atzori, A., Bambi, F., Baviera, M., Bianchini, F., Fenicia, E., Gianfriddo, M., Lonardo, G., Luise, A., Nota, R., Orlando, M. E., Petrolo, R., Pierattini, C., Pierota, V., Ragno, A., Serio, C., Tafi, A., Tellaroli, E., Masson, S., Vago, T., Gramenzi, S., Orso, F., Suliman, I., Nicolis, E., Casola, C., Dall Osso, D., Gorini, M., Bianchini, E., Cabiddu, S., Cangioli, I., Carnaghi, A., Cipressa, M. L., Cipressa, L., Galbiati, L., Lorimer, A., Priami, P., Moccetti, T., Vaghi, F., Capello, A. F., Rossetti, G., Viada, E., Morena, L., Delucchi, M., Reynaud, S. G., Allemano, P., Massobrio, N., Gavazzi, A., Taddei, F., Mor, D. A., Bortolini, F., Lorini, M., Inama, G., Durin, O., Pirelli, S., Spotti, A., Procopio, R., Cuzzucrea, D., Gentile, G., Margonato, A., Bassanelli, G., Tavazzi, L., Buzzi, M. P., Rordorf, R., Gualco, A., Opasich, C., Gronda, E., Genovese, L., Mattioli, R., Donatelli, F., Uriarte, J. A., Rauhe, W., Bertagnolli, C., Canestrini, S., Stefenelli, C., Cioffi, G., Giovanelli, C., Rigatelli, G., Boni, S., Pasini, A., Sitta, N., Sacchetta, A., Borgese, L., Sciascia, R., Targa, L., Raviele, A., Madalosso, M., Bertaglia, E., Franco Zoppo, Capanna, M., Fiorencis, R., Baracca, E., Rossi, R., Rossi, I., Trappolin, R., Morgera, T., Barducci, E., Baldin, M. G., Gobbo, G., Zardo, F., Hrovatin, E., Mos, L., Vriz, O., Sinagra, G., Aleksova, A., Mazzone, C., Fresco, C., Rubartelli, P., Moroni, L. A., Camerieri, A., Piana, M., Mureddu, R., Bertoli, D., Petacchi, R., Pancaldi, L. G., Gabrieli, L., Urbinati, S., Pedone, C., Di Niro, M., Brunelli, A., Bosi, S., Censi, S., Moruzzi, P., Pastori, P., Modena, M. G., Malavasi, V., Mezzetti, M., Melandri, F., Zuppiroli, A., Fazi, A., Testa, R., Venturini, E., Mazzinghi, F., Cosmi, D., Santoro, G. M., Minneci, C., Galli, M., Paperini, L., Bovenzi, F. M., Cortigiani, L., Cocchieri, M., Severini, D., Arcuri, G. M., Bagliani, G., Bernardinangeli, M., Proietti, G., Bocconcelli, P., Pierantozzi, A., Monti, F., Giamundo, L., Tancredi, P., Rossini, E., Bianchi, C., Bettiol, F., Giovannini, E., Fera, M. S., Santini, M., Bianconi, L., Boccanelli, A., Morosetti, P., Volpe, M., Facciolo, C., Vacri, A., Romanazzi, F., Napoletano, C., Piccioni, L. L., Candelmo, F., Marco, G., Arnese, M. R., Vetrano, A., Prinzi, D., Rosa, P., Capuano, V., Torre, S., D Onofrio, A., Ammendola, E., Chiariello, M., Filardi, Pp, Battista, R., Fusco, A., Molero, U., Iervoglini, A., Stefanelli, S., Fattore, L., Bosco, B., Liguori, A., Padula, G., Luca, I., Sorino, M., Colonna, P., D Agostino, C., Pierfelice, O., Pettinati, G., Muscella, A., Lorenzi, E., Falco, M., Giannattasio, C., Baldi, N., Clemente, M. A., D Alessandro, B., Truncellito, L., Arabia, F., Ciconte, V. A., Perticone, F., Ruberto, C., Buffon, A., Tomaselli, C., Rosa, F., Mazza, S., Zampaglione, G., Pirozzi, A. M., Butera, A., Levato, M., Musacchio, D., Polimeni, R. M., Lacquaniti, V., Pulitano, G., Ruggeri, A., Provenzano, A., Cuccurullo, O., Musolino, M., Marrari, A., Anastasio, L., Schiavello, M., Comito, M. G., Gulizia, M. M., Francese, G. M., Vasquez, L., Coppolino, C., Casale, A., D Urso, G., Oliva, G., Giordano, U., Andolina, S., Sanfilippo, N., Ingrilli, F., Accardo, S., Grasso, S., Buffa, L., Serra, E., Disertori, M., Latini, R., Barlera, S., Franzosi, M. G., Staszewsky, L., Maggioni, A. P., Lucci, D., Di Pasquale, G., Tognoni, G., Delise, P., Bertocchi, F., Maiocchi, G., Geraci, E., Correale, E., Lombardi, F., Mugelli, A., Urso, R., Scardi, S., Fabbri, G., Bartolomei, B., Barbato, G., Carbonieri, E., Ciricugno, S., Cosmi, F., Pratola, C., Rossi, M. G., Sciarra, L., Zeni, P., Ceseri, M., Atzori, A., Bambi, F., Baviera, M., Bianchini, F., Fenicia, E., Gianfriddo, M., Lonardo, G., Luise, A., Nota, R., Orlando, M. E., Petrolo, R., Pierattini, C., Pierota, V., Ragno, A., Serio, C., Tafi, A., Tellaroli, E., Masson, S., Vago, T., Gramenzi, S., Orso, F., Suliman, I., Nicolis, E., Casola, C., Dall'Osso, D., Gorini, M., Bianchini, E., Cabiddu, S., Cangioli, I., Carnaghi, A., Cipressa, M. L., Cipressa, L., Galbiati, L., Lorimer, A., Priami, P., Moccetti, T., Vaghi, F., Capello, A. F., Rossetti, G., Viada, E., Morena, L., Delucchi, M., Reynaud, S. G., Allemano, P., Massobrio, N., Gavazzi, A., Taddei, F., Mor, D. A., Bortolini, F., Lorini, M., Inama, G., Durin, O., Pirelli, S., Spotti, A., Procopio, R., Cuzzucrea, D., Gentile, G., Margonato, A., Bassanelli, G., Tavazzi, L., Buzzi, M. P., Rordorf, R., Gualco, A., Opasich, C., Gronda, E., Genovese, L., Mattioli, R., Donatelli, F., Uriarte, J. A., Rauhe, W., Bertagnolli, C., Canestrini, S., Stefenelli, C., Cioffi, G., Giovanelli, C., Rigatelli, G., Boni, S., Pasini, A., Sitta, N., Sacchetta, A., Borgese, L., Sciascia, R., Targa, L., Raviele, A., Madalosso, M., Bertaglia, E., Zoppo, F. C., Capanna, M., Fiorencis, R., Baracca, E., Rossi, R., Rossi, I., Trappolin, R., Morgera, T., Barducci, E., Baldin, M. G., Gobbo, G., Zardo, F., Hrovatin, E., Mos, L., Vriz, O., Sinagra, G., Aleksova, A., Mazzone, C., Fresco, C., Rubartelli, P., Moroni, L. A., Camerieri, A., Piana, M., Mureddu, R., Bertoli, D., Petacchi, R., Pancaldi, L. G., Gabrieli, L., Urbinati, S., Pedone, C., Di Niro, M., Brunelli, A., Bosi, S., Censi, S., Moruzzi, P., Pastori, P., Modena, M. G., Malavasi, V., Mezzetti, M., Melandri, F., Zuppiroli, A., Fazi, A., Testa, R., Venturini, E., Mazzinghi, F., Cosmi, D., Santoro, G. M., Minneci, C., Galli, M., Paperini, L., Bovenzi, F. M., Cortigiani, L., Cocchieri, M., Severini, D., Arcuri, G. M., Bagliani, G., Bernardinangeli, M., Proietti, G., Bocconcelli, P., Pierantozzi, A., Monti, F., Giamundo, L., Tancredi, P., Rossini, E., Bianchi, C., Bettiol, F., Giovannini, E., Fera, M. S., Santini, M., Bianconi, L., Boccanelli, A., Morosetti, P., Volpe, M., Facciolo, C., Vacri, A., Romanazzi, F., Napoletano, C., Piccioni, L. L., Candelmo, F., De Marco, G., Arnese, M. R., Vetrano, A., Prinzi, D., De Rosa, P., Capuano, V., Torre, S., D'Onofrio, A., Ammendola, E., Chiariello, M., Filardi, Pp., Battista, R., De Fusco, A., Molero, U., Iervoglini, A., Stefanelli, S., Fattore, L., Bosco, B., Liguori, A., Padula, G., De Luca, I., Sorino, M., Colonna, P., D'Agostino, C., Pierfelice, O., Pettinati, G., Muscella, A., De Lorenzi, E., Falco, M., Giannattasio, C., Baldi, N., Clemente, M. A., D'Alessandro, B., Truncellito, L., Arabia, F., Ciconte, V. A., Perticone, F., Ruberto, C., Buffon, A., Tomaselli, C., De Rosa, F., Mazza, S., Zampaglione, G., Pirozzi, A. M., Butera, A., Levato, M., Musacchio, D., Polimeni, R. M., Lacquaniti, V., Pulitano, G., Ruggeri, A., Provenzano, A., Cuccurullo, O., Musolino, M., Marrari, A., Anastasio, L., Schiavello, M., Comito, M. G., Gulizia, M. M., Francese, G. M., Vasquez, L., Coppolino, C., Casale, A., D'Urso, G., Oliva, G., Giordano, U., Andolina, S., Sanfilippo, N., Ingrilli, F., Accardo, S., Grasso, S., Buffa, L., Serra, E., Disertori, Marcello, Latini, Roberto, Barlera, Simona, Franzosi, Maria Grazia, Staszewsky, Lidia, Maggioni, Aldo Pietro, Lucci, Donata, Di Pasquale, Giuseppe, and Tognoni, Gianni
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Medicine (all) - Published
- 2009
11. Cardiac expression of hepatocyte growth factor increases adultneovascularization
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Riess, Ilan, Molla, F., Leo, C., Staszewsky, L., Sala, Valentina, Balconi, G., Deangelis, N., Zambelli, V., Latini, R., and Crepaldi, Tiziana
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- 2008
12. Cardiac expression of hepatocyte growth factor increases adult neovascularization
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Crepaldi, Tiziana, Leo, C., Riess, Ilan, Staszewsky, L., Molla, F., Cuccovillo, I., Deangelis, N., Zambelli, V, and Latini, R.
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- 2007
13. n-3PUFA and Holter-derived autonomic variables in patients with heart failure: data from the Gruppo Italiano per lo Studio della Sopravvivenza nell'Insufficienza Cardiaca (GISSI-HF) Holter substudy.
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La Rovere MT, Staszewsky L, Barlera S, Maestri R, Mezzani A, Midi P, Marchioli R, Maggioni AP, Tognoni G, Tavazzi L, Latini R, GISSI-HF Investigators, La Rovere, Maria Teresa, Staszewsky, Lidia, Barlera, Simona, Maestri, Roberto, Mezzani, Alessandro, Midi, Paolo, Marchioli, Roberto, and Maggioni, Aldo P
- Abstract
Background: n-3 Polyunsaturated fatty acid (n-3PUFA) supplementation in the Gruppo Italiano per lo Studio della Sopravvivenza nell'Insufficienza Cardiaca (GISSI-HF) study reduced total mortality in patients with heart failure (HF), but the mechanism of action is still debated. The hypothesis of the present GISSI-HF substudy was that n-3PUFA may have beneficial effects on cardiac autonomic control.Objective: To evaluate the effect of 1 g/day of n-3PUFA vs placebo on heart rate variability variables, deceleration capacity, and turbulence slope.Methods: The GISSI-HF study enrolled patients with HF of any cause and severity. Twenty-four-hour (range 16-24 hours) Holter recordings were performed and analyzed in 388 patients at baseline, 3 months, and 12 months. Baseline characteristics were compared by using the χ(2) test, t test, or nonparametric Wilcoxon 2-sample test. Changes over time were tested by using the analysis of covariance adjusted by baseline values.Results: At baseline, 36% of the patients were older than 70 years, 82% were men, 92% presented a left ventricular ejection fraction<40%, and 80% were in New York Heart Association class II. An increase in mean RR interval, standard deviation of all normal-to-normal RR intervals, very low frequency power (all P<.05), and turbulence slope (P = .05) was observed after 3 months in the n-3PUFA group compared to the placebo group, independently of the frequency of dietary fish consumption or beta-blocker treatment. These differences between study groups were no longer statistically significant at 12 months. A per-protocol analysis in patients compliant with study treatment showed similar results.Conclusions: n-3PUFA supplementation partially restored autonomic modulation in patients with chronic HF; this effect was maximal after 3 months of treatment. [ABSTRACT FROM AUTHOR]- Published
- 2013
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14. Clinical characteristics of patients with asymptomatic recurrences of atrial fibrillation in the Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico-Atrial Fibrillation (GISSI-AF) trial.
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Disertori M, Lombardi F, Barlera S, Maggioni AP, Favero C, Franzosi MG, Lucci D, Staszewsky L, Fabbri G, Quintarelli S, Bianconi L, and Latini R
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- 2011
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15. Cardiac mesoangioblasts are committed, self-renewable progenitors, associated with small vessels of juvenile mouse ventricle.
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Galvez, B. G., Sampaolesi, M., Barbuti, A., Crespi, A., Covarello, D., Brunelli, S., Dellavalle, A., Crippa, S., Balconi, G., Cuccovillo, I., Molla, F., Staszewsky, L., Latini, R., DiFrancesco, D., and Cossu, G.
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HEART cells ,HEART ventricles ,LABORATORY mice ,HEART differentiation ,CORONARY arteries - Abstract
Different cardiac stem/progenitor cells have been recently identified in the post-natal heart. We describe here the identification, clonal expansion and characterization of self-renewing progenitors that differ from those previously described for high spontaneous cardiac differentiation. Unique coexpression of endothelial and pericyte markers identify these cells as cardiac mesoangioblasts and allow prospective isolation and clonal expansion from the juvenile mouse ventricle. Cardiac mesoangioblasts express many cardiac transcription factors and spontaneously differentiate into beating cardiomyocytes that assemble mature sarcomeres and express typical cardiac ion channels. Cells similarly isolated from the atrium do not spontaneously differentiate. When injected into the ventricle after coronary artery ligation, cardiac mesoangioblasts efficiently generate new myocardium in the peripheral area of the necrotic zone, as they do when grafted in the embryonic chick heart. These data identify cardiac mesoangioblasts as committed progenitors, downstream of earlier stem/progenitor cells and suitable for the cell therapy of a subset of juvenile cardiac diseases.Cell Death and Differentiation (2008) 15, 1417–1428; doi:10.1038/cdd.2008.75; published online 23 May 2008 [ABSTRACT FROM AUTHOR]
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- 2008
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16. Valsartan benefits left ventricular structure and function in heart failure: Val-HeFT echocardiographic study.
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Wong M, Staszewsky L, Latini R, Barlera S, Volpi A, Chiang Y, Benza RL, Gottlieb SO, Kleemann TD, Rosconi F, Vandervoort PM, Cohn JN, Val-HeFT Heart Failure Trial Investigators, Wong, Maylene, Staszewsky, Lidia, Latini, Roberto, Barlera, Simona, Volpi, Alberto, Chiang, Yann-Tong, and Benza, Raymond L
- Abstract
Objectives: The objective of the study was to evaluate the effect of an angiotensin receptor blocker on left ventricular (LV) structure and function when added to prescribed heart failure therapy.Background: The clinical benefit derived from heart failure therapy is attributed to the regression of LV remodeling.Methods: At 302 multinational sites, 5,010 patients in New York Heart Association (NYHA) classification II to IV heart failure taking angiotensin-converting enzyme inhibitor (ACEI) and/or beta-blocker (BB) were randomized into valsartan and placebo groups and followed for a mean of 22.4 months. Serial echocardiographic measurements of left ventricular internal diastolic diameter (LVIDd) and ejection fraction (EF) were recorded. Total study reproducibility calculated to 90% power at 5% significance defined detectable differences of 0.09 cm for LVIDd and 0.86% for EF.Results: Baseline LVIDd and EF for valsartan and placebo groups were similar: 3.6 +/- 0.5 versus 3.7 +/- 0.5 (cm/m(2)) and 26.6 +/- 7.3 versus 26.9 +/- 7.0 (%). Mean group changes from baseline over time were compared. Significant decrease in LVIDd and increase in EF began by four months, reached plateau by one year, and persisted to two years in valsartan compared with placebo patients, irrespective of age, gender, race, etiology, NYHA classification, and co-treatment therapy. Changes at 18 months were -0.12 +/- 0.4 versus -0.05 +/- 0.4 (cm/m(2)), p < 0.00001 for LVIDd, and +4.5 +/- 8.9 versus +3.2 +/- 8.6 (%), p < 0.00001 for EF. The exception occurred in patients taking both ACEI and BB as co-treatment, in whom the decrease in LVIDd and increase in EF were no different between valsartan and placebo groups.Conclusions: The Val-HeFT echocardiographic substudy of 5,010 patients with moderate heart failure demonstrated that valsartan therapy taken with either ACEI or BB reversed LV remodeling. [ABSTRACT FROM AUTHOR]- Published
- 2002
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17. The mesoangioblast, a multipotent embryonic cell from dorsal aorta, repairs the infarcted heart: comparative efficacy with bone marrow-derived stem cells and fibroblasts
- Author
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Latini, R., Cossu, G., Dejana, E., Innocenzi, A., Cusella, G., Bai, A., Martinoli, E., Carlo, E., Fiordaliso, F., Zanetta, L., Staszewsky, L., Mavilio, F., and Balconi, G.
- Published
- 2004
- Full Text
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18. ESICM LIVES 2016: part three
- Author
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Velasquez, T., Mackey, G., Lusk, J., Kyle, U. G., Fontenot, T., Marshall, P., Shekerdemian, L. S., Coss-Bu, J. A., Nishigaki, A., Yatabe, T., Tamura, T., Yamashita, K., Yokoyama, M., Ruiz-Rodriguez, J. C., Encina, B., Belmonte, R., Troncoso, I., Tormos, P., Riveiro, M., Baena, J., Sanchez, A., Bañeras, J., Cordón, J., Duran, N., Ruiz, A., Caballero, J., Nuvials, X., Riera, J., Serra, J., Rutten, A. M. F., van Ieperen, S. N. M., Der Kinderen, E. P. H. M., Van Logten, T., Kovacikova, L., Skrak, P., Zahorec, M., Akcan-Arikan, A., Silva, J. C., Goldsworthy, M., Wood, D., Harrison, D., Parslow, R., Davis, P., Pappachan, J., Goodwin, S., Ramnarayan, P., Chernyshuk, S., Yemets, H., Zhovnir, V., Pulitano’, S. M., De Rosa, S., Mancino, A., Villa, G., Tosi, F., Franchi, P., Conti, G., Patel, B., Khine, H., Shah, A., Sung, D., Singer, L., Haghbin, S., Inaloo, S., Serati, Z., Idei, M., Nomura, T., Yamamoto, N., Sakai, Y., Yoshida, T., Matsuda, Y., Yamaguchi, Y., Takaki, S., Yamaguchi, O., Goto, T., Longani, N., Medar, S., Abdel-Aal, I. R., El Adawy, A. S., Mohammed, H. M. E. H., Mohamed, A. N., Parry, S. M., Knight, L. D., Denehy, L., De Morton, N., Baldwin, C. E., Sani, D., Kayambu, G., da Silva, V. Z. M., Phongpagdi, P., Puthucheary, Z. A., Granger, C. L., Rydingsward, J. E., Horkan, C. M., Christopher, K. B., McWilliams, D., Jones, C., Reeves, E., Atkins, G., Snelson, C., Aitken, L. M., Rattray, J., Kenardy, J., Hull, A. M., Ullman, A., Le Brocque, R., Mitchell, M., Davis, C., Macfarlane, B., Azevedo, J. C., Rocha, L. L., De Freitas, F. F. M., Cavalheiro, A. M., Lucinio, N. M., Lobato, M. S., Ebeling, G., Kraegpoeth, A., Laerkner, E., De Brito-Ashurst, I., White, C., Gregory, S., Forni, L. 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Meeting Abstracts - Full Text
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19. 487 Signs and symptoms and relevance to remodeling in chronic heart failure: Val-HeFT data
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Wong, M., Staszewsky, L., Barlera, S., Carretta, E., Latini, R., Tognoni, G., and Cohn, J.N.
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HEART failure , *MEDICAL model - Abstract
An abstract of the article "Signs and Symptoms and Relevance to Remodeling in Chronic Heart Failure: Val-HeFT Data," by M. Wong and colleagues, is presented.
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- 2004
20. 238 Brain natriuretic peptide (BNP) and symptoms as markers of a therapeutic response in chronic heart failure: Val-HeFT substudy
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Wong, M., Masson, S., Latini, R., Carretta, E., Barlera, S., Staszewsky, L., and Cohn, J.N.
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BRAIN natriuretic factor ,HEART failure - Abstract
An abstract of the study "Brain natriuretic peptide (BNP) and symptoms as markers of a therapeutic response in chronic heart failure: Val-HeFT substudy," by M. Wong and colleagues, is presented.
- Published
- 2004
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21. Circulating biomarkers and cardiac function over 3 years after chemotherapy with anthracyclines: the ICOS-ONE trial
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Barbara Bottazzi, Giuseppe Curigliano, Maria Teresa Sandri, Roberto Leone, Jennifer Meessen, Pietro Cortesi, Daniele Nassiacos, Enrico Nicolis, Alessandra Bianchi, Deborah Novelli, Alberto Farolfi, Icos‐One Study Investigators, Cecilia Garlanda, Giovanna Balconi, Alessandro Colombo, Marco Bregni, Enrico Barbieri, Roberto Latini, Daniela Cardinale, Carlo M. Cipolla, Maurizio Civelli, Paolo Pastori, Stefania Gori, Lidia Staszewsky, Alberto Mantovani, Serge Masson, Carlo Milandri, Fabio Ciceri, Francesco Ghisoni, Gianluigi Condorelli, Michela Salvatici, Claudio Verusio, Alessandra Malossi, Maria Grazia Franzosi, Cristina Falci, GianFranco Cucchi, Maurizio Mangiavacchi, Anna Monopoli, Elisabetta Menatti, Meessen, J. M. T. A., Cardinale, D., Ciceri, F., Sandri, M. T., Civelli, M., Bottazzi, B., Cucchi, G., Menatti, E., Mangiavacchi, M., Condorelli, G., Barbieri, E., Gori, S., Colombo, A., Curigliano, G., Salvatici, M., Pastori, P., Ghisoni, F., Bianchi, A., Falci, C., Cortesi, P., Farolfi, A., Monopoli, A., Milandri, C., Bregni, M., Malossi, A., Nassiacos, D., Verusio, C., Staszewsky, L., Leone, R., Novelli, D., Balconi, G., Nicolis, E. B., Franzosi, M. G., Masson, S., Garlanda, C., Mantovani, A., Cipolla, C. M., and Latini, R.
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Cardiac function curve ,lcsh:Diseases of the circulatory (Cardiovascular) system ,medicine.medical_specialty ,030204 cardiovascular system & hematology ,Inducible T-Cell Co-Stimulator Protein ,03 medical and health sciences ,Ventricular Dysfunction, Left ,0302 clinical medicine ,Heart arrhythmia ,Internal medicine ,Original Research Articles ,Troponin I ,Natriuretic Peptide, Brain ,medicine ,Humans ,Anthracyclines ,030212 general & internal medicine ,Original Research Article ,Ejection fraction ,biology ,business.industry ,medicine.disease ,Troponin ,Pulmonary embolism ,Cardio‐oncology ,Cardio-oncology ,lcsh:RC666-701 ,Echocardiography ,Heart failure ,Cardiology ,biology.protein ,Cardiac dysfunction ,Cardiology and Cardiovascular Medicine ,business ,Biomarkers ,Blood sampling - Abstract
Aims: A multicentre trial, ICOS-ONE, showed increases above the upper limit of normality of cardiac troponin (cTn) in 27% of patients within 12months after the end of cancer chemotherapy (CT) with anthracyclines, whether cardiac protection with enalapril was started at study entry in all (prevention arm) or only upon first occurrence on supra-normal cTn (troponin-triggered arm). The aims of the present post hoc analysis were (i) to assess whether anthracycline-based treatment could induce cardiotoxicity over 36month follow-up and (ii) to describe the time course of three cardiovascular biomarkers (i.e. troponin I cTnI-Ultra, B-type natriuretic peptide BNP, and pentraxin 3 PTX3) and of left ventricular (LV) function up to 36months. Methods and results: Eligible patients were those prescribed first-in-life CT, without evidence of cardiovascular disease, normal cTn, LV ejection fraction (EF) >50%, not on renin-angiotensin aldosterone system antagonists. Patients underwent echocardiography and blood sampling at 24 and 36months. No differences were observed in biomarker concentration between the two study arms, ‘prevention' vs. ‘troponin-triggered'. During additional follow-up 13 more deaths occurred, leading to a total of 23 (9.5%), all due to a non-cardiovascular cause. No new occurrences of LV-dysfunction were reported. Two additional patients were admitted to the hospital for cardiovascular causes, both for acute pulmonary embolism. No first onset of raised cTnI-Ultra was reported in the extended follow-up. BNP remained within normal range: at 36months was 23.4ng/L, higher (N.S.) than at baseline, 17.6ng/L. PTX3 peaked at 5.2ng/mL 1month after CT and returned to baseline values thereafter. cTnI-Ultra peaked at 26ng/L 1month after CT and returned to 3ng/L until the last measurement at 36months. All echocardiographic variables remained stable during follow-up with a median LVEF of 63% and left atrial volume index about 24mL/m2. Conclusions: First-in-life CT with median cumulative dose of anthracyclines of 180mg/m2 does not seem to cause clinically significant cardiac injury, as assessed by circulating biomarkers and echocardiography, in patients aged 51years (median), without pre-existing cardiac disease. This may suggest either a 100% efficacy of enalapril (given as preventive or troponin-triggered) or a reassuringly low absolute cardiovascular risk in this cohort of patients, which may not require intensive cardiologic follow-up.
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- 2020
22. Trabectedin and Lurbinectedin Extend Survival of Mice Bearing C26 Colon Adenocarcinoma, without Affecting Tumor Growth or Cachexia
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Giorgia Careccia, Mara Forti, Giulia Benedetta Martinelli, Laura Pasetto, Rosanna Piccirillo, Simonetta Andrea Licandro, Roberto Latini, Giorgio Aquila, Lidia Staszewsky, Andrea David Re Cecconi, Emilie Venereau, Ilaria Russo, Deborah Novelli, Serge Masson, Eugenio Scanziani, Laura Talamini, Roberta Frapolli, Raffaella Giavazzi, Maurizio D'Incalci, Andrea Resovi, Ezia Bello, Aquila, G, Re Cecconi, A, Forti, M, Frapolli, R, Bello, E, Novelli, D, Russo, I, Licandro, S, Staszewsky, L, Martinelli, G, Talamini, L, Pasetto, L, Resovi, A, Giavazzi, R, Scanziani, E, Careccia, G, Vénéreau, E, Masson, S, Latini, R, D'Incalci, M, and Piccirillo, R
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0301 basic medicine ,muscle atrophy ,Cancer Research ,medicine.medical_specialty ,endocrine system ,lurbinectedin ,Inflammation ,lcsh:RC254-282 ,Article ,Cachexia ,Proinflammatory cytokine ,03 medical and health sciences ,0302 clinical medicine ,Internal medicine ,medicine ,Wasting ,Myogenin ,Trabectedin ,splenomegaly ,Myogenesis ,business.industry ,medicine.disease ,lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,Muscle atrophy ,030104 developmental biology ,Endocrinology ,Oncology ,inflammation ,030220 oncology & carcinogenesis ,trabectedin ,lipids (amino acids, peptides, and proteins) ,medicine.symptom ,business ,medicine.drug ,cancer cachexia - Abstract
Trabectedin (ET743) and lurbinectedin (PM01183) limit the production of inflammatory cytokines that are elevated during cancer cachexia. Mice carrying C26 colon adenocarcinoma display cachexia (i.e., premature death and body wasting with muscle, fat and cardiac tissue depletion), high levels of inflammatory cytokines and subsequent splenomegaly. We tested whether such drugs protected these mice from cachexia. Ten-week-old mice were inoculated with C26 cells and three days later randomized to receive intravenously vehicle or 0.05 mg/kg ET743 or 0.07 mg/kg PM01183, three times a week for three weeks. ET743 or PM01183 extended the lifespan of C26-mice by 30% or 85%, respectively, without affecting tumor growth or food intake. Within 13 days from C26 implant, both drugs did not protect fat, muscle and heart from cachexia. Since PM01183 extended the animal survival more than ET743, we analyzed PM01183 further. In tibialis anterior of C26-mice, but not in atrophying myotubes, PM01183 restrained the NF-&kappa, B/PAX7/myogenin axis, possibly reducing the pro-inflammatory milieu, and failed to limit the C/EBP&beta, /atrogin-1 axis. Inflammation-mediated splenomegaly of C26-mice was inhibited by PM01183 for as long as the treatment lasted, without reducing IL-6, M-CSF or IL-1&beta, in plasma. ET743 and PM01183 extend the survival of C26-bearing mice unchanging tumor growth or cachexia but possibly restrain muscle-related inflammation and C26-induced splenomegaly.
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- 2020
23. Ranolazine prevents INaL enhancement and blunts myocardial remodelling in a model of pulmonary hypertension
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Antonio Zaza, Carlotta Ronchi, Luca Sala, Lidia Staszewsky, Jacopo Lucchetti, Claudia Altomare, Vanessa Zambelli, Roberto Latini, Riccardo Rizzetto, Marcella Rocchetti, Ilaria Russo, Marco Gobbi, Laura Cornaghi, Matteo Alemanni, Lucio Barile, Gaspare Mostacciuolo, Rocchetti, M, Sala, L, Rizzetto, R, Staszewsky, L, Alemanni, M, Zambelli, V, Russo, I, Barile, L, Cornaghi, L, Altomare, C, Ronchi, C, Mostacciuolo, G, Lucchetti, J, Gobbi, M, Latini, R, Zaza, A, University of Zurich, and Zaza, Antonio
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Male ,Time Factors ,Physiology ,Piperazines ,Sodium Channels ,Muscle hypertrophy ,Membrane Potentials ,Rats, Sprague-Dawley ,2737 Physiology (medical) ,Ranolazine ,Medicine ,Myocytes, Cardiac ,Monocrotaline ,Ventricular Remodeling ,medicine.anatomical_structure ,Ventricular pressure ,Cardiology ,Collagen ,Cardiology and Cardiovascular Medicine ,Sodium Channel Blockers ,medicine.medical_specialty ,Hypertension, Pulmonary ,Diastole ,610 Medicine & health ,Pulmonary Artery ,Vascular Remodeling ,11171 Cardiocentro Ticino ,2705 Cardiology and Cardiovascular Medicine ,Pulmonary hypertension ,Right ventricular hypertrophy ,Arteriole ,medicine.artery ,Internal medicine ,Late sodium current ,Physiology (medical) ,Animals ,Calcium Signaling ,Hypertrophy, Right Ventricular ,Myosin Heavy Chains ,business.industry ,Sodium ,Remodelling ,1314 Physiology ,Hypertrophy ,medicine.disease ,Fibrosis ,Rats ,Disease Models, Animal ,Blood pressure ,Vascular resistance ,Ventricular Function, Right ,Acetanilides ,Vascular Resistance ,business - Abstract
Aims Pulmonary arterial hypertension (PAH) reflects abnormal pulmonary vascular resistance and causes right ventricular (RV) hypertrophy. Enhancement of the late sodium current ( I NaL) may result from hypertrophic remodelling. The study tests whether: (i) constitutive I NaL enhancement may occur as part of PAH-induced myocardial remodelling; (ii) ranolazine (RAN), a clinically available I NaL blocker, may prevent constitutive I NaL enhancement and PAH-induced myocardial remodelling. Methods and results PAH was induced in rats by a single monocrotaline (MCT) injection [60 mg/kg intraperitoneally (i.p.)]; studies were performed 3 weeks later. RAN (30 mg/kg bid i.p.) was administered 48 h after MCT and washed-out 15 h before studies. MCT increased RV systolic pressure and caused RV hypertrophy and loss of left ventricular (LV) mass. In the RV, collagen was increased; myocytes were enlarged with T-tubule disarray and displayed myosin heavy chain isoform switch. I NaL was markedly enhanced; diastolic Ca2+ was increased and Ca2+ release was facilitated. K+ currents were down-regulated and APD was prolonged. In the LV, I NaL was enhanced to a lesser extent and cell Ca2+ content was strongly depressed. Electrical remodelling was less prominent than in the RV. RAN completely prevented I NaL enhancement and limited most aspects of PAH-induced remodelling, but failed to affect in vivo contractile performance. RAN blunted the MCT-induced increase in RV pressure and medial thickening in pulmonary arterioles. Conclusion PAH induced remodelling with chamber-specific aspects. RAN prevented constitutive I NaL enhancement and blunted myocardial remodelling. Partial mechanical unloading, resulting from an unexpected effect of RAN on pulmonary vasculature, might contribute to this effect.
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- 2014
24. Ibuprofen plus Isosorbide Dinitrate treatment in the mdx mice ameliorates dystrophic heart structure
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Emilio Clementi, Lidia Staszewsky, Vanessa Zambelli, Ilaria Russo, Roberto Latini, Clara Sciorati, Deborah Novelli, Giuseppe Di Grigoli, Rosa Maria Moresco, Monica Salio, Sciorati, C, Staszewsky, L, Zambelli, V, Russo, I, Salio, M, Novelli, D, DI GRIGOLI, G, Moresco, R, Clementi, E, and Latini, R
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medicine.medical_specialty ,Skeletal muscle dystrophy ,Inflammation ,Ibuprofen ,030204 cardiovascular system & hematology ,Isosorbide Dinitrate ,Ventricular Function, Left ,Nitric oxide ,03 medical and health sciences ,chemistry.chemical_compound ,Mice ,0302 clinical medicine ,Fibrosis ,Internal medicine ,medicine ,Animals ,Nitric Oxide Donors ,Cardiac Output ,030304 developmental biology ,Pharmacology ,0303 health sciences ,Non steroidal anti-inflammatory drug ,business.industry ,Myocardium ,Anti-Inflammatory Agents, Non-Steroidal ,Wild type ,Skeletal muscle ,Stroke Volume ,Heart ,medicine.disease ,Non steroidal anti-inflammatory drugs ,3. Good health ,Muscular Dystrophy, Duchenne ,medicine.anatomical_structure ,Endocrinology ,chemistry ,Mice, Inbred mdx ,medicine.symptom ,Isosorbide dinitrate ,business ,Heart structure ,medicine.drug - Abstract
Background: Co-administration of ibuprofen (IBU) and isosorbide dinitrate (ISDN) provides synergistic beneficial effects on dystrophic skeletal muscle. Whether this treatment has also cardioprotective effects in this disease was still unknown. Aims: To evaluate the effects of co-administration of IBU and ISDN (a) on left ventricular (LV) structure and function, and (b) on cardiac inflammatory response and fibrosis in mdx mice. Methods: Three groups of mice were studied: mdx mice treated with IBU (50 mg kg−1) + ISDN (30 mg kg−1) administered daily in the diet, mdx mice that received standard diet without drugs and wild type aged-matched mice. Animals were analysed after 10–11 months of treatment. Structural and functional parameters were evaluated by echocardiography while histological analyses were performed to evaluate inflammatory response, collagen deposition, cardiomyocyte number and area. Results: Treatment for 10–11 months with IBU + ISDN preserved LV wall thickness and LV mass. Drug treatment also preserved the total number of cardiomyocytes in the LV and attenuated the increase in cardiomyocyte size, when compared to untreated mdx mice. Moreover, a trend towards a decreased number of inflammatory cells, a reduced LV myocardial interstitial fibrosis and an enhanced global LV function response to stress was observed in treated mdx mice. Conclusions: Treatment for 10–11 months with IBU + ISDN is effective in preventing the alterations in LV morphology of mdx mice while not reaching statistical significance on LV function and cardiac inflammation.
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- 2013
25. Histone deacetylase inhibition enhances self renewal and cardioprotection by human cord blood-derived CD34 cells
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Giulio Pompilio, Lidia Staszewsky, Annarita Soldo, Simona Nanni, Fabiola Molla, Noeleen De Angelis, Paolo Devanna, Maurizio C. Capogrossi, Simona Cosentino, Antonella Farsetti, Elisa Gambini, Ilaria Russo, Roberto Latini, Marco De Simone, Daniele Avitabile, Antonella Biondi, Ilaria Burba, Carlo Gaetano, Maurizio Pesce, Gualtiero I. Colombo, Burba, I, Colombo, G, Staszewsky, L, De Simone, M, Devanna, P, Nanni, S, Avitabile, D, Molla, F, Cosentino, S, Russo, I, De Angelis, N, Soldo, A, Biondi, A, Gambini, E, Gaetano, C, Farsetti, A, Pompilio, G, Latini, R, Capogrossi, M, and Pesce, M
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medicine.medical_treatment ,Cellular differentiation ,Myocardial Infarction ,Gene Expression ,lcsh:Medicine ,Antigens, CD34 ,Cardiovascular ,Cell Fate Determination ,Mice ,Molecular Cell Biology ,Cluster Analysis ,Stem Cell Niche ,lcsh:Science ,Cardioprotection ,Multidisciplinary ,Stem Cells ,Acetylation ,Cell Differentiation ,Histone Modification ,Stem-cell therapy ,Fetal Blood ,Flow Cytometry ,Adult Stem Cells ,Phenotype ,Cord blood ,cardioprotection ,cardiovascular system ,Medicine ,Stem cell ,Research Article ,Cardiotonic Agents ,Cell Potency ,Biology ,Histone Deacetylases ,Vascular Biology ,Genetics ,medicine ,Animals ,Humans ,Regeneration ,Histone deacetylase ,Progenitor cell ,Cord Blood, CD34 cells ,Cell Proliferation ,Wound Healing ,Gene Expression Profiling ,Valproic Acid ,Regeneration (biology) ,lcsh:R ,Settore MED/50 - SCIENZE TECNICHE MEDICHE APPLICATE ,Clone Cells ,Histone Deacetylase Inhibitors ,Immunology ,Cancer research ,lcsh:Q ,Wound healing ,Biomarkers ,Developmental Biology - Abstract
Background: Use of peripheral blood- or bone marrow-derived progenitors for ischemic heart repair is a feasible option to induce neo-vascularization in ischemic tissues. These cells, named Endothelial Progenitors Cells (EPCs), have been extensively characterized phenotypically and functionally. The clinical efficacy of cardiac repair by EPCs cells remains, however, limited, due to cell autonomous defects as a consequence of risk factors. The devise of "enhancement" strategies has been therefore sought to improve repair ability of these cells and increase the clinical benefit. Principal Findings: Pharmacologic inhibition of histone deacetylases (HDACs) is known to enhance hematopoietic stem cells engraftment by improvement of self renewal and inhibition of differentiation in the presence of mitogenic stimuli in vitro. In the present study cord blood-derived CD34 + were pre-conditioned with the HDAC inhibitor Valproic Acid. This treatment affected stem cell growth and gene expression, and improved ischemic myocardium protection in an immunodeficient mouse model of myocardial infarction. Conclusions: Our results show that HDAC blockade leads to phenotype changes in CD34 + cells with enhanced self renewal and cardioprotection. © 2011 Burba et al.
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- 2011
26. Gene therapy augments the efficacy of hematopoietic cell transplantation and fully corrects Mucopolysaccharidosis type I phenotype in the mouse model
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Angelo Quattrini, Francesca Sanvito, Alessandro Rubinacci, Ubaldo Del Carro, Lidia Staszewsky, Daniela Ungaro, Alessandra Biffi, Merel Stok, Letterio S. Politi, Luigi Naldini, Emanuela Mrak, Katherine P. Ponder, Elisabetta Mariani, Ilaria Visigalli, Ilaria Russo, Francesca Cecere, Claudia Godi, Riccardo Brambilla, Paola Di Natale, Stefania Delai, Federica Cerri, Raffaele d’Isa, Carmela Di Domenico, Visigalli, I, Delai, S, Politi, L, Di Domenico, C, Cerri, F, Mrak, E, D'Isa, R, Ungaro, D, Stok, M, Sanvito, F, Mariani, E, Staszewsky, L, Godi, C, Russo, I, Cecere, Francesca, Del Carro, U, Rubinacci, A, Brambilla, R, Quattrini, A, DI NATALE, Paola, Ponder, K, Naldini, L, Biffi, A., Cecere, F, Di Natale, P, and Naldini, Luigi
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Knockout ,medicine.medical_treatment ,Mucopolysaccharidosis ,Genetic enhancement ,Mucopolysaccharidosis I ,Animals ,Bone and Bones ,Brain ,Disease Models, Animal ,Genetic Therapy ,Genetic Vectors ,Hematopoietic Stem Cell Transplantation ,Iduronidase ,Lentivirus ,Mice ,Mice, Knockout ,Phenotype ,Remission Induction ,Treatment Outcome ,Immunology ,Hepatosplenomegaly ,Hematopoietic stem cell transplantation ,HSC gene therapy ,Biochemistry ,Mucopolysaccharidosis type I ,medicine ,Animal ,business.industry ,MPS I disease ,Cell Biology ,Hematology ,Gene Therapy ,medicine.disease ,Transplantation ,Disease Models ,medicine.symptom ,business - Abstract
Type I mucopolysaccharidosis (MPS I) is a lysosomal storage disorder caused by the deficiency of α-L-iduronidase, which results in glycosaminoglycan accumulation in tissues. Clinical manifestations include skeletal dysplasia, joint stiffness, visual and auditory defects, cardiac insufficiency, hepatosplenomegaly, and mental retardation (the last being present exclusively in the severe Hurler variant). The available treatments, enzyme-replacement therapy and hematopoietic stem cell (HSC) transplantation, can ameliorate most disease manifestations, but their outcome on skeletal and brain disease could be further improved. We demonstrate here that HSC gene therapy, based on lentiviral vectors, completely corrects disease manifestations in the mouse model. Of note, the therapeutic benefit provided by gene therapy on critical MPS I manifestations, such as neurologic and skeletal disease, greatly exceeds that exerted by HSC transplantation, the standard of care treatment for Hurler patients. Interestingly, therapeutic efficacy of HSC gene therapy is strictly dependent on the achievement of supranormal enzyme activity in the hematopoietic system of transplanted mice, which allows enzyme delivery to the brain and skeleton for disease correction. Overall, our data provide evidence of an efficacious treatment for MPS I Hurler patients, warranting future development toward clinical testing.
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- 2010
27. Eplerenone, a selective Aldosterone Blocker, improves diastolic Function in aged Rats with small-to-moderate myocardial Infarction
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Lidia Staszewsky, Beatrice Arosio, Fabio Fiordaliso, Eleonora Carlo, Serge Masson, Eugenio Scanziani, Amy E. Rudolph, Antonio Bai, Giorgio Annoni, Elena Martinoli, Roberto Latini, Monica Salio, Carmen Calabresi, Masson, S, Staszewsky, L, Annoni, G, Carlo, E, Arosio, B, Bai, A, Calabresi, C, Martinoli, E, Salio, M, Fiordaliso, F, Scanziani, E, Rudolph, A, and Latini, R
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Male ,medicine.medical_specialty ,Diastole ,Hemodynamics ,Spironolactone ,Kidney ,Ventricular Function, Left ,chemistry.chemical_compound ,Internal medicine ,medicine ,Animals ,echocardiography ,Myocardial infarction ,Rats, Wistar ,Mineralocorticoid Receptor Antagonists ,Analysis of Variance ,Aldosterone ,aldosterone ,business.industry ,Myocardium ,aging ,diastolic function ,medicine.disease ,Eplerenone ,Rats ,aorta ,Treatment Outcome ,myocardial infarction ,chemistry ,Heart failure ,Cardiology ,MED/09 - MEDICINA INTERNA ,Cardiology and Cardiovascular Medicine ,Isovolumic relaxation time ,business ,medicine.drug - Abstract
Background: The incidence of cardiovascular diseases increases rapidly with age, and the elderly suffer higher morbidity and mortality. Aldosterone blockers have shown. benefits in patients with left ventricular (LV) dysfunction and heart failure after myocardial infarction (MI). However, aldosterone blockade efficacy has not been explored in aged animals with MI. Methods and Results: Small-to-moderate MI was induced by coronary artery ligation in 16-month old rats, divided into 3 groups: sham-operated (control, n = 9), MI (n. = 9), and MI fed a diet containing eplerenone (120 mg/kg/day, MI+Eplerenone, n = 9). given 18 days postsurgery and up to sacrifice 3 months later. At. sacrifice, untreated MI rats did not show overt systolic dysfunctiom but they had (1) echocardiographic evidences of impaired relaxation (increase of E wave deceleration time and of isovolumic relaxation time, decrease of peak E wave velocity), (2) hemodynamically impaired LV relaxation (LV -dP/dt from 7413 +/- 720 to 4956 +/- 475 mm Hg/s, P < .05), and (3) significant increase of collagen content in LV interstitium (from 4.27 +/- 0.23 to 5.34 +/- 0.24%, P < .01), and in aorta. (from 19 +/- 1 to 24 +/- 2%, P < .05). Eplerenone normalized echocardiographic and hemodynamic evidences of diastolic dysfunction, as well as myocardial. interstitial collagen and aortic fibrosis. (all parameters statistically different from untreated MI). Conclusion: In aged rats with small to moderate MI, eplerenone normalized diastolic relaxation, possibly through a reduction of interstitial fibrosis.
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- 2004
28. Post-cardiac arrest temporal evolution of left ventricular function in a rat model: speckle-tracking echocardiography and cardiac circulating biomarkers.
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De Giorgio D, Olivari D, Fumagalli F, Novelli D, Cerrato M, Motta F, Ristagno G, Latini R, and Staszewsky L
- Abstract
Aims: There is little information from experimental studies regarding the evolution of post-resuscitation cardiac arrest [post-return of spontaneous circulation (post-ROSC)] myocardial dysfunction during mid-term follow-up. For this purpose, we assessed left ventricular (LV) function and circulating cardiac biomarkers at different time points in a rat model of cardiac arrest (CA)., Methods and Results: Rats were divided into two groups: control and post-ROSC rats. Eight minutes of untreated ventricular fibrillation were followed by 8 min of cardiopulmonary resuscitation. Conventional and speckle-tracking echocardiographic (STE) parameters and cardiac circulating biomarkers concentrations were assessed, at 3, 4, 72, and 96 h post-ROSC. At 3 and 4 h post-ROSC, LV systolic function was severely impaired, and high-sensitivity cardiac troponin T and N-terminal pro-atrial natriuretic peptide (NT-proANP) plasma concentrations were significantly increased, compared with control rats ( P < 0.0001 for all). At 72 and 96 h post-ROSC, LV ejection fraction (LVEF) normalized. At 96 h, the following variables were significantly different from control rats: early trans-mitral peak velocity, 56.8 ± 3.1 vs. 87.8 ± 3.8 cm/s, P < 0.0001; late trans-mitral peak velocity, 50.6 ± 4.7 vs. 73.7 ± 4.2 cm/s, P < 0.0001; mean s' wave velocity, 4.6 ± 0.3 vs. 5.9 ± 0.3 cm/s, P < 0.0001, global longitudinal strain (GLS) -7.5 ± 0.5 and vs. -11 ± 1.2%, P < 0.01; GLS rate (GLSR) -0.9 ± 0.4 and -2.3 ± 0.2 1/s, P < 0.01; and NT-proANP concentration, 2.5 (0.2; 6.0) vs. 0.4 (0.01; 1.0) nmol/L, P < 0.01., Conclusion: s' velocity, GLS, and GLSR indicated that LV systolic function was still impaired 96 h post-ROSC. These findings agree with NT-proANP concentrations, which continue to be high. Normalization of LVEF supports the use of STE for its greater sensitivity for monitoring post-CA cardiac function. Further investigations are needed to provide evidence of the post-ROSC LV diastolic function pattern., Competing Interests: Conflict of interest: None declared., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.)
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- 2024
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29. Characterization of the Cardiac Structure and Function of Conscious D2.B10- Dmd mdx /J (D2- mdx ) mice from 16-17 to 24-25 Weeks of Age.
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De Giorgio D, Novelli D, Motta F, Cerrato M, Olivari D, Salama A, Fumagalli F, Latini R, Staszewsky L, Crippa L, Steinkühler C, and Licandro SA
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- Animals, Mice, Mice, Inbred mdx, Heart, Fibrosis, Disease Models, Animal, Muscle, Skeletal pathology, Muscular Dystrophy, Duchenne pathology, Cardiomyopathies pathology, Ventricular Dysfunction, Left pathology
- Abstract
Duchenne muscular dystrophy (DMD) is the most common form of muscle degenerative hereditary disease. Muscular replacement by fibrosis and calcification are the principal causes of progressive and severe musculoskeletal, respiratory, and cardiac dysfunction. To date, the D2.B10- Dmd
mdx /J (D2- mdx ) model is proposed as the closest to DMD, but the results are controversial. In this study, the cardiac structure and function was characterized in D2- mdx mice from 16-17 up to 24-25 weeks of age. Echocardiographic assessment in conscious mice, gross pathology, and histological and cardiac biomarker analyses were performed. At 16-17 weeks of age, D2- mdx mice presented mild left ventricular function impairment and increased pulmonary vascular resistance. Cardiac fibrosis was more extended in the right ventricle, principally on the epicardium. In 24-25-week-old D2- mdx mice, functional and structural alterations increased but with large individual variation. High-sensitivity cardiac Troponin T, but not N-terminal pro-atrial natriuretic peptide, plasma levels were increased. In conclusion, left ventricle remodeling was mild to moderate in both young and adult mice. We confirmed that right ventricle epicardial fibrosis is the most outstanding finding in D2- mdx mice. Further long-term studies are needed to evaluate whether this mouse model can also be considered a model of DMD cardiomyopathy.- Published
- 2023
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30. Scientific and ethical issues in add-on designs for antidiabetic drugs.
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Staszewsky L and Garattini S
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- Clinical Trials as Topic, Drug Therapy, Combination, Humans, Metformin therapeutic use, Sulfonylurea Compounds, Diabetes Mellitus, Type 2 drug therapy, Hypoglycemic Agents therapeutic use
- Abstract
This editorial describes the clinical trials related to antidiabetic drugs, most of them following an "add-on" design of where the new drug is added to metformin and the comparative arm is metformin plus placebo. Many drugs are already approved for therapy following this design; the authors believe that it is unethical to continue this trend because it makes it impossible to stratify the many antidiabetic drugs according to their efficacy and toxicity., (© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)
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- 2022
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31. Circulating levels and prognostic cut-offs of sST2, hs-cTnT, and NT-proBNP in women vs. men with chronic heart failure.
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Vergaro G, Gentile F, Aimo A, Januzzi JL Jr, Richards AM, Lam CSP, de Boer RA, Meems LMG, Latini R, Staszewsky L, Anand IS, Cohn JN, Ueland T, Gullestad L, Aukrust P, Brunner-La Rocca HP, Bayes-Genis A, Lupón J, Yoshihisa A, Takeishi Y, Egstrup M, Gustafsson I, Gaggin HK, Eggers KM, Huber K, Gamble GD, Ling LH, Leong KTG, Yeo PSD, Ong HY, Jaufeerally F, Ng TP, Troughton R, Doughty RN, Devlin G, Lund M, Giannoni A, Passino C, and Emdin M
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- Aged, Biomarkers, Chronic Disease, Female, Humans, Male, Middle Aged, Peptide Fragments, Prognosis, Stroke Volume, Troponin T, Ventricular Function, Left, Heart Failure diagnosis, Interleukin-1 Receptor-Like 1 Protein blood, Natriuretic Peptide, Brain
- Abstract
Aims: To define plasma concentrations, determinants, and optimal prognostic cut-offs of soluble suppression of tumorigenesis-2 (sST2), high-sensitivity cardiac troponin T (hs-cTnT), and N-terminal pro-B-type natriuretic peptide (NT-proBNP) in women and men with chronic heart failure (HF)., Methods and Results: Individual data of patients from the Biomarkers In Heart Failure Outpatient Study (BIOS) Consortium with sST2, hs-cTnT, and NT-proBNP measured were analysed. The primary endpoint was a composite of 1 year cardiovascular death and HF hospitalization. The secondary endpoints were 5 year cardiovascular and all-cause death. The cohort included 4540 patients (age 67 ± 12 years, left ventricular ejection fraction 33 ± 13%, 1111 women, 25%). Women showed lower sST2 (24 vs. 27 ng/mL, P < 0.001) and hs-cTnT level (15 vs. 20 ng/L, P < 0.001), and similar concentrations of NT-proBNP (1540 vs. 1505 ng/L, P = 0.408). Although the three biomarkers were confirmed as independent predictors of outcome in both sexes, the optimal prognostic cut-off was lower in women for sST2 (28 vs. 31 ng/mL) and hs-cTnT (22 vs. 25 ng/L), while NT-proBNP cut-off was higher in women (2339 ng/L vs. 2145 ng/L). The use of sex-specific cut-offs improved risk prediction compared with the use of previously standardized prognostic cut-offs and allowed to reclassify the risk of many patients, to a greater extent in women than men, and for hs-cTnT than sST2 or NT-proBNP. Specifically, up to 18% men and up to 57% women were reclassified, by using the sex-specific cut-off of hs-cTnT for the endpoint of 5 year cardiovascular death., Conclusions: In patients with chronic HF, concentrations of sST2 and hs-cTnT, but not of NT-proBNP, are lower in women. Lower sST2 and hs-cTnT and higher NT-proBNP cut-offs for risk stratification could be used in women., (© 2022 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.)
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- 2022
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32. Transthoracic Echocardiography to Assess Post-Resuscitation Left Ventricular Dysfunction After Acute Myocardial Infarction and Cardiac Arrest in Pigs.
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De Giorgio D, Olivari D, Fumagalli F, Staszewsky L, and Ristagno G
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- Animals, Diastole, Echocardiography, Echocardiography, Doppler, Pulsed adverse effects, Echocardiography, Doppler, Pulsed methods, Swine, Ventricular Function, Left, Heart Arrest diagnostic imaging, Heart Arrest etiology, Heart Arrest therapy, Myocardial Infarction complications, Myocardial Infarction diagnostic imaging, Ventricular Dysfunction, Left
- Abstract
One of the main causes of out-of-hospital cardiac arrest is acute myocardial infarction (AMI). After successful resuscitation from cardiac arrest, approximately 70% of patients die before hospital discharge due to post-resuscitation myocardial and cerebral dysfunction. In experimental models, myocardial dysfunction after cardiac arrest, characterized by an impairment in both left ventricular (LV) systolic and diastolic function, has been described as reversible but very little data are available in cardiac arrest models associated with AMI in pigs. Transthoracic echocardiography is the first-line diagnostic test for the assessment of myocardial dysfunction, structural changes and/or AMI extension. In this pig model of ischemic cardiac arrest, echocardiography was done at baseline and 2-4 and 96 hours after resuscitation. In the acute phase, the examinations are done in anesthetized, mechanically ventilated pigs (weight 39.8 ± 0.6 kg) and ECG is recorded continuously. Mono- and bi-dimensional, Doppler and tissue Doppler recordings are acquired. Aortic and left atrium diameter, end-systolic and end-diastolic left ventricular wall thicknesses, end-diastolic and end-systolic diameters and shortening fraction (SF) are measured. Apical 2-, 3-, 4-, and 5-chamber views are acquired, LV volumes and ejection fraction are calculated. Segmental wall motion analysis is done to detect the localization and estimate the extent of myocardial infarction. Pulsed Wave Doppler echocardiography is used to record trans-mitral flow velocities from a 4-apical chamber view and trans-aortic flow from a 5-chamber view to calculate LV cardiac output (CO) and stroke volume (SV). Tissue Doppler Imaging (TDI) of LV lateral and septal mitral anulus is recorded (TDI septal and lateral s', e', a' velocities). All the recordings and measurements are done according to the recommendations of the American and European Societies of Echocardiography Guidelines.
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- 2022
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33. Rationale and design of the pragmatic clinical trial tREatment with Beta-blockers after myOcardial infarction withOut reduced ejection fracTion (REBOOT).
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Rossello X, Raposeiras-Roubin S, Latini R, Dominguez-Rodriguez A, Barrabés JA, Sánchez PL, Anguita M, Fernández-Vázquez F, Pascual-Figal D, De la Torre Hernandez JM, Ferraro S, Vetrano A, Pérez-Rivera JA, Prada-Delgado O, Escalera N, Staszewsky L, Pizarro G, Agüero J, Pocock S, Ottani F, Fuster V, and Ibáñez B
- Subjects
- Adrenergic beta-Antagonists adverse effects, Humans, Prospective Studies, Stroke Volume, Ventricular Function, Left, Myocardial Infarction complications, Myocardial Infarction diagnosis, Myocardial Infarction drug therapy, Ventricular Dysfunction, Left drug therapy
- Abstract
Aims: There is a lack of evidence regarding the benefits of β-blocker treatment after invasively managed acute myocardial infarction (MI) without reduced left ventricular ejection fraction (LVEF)., Methods and Results: The tREatment with Beta-blockers after myOcardial infarction withOut reduced ejection fracTion (REBOOT) trial is a pragmatic, controlled, prospective, randomized, open-label blinded endpoint (PROBE design) clinical trial testing the benefits of β-blocker maintenance therapy in patients discharged after MI with or without ST-segment elevation. Patients eligible for participation are those managed invasively during index hospitalization (coronary angiography), with LVEF >40%, and no history of heart failure (HF). At discharge, patients will be randomized 1:1 to β-blocker therapy (agent and dose according to treating physician) or no β-blocker therapy. The primary endpoint is a composite of all-cause death, non-fatal reinfarction, or HF hospitalization over a median follow-up period of 2.75 years (minimum 2 years, maximum 3 years). Key secondary endpoints include the incidence of the individual components of the primary composite endpoint, the incidence of cardiac death, and incidence of malignant ventricular arrhythmias or resuscitated cardiac arrest. The primary endpoint will be analysed according to the intention-to-treat principle., Conclusion: The REBOOT trial will provide robust evidence to guide the prescription of β-blockers to patients discharged after MI without reduced LVEF., (© The Author(s) 2021. Published by Oxford University Press on behalf of the European Society of Cardiology.)
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- 2022
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34. Insulin treatment in patients with diabetes mellitus and heart failure in the era of new antidiabetic medications.
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Staszewsky L, Baviera M, Tettamanti M, Colacioppo P, Robusto F, D'Ettorre A, Lepore V, Fortino I, Bisceglia L, Attolini E, Graps EA, Caldo G, Roncaglioni MC, Garattini S, and Latini R
- Subjects
- Female, Glucagon-Like Peptide-1 Receptor agonists, Humans, Hypoglycemic Agents therapeutic use, Insulin therapeutic use, Male, Middle Aged, Diabetes Mellitus, Type 2 complications, Diabetes Mellitus, Type 2 drug therapy, Heart Failure complications, Heart Failure drug therapy, Heart Failure epidemiology, Sodium-Glucose Transporter 2 Inhibitors therapeutic use
- Abstract
Background: Coexistent heart failure (HF) and diabetes mellitus (DM) are associated with marked morbidity and mortality. Optimizing treatment strategies can reduce the number and severity of events. Insulin is frequently used in these patients, but its benefit/risk ratio is still not clear, particularly since new antidiabetic drugs that reduce major adverse cardiac events (MACEs) and renal failure have recently come into use. Our aim is to compare the clinical effects of insulin in a real-world setting of first-time users, with sodium-glucose cotransporter-2 inhibitor (SGLT-2i), glucagon-like peptide-1 receptor agonist (GLP-1RA) and the other antihyperglycemic agents (other-AHAs)., Methods: We used the administrative databases of two Italian regions, during the years 2010-2018. Outcomes in whole and propensity-matched cohorts were examined using Cox models. A meta-analysis was also conducted combining the data from both regions., Results: We identified 34 376 individuals ≥50 years old with DM and HF; 42.0% were aged >80 years and 46.7% were women. SGLT-2i and GLP-1RA significantly reduced MACE compared with insulin and particularly death from any cause (SGLT-2i, hazard ratio (95% CI) 0.29 (0.23 to 0.36); GLP-1RA, 0.482 (0.51 to 0.42)) and first hospitalization for HF (0.57 (0.40 to 0.81) and 0.67 (0.59 to 0.76))., Conclusions: In patients with DM and HF, SGLT-2i and GLP-1RA significantly reduced MACE compared with insulin, and particularly any cause of death and first hospitalization for HF. These groups of medications had high safety profiles compared with other-AHAs and particularly with insulin. The inadequate optimization of HF and DM cotreatment in the insulin cohort is noteworthy., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)
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- 2022
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35. Cancer Incidence and Mortality According to Pre-Existing Heart Failure in a Community-Based Cohort.
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Bertero E, Robusto F, Rulli E, D'Ettorre A, Bisceglia L, Staszewsky L, Maack C, Lepore V, Latini R, and Ameri P
- Abstract
Background: Studies assessing whether heart failure (HF) is associated with cancer and cancer-related mortality have yielded conflicting results., Objectives: This study assessed cancer incidence and mortality according to pre-existing HF in a community-based cohort., Methods: Among individuals ≥50 years of age from the Puglia region in Italy with administrative health data from 2002 to 2018, no cancer within 3 years before the baseline evaluation, and ≥5-year follow-up, the study matched 104,020 subjects with HF at baseline with 104,020 control subjects according to age, sex, drug-derived complexity index, Charlson comorbidity index, and follow-up duration. Cancer incidence and mortality were defined based on International Classification of Diseases-Ninth Revision codes in hospitalization records or death certificates., Results: The incidence rate of cancer in HF patients and control subjects was 21.36 (95% CI: 20.98-21.74) and 12.42 (95% CI: 12.14-12.72) per 1000 person-years, respectively, with the HR being 1.76 (95% CI: 1.71-1.81). Cancer mortality was also higher in HF patients than control subjects (HR: 4.11; 95% CI: 3.86-4.38), especially in those <70 years of age (HR: 7.54; 95% CI: 6.33-8.98 vs HR: 3.80; 95% CI: 3.44-4.19 for 70-79 years of age; and HR: 3.10; 95% CI: 2.81-3.43 for ≥80 years of age). The association between HF and cancer mortality was confirmed in a competing risk analysis (subdistribution HR: 3.48; 95% CI: 3.27-3.72). The HF-related excess risk applied to the majority of cancer types. Among HF patients, prescription of high-dose loop diuretic was associated with higher cancer incidence (HR: 1.11; 95% CI: 1.03-1.21) and mortality (HR: 1.35; 95% CI: 1.19-1.53)., Conclusions: HF is associated with an increased risk of cancer and cancer-related mortality, which may be heightened in decompensated states., Competing Interests: This research was supported by the Italian Ministry of Health (GR-2018-12365661 - CHANGE Study, principal investigator Pietro Ameri) and is part of the work covered by the 2015-2020 Collaboration between the Regional Healthcare Agency of Puglia Region (AReSS Puglia) and the Istituto di Ricerche Farmacologiche Mario Negri IRCCS. Dr Maack was supported by the Barth Syndrome Foundation, the German Research Foundation (Ma 2528/7-1, SFB 894, TRR-219), and the German Federal Agency for Education and Research (01EO1504). The authors have reported that they have no relationships relevant to the contents of this paper to disclose., (© 2022 The Authors.)
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- 2022
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36. Cardiac biomarkers retain prognostic significance in patients with heart failure and chronic obstructive pulmonary disease.
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Vergaro G, Aimo A, Januzzi JL Jr, Richards AM, Lam CSP, Latini R, Staszewsky L, Anand IS, Ueland T, Rocca HB, Bayes-Genis A, Lupón J, de Boer RA, Yoshihisa A, Takeishi Y, Gustafsson I, Eggers KM, Huber K, Gamble GD, Leong KTG, Yeo PSD, Ong HY, Jaufeerally F, Ng TP, Troughton R, Doughty RN, Emdin M, and Passino C
- Subjects
- Aged, Biomarkers blood, Female, Forced Expiratory Volume, Humans, Interleukin-1 Receptor-Like 1 Protein blood, Male, Middle Aged, Natriuretic Peptide, Brain blood, Peptide Fragments blood, Prognosis, Severity of Illness Index, Troponin T blood, Heart Failure mortality, Hospitalization, Pulmonary Disease, Chronic Obstructive mortality
- Abstract
Aims: Chronic obstructive pulmonary disease (COPD) is a frequent comorbidity in patients with heart failure (HF). We assessed the influence of COPD on circulating levels and prognostic value of three HF biomarkers: N-terminal pro-B-type natriuretic peptide (NT-proBNP), high-sensitivity troponin T (hs-TnT), and soluble suppression of tumorigenesis-2 (sST2)., Methods: Individual data from patients with chronic HF, known COPD status, NT-proBNP and hs-TnT values (n = 8088) were analysed. A subgroup (n = 3414) had also sST2 values., Results: Patients had a median age of 66 years (interquartile interval 57-74), 77% were men and 82% had HF with reduced ejection fraction. NT-proBNP, hs-TnT and sST2 were 1207 ng/l (487-2725), 17 ng/l (9-31) and 30 ng/ml (22-44), respectively. Patients with COPD (n = 1249, 15%) had higher NT-proBNP (P = 0.042) and hs-TnT (P < 0.001), but not sST2 (P = 0.165). Over a median 2.0-year follow-up (1.5-2.5), 1717 patients (21%) died, and 1298 (16%) died from cardiovascular causes; 2255 patients (28%) were hospitalized for HF over 1.8 years (0.9-2.1). NT-proBNP, hs-TnT and sST2 predicted the three end points regardless of COPD status. The best cut-offs from receiver-operating characteristics analysis were higher in patients with COPD than in those without. Patients with all three biomarkers higher than or equal to end-point- and COPD-status-specific cut-offs were also those with the worst prognosis., Conclusions: Among patients with HF, those with COPD have higher NT-proBNP and hs-TnT, but not sST2. All these biomarkers yield prognostic significance regardless of the COPD status., (Copyright © 2021 Italian Federation of Cardiology - I.F.C. All rights reserved.)
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- 2022
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37. Brain Kynurenine Pathway and Functional Outcome of Rats Resuscitated From Cardiac Arrest.
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Lucchetti J, Fumagalli F, Olivari D, Affatato R, Fracasso C, De Giorgio D, Perego C, Motta F, Passoni A, Staszewsky L, Novelli D, Magliocca A, Garattini S, Latini R, Ristagno G, and Gobbi M
- Subjects
- Animals, Rats, Functional Status, Treatment Outcome, Tryptophan metabolism, Brain physiopathology, Cardiopulmonary Resuscitation, Heart Arrest therapy, Kynurenine metabolism
- Abstract
Background Brain injury and neurological deficit are consequences of cardiac arrest (CA), leading to high morbidity and mortality. Peripheral activation of the kynurenine pathway (KP), the main catabolic route of tryptophan metabolized at first into kynurenine, predicts poor neurological outcome in patients resuscitated after out-of-hospital CA. Here, we investigated KP activation in hippocampus and plasma of rats resuscitated from CA, evaluating the effect of KP modulation in preventing CA-induced neurological deficit. Methods and Results Early KP activation was first demonstrated in 28 rats subjected to electrically induced CA followed by cardiopulmonary resuscitation. Hippocampal levels of the neuroactive metabolites kynurenine, 3-hydroxy-anthranilic acid, and kynurenic acid were higher 2 hours after CA, as in plasma. Further, 36 rats were randomized to receive the inhibitor of the first step of KP, 1-methyl-DL-tryptophan, or vehicle, before CA. No differences were observed in hemodynamics and myocardial function. The CA-induced KP activation, sustained up to 96 hours in hippocampus (and plasma) of vehicle-treated rats, was counteracted by the inhibitor as indicated by lower hippocampal (and plasmatic) kynurenine/tryptophan ratio and kynurenine levels. 1-Methyl-DL-tryptophan reduced the CA-induced neurological deficits, with a significant correlation between the neurological score and the individual kynurenine levels, as well as the kynurenine/tryptophan ratio, in plasma and hippocampus. Conclusions These data demonstrate the CA-induced lasting activation of the first step of the KP in hippocampus, showing that this activation was involved in the evolving neurological deficit. The degree of peripheral activation of KP may predict neurological function after CA.
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- 2021
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38. Total NT-proBNP, a novel biomarker related to recurrent atrial fibrillation.
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Staszewsky L, Meessen JMTA, Novelli D, Wienhues-Thelen UH, Disertori M, Maggioni AP, Masson S, Tognoni G, Franzosi MG, Lucci D, and Latini R
- Subjects
- Aged, Atrial Fibrillation diagnosis, Biomarkers blood, Double-Blind Method, Echocardiography, Electrocardiography, Female, Glycosylation, Hospitalization, Humans, Male, Middle Aged, Predictive Value of Tests, Protein Processing, Post-Translational, Recurrence, Risk Assessment, Risk Factors, Time Factors, Treatment Outcome, Atrial Fibrillation blood, Natriuretic Peptide, Brain blood, Peptide Fragments blood
- Abstract
Background: Novel circulating biomarkers may help in understanding the underlying mechanisms of atrial fibrillation (AF), a challenge for AF management and prevention of cardiovascular (CV) events. Whether glycosylation affects the prognostic value of N-terminal pro-B type natriuretic peptide (NT-proBNP) in AF is still unknown., Objectives: To test how deglycosylated total NT-proBNP, NT-proBNP and a panel of biomarkers are associated with: (1) recurrent AF, (2) first hospitalization for CV reasons., Methods: A total of 382 patients of the GISSI-AF trial in sinus rhythm with a history of AF, echocardiographic variables, total NT-proBNP, NT-proBNP and nine additional biomarkers [Total N-terminal pro-B type natriuretic peptide (Total NT proBNP), N-terminal pro-B type natriuretic peptide (NTproBNP), Angiopoietin 2 (Ang2), Bone morphogenic protein-10 (BMP10), Dickkopf-related protein-3 (DKK3), Endothelial cell specific molecule-1 (ESM1), Fatty acid-binding protein 3 (FABP3), Fibroblast growth factor 23 (FGF23), Growth differentiation factor-15 (GDF15), Insulin-like growth factor-binding protein-7 (IGFBP7) and Myosin binding protein C3 (MYPBC3)]. were assayed at baseline, 6 and 12 months under blind conditions in a laboratory at Roche Diagnostics, Penzberg, Germany. The associations between circulating biomarkers and AF at the 6- and 12-month visits, and their predictive value, were assessed in multivariable models with logistic regression analysis and Cox proportional hazards regression analysis. Biomarkers associations were modelled for 1SD increase in their level., Results: Over a median follow-up of 365 days, 203/382 patients (53.1%) had at least one recurrence of AF and 16.3% were hospitalized for CV reasons. Total NT-proBNP, NT-proBNP, Ang2 and BMP10 showed the strongest associations with ongoing AF. Natriuretic peptides also predicted recurrent AF (total NT-proBNP: HR:1.19[1.04-1.36], p = 0.026; NT-proBNP: HR:1.19[1.06-1.35], p = 0.016; Ang2: HR:1.07[0.95-1.20], p = 0.283; BMP10: HR:1.09[0.96-1.25], p = 0.249) and CV hospitalization (total NT-proBNP: HR:1.57[1.29-1.90], p < 0.001 1.63], p = 0.097)., Conclusions: The association of total NT-proBNP with the risk of AF first recurrence was similar to that of NT-proBNP, suggesting no influence of glycosylation. Analogous results were obtained for the risk of first hospitalization for CV reasons. Natriuretic peptides, Ang2 and BMP10 were associated with ongoing AF. Findings from the last two biomarkers point to a pathogenic role of cardiac extracellular matrix and cardiomyocyte growth in the myocardium of the right atrium and ventricle., (© 2021. The Author(s).)
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- 2021
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39. NT-proBNP for Risk Prediction in Heart Failure: Identification of Optimal Cutoffs Across Body Mass Index Categories.
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Vergaro G, Gentile F, Meems LMG, Aimo A, Januzzi JL Jr, Richards AM, Lam CSP, Latini R, Staszewsky L, Anand IS, Cohn JN, Ueland T, Gullestad L, Aukrust P, Brunner-La Rocca HP, Bayes-Genis A, Lupón J, Yoshihisa A, Takeishi Y, Egstrup M, Gustafsson I, Gaggin HK, Eggers KM, Huber K, Gamble GD, Ling LH, Leong KTG, Yeo PSD, Ong HY, Jaufeerally F, Ng TP, Troughton R, Doughty RN, Devlin G, Lund M, Giannoni A, Passino C, de Boer RA, and Emdin M
- Subjects
- Aged, Biomarkers, Body Mass Index, Female, Humans, Male, Middle Aged, Peptide Fragments, Prognosis, Stroke Volume, Ventricular Function, Left, Heart Failure, Natriuretic Peptide, Brain
- Abstract
Objectives: The goal of this study was to assess the predictive power of N-terminal pro-B-type natriuretic peptide (NT-proBNP) and the decision cutoffs in heart failure (HF) across body mass index (BMI) categories., Background: Concentrations of NT-proBNP predict outcome in HF. Although the influence of BMI to reduce levels of NT-proBNP is known, the impact of obesity on prognostic value remains uncertain., Methods: Individual data from the BIOS (Biomarkers In Heart Failure Outpatient Study) consortium were analyzed. Patients with stable HF were classified as underweight (BMI <18.5 kg/m
2 ), normal weight (BMI 18.5-24.9 kg/m2 ), overweight (BMI 25-29.9 kg/m2 ), and mildly (BMI 30-34.9 kg/m2 ), moderately (BMI 35-39.9 kg/m2 ), or severely (BMI ≥40 kg/m2 ) obese. The prognostic role of NT-proBNP was tested for the endpoints of all-cause and cardiac death., Results: The study population included 12,763 patients (mean age 66 ± 12 years; 25% women; mean left ventricular ejection fraction 33% ± 13%). Most patients were overweight (n = 5,176), followed by normal weight (n = 4,299), mildly obese (n = 2,157), moderately obese (n = 612), severely obese (n = 314), and underweight (n = 205). NT-proBNP inversely correlated with BMI (β = -0.174 for 1 kg/m2 ; P < 0.001). Adding NT-proBNP to clinical models improved risk prediction across BMI categories, with the exception of severely obese patients. The best cutoffs of NT-proBNP for 5-year all-cause death prediction were lower as BMI increased (3,785 ng/L, 2,193 ng/L, 1,554 ng/L, 1,045 ng/L, 755 ng/L, and 879 ng/L, for underweight, normal weight, overweight, and mildly, moderately, and severely obese patients, respectively) and were higher in women than in men., Conclusions: NT-proBNP maintains its independent prognostic value up to 40 kg/m2 BMI, and lower optimal risk-prediction cutoffs are observed in overweight and obese patients., Competing Interests: Funding Support and Author Disclosures Dr Januzzi is supported in part by the Hutter Family Professorship; is a Trustee of the American College of Cardiology; has received grant support from Novartis Pharmaceuticals, Roche Diagnostics, Abbott, Singulex and Prevencio; has received consulting income from Abbott, Janssen, Novartis, Pfizer, Merck, and Roche Diagnostics; and participates in clinical endpoint committees/data safety monitoring boards for Abbott, AbbVie, Amgen, Boehringer Ingelheim, Janssen, and Takeda. Dr Richards has sat on advisory boards and/or received speakers honoraria, travel support, and/or grants from Novartis, Roche Diagnostics, Abbott Laboratories, Thermo Fisher, and Critical Diagnostics. Dr Lam is supported by a Clinician Scientist Award from the National Medical Research Council of Singapore; has received research support from Boston Scientific, Bayer, Roche Diagnostics, AstraZeneca, Medtronic, and Vifor Pharma; has served as consultant or on the Advisory Board/ Steering Committee/Executive Committee for Boston Scientific, Bayer, Roche Diagnostics, AstraZeneca, Medtronic, Vifor Pharma, Novartis, Amgen, Merck, Janssen Research & Development LLC, Menarini, Boehringer Ingelheim, Novo Nordisk, Abbott Diagnostics, Corvia, Stealth BioTherapeutics, JanaCare, Biofourmis, Darma, Applied Therapeutics, MyoKardia, WebMD Global LLC, Radcliffe Group Ltd, and Corpus. Dr Latini has received grant support and travel reimbursements from Roche Diagnostics. Dr Brunner-La Rocca reports unrestricted research grants and consulting fees from Roche Diagnostics, as well as unrestricted research grants from Novartis and GlaxoSmithKline outside this work. Dr Bayes-Genis has received grant support from Roche Diagnosis, lecture honoraria from Roche Diagnostics and Critical Diagnostics, and consulting income from Roche Diagnostics, Critical Diagnostics, and Novartis. Dr Lupón has received lecture honoraria from Roche Diagnostics and Critical Diagnostics. The University Medical Centre Groningen, which employs Drs De Boer and Meems, has received research grants and/or fees from AstraZeneca, Abbott, Boehringer Ingelheim, Cardior Pharmaceuticals Gmbh, Ionis Pharmaceuticals, Inc, Novo Nordisk, and Roche. Dr de Boer received speaker fees from Abbott, AstraZeneca, Bayer, Novartis, and Roche, outside the submitted work. Dr Gaggin has received grant support from Roche and Portola; consulting income from Roche Diagnostics, Amgen, and Ortho Clinical; and research payments for clinical endpoint committees for EchoSense and Radiometer. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Copyright © 2021 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)- Published
- 2021
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40. IGFBP7 and GDF-15, but not P1NP, are associated with cardiac alterations and 10-year outcome in an elderly community-based study.
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Meessen JMTA, Cesaroni G, Mureddu GF, Boccanelli A, Wienhues-Thelen UH, Kastner P, Ojeda-Fernandez L, Novelli D, Bazzoni G, Mangiavacchi M, Agabiti N, Masson S, Staszewsky L, and Latini R
- Subjects
- Age Factors, Aged, Aged, 80 and over, Biomarkers blood, Cause of Death, Cross-Sectional Studies, Female, Heart Failure diagnosis, Heart Failure mortality, Heart Failure physiopathology, Humans, Italy epidemiology, Male, Peptide Fragments blood, Prevalence, Procollagen blood, Prognosis, Registries, Risk Assessment, Risk Factors, Time Factors, Ventricular Dysfunction, Left diagnosis, Ventricular Dysfunction, Left mortality, Ventricular Dysfunction, Left physiopathology, Growth Differentiation Factor 15 blood, Heart Failure blood, Insulin-Like Growth Factor Binding Proteins blood, Ventricular Dysfunction, Left blood
- Abstract
Background: Little is known about the clinical value of Insulin-like growth factor-binding protein-7 (IGFBP7), a cellular senescence marker, in an elderly general population with multiple co-morbidities and high prevalence of asymptomatic cardiovascular ventricular dysfunction. Inflammation and fibrosis are hallmarks of cardiac aging and remodelling. Therefore, we assessed the clinical performance of IGFBP7 and two other biomarkers reflecting these pathogenic pathways, the growth differentiation factor-15 (GFD-15) and amino-terminal propeptide of type I procollagen (P1NP), for their association with cardiac phenotypes and outcomes in the PREDICTOR study., Methods: 2001 community-dwelling subjects aged 65-84 years who had undergone centrally-read echocardiography, were selected through administrative registries. Atrial fibrillation (AF) and 4 echocardiographic patterns were assessed: E/e' (> 8), enlarged left atrial area, left ventricular hypertrophy (LVH) and reduced midwall circumference shortening (MFS). All-cause and cardiovascular mortality and hospitalization were recorded over a median follow-up of 10.6 years., Results: IGFBP7 and GDF-15, but not P1NP, were independently associated with prevalent AF and echocardiographic variables after adjusting for age and sex. After adjustment for clinical risk factors and cardiac patterns or NT-proBNP and hsTnT, both IGFBP7 and GDF-15 independently predicted all-cause mortality, hazard ratios 2.13[1.08-4.22] and 2.03[1.62-2.56] per unit increase of Ln-transformed markers, respectively., Conclusions: In a community-based elderly cohort, IGFBP7 and GDF-15 appear associated to cardiac alterations as well as to 10-year risk of all-cause mortality.
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- 2021
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41. Ventilation with the noble gas argon in an in vivo model of idiopathic pulmonary arterial hypertension in rats.
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De Giorgio D, Magliocca A, Fumagalli F, Novelli D, Olivari D, Staszewsky L, Latini R, and Ristagno G
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- Animals, Argon, Familial Primary Pulmonary Hypertension, Rats, Lung, Respiration
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- 2021
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42. Esmolol during cardiopulmonary resuscitation reduces neurological injury in a porcine model of cardiac arrest.
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Ruggeri L, Nespoli F, Ristagno G, Fumagalli F, Boccardo A, Olivari D, Affatato R, Novelli D, De Giorgio D, Romanelli P, Minoli L, Cucino A, Babini G, Staszewsky L, Zani D, Pravettoni D, Belloli A, Scanziani E, Latini R, and Magliocca A
- Subjects
- Animals, Blood Gas Analysis, Brain pathology, Disease Models, Animal, Heart Arrest blood, Heart Arrest complications, Heart Arrest physiopathology, Hemodynamics drug effects, Male, Nerve Degeneration blood, Nerve Degeneration complications, Nerve Degeneration pathology, Neurons drug effects, Perfusion, Phosphopyruvate Hydratase blood, Pressure, Propanolamines pharmacology, Swine, Cardiopulmonary Resuscitation, Heart Arrest drug therapy, Neurons pathology, Propanolamines therapeutic use
- Abstract
Primary vasopressor efficacy of epinephrine during cardiopulmonary resuscitation (CPR) is due to its α-adrenergic effects. However, epinephrine plays β1-adrenergic actions, which increasing myocardial oxygen consumption may lead to refractory ventricular fibrillation (VF) and poor outcome. Effects of a single dose of esmolol in addition to epinephrine during CPR were investigated in a porcine model of VF with an underlying acute myocardial infarction. VF was ischemically induced in 16 pigs and left untreated for 12 min. During CPR, animals were randomized to receive epinephrine (30 µg/kg) with either esmolol (0.5 mg/kg) or saline (control). Pigs were then observed up to 96 h. Coronary perfusion pressure increased during CPR in the esmolol group compared to control (47 ± 21 vs. 24 ± 10 mmHg at min 5, p < 0.05). In both groups, 7 animals were successfully resuscitated and 4 survived up to 96 h. No significant differences were observed between groups in the total number of defibrillations delivered prior to final resuscitation. Brain histology demonstrated reductions in cortical neuronal degeneration/necrosis (score 0.3 ± 0.5 vs. 1.3 ± 0.5, p < 0.05) and hippocampal microglial activation (6 ± 3 vs. 22 ± 4%, p < 0.01) in the esmolol group compared to control. Lower circulating levels of neuron specific enolase were measured in esmolol animals compared to controls (2[1-3] vs. 21[16-52] ng/mL, p < 0.01). In this preclinical model, β1-blockade during CPR did not facilitate VF termination but provided neuroprotection.
- Published
- 2021
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43. Semaglutide and effective weight control.
- Author
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Latini R and Staszewsky L
- Subjects
- Adult, Double-Blind Method, Glucagon-Like Peptides, Humans, Obesity drug therapy, Obesity prevention & control, Overweight, Diabetes Mellitus, Type 2 drug therapy
- Published
- 2021
- Full Text
- View/download PDF
44. Ventilation With Argon Improves Survival With Good Neurological Recovery After Prolonged Untreated Cardiac Arrest in Pigs.
- Author
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Fumagalli F, Olivari D, Boccardo A, De Giorgio D, Affatato R, Ceriani S, Bariselli S, Sala G, Cucino A, Zani D, Novelli D, Babini G, Magliocca A, Russo I, Staszewsky L, Salio M, Lucchetti J, Maisano AM, Fiordaliso F, Furlan R, Gobbi M, Luini MV, Pravettoni D, Scanziani E, Belloli A, Latini R, and Ristagno G
- Subjects
- Animals, Argon administration & dosage, Biomarkers blood, Brain pathology, Brain ultrastructure, Brain Injuries blood, Brain Injuries metabolism, Brain Injuries physiopathology, Cardiopulmonary Resuscitation statistics & numerical data, Case-Control Studies, Hemodynamics drug effects, Male, Models, Animal, Neuroprotective Agents pharmacology, Nitrogen administration & dosage, Oxygen administration & dosage, Recovery of Function physiology, Safety, Survival Analysis, Swine, Treatment Outcome, Argon pharmacology, Cardiopulmonary Resuscitation methods, Heart Arrest therapy, Recovery of Function drug effects, Ventilation methods
- Abstract
Background Ventilation with the noble gas argon (Ar) has shown neuroprotective and cardioprotective properties in different in vitro and in vivo models. Hence, the neuroprotective effects of Ar were investigated in a severe, preclinically relevant porcine model of cardiac arrest. Methods and Results Cardiac arrest was ischemically induced in 36 pigs and left untreated for 12 minutes before starting cardiopulmonary resuscitation. Animals were randomized to 4-hour post-resuscitation ventilation with: 70% nitrogen-30% oxygen (control); 50% Ar-20% nitrogen-30% oxygen (Ar 50%); and 70% Ar-30% oxygen (Ar 70%). Hemodynamic parameters and myocardial function were monitored and serial blood samples taken. Pigs were observed up to 96 hours for survival and neurological recovery. Heart and brain were harvested for histopathology. Ten animals in each group were successfully resuscitated. Ninety-six-hour survival was 60%, 70%, and 90%, for the control, Ar 50%, and Ar 70% groups, respectively. In the Ar 50% and Ar 70% groups, 60% and 80%, respectively, achieved good neurological recovery, in contrast to only 30% in the control group ( P <0.0001). Histology showed less neuronal degeneration in the cortex ( P <0.05) but not in the hippocampus, and less reactive microglia activation in the hippocampus ( P =0.007), after Ar compared with control treatment. A lower increase in circulating biomarkers of brain injury, together with less kynurenine pathway activation ( P <0.05), were present in Ar-treated animals compared with controls. Ar 70% pigs also had complete left ventricular function recovery and smaller infarct and cardiac troponin release ( P <0.01). Conclusions Post-resuscitation ventilation with Ar significantly improves neurologic recovery and ameliorates brain injury after cardiac arrest with long no-flow duration. Benefits are greater after Ar 70% than Ar 50%.
- Published
- 2020
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45. Trabectedin and Lurbinectedin Extend Survival of Mice Bearing C26 Colon Adenocarcinoma, without Affecting Tumor Growth or Cachexia.
- Author
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Aquila G, Re Cecconi AD, Forti M, Frapolli R, Bello E, Novelli D, Russo I, Licandro SA, Staszewsky L, Martinelli GB, Talamini L, Pasetto L, Resovi A, Giavazzi R, Scanziani E, Careccia G, Vénéreau E, Masson S, Latini R, D'Incalci M, and Piccirillo R
- Abstract
Trabectedin (ET743) and lurbinectedin (PM01183) limit the production of inflammatory cytokines that are elevated during cancer cachexia. Mice carrying C26 colon adenocarcinoma display cachexia (i.e., premature death and body wasting with muscle, fat and cardiac tissue depletion), high levels of inflammatory cytokines and subsequent splenomegaly. We tested whether such drugs protected these mice from cachexia. Ten-week-old mice were inoculated with C26 cells and three days later randomized to receive intravenously vehicle or 0.05 mg/kg ET743 or 0.07 mg/kg PM01183, three times a week for three weeks. ET743 or PM01183 extended the lifespan of C26-mice by 30% or 85%, respectively, without affecting tumor growth or food intake. Within 13 days from C26 implant, both drugs did not protect fat, muscle and heart from cachexia. Since PM01183 extended the animal survival more than ET743, we analyzed PM01183 further. In tibialis anterior of C26-mice, but not in atrophying myotubes, PM01183 restrained the NF-κB/PAX7/myogenin axis, possibly reducing the pro-inflammatory milieu, and failed to limit the C/EBP β /atrogin-1 axis. Inflammation-mediated splenomegaly of C26-mice was inhibited by PM01183 for as long as the treatment lasted, without reducing IL-6, M-CSF or IL-1β in plasma. ET743 and PM01183 extend the survival of C26-bearing mice unchanging tumor growth or cachexia but possibly restrain muscle-related inflammation and C26-induced splenomegaly.
- Published
- 2020
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- View/download PDF
46. Circulating biomarkers and cardiac function over 3 years after chemotherapy with anthracyclines: the ICOS-ONE trial.
- Author
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Meessen JMTA, Cardinale D, Ciceri F, Sandri MT, Civelli M, Bottazzi B, Cucchi G, Menatti E, Mangiavacchi M, Condorelli G, Barbieri E, Gori S, Colombo A, Curigliano G, Salvatici M, Pastori P, Ghisoni F, Bianchi A, Falci C, Cortesi P, Farolfi A, Monopoli A, Milandri C, Bregni M, Malossi A, Nassiacos D, Verusio C, Staszewsky L, Leone R, Novelli D, Balconi G, Nicolis EB, Franzosi MG, Masson S, Garlanda C, Mantovani A, Cipolla CM, and Latini R
- Subjects
- Biomarkers, Humans, Inducible T-Cell Co-Stimulator Protein, Natriuretic Peptide, Brain, Troponin I, Anthracyclines adverse effects, Ventricular Dysfunction, Left
- Abstract
Aims: A multicentre trial, ICOS-ONE, showed increases above the upper limit of normality of cardiac troponin (cTn) in 27% of patients within 12 months after the end of cancer chemotherapy (CT) with anthracyclines, whether cardiac protection with enalapril was started at study entry in all (prevention arm) or only upon first occurrence on supra-normal cTn (troponin-triggered arm). The aims of the present post hoc analysis were (i) to assess whether anthracycline-based treatment could induce cardiotoxicity over 36 month follow-up and (ii) to describe the time course of three cardiovascular biomarkers (i.e. troponin I cTnI-Ultra, B-type natriuretic peptide BNP, and pentraxin 3 PTX3) and of left ventricular (LV) function up to 36 months., Methods and Results: Eligible patients were those prescribed first-in-life CT, without evidence of cardiovascular disease, normal cTn, LV ejection fraction (EF) >50%, not on renin-angiotensin aldosterone system antagonists. Patients underwent echocardiography and blood sampling at 24 and 36 months. No differences were observed in biomarker concentration between the two study arms, 'prevention' vs. 'troponin-triggered'. During additional follow-up 13 more deaths occurred, leading to a total of 23 (9.5%), all due to a non-cardiovascular cause. No new occurrences of LV-dysfunction were reported. Two additional patients were admitted to the hospital for cardiovascular causes, both for acute pulmonary embolism. No first onset of raised cTnI-Ultra was reported in the extended follow-up. BNP remained within normal range: at 36 months was 23.4 ng/L, higher (N.S.) than at baseline, 17.6 ng/L. PTX3 peaked at 5.2 ng/mL 1 month after CT and returned to baseline values thereafter. cTnI-Ultra peaked at 26 ng/L 1 month after CT and returned to 3 ng/L until the last measurement at 36 months. All echocardiographic variables remained stable during follow-up with a median LVEF of 63% and left atrial volume index about 24 mL/m
2 ., Conclusions: First-in-life CT with median cumulative dose of anthracyclines of 180 mg/m2 does not seem to cause clinically significant cardiac injury, as assessed by circulating biomarkers and echocardiography, in patients aged 51 years (median), without pre-existing cardiac disease. This may suggest either a 100% efficacy of enalapril (given as preventive or troponin-triggered) or a reassuringly low absolute cardiovascular risk in this cohort of patients, which may not require intensive cardiologic follow-up., (© 2020 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of the European Society of Cardiology.)- Published
- 2020
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47. Cardiovascular mortality and morbidity burden in successive and age pre-stratified case-control cohorts of breast cancer women. A population-based study.
- Author
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Staszewsky L, Robusto F, Lepore V, Bisceglia L, Petrarolo V, D'Ettorre A, Tognoni G, and Latini R
- Subjects
- Age Distribution, Aged, Cardiovascular Diseases mortality, Case-Control Studies, Cause of Death, Female, Follow-Up Studies, Heart Failure epidemiology, Heart Failure mortality, Hospitalization statistics & numerical data, Humans, Incidence, Italy epidemiology, Middle Aged, Proportional Hazards Models, Prospective Studies, Treatment Outcome, Breast Neoplasms epidemiology, Cardiovascular Diseases epidemiology
- Abstract
Aims: To assess the existence, components and clinical relevance of cardiac causes of death and cardiovascular (CV) hospitalizations in a population-wide database of patients with breast cancer (BC)., Methods and Results: A population-wide database of the Puglia Region, Italy was analyzed, with a prospective comparative design. Three successive closely matched case/control cohorts representing current care in the period 2007-2014 were also stratified according to age to focus specifically on the potential interaction of treatment-related cardiac toxicity and the expected different baseline CV risk profiles., Results: At 3-year follow-up, in the successive cohorts the incidence of BC-related (7.7, 7.0, 6.5%) and cardiac causes of death, specifically attributed to heart failure (HF, 1.3, 0.5, 0.5%), decreased. Significant mortality hazard ratio (HR) for HF was found in the total population (1.47, 95% CI 1.14-1.90), in particular in the 2007-2009 cohort (1.71, 95% CI 1.19-2.46) and in the 50-69 age group (7.96, 95% CI 2.81-22.55). Results at 5 years confirm the mortality findings, and a significant HR for hospitalizations for HF, non-atrial arrhythmias and ischemic heart disease in the younger than 50 subpopulation pointed to a late expression of toxicity in the youngest BC population., Conclusions: The incidence of CV causes of death 3 and 5 years after BC diagnosis was very low, even if an excess in risk of death for HF as compared with the control cohort was observed. While younger patients seems to tolerate BC and BC therapy better in the short term, HF mortality and morbidity resulted significantly increased at 5-year follow-up. As the risk for hospitalization for CV reasons increased at 5-year follow-up in particular in women aged less than 50 years, CV monitoring in this subgroup of patients seems mandatory.
- Published
- 2020
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- View/download PDF
48. Primary pulmonary arterial hypertension: Protocol to assess comprehensively in the rat the response to pharmacologic treatments.
- Author
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Novelli D, Fumagalli F, Staszewsky L, Ristagno G, Olivari D, Masson S, De Giorgio D, Ceriani S, Massafra R, De Logu F, Nassini R, Milioli M, Facchinetti F, Cantoni S, Trevisani M, Letizia T, Russo I, Salio M, and Latini R
- Abstract
The identification of new treatments for primary pulmonary arterial hypertension (PAH) is a critical unmet need since there is no a definitive cure for this disease yet. Due to the complexity of PAH, a wide set of methods are necessary to assess the response to a pharmacological intervention. Thus, a rigorous protocol is crucial when experimental studies are designed. In the present experimental protocol, a stepwise approach was followed in a monocrotaline-induced PAH model in the rat, moving from the dose finding study of treatment compounds to the recognition of the onset of disease manifestation, in order to identify when to start a curative treatment. A complete multidimensional evaluation of treatment effects represented the last step. The primary study endpoint was the change in right ventricular systolic pressure after 14 days of treatment; echocardiographic and biohumoral markers together with heart and pulmonary arterial morphometric parameters were considered as secondary efficacy and/or safety endpoints and for the evaluation of the biologic coherence in the different results., Competing Interests: Marco Milioli, Fabrizio Facchinetti, Silvia Cantoni, Marcello Trevisani are employees of Chiesi Farmaceutici S.p.A. The other authors have no conflicts of interest to declare., (© 2019 The Authors.)
- Published
- 2019
- Full Text
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49. Monocrotaline-induced pulmonary arterial hypertension: Time-course of injury and comparative evaluation of macitentan and Y-27632, a Rho kinase inhibitor.
- Author
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Novelli D, Fumagalli F, Staszewsky L, Ristagno G, Olivari D, Masson S, De Giorgio D, Ceriani S, Affatato R, De Logu F, Nassini R, Milioli M, Facchinetti F, Cantoni S, Trevisani M, Letizia T, Russo I, Salio M, and Latini R
- Subjects
- Animals, Heart Ventricles pathology, Hemodynamics drug effects, Hypertrophy, Right Ventricular chemically induced, Hypertrophy, Right Ventricular drug therapy, Male, Monocrotaline, Pulmonary Arterial Hypertension chemically induced, Pulmonary Arterial Hypertension pathology, Pulmonary Artery drug effects, Pulmonary Artery pathology, Rats, Wistar, Amides therapeutic use, Endothelin Receptor Antagonists therapeutic use, Protein Kinase Inhibitors therapeutic use, Pulmonary Arterial Hypertension drug therapy, Pyridines therapeutic use, Pyrimidines therapeutic use, Sulfonamides therapeutic use, rho-Associated Kinases antagonists & inhibitors
- Abstract
Novel pharmacological approaches are needed to improve outcomes of patients with idiopathic pulmonary hypertension. Rho-associated protein kinase (ROCK) inhibitors have shown beneficial effects in preclinical models of pulmonary arterial hypertension (PAH), because of their role in the regulation of pulmonary artery vasoconstrictor tone and remodeling. We compared a ROCK inhibitor, Y-27632, for the first time with the dual endothelin receptor antagonist, macitentan, in a monocrotaline-induced rat pulmonary hypertension model. Different methods (echocardiography, hemodynamics, histology of right ventricle and pulmonary vessels, and circulating biomarkers) showed consistently that 100 mg/kg daily of Y-27632 and 10 mg/kg daily of macitentan slowed the progression of PAH both at the functional and structural levels. Treatments started on day 14 after monocrotaline injection and lasted 14 days. The findings of all experimental methods show that the selective ROCK inhibitor Y-27632 has more pronounced effects than macitentan, but a major limitation to its use is its marked peripheral vasodilating action., (Copyright © 2019 Elsevier B.V. All rights reserved.)
- Published
- 2019
- Full Text
- View/download PDF
50. Adrenomedullin, a circulating biomarker of congestion: in search of evidence.
- Author
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Staszewsky L, De Giorgio D, and Latini R
- Subjects
- Biomarkers, Humans, Adrenomedullin, Heart Failure
- Published
- 2019
- Full Text
- View/download PDF
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