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4. Major adverse cardiovascular events in non-valvular atrial fibrillation with chronic obstructive pulmonary disease: the ARAPACIS study

Author

Raparelli, Valeria, Pastori, Daniele, Pignataro, Serena Francesca, Vestri, Anna Rita, Pignatelli, Pasquale, Cangemi, Roberto, Proietti, Marco, Davì, Giovanni, Hiatt, William Robert, Lip, Gregory Yoke Hong, Corazza, Gino Roberto, Perticone, Francesco, Violi, Francesco, Basili, Stefania, Alessandri, C., Serviddio, G., Palange, P., Greco, E., Bruno, G., Averna, M., Giammanco, A., Sposito, P., de Cristofaro, R., Carulli, L., de Gennaro, L., Pellegrini, E., Cominacini, L., Mozzini, C., Pasini, A. F., Sprovieri, M., Spagnuolo, V., Cerqua, G., Cerasola, G., Mulé, G., Barbagallo, M., Lo Sciuto, S., Monteverde, A., Saitta, A., Lo Gullo, A., Malatino, L., Cilia, C., Terranova, V., Pisano, M., Pinto, A., Di Raimondo, D., Tuttolomondo, A., Conigliaro, R., Signorelli, S., de Palma, D., Galderisi, M., Cudemo, G., Galletti, F., Fazio, V., de Luca, N., Meccariello, A., Caputo, D., de Donato, M. T., Iannuzi, A., Bresciani, A., Giunta, R., Utili, R., Iorio, V., Adinolfi, L. E., Sellitto, C., Iuliano, N., Bellis, P., Tirelli, P., Sacerdoti, D., Vanni, D., Iuliano, L., Ciacciarelli, M., Pacelli, A., Palazzuoli, A., Cacciafesta, M., Gueli, N., Lo Iacono, C., Brusco, S., Verrusio, W., Nobili, L., Tarquinio, N., Pellegrini, F., Vincentelli, G. M., Ravallese, F., Santini, C., Letizia, C., Petramala, L., Zinnamosca, L., Minisola, S., Cilli, M., Colangelo, L., Falaschi, P., Martocchia, A., Pastore, F., Bertazzoni, G., Attalla El Halabieh, E., Paradiso, M., Lizzi, E. M., Timmi, S., Battisti, P., Cerci, S., Ciavolella, M., Di Veroli, C., Malci, F., de Ciocchis, A., Abate, D., Castellino, P., Zanoli, L., Fidone, F., Mannarino, E., Pasqualini, L., Oliverio, G., Pende, A., Artom, N., Ricchio, R., Fimognari, F. L., Alletto, M., Messina, S., Sesti, G., Arturi, F., Succurro, E., Fiorentino, T. V., Pedace, E., Scarpino, P. E., Carullo, G., Maio, R., Sciacqua, A., Frugiuele, P., Battaglia, G., Atzori, S., Delitala, G., Angelucci, E., Sestili, S., Traisci, G., de Feudis, L., Di Michele, D., Fava, A., Balsano, C., de Ciantis, P., Desideri, G., Camerota, A., Mezzetti, M., Gresele, P., Vedovati, C., Fierro, T., Puccetti, L., Bertolotti, M., Mussi, C., Boddi, M., Savino, A., Contri, S., Degl’Innocenti, G., Saller, A., Fabris, F., Pesavento, R., Filippi, L., Vedovetto, V., Puato, M., Treleani, M., de Luca, E., de Zaiacomo, F., Giantin, V., Semplicini, A., Minuz, P., Romano, S., Fantin, F., Manica, A., Stockner, I., Pattis, P., Gutmann, B., Catena, C., Colussi, G., Sechi, L. A., Annoni, G., Bruni, A. A., Castagna, A., Spinelli, D., Miceli, E., Padula, D., Schinco, G., Spreafico, S., Secchi, B., Vanoli, M., Casella, G., Pulixi, E. A., Sansone, L., Serra, M. G., Longo, S., Antonaci, S., Belfiore, A., Frualdo, M., Palasciano, G., Ricci, L., Ventrella, F., Bianco, C., Santovito, D., Cipollone, F., Nicolai, S., Salvati, F., Rini, G. B., Scozzari, F., Muiesan, M. L., Salvetti, M., Bazza, A., Picardi, A., Vespasiani-Gentilucci, U., de Vincentis, A., Cosio, P., Terzolo, M., Madaffari, B., Parasporo, B., Fenoglio, L., Bracco, C., Melchio, R., Gentili, T., Salvi, A., Nitti, C., Gabrielli, A., Martino, G. P., Capucci, A., Brambatti, M., Sparagna, A., Tirotta, D., Andreozzi, P., Ettorre, E., Viscogliosi, G., Servello, A., Musumeci, M., Delfino, M., Giorgi, A., Glorioso, N., Melis, G., Marras, G., Matta, M., Sacco, A., Stellitano, E., Scordo, A., Russo, F., Caruso, A. A., Porreca, E., Tana, M., Ferri, C., Cheli, P., Portincasa, P., Muscianisi, G., Giordani, S., Stanghellini, V., Sabbà, C., Mancuso, G., Bartone, M., Calipari, D., Arcidiacono, G., Bellanuova, I., Ferraro, M., Marigliano, G., Cozzolino, D., Lampitella, A., Acri, V., Galasso, D., Mazzei, F., Buratti, A., Galasso, S., Porta, M., Brizzi, M. F., Fattorini, A., Sampietro, F., D’Angelo, A., Manfredini, R., Pala, M., Fabbian, F., Moroni, C., Valente, L., Lopreiato, F., Parente, F., Granata, M., Moia, M., Braham, S., Rossi, M., Pesce, M., Gentile, A., Catozzo, V., Baciarello, G., Cosimati, A., Ageno, W., Rancan, E., Guasti, L., Ciccaglioni, A., Negri, S., Polselli, M., Prisco, D., Marcucci, R., Ferro, D., Perri, L., Cangemi, R., Saliola, M., Del Ben, M., Angelico, F., Baratta, F., Migliacci, R., Porciello, G., Corrao, S., Proietti, M., Raparelli, V., Napoleone, L., Talerico, G., Amoroso, D., Romiti, G. F., Ruscio, E., Toriello, F., Sperduti, N., Todisco, T., Di Tanna, G., Sacchetti, M. L., Puddu, P. E., Farcomeni, A., Anzaldi, M., Bazzini, C., Bianchi, P. I., Boari, B., Buonauro, A., Buttà, C., Buzzetti, E., Calabria, S., Capeci, W., Caradio, F., Carleo, P., Carrabba, M. D., Castorani, L., Cecchetto, L., Cicco, S., Cimini, C., Colombo, B. M., de Giorgi, A., de Vuono, S., Del Corso, L., Denegri, A., Di Giosia, P., Durante Mangoni, E., Falsetti, L., Forgione, A., Giorgini, P., Grassi, D., Grembiale, A., Hijazi, D., Iamele, L., Lorusso, G., Marchese, A., Marra, A. M., Masala, M., Miceli, G., Montebianco Abenavoli, L., Murgia, G., Naccarato, P., Pattoneri, P., Perego, F., Pesce, P., Piano, S., Pinna, M., Pinto, D., Pretti, V., Pucci, G., Salinaro, F., Salzano, A., Santilli, F., Scarpini, F., Scicali, R., Sirico, D., Suppressa, P., Talia, M., Tassone, E. J., Torres, D., Vazzana, N., Vecchio, C. R., Vidili, G., Vitale, F., Zaccone, V., ARAPACIS Study Collaborators, Raparelli, V, Pastori, D, Pignataro, S, Vestri, A, Pignatelli, P, Cangemi, R, Proietti, M, Davi, G, Hiatt, W, Lip, G, Corazza, G, Perticone, F, Violi, F, Basili, S, Alessandri, C, Serviddio, G, Palange, P, Greco, E, Bruno, G, Averna, M, Giammanco, A, Sposito, P, Decristofaro, R, Carulli, L, Degennaro, L, Pellegrini, E, Cominacini, L, Mozzini, C, Pasini, A, Sprovieri, M, Spagnuolo, V, Cerqua, G, Cerasola, G, Mule, G, Barbagallo, M, Lo Sciuto, S, Monteverde, A, Saitta, A, Lo Gullo, A, Malatino, L, Cilia, C, Terranova, V, Pisano, M, Pinto, A, Diraimondo, D, Tuttolomondo, A, Conigliaro, R, Signorelli, S, Depalma, D, Galderisi, M, Cudemo, G, Galletti, F, Fazio, V, Deluca, N, Meccariello, A, Caputo, D, Dedonato, M, Iannuzi, A, Bresciani, A, Giunta, R, Utili, R, Iorio, V, Adinolfi, L, Sellitto, C, Iuliano, N, Bellis, P, Tirelli, P, Sacerdoti, D, Vanni, D, Iuliano, L, Ciacciarelli, M, Pacelli, A, Palazzuoli, A, Cacciafesta, M, Gueli, N, Lo Iacono, C, Brusco, S, Verrusio, W, Nobili, L, Tarquinio, N, Pellegrini, F, Vincentelli, G, Ravallese, F, Santini, C, Letizia, C, Petramala, L, Zinnamosca, L, Minisola, S, Cilli, M, Colangelo, L, Falaschi, P, Martocchia, A, Pastore, F, Bertazzoni, G, Attalla El Halabieh, E, Paradiso, M, Lizzi, E, Timmi, S, Battisti, P, Cerci, S, Ciavolella, M, Diveroli, C, Malci, F, Deciocchis, A, Abate, D, Castellino, P, Zanoli, L, Fidone, F, Mannarino, E, Pasqualini, L, Oliverio, G, Pende, A, Artom, N, Ricchio, R, Fimognari, F, Alletto, M, Messina, S, Sesti, G, Arturi, F, Succurro, E, Fiorentino, T, Pedace, E, Scarpino, P, Carullo, G, Maio, R, Sciacqua, A, Frugiuele, P, Battaglia, G, Atzori, S, Delitala, G, Angelucci, E, Sestili, S, Traisci, G, Defeudis, L, Dimichele, D, Fava, A, Balsano, C, Deciantis, P, Desideri, G, Camerota, A, Mezzetti, M, Gresele, P, Vedovati, C, Fierro, T, Puccetti, L, Bertolotti, M, Mussi, C, Boddi, M, Savino, A, Contri, S, Degl'Innocenti, G, Saller, A, Fabris, F, Pesavento, R, Filippi, L, Vedovetto, V, Puato, M, Treleani, M, Deluca, E, Dezaiacomo, F, Giantin, V, Semplicini, A, Minuz, P, Romano, S, Fantin, F, Manica, A, Stockner, I, Pattis, P, Gutmann, B, Catena, C, Colussi, G, Sechi, L, Annoni, G, Bruni, A, Castagna, A, Spinelli, D, Miceli, E, Padula, D, Schinco, G, Spreafico, S, Secchi, B, Vanoli, M, Casella, G, Pulixi, E, Sansone, L, Serra, M, Longo, S, Antonaci, S, Belfiore, A, Frualdo, M, Palasciano, G, Ricci, L, Ventrella, F, Bianco, C, Santovito, D, Cipollone, F, Nicolai, S, Salvati, F, Rini, G, Scozzari, F, Muiesan, M, Salvetti, M, Bazza, A, Picardi, A, Vespasiani-Gentilucci, U, Devincentis, A, Cosio, P, Terzolo, M, Madaffari, B, Parasporo, B, Fenoglio, L, Bracco, C, Melchio, R, Gentili, T, Salvi, A, Nitti, C, Gabrielli, A, Martino, G, Capucci, A, Brambatti, M, Sparagna, A, Tirotta, D, Andreozzi, P, Ettorre, E, Viscogliosi, G, Servello, A, Musumeci, M, Delfino, M, Giorgi, A, Glorioso, N, Melis, G, Marras, G, Matta, M, Sacco, A, Stellitano, E, Scordo, A, Russo, F, Caruso, A, Porreca, E, Tana, M, Ferri, C, Cheli, P, Portincasa, P, Muscianisi, G, Giordani, S, Stanghellini, V, Sabba, C, Mancuso, G, Bartone, M, Calipari, D, Arcidiacono, G, Bellanuova, I, Ferraro, M, Marigliano, G, Cozzolino, D, Lampitella, A, Acri, V, Galasso, D, Mazzei, F, Buratti, A, Galasso, S, Porta, M, Brizzi, M, Fattorini, A, Sampietro, F, D'Angelo, A, Manfredini, R, Pala, M, Fabbian, F, Moroni, C, Valente, L, Lopreiato, F, Parente, F, Granata, M, Moia, M, Braham, S, Rossi, M, Pesce, M, Gentile, A, Catozzo, V, Baciarello, G, Cosimati, A, Ageno, W, Rancan, E, Guasti, L, Ciccaglioni, A, Negri, S, Polselli, M, Prisco, D, Marcucci, R, Ferro, D, Perri, L, Saliola, M, Delben, M, Angelico, F, Baratta, F, Migliacci, R, Porciello, G, Corrao, S, Napoleone, L, Talerico, G, Amoroso, D, Romiti, G, Ruscio, E, Toriello, F, Sperduti, N, Todisco, T, Ditanna, G, Sacchetti, M, Puddu, P, Farcomeni, A, Anzaldi, M, Bazzini, C, Bianchi, P, Boari, B, Buonauro, A, Butta, C, Buzzetti, E, Calabria, S, Capeci, W, Caradio, F, Carleo, P, Carrabba, M, Castorani, L, Cecchetto, L, Cicco, S, Cimini, C, Colombo, B, De Giorgi, A, Devuono, S, Delcorso, L, Denegri, A, Digiosia, P, Durante Mangoni, E, Falsetti, L, Forgione, A, Giorgini, P, Grassi, D, Grembiale, A, Hijazi, D, Iamele, L, Lorusso, G, Marchese, A, Marra, A, Masala, M, Miceli, G, Montebianco Abenavoli, L, Murgia, G, Naccarato, P, Pattoneri, P, Perego, F, Pesce, P, Piano, S, Pinna, M, Pinto, D, Pretti, V, Pucci, G, Salinaro, F, Salzano, A, Santilli, F, Scarpini, F, Scicali, R, Sirico, D, Suppressa, P, Talia, M, Tassone, E, Torres, D, Vazzana, N, Vecchio, C, Vidili, G, Vitale, F, Zaccone, V, Raparelli, V1, Pastori, D1, Pignataro, Sf1, Vestri, Ar2, Pignatelli, P1, Cangemi, R1, Proietti, M3, Davì, G4, Hiatt, Wr5, Lip, Gyh3, Corazza, Gr6, Perticone, F7, Violi, F8, Basili, S1, De Cristofaro, R, De Gennaro, L, Pasini, Af, Mulé, G, Di Raimondo, D, De Palma, D, De Luca, N, De Donato, Mt, Adinolfi, Le, Vincentelli, Gm, Lizzi, Em, Di Veroli, C, De Ciocchis, A, Fimognari, Fl, Fiorentino, Tv, Scarpino, Pe, De Feudis, L, Di Michele, D, De Ciantis, P, De Luca, E, De Zaiacomo, F, Sechi, La, Bruni, Aa, Pulixi, Ea, Serra, Mg, Rini, Gb, Muiesan, Ml, De Vincentis, A, Martino, Gp, Caruso, Aa, Sabbà, C, Brizzi, Mf, Del Ben, M, Romiti, Gf, Di Tanna, G, Sacchetti, Ml, Puddu, Pe, Bianchi, Pi, Buttà, C, Carrabba, Md, Colombo, Bm, De Vuono, S, Del Corso, L, Di Giosia, P, Marra, Am, Tassone, Ej, Vecchio, Cr, Zaccone, V., Pignataro, Sf, Vestri, Ar, Davì, G, Hiatt, Wr, Lip, Gyh, Corazza, Gr, Raparelli, Valeria, Pastori, Daniele, Pignataro, Serena Francesca, Vestri, Anna Rita, Pignatelli, Pasquale, Cangemi, Roberto, Proietti, Marco, Davì, Giovanni, Hiatt, William Robert, Lip, Gregory Yoke Hong, Corazza, Gino Roberto, Perticone, Francesco, Violi, Francesco, Basili, Stefania, Alessandri C., Serviddio G., Palange P., Greco E., Bruno G., Averna M., Giammanco A., Sposito P., De Cristofaro R., Carulli L., De Gennaro L., Pellegrini E. Cominacini L., Mozzini C., Pasini A.F., Sprovieri M., Spagnuolo V., Cerqua G., Cerasola G., Mulé G., Barbagallo M., Lo Sciuto S., Monteverde A., Saitta A., Lo Gullo A., Malatino L., Cilia C., Terranova V., Pisano M., Pinto A., Di Raimondo D., Tuttolomondo A., Conigliaro R., Signorelli S., De Palma D., Galderisi M., Cudemo G., Galletti F., Fazio V., De Luca N., Meccariello A., Caputo D., De Donato M. T., Iannuzi A., Bresciani A., Giunta R., Utili R., Iorio V., Adinolfi L.E., Sellitto C., Iuliano N., Bellis P., Tirelli P., Sacerdoti D., Vanni D., Iuliano L., Ciacciarelli M., Pacelli A., Palazzuoli A., Cacciafesta M., Gueli N., Lo Iacono C., Brusco S., Verrusio W., Nobili L., Tarquinio N., Pellegrini F., Vincentelli G.M., Ravallese F., Santini C., Letizia C., Petramala L., Zinnamosca L., Minisola S., Cilli M., Colangelo L., Falaschi P., Martocchia A., Pastore F., Bertazzoni G., Attalla El Halabieh E., Paradiso M., Lizzi E.M., Timmi S., Battisti P., Cerci S., Ciavolella M., Di Veroli C., Malci F., De Ciocchis A., Abate D., Castellino P., Zanoli L., Fidone F., Mannarino E., Pasqualini L., Oliverio G., Pende A., Artom N., Ricchio R., Fimognari F.L., Alletto M., Messina S., Sesti G., Arturi F., Succurro E, Fiorentino T.V., Pedace E., Scarpino P.E., Carullo G., Maio R., Sciacqua A., Frugiuele P., Spagnuolo V., Battaglia G., Atzori S., Delitala G., Angelucci E., Sestili S., Traisci G., De Feudis L., Di Michele D., Fava A., Balsano C., De Ciantis P., Desideri G., Camerota A., Mezzetti M., Gresele P., Vedovati C., Fierro T., Puccetti L., Bertolotti M., Mussi C., Boddi M., Savino A., Contri S., Degl’Innocenti G., Saller A., Fabris F., Pesavento R., Filippi L., Vedovetto V., Puato M., Fabris F., Treleani M., De Luca E., De Zaiacomo F., Giantin V., Semplicini A., Minuz P., Romano S., Fantin F., Manica A., Stockner I., Pattis P., Gutmann B., Catena C., Colussi G., Sechi L.A., Annoni G., Bruni A.A., Castagna A., Spinelli D., Miceli E., Padula D., Schinco G., Spreafico S., Secchi B., Vanoli M., Casella G., Pulixi E.A., Sansone L., Serra M.G., Longo S., Antonaci S., Belfiore A., Frualdo M., Palasciano G., Ricci L., Ventrella F., Bianco C., Santovito D., Cipollone F., Nicolai S., Salvati F., Rini G. B., Scozzari F., Muiesan M.L., Salvetti M., Bazza A., Picardi A., Vespasiani-Gentilucci U., De Vincentis A., Cosio P., Terzolo M., Madaffari B., Parasporo B., Fenoglio L., Bracco C., Melchio R., Gentili T., Salvi A., Nitti C., Gabrielli A., Martino G.P., Capucci A., Brambatti M., Sparagna A., Tirotta D., Andreozzi P., Ettorre E., Viscogliosi G., Servello A., Musumeci M., Delfino M., Giorgi A., Glorioso N., Melis G., Marras G., Matta M., Sacco A., Stellitano E., Scordo A., Russo F., Caruso A.A., Porreca E., Tana M., Ferri C., Cheli P., Portincasa P., Muscianisi G., Giordani S., Stanghellini V., Sabbà C., Mancuso G., Bartone M., Calipari D., Arcidiacono G., Bellanuova I., Ferraro M., Marigliano G., Cozzolino D., Lampitella A., Acri V., Galasso D., Mazzei F., Buratti A., Galasso S., Porta M., Brizzi M.F., Fattorini A., Sampietro F., D’Angelo A., Manfredini R., Pala M., Fabbian F., Moroni C., Valente L., Lopreiato F., Parente F., Granata M., Moia M., Braham S., Rossi M., Pesce M., Gentile A., Catozzo V., Baciarello G., Cosimati A., Ageno W., Rancan E., Guasti L., Ciccaglioni A., Negri S., Polselli M., Prisco D., Marcucci R., Ferro D., Perri L., Cangemi R., Saliola M., Del Ben M., Angelico F., Baratta F., Migliacci R., Porciello G., Corrao S. Data entry and Safety Monitoring Board: Proietti M., Raparelli V., Napoleone L., Talerico G., Amoroso D., Romiti G.F., Ruscio E., Toriello F., Sperduti N., Todisco T., Di Tanna G., Sacchetti M.L., Puddu P.E., Farcomeni A. Simi Young Internists Group: Anzaldi M., Bazzini C., Bianchi P.I., Boari B., Bracco C., Buonauro A., Buttà C., Buzzetti E., Calabria S., Capeci W., Caradio F., Carleo P., Carrabba M.D., Castorani L., Cecchetto L., Cicco S., Cimini C., Colombo B.M., De Giorgi A., De Vuono S., Del Corso L., Denegri A., Di Giosia P., Durante Mangoni E., Falsetti L., Forgione A., Giorgini P., Grassi D., Grembiale A., Hijazi D., Iamele L., Lorusso G., Marchese A., Marra A.M., Masala M., Miceli G., Montebianco Abenavoli L., Murgia G., Naccarato P., Padula D., Pattoneri P., Perego F., Pesce P., Piano S., Pinna M., Pinto D., Pretti V., Pucci G., Salinaro F., Salzano A., Santilli F., Scarpini F., Scicali R., Sirico D., Suppressa P., Talia M., Tassone E.J., Torres D., Vazzana N., Vecchio C.R., Vidili G., Vitale F., Zaccone V., Raparelli Valeria, Pastori Daniele, Pignataro Serena Francesca, Vestri Anna Rita, Pignatelli Pasquale, Cangemi Roberto, Proietti Marco, Davì Giovanni, Hiatt William Robert, Lip Gregory Yoke Hong, Corazza Gino Roberto, Perticone Francesco, Violi Francesco, Basili Stefania, Alessandri C, Serviddio G, Palange P, Greco E, Bruno G, Averna M, Giammanco A, Sposito P, De Cristofaro R, Carulli L, De Gennaro L, Pellegrini E, Cominacini L, Mozzini C, Pasini AF, Sprovieri M, Spagnuolo V, Cerqua G, Cerasola G, Mulé G, Barbagallo M, Lo Sciuto S, Monteverde A, Saitta A, Lo Gullo A, Malatino L, Cilia C, Terranova V, Pisano M, Pinto A, Di Raimondo D, Tuttolomondo A, Conigliaro R, Signorelli S, De Palma D, Galderisi M, Cudemo G, Galletti F, Fazio V, De Luca N, Meccariello A, Caputo D, De Donato MT, Iannuzi A, Bresciani A, Giunta R, Utili R, Iorio V, Adinolfi LE, Sellitto C, Iuliano N, Bellis P, Tirelli P, Sacerdoti D, Vanni D, Iuliano L, Ciacciarelli M, Pacelli A, Palazzuoli A, Cacciafesta M, Gueli N, Lo Iacono C, Brusco S, Verrusio W, Nobili L, Tarquinio N, Pellegrini F, Vincentelli GM, Ravallese F, Santini C, Letizia C, Petramala L, Zinnamosca L, Minisola S, Cilli M, Colangelo L, Falaschi P, Martocchia A, Pastore F, Bertazzoni G, Attalla El Halabieh E, Paradiso M, Lizzi EM, Timmi S, Battisti P, Cerci S, Ciavolella M, Di Veroli C, Malci F, De Ciocchis A, Abate D, Castellino P, Zanoli L, Fidone F, Mannarino E, Pasqualini L, Oliverio G, Pende A, Artom N, Ricchio R, Fimognari FL, Alletto M, Messina S, Sesti G, Arturi F, Succurro E, Fiorentino TV, Pedace E, Scarpino PE, Carullo G, Maio R, Sciacqua A, Frugiuele P, Battaglia G, Atzori S, Delitala G, Angelucci E, Sestili S, Traisci G, De Feudis L, Di Michele D, Fava A, Balsano C, De Ciantis P, Desideri G, Camerota A, Mezzetti M, Gresele P, Vedovati C, Fierro T, Puccetti L, Bertolotti M, Mussi C, Boddi M, Savino A, Contri S, Degl’Innocenti G, Saller A, Fabris F, Pesavento R, Filippi L, Vedovetto V, Puato M, Treleani M, De Luca E, De Zaiacomo F, Giantin V, Semplicini A, Minuz P, Romano S, Fantin F, Manica A, Stockner I, Pattis P, Gutmann B, Catena C, Colussi G, Sechi LA, Annoni G, Bruni AA, Castagna A, Spinelli D, Miceli E, Padula D, Schinco G, Spreafico S, Secchi B, Vanoli M, Casella G, Pulixi EA, Sansone L, Serra MG, Longo S, Antonaci S, Belfiore A, Frualdo M, Palasciano G, Ricci L, Ventrella F, Bianco C, Santovito D, Cipollone F, Nicolai S, Salvati F, Rini GB, Scozzari F, Muiesan ML, Salvetti M, Bazza A, Picardi A, Vespasiani-Gentilucci U, De Vincentis A, Cosio P, Terzolo M, Madaffari B, Parasporo B, Fenoglio L, Bracco C, Melchio R, Gentili T, Salvi A, Nitti C, Gabrielli A, Martino GP, Capucci A, Brambatti M, Sparagna A, Tirotta D, Andreozzi P, Ettorre E, Viscogliosi G, Servello A, Musumeci M, Delfino M, Giorgi A, Glorioso N, Melis G, Marras G, Matta M, Sacco A, Stellitano E, Scordo A, Russo F, Caruso AA, Porreca E, Tana M, Ferri C, Cheli P, Portincasa P, Muscianisi G, Giordani S, Stanghellini V, Sabbà C, Mancuso G, Bartone M, Calipari D, Arcidiacono G, Bellanuova I, Ferraro M, Marigliano G, Cozzolino D, Lampitella A, Acri V, Galasso D, Mazzei F, Buratti A, Galasso S, Porta M, Brizzi MF, Fattorini A, Sampietro F, D’Angelo A, Manfredini R, Pala M, Fabbian F, Moroni C, Valente L, Lopreiato F, Parente F, Granata M, Moia M, Braham S, Rossi M, Pesce M, Gentile A, Catozzo V, Baciarello G, Cosimati A, Ageno W, Rancan E, Guasti L, Ciccaglioni A, Negri S, Polselli M, Prisco D, Marcucci R, Ferro D, Perri L, Cangemi R, Saliola M, Del Ben M, Angelico F, Baratta F, Migliacci R, Porciello G, Corrao S, Proietti M, Raparelli V, Napoleone L, Talerico G, Amoroso D, Romiti GF, Ruscio E, Toriello F, Sperduti N, Todisco T, Di Tanna G, Sacchetti ML, Puddu PE, Farcomeni A, Anzaldi M, Bazzini C, Bianchi PI, Boari B, Buonauro A, Buttà C, Buzzetti E, Calabria S, Capeci W, Caradio F, Carleo P, Carrabba MD, Castorani L, Cecchetto L, Cicco S, Cimini C, Colombo BM, De Giorgi A, De Vuono S, Del Corso L, Denegri A, Di Giosia P, Durante Mangoni E, Falsetti L, Forgione A, Giorgini P, Grassi D, Grembiale A, Hijazi D, Iamele L, Lorusso G, Marchese A, Marra AM, Masala M, Miceli G, Montebianco Abenavoli L, Murgia G, Naccarato P, Pattoneri P, Perego F, Pesce P, Piano S, Pinna M, Pinto D, Pretti V, Pucci G, Salinaro F, Salzano A, Santilli F, Scarpini F, Scicali R, Sirico D, Suppressa P, Talia M, Tassone EJ, Torres D, Vazzana N, Vecchio CR, Vidili G, Vitale F, and Zaccone V

Subjects
Male, Settore MED/09 - Medicina Interna, 030204 cardiovascular system & hematology, Pulmonary Disease, Chronic Obstructive, 0302 clinical medicine, Risk Factors, Major cardiovascular event, Cause of Death, Risk of mortality, Prevalence, Medicine, 030212 general & internal medicine, Prospective Studies, Registries, Prospective cohort study, Stroke, Cause of death, COPD, Chronic obstructive pulmonary disease, Incidence, Hazard ratio, Atrial fibrillation, Cardiovascular mortality, Major cardiovascular events, Aged, Atrial Fibrillation, Cardiovascular Diseases, Endpoint Determination, Female, Follow-Up Studies, Humans, Italy, Predictive Value of Tests, Internal Medicine, Emergency Medicine, Atrial fibrillation, Cardiovascular mortality, Chronic obstructive pulmonary disease, Major cardiovascular events, Cardiology, Settore SECS-S/01 - Statistica, medicine.medical_specialty, Chronic Obstructive, Socio-culturale, Pulmonary Disease, 03 medical and health sciences, Internal medicine, cardiovascular diseases, business.industry, medicine.disease, business, Mace
Abstract

Chronic obstructive pulmonary disease (COPD) increases the risk of mortality in non-valvular atrial fibrillation (NVAF) patients. Data on the relationship of COPD to major cardiovascular events (MACE) in AF have not been defined. The aim of the study is to assess the predictive value of COPD on incident MACE in NVAF patients over a 3-year follow-up. In the Atrial Fibrillation Registry for Ankle-Brachial Index Prevalence Assessment-Collaborative Italian Study (ARAPACIS) cohort, we evaluate the impact of COPD on the following clinical endpoints: MACE (including vascular death, fatal/non-fatal MI and stroke/TIA), cardiovascular (CV) death and all-cause mortality. Among 2027 NVAF patients, patients with COPD (9%) are more commonly male, elderly and at higher thromboembolic risk. During a median 36.0months follow-up, 186 patients experienced MACE: vascular death (n = 72), MI (n = 57), stroke/TIA (n = 57). All major outcomes (including stroke/TIA, MI, vascular death, and all-cause death) are centrally adjudicated. Kaplan–Meier curves show that NVAF patients with COPD are at higher risk for MACE (p < 0.001), CV death (p < 0.001) and all-cause death (p < 0.001). On Cox proportional hazard analysis, COPD is an independent predictor of MACE (Hazard ratio [HR] 1.77, 95% Confidence Intervals [CI] 1.20–2.61; p = 0.004), CV death (HR 2.73, 95% CI 1.76–4.23; p < 0.0001) and all-cause death (HR 2.16, 95% CI 1.48–3.16; p < 0.0001). COPD is an independent predictor of MACE, CV death and all-cause death during a long-term follow-up of NVAF patients.

Published
2018

5. Ankle-Brachial Index and cardiovascular events in atrial fibrillation The ARAPACIS Study

Author

Violi, F., Davi, G., Proietti, M., Pastori, D., Hiatt, W. R., Corazza, G. R., Perticone, F., Pignatelli, P., Farcomeni, A., Vestri, A. R., Lip, G. Y. H., Basili, S, ARAPACIS (Atrial Fibrillation Registry for Ankle-Brachial Index Prevalence Assessment-Collaborative Italian Study) STUDY Investigators. Alessandri C. (Dipartimento di Scienze e Biotecnologie Medico-Chirurgiche, Sapienza-Università di Roma), Serviddio G. (Department of Medical and Surgical Sciences, University of Foggia), (UOC Medicina Generale, Fascetti S., USL 12 Viareggio, Toscana), (UOC Medicina Interna I, Palange P., Dipartimento di Sanità Pubblica, e Malattie Infettive, Sapienza-Università di Roma), Greco, E., (Medicina 3, Bruno G., Department of Medical Sciences, Città della Salute e della Scienza, A. O., University of Turin), Averna, M., (Dipartimento Biomedico di Medicina Interna e Specialistica, Giammanco A., Università di Palermo), Sposito P. (Azienda Ospedaliera Ospedali Riuniti Papardo Piemonte, Messina), De Cristofaro, R., (Istituto di Medicina Interna e Geriatria, De Gennaro L., Centro Emostasi, e Trombosi, Gemelli, Policlinico A., Roma), Carulli, L., (UO di Medicina a Indirizzo Nutrizionistico e Metabolico, Pellegrini E., Università degli Studi di Modena e Reggio Emilia), Dipartimento Integrato di Medicina Endocrinologia Metabolismo e Geriatria., Cominacini, L., Mozzini, C., (Dipartimento di Medicina, Pasini A. F., Sezione di Medicina Interna, D, Università di Verona), Sprovieri, M., (UOC Medicina d'Urgenza e PS, Spagnuolo V., Stabilimento Ospedaliero dell'Annunziata, Cosenza), (UOC Medicina Interna per l'Urgenza, Cerqua G., S Giovanni Addolorata, Ao, Cerasola G., Mulé G. (Università degli Studi di Palermo), Barbagallo, M., Lo Sciuto, S., (UOC di Geriatria e Lungodegenza, Monteverde A., Azienda Ospedaliera Universitaria Policlinico, Aoup, Palermo), Saitta, A., (UOC Medicina Interna, Lo Gullo A., Università di Messina), Malatino, L., Cilia, C., Terranova, V., (Clinica Medica, Pisano M., Ospedale, Cannizzaro, Università degli Studi di Catania), Pinto, A., Di Raimondo, D., Tuttolomondo, A., (Internal Medicine and Cardio-Angiology Ward, Conigliaro R., Department of Biomedicine and Internal Medicine, University of Palermo), Signorelli S. (Dipartimento di Medicina Interna e Patologia, Università degli Studi di Catania), De Palma, D., Galderisi, M., (Dipartimento di Medicina Clinica e Sperimentale, Cudemo G., AUP Federico II di Napoli), Galletti, F., (Dipartimento di Medicina Clinica e Chirurgia, Fazio V., Università di Napoli Federico II), De Luca, N., (Centro Ipertensione, Meccariello A., AUO Federico II, Napoli), Caputo, D., (UO Medicina Interna, De Donato M. T., Azienda Ospedaliera Universitaria San Giovanni di Dio, e Ruggi D'Aragona, Salerno), Iannuzi, A., (Divisione di Medicina Interna, Bresciani A., Cardarelli, Osp. A., (V Divisione Medicina Interna ed Immunoallergologia, Giunta R., Policlinico, Sun, Utili, R., (Medicina Infettivologica e dei Trapianti, Iorio V., Seconda Università di Napoli, AORN dei Colli-Monaldi), Adinolfi, L. E., Sellitto, A., (Medicina Interna, Iuliano N., Ospedale di Marcianise), Bellis, P., (UOC Medicina Interna e di Urgenza e Pronto Soccorso, Tirelli P., del Loreto Nuovo, P. O. S. M., Loreto, Mare), (Clinica Medica 5, Sacerdoti D., Dipartimento di Medicina DIMED, Università degli Studi di Padova), (UO Medicina Interna Arezzo, Vanni D., Ospedale San Donato, Azienda USL, 8 Arezzo), Iuliano, L., Ciacciarelli, M., (Department of Medico-Surgical Sciences and Biotechnology, Pacelli A., Vascular Biology, Mass Spectrometry Lab, Sapienza-University of Rome), Palazzuoli A. (UOS Malattie Cardiovascolari Dipartimento di Scienze Mediche Chirurgiche e Neuroscienze, Università di Siena), Cacciafesta, M., Gueli, N., Lo Iacono, C., Brusco, S., (UOC di Medicina Geriatrica e Riabilitazione, Verrusio W., Sapienza-Università di Roma, Nobili, L., Tarquinio, N., (UO Medicina 'SS Benvenuto e Rocco', Pellegrini F., Dipartimento di Medicina Interna, Asur, Marche, Area Vasta, n. 2., ex ZT 7), (UOS Breve Osservazione, Vincentelli G. M., Calibita 'Fatebenefratelli' Isola Tiberina, Ospedale S. G., Ravallese, F., (UOC Medicina Interna, Santini C., Ospedale, Vannini, Letizia, C., Petramala, L., (UOD Ipertensione Secondaria, Zinnamosca L., Dipartimento di Medicina Interna, e Specialità Mediche, Minisola, S., Cilli, M., Savoriti, C., (UOC Medicina Interna F e Malattie Metaboliche dell'osso- Sapienza-Università di Roma), Colangelo L., Falaschi, P., Martocchia, A., (UO Geriatria, Pastore F., Andrea, Azienda Ospedaliera S., Facoltà diMedicina, e Psicologia, Bertazzoni, G., (UOC Medicina d’Urgenza, Attalla El Halabieh E., Dipartimento di Emergenza ed Accettazione, Paradiso, M., Lizzi, E. M., (Ospedale San Giovanni Battista, Timmi S., Ordine di Malta, (Medicina Interna II, Battisti P., Ospedale San Giovanni-Addolorata, (UOC Medicina Interna, Cerci S., Ospedali Riuniti Frascati, Marino), (UOC Cardiologia-UTIC, Ciavolella M., Ospedale di Frascati, (Centro dell’Ipertensione Arteriosa e delle Malattie Metaboliche e Renali, Di Veroli C., Casa di Cura 'San Domenico', Malci, F., (UOC di Medicina Interna, De Ciocchis A., Ospedale, ASL Roma, G, Subiaco), Abate, D. (Az., Castellino, P., Zanoli, L., (UOC Medicina Interna, Fidone F., Dipartimento di Medicina Clinica, e Sperimentale, Mannarino, E., Pasqualini, L., (Medicina Interna, Oliverio G., Università degli Studi di Perugia), Pende, A., (Clinica di Medicina Interna 1, Artom N., Università di Genova, San Martino - IST), IRCCS Az. Osp. Univ., Ricchio, R., (UOC Geriatria, Fimognari F. L., Azienda Ospedaliera di Cosenza, Alletto, M., (Unità Operativa di Medicina, Messina S., Elia, Ospedale S., Caltanissetta), Sesti, G., Arturi, F., Fiorentino, T. V., (Università degli Studi, Pedace E., UOC Medicina Interna, Policlinico Universitario 'Mater Domini'), Scarpino, P. E., Carullo, G., Maio, R., (Cattedra di Medicina Interna, Sciacqua A., UO Malattie Cardiovascolari, Campus Universitario di Germaneto, Università Magna Graecia di Catanzaro), Frugiuele, P., (UOC Medicina Interna e Reumatologia, Spagnuolo V., Stabilimento Ospedaliero Annunziata, Azienda Ospedaliera Cosenza), (UO Lungodegenza, Battaglia G., Serra San Bruno, S. O., ASP Vibo Valentia), Atzori, S., (Clinica Medica, Delitala G., Aou, Sassari), Angelucci, E., (UOC di Clinica Medica, Sestili S., PO Clinicizzato di Chieti), Traisci, G., (UOC Medicina Interna 2, De Feudis L., PO di Pescara), Di Michele, D., (UOC Medicina Interna, Fava A., Asl, Teramo), Balsano, C., (Dipartimento di Medicina Interna e Sanità Pubblica, De Ciantis P., Università, dell'Aquila), Desideri, G., (UOC Geriatria e Lungodegenza Geriatrica, Camerota A., Dipartimento Medico ORM, Avezzano), Po, Mezzetti M. (UOC Medicina Interna Ospedale del Casentino-Direttore Dr. Emilio Santoro, AUSL8 Arezzo), Gresele, P., Vedovati, C., (Dipartimento di Medicina Interna, Fierro T., Sezione di Medicina Interna, e Cardiovascolare, Università di Perugia), (Centro Aterosclerosi, Puccetti L., Trombosi, e Coagulopatie, Università degli Studi di Siena, Azienda Ospedaliero-Universitaria Senese), Bertolotti, M., (UO Geriatria, Mussi C., Boddi, M., Savino, A., Contri, S., (Dipartimento di Medicina Sperimentale e Clinica, Degl'Innocenti G., Università degli Studi di Firenze), Saller, A., (Clinica Medica 1, Fabris F., Medicina Interna CLOPD, Departement of Medicine DIMED, University of Padova), Pesavento, R., Filippi, L., (Dipartimento di Scienze Cardiologiche, Vedovetto V., Toraciche, e Vascolari, Clinica Medica, 2, Azienda Ospedaliera-Università di Padova), (Clinica Medica IV, Puato M., Dipartimento di Medicina, Azienda Ospedaliera Universitaria Padova, Padova), Fabris, F., (UOA Medicina, Treleani M., Policlinico, Universitario, De Luca, E., De Zaiacomo, F., (Clinica Geriatrica, Giantin V., Università di Padova), (Medicina Interna 1, Semplicini A., Giovanni e Paolo, Ospedale SS., Venezia), Minuz, P., (Sezione di Medicina Interna C, Romano S., Università di Verona, Aoui, Verona), Fantin, F., (Dipartimento di Medicina, Manica A., Sezione di Geriatria, Stockner, I., Pattis, P., Wiedermann, Gutmann B. (Divisione di Medicina Interna-Direttore Prof. J., Ospedale Centrale di Bolzano), Catena, C., Colussi, G., (Clinica Medica, Sechi L. A., Dipartimento di Scienze Mediche Sperimentali, e Cliniche, Università di Udine, Italy), Annoni, G., Bruni, A. A., (Clinica Geriatrica, Castagna A., Università degli Studi di Milano-Bicocca, Dipartimento di Medicina, e Chirurgia, AO San Gerardo, Monza), (Medicina Interna 1, Spinelli D., Dipartimento di Scienze Cliniche, e di Comunità, Fondazione, Irccs, Università di Milano), (Clinica Medica I, Miceli E., Reparto, 11, IRCCS Policlinico San Matteo di Pavia), Schinco, G., (UOC Geriatria, Spreafico S., Fondazione IRCCS Cà Granda, Ospedale Maggiore Policlinico), (UOC Medicina Interna, Secchi B., Ospedale, Bassini, Milano), Vanoli, M., Casella, G., (SC Medicina Interna, Pulixi E. A., Azienda Ospedaliera della Provincia di Lecco, Ospedale di Merate, Lecco), Sansone, L., (UOC Medicina, Serra M. G., Panico', Azienda Ospedaliera 'Cardinale G., Tricase, (Lecce), Longo, S., (UOC Medicina Interna, Antonaci S., Azienda Ospedaliera Policlinico, Bari), Belfiore, A., Frualdo, M., Palasciano, G., Murri'- Bari), Ricci L. (Clinica Medica 'A., (Struttura Complessa di Medicina Interna, Ventrella F., Cerignola, Asl, Foggia), (UOC Medicina Interna, Bianco C., Tropea), Santovito, D., (Centro di Eccellenza Europeo e di Riferimento Regionale per l'Aterosclerosi, Cipollone F., l'Ipertensione Arteriosa, e le Dislipidemie, Università, Chieti), Nicolai, S., (UO Medicina Interna, Salvati F., Ospedale di Ortona, ASL 02 Abruzzo), Rini, G. B., (UOC Medicina Interna ed Ipertensione, Scozzari F., Dipartimento Biomedico di Medicina Interna, e Specialistica, Giaccone' di Palermo), Policlinico 'P., Muiesan, M. L., Salvetti, M., (Dipartimento di Scienze Cliniche e Sperimentali, Bazza A., Università di Brescia, 2° Medicina Generale Spedali Civili), Picardi, A., Vespasiani-Gentilucci, U., (Medicina Interna e Epatologia, De Vincentis A., Università Campus Bio-Medico, Cosio, P., (Medicina Interna 1, Terzolo M., Dipartimento di Scienze Cliniche, e Biologiche, AOU San Luigi Gonzaga, Università di Torino), Madaffari, B., (UO Medicina Interna, Parasporo B., Azienda Ospedaliera Bianchi Melacrino Morelli, Reggio, Calabria), Fenoglio, L., Bracco, C., (SC Medicina Interna, Melchio R., Croce e Carle, AO S., Cuneo), Gentili, T., (Medicina Generale - Settore Subintensivo, Salvi A., Azienda Ospedaliero- Universitaria, Ancona), (Medicina Generale - Settore Ordinario, Nitti C., Azienda, Ospedaliero-Universitaria, Gabrielli, A., (Clinica Medica, Martino G. P., Capucci, A., Brambatti, M., (Clinica di Cardiologia, Sparagna A., Ospedale, Torrette, (UO Medicina Generale IV, Tirotta D., Ospedale, Cervesi, Cattolica), Andreozzi, P., Ettorre, E., Viscogliosi, G., Servello, A., (Area Geriatria, Musumeci M., DAI Medicina Interna, Rossi Fanelli, F., Delfino, M., (UOC Medicina Interna H, Giorgi A., Sapienza- Università di Roma), Glorioso, N., Melis, G., Marras, G., (Ambulatorio Ipertensione Arteriosa e Patologie Correlate, Matta M., (UOC Medicina Interna, Sacco A., PO Madonna delle Grazie, Matera), Stellitano, E., (UO Medicina, Scordo A., PO 'Tiberio Evoli', Melito Porto Salvo), Russo, F., (UOC Medicina Generale di Rogliano, Caruso A. A., AO di Cosenza), Porreca, E., (UO Medicina Interna e Geriatria, Tana M., D'Annunzio, Università G., Chieti-Pescara), Ferri, C., (Divisione di Medicina Interna e Nefrologia - Ospedale San Salvatore, Cheli P., Dipartimento, Mesva, (Clinica Medica 'Murri', Portincasa P., Dipartimento di Scienze Mediche, e Oncologia Umana, Università degli Studi di Bari), Muscianisi G. (ASP Reggio Calabria, Saline Joniche), Giordani, S., (Dipartimento di Scienze Mediche e Chirurgiche, Stanghellini V., Università degli Studi di Bologna), Sabbà C. (UOC Geriatria e Centro di assistenza e ricerca sovraziendale per le malattie rare, Bari), Mancuso, G., Bartone, M., (UOC Medicina Interna, Calipari D., Presidio, Ospedaliero, ASP di Catanzaro), Arcidiacono, G., (UOC Cardiologia e UTIC, Bellanuova I., Catania), Ferraro M., Marigliano G. (ASP Cosenza), Cozzolino, D., Lampitella, A., (Dipartimento di Internistica Clinica e Sperimentale, Acri V., Seconda Università di Napoli), Galasso, D., Mazzei, F., (RSA Madonna di Porto Gimigliano, Galasso S., Catanzaro), (Azienda Ospedaliera della Provincia di Pavia, Buratti A., UO Medicina Interna, Ospedale, Civile, Casorate, Primo, Pavia), Porta, M., (SC Medicina Interna 1U, Brizzi M. F., Azienda, Ospedaliera, Torino), Fattorini, A., Sampietro, F., (Servizio di Coagulazione ed Unità Ricerca Trombosi, D’Angelo A., IRCCS Ospedale San Raffaele, Manfredini, R., Pala, M., (UOC Clinica Medica, Fabbian F., Anna, Azienda Ospedaliera- Universitaria S., Ferrara), Moroni, C., Valente, L., (Laboratorio di Ecocardiografia- Cardiologia Preventiva, Lopreiato F., DAI Cuore, e Grossi Vasi, (UOC Medicina Interna, Parente F., Lecce), (Immunologia Clinica A, Granata M., Moia, M., (Fondazione IRCCS Ca'Granda, Braham S., Ospedale Maggiore Policlinico, Rossi, M., (Dipartimento di Medicina Clinica e Sperimentale, Pesce M., Università di Pisa), Gentile, A., (UO Medicina, Catozzo V., Ldp, Loreto, Baciarello, G., (UOC Cardiologia Preventiva e Riabilitativa, Cosimati A., Ageno, W., Rancan, E., (Dipartimento di Medicina Clinica e Sperimentale, Guasti L., Università, Dell'Insubria, Varese), Ciccaglioni, A., Negri, S., (Centro Elettro-Stimolazione Cardiaca, Polselli M., Prisco, D., (SOD Patologia Medica, Marcucci R., Aou, Careggi, Firenze), Ferro, D., Cangemi, R., Perri, L., Polimeni, L., Catasca, E., Vicario, T., Russo, R., Saliola, M., Del Ben, M., Angelico, F., Calvieri, C., Bucci, T., (I Clinica Medica, Baratta F., Migliacci, R., Medicina Interna, Porciello G. (S. C., Ospedale della Valdichiana, Cortona, Usl, 8 Arezzo), (Dipartimento BioMedico di Medicina Interna e Specialistica, Corrao S., Università degli Studi di, Palermo). Simi Young Internists (GIS) Group: Anzaldi M., Bazzini, C., Bianchi, P. I., Boari, B., Buonauro, A., Buttà, C., Buzzetti, E., Calabria, S., Capeci, W., Caradio, F., Carleo, P., Carrabba, M. D., Castorani, L., Cecchetto, L., Cicco, S., Cimini, C., Colombo, B. M., De Giorgi, A., De Vuono, S., Del Corso, L., Denegri, A., Di Giosia, P., Durante Mangoni, E., Falsetti, L., Forgione, A., Giorgini, P., Grassi, D., Grembiale, A., Hijazi, D., Iamele, L., Lorusso, G., Marchese, A., Marra, A. M., Masala, M., Miceli, G., Montebianco Abenavoli, L., Murgia, G., Naccarato, P., Padula, D., Pattoneri, P., Perego, F., Pesce, P., Piano, S., Pinna, M., Pinto, D., Pretti, V., Pucci, G., Raparelli, V., Salinaro, F., Salzano, A., Santilli, F., Scarpini, F., Scicali, R., Sirico, D., Suppressa, P., Talia, M., Tassone, E. J., Torres, D., Vazzana, N., Vecchio, C. R., Vidili, G., Vitale, F., Zaccone, V., Alessandri, C., Serviddio, G., Palange, P, Greco, E, Bruno, G, Averna, M, Giammanco, A, Sposito, P, De Cristofaro, R., De Gennaro, L, Carulli, L, Pellegrini, E, Cominacini, L, Mozzini, C, Pasini, Af, Sprovieri, M, Spagnuolo, V, Cerqua, G, Cerasola, G, Mulé, G, Barbagallo, M, Lo Sciuto, S, Monteverde, A, Saitta, A, Lo Gullo, A, Malatino, L, Cilia, C, Terranova, V, Pisano, M, Pinto, A, Di Raimondo, D, Tuttolomondo, A, Conigliaro, R, Signorelli, S, De Palma, D, Galderisi, M, Cudemo, G, Galletti, F, Fazio, V, De Luca, N, Meccariello, A, Caputo, D, De Donato, Mt, Iannuzi, A, Bresciani, A, Giunta, R, Utili, R, Iorio, V, Adinolfi, Luigi Elio, Sellitto, A, Iuliano, N, Bellis, P, Tirelli, P, Sacerdoti, D, Vanni, D, Iuliano, L, Ciacciarelli, M, Pacelli, A, Palazzuoli, A, Cacciafesta, M, Gueli, N, Lo Iacono, C, Brusco, S, Verrusio, W, Nobili, L., Tarquinio, N., Pellegrini, F, Vincentelli, G. M., Ravallese, F, Santini, C, Letizia, C, Petramala, L, Zinnamosca, L, Minisola, S., Cilli, M, Savoriti, C, Colangelo, L, Falaschi, P, Martocchia, A, Pastore, F., and DURANTE MANGONI, Emanuele

Subjects
Male, Risk, ABI, ARAPACIS, Atrial fibrillation, Myocardial infarction, Vascular events, Hematology, medicine.medical_specialty, Aged, Aged, 80 and over, Ankle Brachial Index, Atrial Fibrillation, Female, Follow-Up Studies, Humans, Italy, Middle Aged, Predictive Value of Tests, Prospective Studies, Survival Analysis, Vascular Diseases, Population, Socio-culturale, 030204 cardiovascular system & hematology, 03 medical and health sciences, 0302 clinical medicine, atrial fibrillation, ABI, ARAPACIS, myocardial infarction, vascular events, Interquartile range, Internal medicine, myocardial infarction, vascular events, 80 and over, Medicine, Cumulative incidence, 030212 general & internal medicine, education, Prospective cohort study, Stroke, education.field_of_study, business.industry, Hazard ratio, medicine.disease, Cardiology, business, Settore SECS-S/01 - Statistica
Abstract

SummaryAtrial fibrillation (AF) patients are at high risk for thrombotic and vascular events related to their cardiac arrhythmia and underlying systemic atherosclerosis. Ankle-Brachial Index (ABI) is a non-invasive tool in evaluating systemic atherosclerosis, useful in predicting cardiovascular events in general population; no data are available in AF patients. ARAPACIS is a prospective multicentre observational study performed by the Italian Society of Internal Medicine, analysing association between low ABI (≤0.90) and vascular events in NVAF out- or in-patients, enrolled in 136 Italian centres. A total of 2,027 non-valvular AF (NVAF) patients aged > 18 years from both sexes followed for a median time of 34.7 (interquartile range: 22.0–36.0) months, yielding a total of 4,614 patient-years of observation. Mean age was 73 ± 10 years old with 55% male patients. A total of 176 patients (8.7%) experienced a vascular event, with a cumulative incidence of 3.81%/patient-year. ABI≤ 0.90 was more prevalent in patients with a vascular event compared with patients free of vascular events (32.2 vs 20.2%, p< 0.05). On Cox proportional hazard analysis, ABI≤ 0.90 was an independent predictor of vascular events (hazard ratio (HR): 1.394, 95% confidence interval (CI): 1.042–1.866; p=0.02), vascular death (HR: 2.047, 95% CI: 1.255-3.338; p=0.004) and MI (HR: 2.709, 95%> CI: 1.485-5.083; p=0.001). This latter association was also confirmed after excluding patients with previous MI (HR: 2.901, 95% CI: 1.408-5.990, p=0.004). No association was observed between low ABI and stroke/transient ischaemic attack (p=0.91). In conclusion, low ABI is useful to predict MI and vascular death in NVAF patients and may independently facilitate cardiovascular risk assessment in NVAF patients.Note: The review process for this paper was fully handled by C. Weber, Editor in Chief.Listed in the Supplementary Online Appendix Material which is available online at www.thrombosis-online.com.

Published
2016

6. The atherosclerotic plaque vulnerability: focus on the oxidative and endoplasmic reticulum stress in orchestrating the macrophage apoptosis in the formation of the necrotic core.

Author

Cominacini L, Garbin U, Mozzini C, Stranieri C, Pasini A, Solani E, Tinelli IA, and Pasini AF

Subjects
Animals, Humans, Plaque, Atherosclerotic immunology, Apoptosis, Endoplasmic Reticulum Stress, Macrophages cytology, Necrosis, Oxidative Stress, Plaque, Atherosclerotic metabolism, Plaque, Atherosclerotic pathology
Abstract

Although the understanding the pathophysiology of atherogenesis and atherosclerosis progression has been one of the major goals of cardiovascular research during the last decades, the precise mechanisms underlying plaque destabilization are still unknown. The disruption of the plaque and the thrombosis in the lumen that are mostly determined by the expansion of the necrotic core (NC) are driven by various mechanisms, including accelerated macrophage apoptosis and defective phagocytic clearance (defective efferocytosis). Oxidative stress is implicated in the expansion of the NC: in fact, many oxidized compounds and processes contribute to the macrophage apoptosis; in addition, the oxidized derivatives of polyunsatured fatty acids promote defective efferocytosis, with the final result of NC expansion. In the last years the role of the endoplasmic reticulum (ER) stress is under investigation to better define its possible contribution in affecting the NC expansion. The abnormal amount of apoptotic cells in the vulnerable plaque has been demonstrated to be related both to the sustained ER stress and to the expression of survival and protective genes, such as the unfolded protein response or/and the nuclear erytroid- related factor 2. In this review the authors focus on the promising results of the oxidative and ER stress in contributing to triggering and orchestrating the atherosclerotic plaque vulnerability.

Published
2015
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7. Role of MDCT coronary angiography in the clinical setting: economic implications.

Author

Malagò R, Pezzato A, Barbiani C, Tavella D, Vallerio P, Pasini AF, Cominacini L, and Mucelli RP

Subjects
Aged, Cost-Benefit Analysis, Exercise Test, Female, Humans, Male, Middle Aged, Predictive Value of Tests, Risk Factors, Sensitivity and Specificity, Coronary Angiography economics, Coronary Artery Disease diagnostic imaging, Coronary Artery Disease economics, Multidetector Computed Tomography economics
Abstract

Purpose: This study evaluated the incremental value and cost-effectiveness ratio of introducing coronary angiography (CA) with multidetector computed tomography (MDCT-CA) in the diagnostic management of patients with suspected coronary artery disease (CAD) compared with the traditional diagnostic workup., Material and Methods: Five hundred and fifty consecutive patients who underwent MDCT-CA between January 2009 and June 2011 were considered. Patients with atypical chest pain and suspected obstructive CAD were directed to one of two diagnostic pathways: the traditional protocol (examination, stress test, CA) and the current protocol (examination, stress test, MDCT-CA, and CA, if necessary). The costs of each protocol and for the individual method were calculated. Based on the results, the cost-effectiveness ratio of the two diagnostic pathways was compared. A third, modified, diagnostic pathway has been proposed with its relative cost-effectiveness ratio (examination, MDCT-CA, stress test, and CA, if necessary)., Results: Stress test vs. MDCT-CA had an accuracy of 66%, a sensitivity and specificity of 21% and 87%, respectively, and a positive (PPV) and negative (NPV) predictive value of 40% and 70%, respectively. Comparison between conventional CA (CCA) and MDCT-CA showed a sensitivity and specificity of 92% and 89%, respectively, a PPV and NPV of 89%, and an accuracy of 92%. The traditional protocol has higher costs than the second protocol: 1,645 euro against 322 euro (mean), but it shows a better cost-effectiveness ratio. The new proposed protocol has lower costs, mean 261 euro, with a better costeffectiveness ratio than the traditional protocol., Conclusions: The diagnostic protocol for patients with suspected CAD has been modified by the introduction of MDCT-CA. Our study confirms the greater diagnostic performance of MDCT-CA compared with stress test and its similar accuracy to CCA. The use of MDCT-CA to select patients for CCA has a favourable cost-effectiveness profile.

Published
2013
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8. Nebivolol treatment reduces serum levels of asymmetric dimethylarginine and improves endothelial dysfunction in essential hypertensive patients.

Author

Pasini AF, Garbin U, Stranieri C, Boccioletti V, Mozzini C, Manfro S, Pasini A, Cominacini M, and Cominacini L

Subjects
Adrenergic beta-Antagonists therapeutic use, Aged, Amidohydrolases metabolism, Antihypertensive Agents pharmacology, Antihypertensive Agents therapeutic use, Arginine blood, Atenolol pharmacology, Atenolol therapeutic use, Benzopyrans therapeutic use, Double-Blind Method, Endothelium, Vascular drug effects, Ethanolamines therapeutic use, Female, Humans, Hypertension drug therapy, Male, Middle Aged, Nebivolol, Nitric Oxide Synthase Type III metabolism, Vasodilation drug effects, Adrenergic beta-Antagonists pharmacology, Arginine analogs & derivatives, Benzopyrans pharmacology, Endothelium, Vascular physiopathology, Ethanolamines pharmacology, Hypertension blood, Hypertension physiopathology
Abstract

Background: This study was conducted to evaluate (i) the effect of nebivolol, a selective beta1-adrenergic receptor antagonist, on plasma concentration of asymmetric dimethylarginine (ADMA) and on flow-mediated dilation (FMD) in essential hypertensive patients; (ii) the effect of serum derived from the treated hypertensive patients on ADMA and on dimethylarginine dimethylaminohydrolase 2 (DDAH2), the enzyme that selectively degrades ADMA, in human umbilical vein endothelial cells (HUVECs)., Methods: Forty healthy subjects and 40 matched essential hypertensive patients treated with atenolol and nebivolol according to a double-blind, randomized design participated in the study. Evaluation of brachial artery (BA) reactivity was performed by a longitudinal B-mode scan of the right BA. ADMA and L-arginine were measured by high-performance liquid chromatography. DDAH2 expression and endothelial nitric oxide synthase activity (eNOS) were also evaluated in HUVECs., Results: ADMA levels were significantly decreased and FMD increased only in patients receiving nebivolol (P < 0.01). Furthermore, in nebivolol group, we found a significant correlation between changes in ADMA levels and changes in FMD (P < 0.01). Sera derived from patients treated with nebivolol but not with atenolol decreased ADMA and increased DDAH2 expression and eNOS activity (P < 0.001) in HUVECs., Conclusions: The results of this study demonstrate that the improvement of endothelial dysfunction induced by nebivolol in hypertensive patients may be related to its effect on circulating ADMA levels. Although the mechanism by which nebivolol reduces circulating ADMA in hypertensive patients remains unclear, our ex vivo results suggest that the upregulation of DDAH2 expression may have a role.

Published
2008
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9. Nebivolol reduces asymmetric dimethylarginine in endothelial cells by increasing dimethylarginine dimethylaminohydrolase 2 (DDAH2) expression and activity.

Author

Garbin U, Pasini AF, Stranieri C, Manfro S, Boccioletti V, and Cominacini L

Subjects
Amidohydrolases genetics, Arginine metabolism, Atenolol pharmacology, Cell Line, Endothelial Cells metabolism, Female, Humans, Male, Nebivolol, Nitric Oxide Synthase Type III metabolism, RNA, Messenger metabolism, Adrenergic beta-Antagonists pharmacology, Amidohydrolases metabolism, Antihypertensive Agents pharmacology, Arginine analogs & derivatives, Benzopyrans pharmacology, Endothelial Cells drug effects, Ethanolamines pharmacology
Abstract

Asymmetric dimethylarginine (ADMA) has been reported to affect the synthesis of nitric oxide (NO) in endothelial cells by inhibiting endothelial NO synthase (eNOS) activity and to cause endothelial dysfunction in humans. This study was conducted in human umbilical vein endothelial cells (HUVECs) to evaluate the effect of nebivolol, a selective beta1-adrenergic receptor antagonist, on ADMA concentration and on dimethylarginine dimethylaminohydrolase (DDAH2), the enzyme that regulates ADMA catabolism. Nebivolol dose-dependently decreased ADMA/symmetric dimethylarginine (SDMA) ratio (p from <0.01 to <0.001). This was parallelled by a dose-dependent increase in DDAH2 mRNA (p from <0.01 to <0.001) and protein expression (p from <0.01 to <0.001) and activity (p from <0.01 to <0.001). The small interference RNA (siRNA)-mediated knockdown of DDAH2 abolished the modification of DDAH2 expression (p<0.001) and ADMA/SDMA ratio (p<0.001) induced by nebivolol. In conclusion, the results of this study demonstrate that nebivolol reduces ADMA concentration by increasing DDAH2 expression and activity. Our in vitro findings describe a novel vascular effect of nebivolol and clearly identify this compound as the first antihypertensive agent that modulates DDAH2 in endothelial cells.

Published
2007
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10. Enhanced levels of oxidized low-density lipoprotein prime monocytes to cytokine overproduction via upregulation of CD14 and toll-like receptor 4 in unstable angina.

Author

Pasini AF, Anselmi M, Garbin U, Franchi E, Stranieri C, Nava MC, Boccioletti V, Vassanelli C, and Cominacini L

Subjects
Aged, Angina, Unstable blood, Female, Humans, Interleukin-1beta metabolism, Interleukin-6 metabolism, Male, Middle Aged, Up-Regulation, Angina, Unstable metabolism, Lipopolysaccharide Receptors metabolism, Lipoproteins, LDL physiology, Monocytes metabolism, Toll-Like Receptor 4 metabolism
Abstract

Objectives: The purpose of this study was to establish whether oxidized low-density lipoprotein (oxLDL) contributes to cytokine overproduction via upregulation of CD14 and toll-like receptor-4 (TLR-4) expression on circulating monocytes of unstable angina (UA) patients., Methods and Results: Expression of CD14 and TLR-4 on circulating monocytes, and the concentration of plasma oxLDL, (interleukin [IL])-6, IL-1 beta, IL-8, tumor necrosis factor (TNF)-alpha, monocyte chemoattractant protein-1 (MCP-1) were measured in 27 control (C) subjects, 29 patients with stable angina (SA), and 27 with UA. CD14 and TLR-4 expression on monocytes and circulating IL-6, IL-1 beta, and oxLDL were higher in UA than in SA and C subjects (P<0.001). In in vitro experiments, oxLDL increased CD14 and TLR-4 expression (P<0.001) in control monocytes as well as IL-6, IL-1 beta, and at a lower extent TNF-alpha and MCP-1 levels in the supernatant (P from <0.05 to <0.001). The preincubation of sera derived from UA patients but with control monocytes also induced a significant increase of CD14 and TLR-4 expression (P<0.001) and of IL-6 and IL-1 beta production (P<0.001) in the supernatant., Conclusions: In UA patients oxLDL may contribute to monocyte overproduction of some cytokines by upregulating CD14 and TLR-4 expression.

Published
2007
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11. Effect of sulfhydryl and non-sulfhydryl angiotensin-converting enzyme inhibitors on endothelial function in essential hypertensive patients.

Author

Pasini AF, Garbin U, Nava MC, Stranieri C, Pellegrini M, Boccioletti V, Luchetta ML, Fabrizzi P, Lo Cascio V, and Cominacini L

Subjects
Adrenergic beta-Antagonists pharmacology, Adrenergic beta-Antagonists therapeutic use, Adult, Angiotensin-Converting Enzyme Inhibitors pharmacology, Atenolol pharmacology, Atenolol therapeutic use, Blood Glucose metabolism, Blood Pressure drug effects, Blood Pressure physiology, Captopril pharmacology, Captopril therapeutic use, Cell Adhesion Molecules blood, Cell Adhesion Molecules drug effects, Cholesterol, HDL blood, Endothelium, Vascular drug effects, Female, Heart Rate drug effects, Heart Rate physiology, Humans, Hypertension physiopathology, Male, Middle Aged, Oxidative Stress drug effects, Oxidative Stress physiology, Ramipril pharmacology, Sulfhydryl Compounds pharmacology, Triglycerides blood, Vasodilation drug effects, Angiotensin-Converting Enzyme Inhibitors therapeutic use, Captopril analogs & derivatives, Endothelium, Vascular physiopathology, Hypertension drug therapy, Ramipril therapeutic use, Sulfhydryl Compounds therapeutic use
Abstract

Background: Oxidative inactivation of nitric oxide (NO) is regarded as an important cause of reduced endothelium-dependent vasodilation in essential hypertension. Because zofenopril, an angiotensin-converting enzyme (ACE) inhibitor with a sulfhydryl (SH) group, has demonstrated antioxidant properties and to reduce adhesion molecule expression in vitro, in this study we evaluated the effect of this drug in comparison with the carboxylic ACE inhibitor ramipril and the beta-adrenoreceptor blocker atenolol on (1) circulating adhesion molecules and some oxidative stress parameters and (2) endothelium-dependent vasodilation in essential mildly hypertensive patients., Methods: A total of 45 healthy subjects and 45 matched hypertensive patients participated in the study. Hypertensive patients were randomly treated with zofenopril (15 to 30 mg/d), ramipril (2.5 to 5 mg/d), and atenolol (50 to 100 mg/d). At baseline and after an 8-week therapy we evaluated blood pressure (BP) values, plasma and LDL hydroperoxides, plasma 8-isoprostanes, circulating levels of oxidized-(ox)LDL and of adhesion molecules (intercellular cell adhesion molecule-1 [ICAM-1], and vascular cell adhesion molecule-1 [VCAM-1], and E-selectin). Furthermore, all patients underwent ultrasound detection of brachial artery reactivity and endothelium-dependent dilation (flow-mediated dilation, FMD) was evaluated., Results: All the treatments determined similar significant (P < .001) reduction of both systolic and diastolic BP values. Plasma (P < .01) and LDL hydroperoxides (P < .01), plasma 8-isoprostanes (P < .05), circulating oxLDL (P < .05), and adhesion molecules (P < .05) were significantly reduced only in patients receiving zofenopril. Similarly FMD was significantly increased (P < .001) in the zofenopril-treated group., Conclusions: Our results suggest that in mildly hypertensive patients without organ damage zofenopril, beyond its BP-lowering effects and through its sustained antioxidant activity, offers important advantages in reducing endothelial activation.

Published
2007
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12. Effect of DL-nebivolol, its enantiomers and metabolites on the intracellular production of superoxide and nitric oxide in human endothelial cells.

Author

Evangelista S, Garbin U, Pasini AF, Stranieri C, Boccioletti V, and Cominacini L

Subjects
Adrenergic beta-Antagonists chemistry, Adrenergic beta-Antagonists metabolism, Antioxidants chemistry, Antioxidants metabolism, Benzopyrans chemistry, Benzopyrans metabolism, Biotransformation, Bupranolol pharmacology, Calcium metabolism, Cells, Cultured, Endothelial Cells metabolism, Enzyme Activation drug effects, Ethanolamines chemistry, Ethanolamines metabolism, Humans, Lipoproteins, LDL metabolism, Nadolol pharmacology, Nebivolol, Nitric Oxide Synthase Type III metabolism, Propanolamines pharmacology, Receptors, Adrenergic, beta drug effects, Receptors, Adrenergic, beta metabolism, Stereoisomerism, Adrenergic beta-Antagonists pharmacology, Antioxidants pharmacology, Benzopyrans pharmacology, Endothelial Cells drug effects, Ethanolamines pharmacology, Nitric Oxide metabolism, Oxidative Stress drug effects, Superoxides metabolism
Abstract

Nebivolol, a third generation selective beta(1)-adrenoceptor (beta(1)-AR) antagonist, has been reported to reduce intracellular oxidative stress and to induce the release of nitric oxide (NO) from the endothelium. Nebivolol is also subjected to a complex metabolic process where glucuronidation, aromatic and alicyclic hydroxylation are the major pathways leading to several metabolites. We have studied the effect of nebivolol, its enantiomers and metabolites on intracellular oxidative stress and NO availability in human umbilical vein endothelial cells (HUVECs). Furthermore, since the receptors involved in this endothelial effect of nebivolol remain controversial, we have studied this matter by the use of antagonists of beta-AR. dl-Nebivolol, d-nebivolol and l-nebivolol significantly reduced the formation of reactive oxygen species (ROS) and superoxide induced by oxidized-low density lipoprotein (ox-LDL), although the racemic and l-form were significantly more active than d-nebivolol in this activity. A marked decrease in the availability of intracellular NO was found in HUVECs exposed to ox-LDL and this parameter was normalized by the prior incubation with dl-nebivolol, d-nebivolol and l-nebivolol; the effect of racemate was mainly mimicked by its l-enantiomer. eNOS activity significantly increased by a 5-min contact of HUVECs with dl-nebivolol and l-nebivolol, but not with d-nebivolol, and a similar pattern was observed when the intracellular calcium increase was measured. The metabolites A2, A3', A12 and A14 but not A1, A3 and R 81,928, derived from different metabolic pathways, retained the antioxidant activity of the parent racemic compound dl-nebivolol, reducing the intracellular formation of ROS and superoxide. The effects of dl-nebivolol on intracellular formation of NO, eNOS activity and intracellular Ca(2+) were partially antagonized by the antagonists of beta(1-2)-AR nadolol or by the beta(3)-AR antagonist SR59230A and further antagonized by their combination or by (beta(1-2-3)-AR antagonist bupranolol. In conclusion, this study shows that the NO releasing effect of nebivolol is mainly due to its l-enantiomer; the racemate and its enantiomers possess a remarkable antioxidant activity that contributes to its effect on the cellular NO metabolism and the activation of beta(3)-AR through a calcium dependent pathway is involved in the mechanisms leading to the NO release.

Published
2007
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13. Plasma levels of oxidized-low-density lipoproteins are higher in patients with unstable angina and correlated with angiographic coronary complex plaques.

Author

Anselmi M, Garbin U, Agostoni P, Fusaro M, Pasini AF, Nava C, Keta D, Turri M, Zardini P, Vassanelli C, Lo Cascio V, and Cominacini L

Subjects
Aged, Angina, Unstable diagnostic imaging, Angina, Unstable etiology, Biomarkers blood, Coronary Artery Disease complications, Coronary Artery Disease diagnostic imaging, Enzyme-Linked Immunosorbent Assay, Female, Humans, Male, Middle Aged, Oxidation-Reduction, Prognosis, Severity of Illness Index, Angina, Unstable blood, Coronary Angiography, Coronary Artery Disease blood, Lipoproteins, LDL blood
Abstract

Objectives: To measure circulating levels of oxidized-low-density lipoproteins (ox-LDL) in patients with stable and unstable angina and controls, and to investigate their correlation with the extent of coronary artery disease (CAD) and the presence of complex plaques at coronary angiography., Methods and Results: Circulating ox-LDL were assessed, using ELISA, in patients with unstable angina (UA, n=26), stable angina (SA, n=29) and in controls (C, n=27). All patients underwent coronary angiography. The extent of CAD was evaluated using a quantitative score, while the presence of complex, vulnerable plaques was angiographically assessed. Ox-LDL were higher in UA patients than in SA patients and in C subjects, and in SA patients than in C subjects (C, 45.6+/-12.8 U/L; SA, 58.8+/-11.0 U/L; UA, 73.7+/-13.6 U/L; p<0.001). No correlation was found with the extent of atherosclerotic disease in the coronary tree. Patients with angiographic complex lesions showed significantly higher levels of ox-LDL (68.4+/-13.9 U/L versus 55.2+/-16.4 U/L, p<0.001). Multiple regression analysis showed that ox-LDL were independent predictors of the presence of complex plaques (p<0.023)., Conclusions: Ox-LDL levels are higher in unstable patients and correlate with the presence of angiographically documented complex plaques. Ox-LDL might be markers of destabilization of CAD.

Published
2006
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14. Reduced progression of atherosclerosis in apolipoprotein E-deficient mice treated with lacidipine is associated with a decreased susceptibility of low-density lipoprotein to oxidation.

Author

Cristofori P, Crivellente F, Campagnola M, Pasini AF, Garbin U, Rigoni A, Tosetti M, Turton J, Faustinelli I, and Cominacini L

Subjects
Animals, Apolipoproteins E genetics, Arteriosclerosis genetics, Arteriosclerosis metabolism, Disease Susceptibility, Dose-Response Relationship, Drug, Female, Lipid Peroxidation drug effects, Lipoproteins, LDL metabolism, Malondialdehyde metabolism, Mice, Mice, Knockout, Random Allocation, Vitamin E metabolism, Antioxidants therapeutic use, Apolipoproteins E deficiency, Arteriosclerosis drug therapy, Calcium Channel Blockers therapeutic use, Dihydropyridines therapeutic use
Abstract

A study has been carried out in the apolipoprotein (apo) E-deficient mouse to investigate the activity of lacidipine (a calcium antagonist with antioxidant properties) in inhibiting the development of atherosclerotic lesions; of particular interest were changes in the susceptibility of low-density lipoproteins (LDL) to oxidation. Mice receiving a Western-type diet to accelerate the development of atherosclerosis were treated orally with vehicle or lacidipine at 3 or 10 mg/kg/day for 8 weeks. Lacidipine treatment (at 3 or 10 mg/kg) had no effect on the plasma lipid profile. However, a significant (P < 0.01) dose-related reduction of 43 and 50% of the aortic lesion area in respect to vehicle-treated mice was observed. Moreover, the resistance of mouse plasma LDL to undergo lipid peroxidation was significantly (P < 0.01) increased in apo E-deficient mice treated with lacidipine. The native LDL-like particle, derived from apo E-deficient mice treated with lacidipine, contained significantly lower concentrations of malonyldialdehyde than the vehicle-treated control group (P < 0.01). After exposure to human umbilical vein endothelial cells, LDL-like particle vitamin E levels (expressed as area under the curve; AUC), were significantly higher (P < 0.01) in both the 3 and 10 mg/kg lacidipine-treated groups, in comparison with the vehicle-treated control animals. We conclude that lacidipine reduced the extent of the atherosclerotic area in hypercholesterolaemic apo E-deficient mice, and that this reduction may be associated with the capacity of the drug to decrease the susceptibility of LDL to oxidation.

Published
2004
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15. Beta2 integrin-dependent neutrophil adhesion induced by minimally modified low-density lipoproteins is mainly mediated by F2-isoprostanes.

Author

Fontana L, Giagulli C, Cominacini L, Pasini AF, Minuz P, Lechi A, Sala A, and Laudanna C

Subjects
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid pharmacology, Blood Platelets cytology, Blood Platelets physiology, Bridged Bicyclo Compounds, Heterocyclic, Cell Adhesion drug effects, Cell Adhesion immunology, Fatty Acids, Unsaturated, Fibrinogen metabolism, GTP-Binding Protein alpha Subunits, Gi-Go drug effects, GTP-Binding Protein alpha Subunits, Gi-Go metabolism, Humans, Hydrazines pharmacology, Intercellular Adhesion Molecule-1 metabolism, Lipoproteins, LDL chemistry, Lipoproteins, LDL radiation effects, Neutrophils cytology, Neutrophils drug effects, Pertussis Toxin pharmacology, Receptors, Thromboxane agonists, Receptors, Thromboxane antagonists & inhibitors, Signal Transduction drug effects, Signal Transduction physiology, Ultraviolet Rays, CD18 Antigens metabolism, F2-Isoprostanes metabolism, Lipoproteins, LDL pharmacology, Neutrophils physiology
Abstract

Background: Oxidation of LDL produces a series of biologically active, oxidized lipids. Among them, isoprostanes, and in particular iPF(2alpha)-III, seem to be crucial in mediating some of the key cellular events seen in myocardial ischemia-reperfusion injury., Methods and Results: Minimally modified LDL (MM-LDL) triggers a dose-dependent, very rapid neutrophil adhesion to human fibrinogen. Rapid adhesion triggering correlates with degree of LDL oxidation and accumulation of isoprostanes. Isoprostanes accumulated in MM-LDL are major determinants of the proadhesive effect of oxidized LDL, as shown by experiments of receptor functional deletion. Moreover, evidence is provided of expression on human neutrophils of a biological active isoprostane receptor distinct from the classical thromboxane A2 receptor., Conclusions: These data suggest that isoprostanes are major contributors to the proadhesive effect induced by MM-LDL on neutrophils and provide additional evidence for the involvement of isoprostanes in the pathogenesis of myocardial ischemia/reperfusion injury.

Published
2002
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16. Effect of calcium antagonist or beta blockade treatment on nitric oxide-dependent vasodilation and oxidative stress in essential hypertensive patients.

Author

Taddei S, Virdis A, Ghiadoni L, Magagna A, Pasini AF, Garbin U, Cominacini L, and Salvetti A

Subjects
Adult, Biological Availability, Biomarkers, Double-Blind Method, Female, Humans, Male, Middle Aged, Nitric Oxide blood, Adrenergic beta-Antagonists therapeutic use, Antioxidants therapeutic use, Atenolol therapeutic use, Calcium Channel Blockers therapeutic use, Dihydropyridines therapeutic use, Hypertension drug therapy, Hypertension physiopathology, Nitric Oxide physiology, Oxidative Stress drug effects, Vasodilation drug effects, Vasodilation physiology
Abstract

Objectives: Essential hypertension is associated with impaired endothelium-dependent vasodilation caused by oxygen free radical-induced nitric oxide (NO) breakdown. Since calcium antagonists can improve endothelial function in hypertensive patients, we tested whether this beneficial effect could be related to restoration of NO availability by antioxidant activity., Methods: In 10 healthy subjects and 20 essential hypertensive patients, we studied forearm blood flow (strain-gauge plethysmography) modifications induced by intrabrachial acetylcholine (from 0.15-15 microg/100 ml per min), bradykinin (0.005-0.05 microg/100 ml per min), two endothelium-dependent vasodilators, and sodium nitroprusside (1-4 microg/100 ml forearm tissue per min), an endothelium independent vasodilator, in the absence and presence of NG-monomethyl-L-arginine (L-NMMA) (100 microg/100 ml forearm tissue per min), an NO synthase inhibitor., Results: In controls, vasodilation to acetylcholine and bradykinin was inhibited by L-NMMA. In hypertensive patients, vasodilation to acetylcholine and bradykinin, but not to sodium nitroprusside, was blunted and resistant to L-NMMA. Hypertensive patients were randomized to a 12-week treatment with lacidipine (4-6 mg/daily) or atenolol (50-100 mg/daily) (n = 10 each group). Lacidipine but not atenolol increased the vasodilation to acetylcholine and bradykinin and restored the inhibiting effect of L-NMMA on endothelium-dependent vasodilation, without affecting the response to sodium nitroprusside. Moreover, lacidipine reduced circulating markers of oxidative stress including plasma and low-density lipoprotein (LDL) hydroperoxides, the susceptibility of LDL to Cu2+-induced oxidation and the reactive oxygen species generated from human umbilical vein endothelial cells after incubation with LDL derived from plasma of the patients., Conclusions: Lacidipine increases endothelium-dependent vasodilation by restoring NO availability, and this effect possibly is related to antioxidant activity.

Published
2001
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17. The binding of oxidized low density lipoprotein (ox-LDL) to ox-LDL receptor-1 reduces the intracellular concentration of nitric oxide in endothelial cells through an increased production of superoxide.

Author

Cominacini L, Rigoni A, Pasini AF, Garbin U, Davoli A, Campagnola M, Pastorino AM, Lo Cascio V, and Sawamura T

Subjects
Allopurinol pharmacology, Animals, Antibodies, Monoclonal pharmacology, Antioxidants pharmacology, Aorta metabolism, Ascorbic Acid pharmacology, Aspirin pharmacology, Bradykinin pharmacology, CHO Cells, Catecholamines pharmacology, Cattle, Cells, Cultured, Chromans pharmacology, Cricetinae, Dose-Response Relationship, Drug, Endothelium, Vascular metabolism, Enzyme Inhibitors pharmacology, Flow Cytometry, Free Radical Scavengers pharmacology, Hemostatics pharmacology, Humans, Mice, Probucol pharmacology, Protein Binding, Reactive Oxygen Species metabolism, Receptors, Oxidized LDL, Scavenger Receptors, Class E, Thrombin pharmacology, Time Factors, omega-N-Methylarginine pharmacology, Imidazolines, Lipoproteins, LDL metabolism, Nitric Oxide metabolism, Oxygen metabolism, Receptors, LDL metabolism, Superoxides metabolism
Abstract

Oxidized low density lipoprotein (ox-LDL) has been suggested to affect endothelium-dependent vascular tone through a decreased biological activity of endothelium-derived nitric oxide (NO). Oxidative inactivation of NO is regarded as an important cause of its decreased biological activity, and in this context superoxide (O(2)) is known to inactivate NO in a chemical reaction during which peroxynitrite is formed. In this study we examined the effect of ox-LDL on the intracellular NO concentration in bovine aortic endothelial cells and whether this effect is influenced by ox-LDL binding to the endothelial receptor lectin-like ox-LDL receptor-1 (LOX-1) through the formation of reactive oxygen species and in particular of O(2). ox-LDL induced a significant dose-dependent decrease in intracellular NO concentration both in basal and stimulated conditions after less than 1 min of incubation with bovine aortic endothelial cells (p < 0.01). In the same experimental conditions ox-LDL also induced O(2) generation (p < 0.001). In the presence of radical scavengers and anti-LOX-1 monoclonal antibody, O(2) formation induced by ox-LDL was reduced (p < 0.001) with a contemporary rise in intracellular NO concentration (p < 0.001). ox-LDL did not significantly modify the ability of endothelial nitric oxide synthase to metabolize l-arginine to l-citrulline. The results of this study show that one of the pathophysiological consequences of ox-LDL binding to LOX-1 may be the inactivation of NO through an increased cellular production of O(2).

Published
2001
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18. Oxidized low density lipoprotein (ox-LDL) binding to ox-LDL receptor-1 in endothelial cells induces the activation of NF-kappaB through an increased production of intracellular reactive oxygen species.

Author

Cominacini L, Pasini AF, Garbin U, Davoli A, Tosetti ML, Campagnola M, Rigoni A, Pastorino AM, Lo Cascio V, and Sawamura T

Subjects
Animals, Anticholesteremic Agents pharmacology, Antioxidants pharmacology, Ascorbic Acid pharmacology, CHO Cells, Cattle, Cells, Cultured, Chromans pharmacology, Cricetinae, Fluoresceins metabolism, Humans, Hydrogen Peroxide metabolism, Probucol pharmacology, Protein Binding, Receptors, Oxidized LDL, Scavenger Receptors, Class E, Time Factors, Endothelium, Vascular metabolism, Lipoproteins, LDL metabolism, NF-kappa B metabolism, Reactive Oxygen Species metabolism, Receptors, LDL metabolism
Abstract

In this study we examined the effect of oxidized low density lipoprotein (ox-LDL) on the intracellular production of reactive oxygen species (ROS) in bovine aortic endothelial cells (BAECs) and whether this increase occurs through its binding to the endothelial receptor lectin-like ox-LDL receptor-1 (LOX-1). Furthermore, this study also aimed to ascertain whether the binding of ox-LDL to LOX-1 is associated with NF-kappaB activation. ox-LDL induced a significant dose-dependent increase in ROS production after a 30-s incubation with BAECs (p < 0.01). ROS formation was markedly reduced in BAECs incubated with anti-LOX-1 monoclonal antibody (p < 0.001), while control nonimmune IgG produced no effect. ox-LDL induced a time- and dose-dependent significant increase in ROS formation only in CHO-K1 cells stably expressing bovine LOX-1 (p < 0.001), while no increase was present in CHO-K1 cells. The activation of the transcription factor NF-kappaB in BAECs was evident after a 5-min incubation with ox-LDL and was attenuated by anti-LOX-1 monoclonal antibody. The conclusion is that one of the pathophysiological consequences of ox-LDL binding to LOX-1 may be the activation of NF-kappaB through an increased ROS production.

Published
2000
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19. The expression of adhesion molecules on endothelial cells is inhibited by troglitazone through its antioxidant activity.

Author

Cominacini L, Garbin U, Pasini AF, Davoli A, Campagnola M, Rigoni A, Tosetti L, and Lo Cascio V

Subjects
Cell Adhesion drug effects, Cells, Cultured, Dose-Response Relationship, Drug, E-Selectin biosynthesis, Endothelium, Vascular drug effects, Humans, Intercellular Adhesion Molecule-1 biosynthesis, Lipoproteins, LDL metabolism, NF-kappa B metabolism, Signal Transduction drug effects, Troglitazone, Tumor Necrosis Factor-alpha pharmacology, Umbilical Veins, Vascular Cell Adhesion Molecule-1 biosynthesis, Vitamin E pharmacology, Antioxidants pharmacology, Cell Adhesion Molecules biosynthesis, Chromans pharmacology, Endothelium, Vascular metabolism, Thiazoles pharmacology, Thiazolidinediones
Abstract

The adhesion of monocytes to endothelium, an early event in atherosclerosis, is mediated by cell adhesion molecules. Signal-transduction pathways for these binding molecules include the translocation of the transcription factor NF-kappaB; moreover, intracellularly generated oxygen-derived free radicals (ODFR) play a major role in this process. This study evaluated the extent to which troglitazone, an oral antidiabetic agent with antioxidant properties, affects the expression of intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin on human umbilical vein endothelial cells (HUVECs), induced by different prooxidant signals such as oxidized LDL and tumor necrosis factor-alpha (TNF-alpha). Furthermore we assessed whether the NF-kappaB activation is modulated by the antioxidative effect of troglitazone. Oxidized LDL not only caused a dose-dependent increase of ICAM-1, VCAM-1 and E-selectin (p<0.001), but also synergically increased their TNF-alpha-induced expression (p<0.001). Troglitazone reduced in a dose-dependent manner the expression of VCAM-1, ICAM-1 and E-selectin induced by different amounts of oxidized LDL (p<0.001). The addition of troglitazone to HUVECs significantly reduced the expression of ICAM-1, VCAM-1 and E-selectin induced by TNF-alpha alone or in combination with oxidized LDL (p<0.001); this reduction was paralleled by a significant fall in NF-kappaB translocation. The results suggest that troglitazone may have prevented NF-kappaB-mediated adhesion molecule expression by exerting its antioxidant effect on ODFR.

Published
1999
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20. Systemic lupus erythematosus and thrombotic thrombocytopenic purpura. Report of three cases and review of the literature.

Author

Caramaschi P, Riccetti MM, Pasini AF, Savarin T, Biasi D, and Todeschini G

Subjects
Adolescent, Adult, Female, Humans, Middle Aged, Purpura, Thrombotic Thrombocytopenic therapy, Lupus Erythematosus, Systemic complications, Purpura, Thrombotic Thrombocytopenic complications
Abstract

We describe three female patients affected by both systemic lupus erythematosus and thrombotic thrombocytopenic purpura, one with a fatal outcome. The literature about this disease association is reviewed.

Published
1998
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21. Antioxidants inhibit the expression of intercellular cell adhesion molecule-1 and vascular cell adhesion molecule-1 induced by oxidized LDL on human umbilical vein endothelial cells.

Author

Cominacini L, Garbin U, Pasini AF, Davoli A, Campagnola M, Contessi GB, Pastorino AM, and Lo Cascio V

Subjects
Cells, Cultured, Dialysis, E-Selectin biosynthesis, Endothelium, Vascular cytology, Endothelium, Vascular metabolism, Free Radical Scavengers pharmacology, Free Radicals, Humans, Oxidation-Reduction, Reactive Oxygen Species, Ultrafiltration, Umbilical Veins cytology, Umbilical Veins drug effects, Umbilical Veins metabolism, Antioxidants pharmacology, Endothelium, Vascular drug effects, Intercellular Adhesion Molecule-1 biosynthesis, Lipoproteins, LDL pharmacology, Vascular Cell Adhesion Molecule-1 biosynthesis
Abstract

The oxidative modification of low density lipoprotein (LDL) and the endothelial expression of adhesion molecules are key events in the pathogenesis of atherosclerosis. In this study we evaluated the effect of oxidized LDL on the expression of intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin on human umbilical vein endothelial cells (HUVECs). The hypothesis that oxidized LDL functions as a prooxidant signal was also evaluated, by studying the effect of different radical-scavenging antioxidants on expression of adhesion molecules. LDL was oxidized by using Cu2+, HUVECs or phospholipase A2 (PLA2)/ soybean lipoxygenase (SLO), the degree of oxidation being measured as thiobarbituric acid-reactive substances (TBARS) and conjugated dienes (CD). Exposure of 200 micrograms/ml of native LDL to 1 microns Cu2+, HUVECs and to PLA2/ SLO resulted in four- to fivefold higher levels of TBARS and CD than in native LDL. Cu(2+)-(1 microM), HUVEC-, and PLA2/SLO-oxidized LDL caused a dose-dependent, significant increase of ICAM-1 and VCAM-1 (p < .01). The expression of E-selectin did not change. LDL oxidized with a 2.5 and 5 microM Cu2+ did not increase ICAM-1 and VCAM-1 significantly. Both the Cu(2+)- and HUVEC-oxidized LDL, subjected to dialysis and ultrafiltration, induced ICAM-1 and VCAM-1 expression. After incubation with the ultrafiltrate, the expression of ICAM-1 and VCAM-1 was not significantly different from that obtained with native LDL. LDL pretreated with different antioxidants (vitamin E and probucol) and subjected to oxidation by Cu2+ and HUVECs induced a significantly lower expression of ICAM-1 and VCAM-1 than nonloaded LDL (p < .01). The pretreatment of HUVECs with vitamin E and probucol significantly reduced the expression of VCAM-1 on HUVECs induced by oxidized LDL (p < .01); the effect on ICAM-1 was much less evident. In conclusion, oxidized LDL can induce the expression of different adhesion molecules on HUVECs; this induction can be prevented by pretreating either the LDL or the cells with radical-scavenging antioxidant.

Published
1997
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22. Mechanisms involved in the in vitro modification of low density lipoprotein by human umbilical vein endothelial cells and copper ions.

Author

Cominacini L, Garbin U, De Santis A, Campagnola M, Davoli A, Pasini AF, Faccini G, Pasqualini E, Bertozzo L, Micciolo R, Pastorino AM, and Lo Cascio V

Subjects
5,8,11,14-Eicosatetraynoic Acid pharmacology, Arachidonic Acid metabolism, Cells, Cultured, Culture Media, Eicosapentaenoic Acid metabolism, Electrophoresis, Endothelium, Vascular cytology, Fatty Acids, Unsaturated metabolism, Fluorescence, Guanidines pharmacology, Humans, Kinetics, Lipid Peroxidation, Lipid Peroxides metabolism, Malondialdehyde metabolism, Oleic Acid metabolism, Umbilical Veins, Vitamin E metabolism, Copper pharmacology, Endothelium, Vascular physiology, Lipoproteins, LDL metabolism
Abstract

In this study we evaluated the time course and mechanism of low density lipoprotein (LDL) oxidation induced by human umbilical vein endothelial cells (HUVECs), cell-free medium (CFM) and Cu2+. After incubating LDL (200 micrograms/ml) with HUVECs, CFM and Cu2+ (concentration adjusted to obtain the same degree of LDL modification as with HUVECs), the extent of LDL lipid peroxidation and apoprotein B modification was monitored at different times from 0 to 24 h. This involved evaluating the time course of LDL conjugated diene, peroxide, malonyldialdehyde (MDA), fluorescence, relative electrophoretic mobility (REM), vitamin E and monounsaturated and polyunsaturated fatty acids. After incubation with HUVECs, the LDL REM was significantly higher than that obtained in CFM (p < 0.01). When balanced for the same degree of LDL modification as obtained with HUVECs, Cu2+ gave a REM similar to that obtained with HUVECs. At the different times of incubation there was no statistical difference between conjugated diene and peroxide values after incubation with HUVECs and with CFM. The values obtained with Cu2+ were significantly higher than those obtained with HUVECs and CFM (p < 0.01). MDA and LDL fluorescence were significantly higher after exposure to HUVECs than to CFM (p < 0.01), values being similar to those obtained with Cu2+. There was no statistical difference between the values of LDL oleic, linoleic, arachidonic and eicosapentaenoic acids after incubation with HUVECs and CFM. Eicosatetraynoic acid (ETYA), a lipoxygenase inhibitor, determined dose-dependent reduction of MDA formation induced by the incubation of LDL with HUVECs; it did not affect LDL conjugated diene. ETYA did not have any effect on the MDA derived from LDL after incubation with Cu2+ or CFM. The results of this study demonstrate that, unlike Cu2+, the contribution of HUVECs to LDL modification does not involve only lipid peroxidation of the lipoprotein; it also includes intracellular radical and non-radical processes.

Published
1996
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23. The susceptibility of low-density lipoprotein to in vitro oxidation is increased in hypercholesterolemic patients.

Author

Cominacini L, Pastorino AM, Garbin U, Campagnola M, de Santis A, Davoli A, Faccini G, Bertozzo L, Pasini F, and Pasini AF

Subjects
Adult, Anthropometry, Antioxidants metabolism, Arachidonic Acid blood, Arachidonic Acid metabolism, Cholesterol, LDL blood, Cholesterol, LDL metabolism, Copper pharmacology, Fatty Acids, Unsaturated blood, Fatty Acids, Unsaturated metabolism, Female, Humans, Hypercholesterolemia blood, Hypercholesterolemia genetics, Linoleic Acid, Linoleic Acids blood, Linoleic Acids metabolism, Lipid Peroxidation, Lipoproteins, LDL blood, Male, Middle Aged, Oxidation-Reduction, Time Factors, Vitamin E blood, Vitamin E metabolism, Hypercholesterolemia metabolism, Lipoproteins, LDL metabolism
Abstract

It has been suggested that the oxidative modification of low-density lipoprotein (LDL) plays a major role in atherogenesis. We evaluated the oxidative resistance to copper-induced oxidative changes of LDL derived from patients affected by type IIa hyperlipoproteinemia compared with healthy subjects and faced the question of the importance of the antioxidants and polyunsaturated fatty acids (PUFAs) contained in LDL in determining its variability. LDL isolated from the plasmas of 25 subjects affected by familial hypercholesterolemia and 15 control subjects was oxidatively modified with Cu2+ in vitro, and the differences in LDL susceptibilities (lag and propagation phases) to lipid peroxidation were studied by measuring the changes in fluorescence intensity. LDL alpha-tocopherol and PUFAs were also measured. The lag phase was significantly lower and the propagation phase significantly higher in the type IIa patients than in control subjects (p < 0.01). The linoleic and arachidonic acids, expressed as percentage of total LDL fatty acids, were significantly higher in type IIa patients than in the control subjects (p < 0.01). There was a positive significant correlation between the LDL cholesterol and the linoleic and arachidonic acids as percentage of total LDL fatty acids (p < 0.01). Both linoleic and arachidonic acids turned out to be negatively correlated with the lag phase and positively with the propagation phase (p < 0.01). The concentration of LDL alpha-tocopherol was similar in the two groups. Therefore, type IIa patients have a greater susceptibility to LDL oxidation than control subjects. This may be due to a relative higher concentration of linoleic and arachidonic acids in LDL derived from patients with familial hypercholesterolemia.

Published
1994

24. Effect of bisphosphonate therapy and parathyroidectomy on the urinary excretion of galactosylhydroxylysine in primary hyperparathyroidism.

Author

LoCascio V, Braga V, Bertoldo F, Bettica P, Pasini AF, Stefani L, and Moro L

Subjects
Aged, Alendronate, Biomarkers urine, Bone Resorption urine, Female, Humans, Hydroxylysine urine, Hydroxyproline urine, Hyperparathyroidism urine, Middle Aged, Diphosphonates therapeutic use, Hydroxylysine analogs & derivatives, Hyperparathyroidism drug therapy, Parathyroidectomy
Abstract

Background: In patients with mild or asymptomatic primary hyperparathyroidism a reliable index of bone resorption might be useful for appropriate management. Hydroxyproline is the most commonly used marker of bone resorption but its low specificity and sensitivity are known. Galactosylhydroxylysine, an amino acid mainly represented in bone collagen, has been proposed as a more suitable index of bone resorption. In this study we evaluated the sensitivity of galactosylhydroxylysine and hydroxyproline assays in following the changes of their urinary levels in 12 patients with mild primary hyperparathyroidism before and after treatment with bisphosphonate and surgery., Methods: Serum and fasting urine specimens were obtained from 12 women with mild primary hyperparathyroidism before and after bisphosphonate treatment (2.5 mg daily for 5 days, intravenously) and after a further 25 days; in 7 patients biochemical tests were also performed 1 and 6 days after parathyroidectomy. Galactosylhydroxylysine was assayed by an HPLC method and hydroxyproline by a RIA commercial kit., Results: Baseline galactosylhydroxylysine urinary levels were far above the normal range in all the patients whilst in 8 of them baseline hydroxyproline levels were normal. Bisphosphonate treatment significantly decreased bone turnover as shown by a significant fall in serum calcium (from 2.9 to 2.6 mmol/l; P < 0.001) and in galactosylhydroxylysine and hydroxyproline (-55 and -31% respectively). Twenty-five days after the end of treatment, resorption increased again and serum calcium and galactosylhydroxylysine, but not hydroxyproline, rose significantly towards basal levels. One day after parathyroidectomy serum calcium, galactosylhydroxylysine and PTH showed reduction below normal ranges. PTH and galactosylhydroxylysine returned to normal values at day 6 after parathyroidectomy. No changes in hydroxyproline levels were seen. Galactosylhydroxylysine, but not hydroxyproline, correlated significantly with serum calcium and PTH., Conclusion: Galactosylhydroxylysine appears to be a sensitive index of bone resorption, useful in the clinical assessment of bone involvement and in the management of patients with mild primary hyperparathyroidism.

Published
1994
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25. Nd:YAG laser versus polidocanol injection for palliation of esophageal malignancy: a prospective, randomized study.

Author

Angelini G, Pasini AF, Ederle A, Castagnini A, Talamini G, and Bulighin G

Subjects
Adenocarcinoma complications, Adenocarcinoma therapy, Aged, Aged, 80 and over, Carcinoma, Squamous Cell complications, Carcinoma, Squamous Cell therapy, Deglutition Disorders etiology, Deglutition Disorders therapy, Esophageal Neoplasms complications, Esophagoscopy, Female, Humans, Injections, Male, Middle Aged, Polidocanol, Polyethylene Glycols adverse effects, Prospective Studies, Sclerosing Solutions adverse effects, Esophageal Neoplasms therapy, Laser Therapy adverse effects, Laser Therapy methods, Palliative Care, Polyethylene Glycols administration & dosage, Sclerosing Solutions administration & dosage
Abstract

Palliation is often the only treatment that can be offered to patients affected by esophageal malignancy. This prospective study was carried out in order to compare two endoscopic palliative treatments: Nd:YAG laser and local injection of 3% polidocanol. We randomized 34 patients with inoperable malignancies to one of the two treatments. After the first course, 88.8% of the patients in the laser group and 81.5% in the polidocanol group were able to swallow a normal oral caloric intake. Only one major complication (esophageal perforation) was observed (polidocanol group) and was successfully treated with endoscopic placement of a prosthesis. We believe that both techniques are safe and effective for the palliation of esophageal malignant strictures but that polidocanol injection is cheap, simple, and more widely available.

Published
1991
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26. Treatment of reflux gastritis: double blind comparison between clebopride and domperidone. A preliminary report.

Author

Angelini G, Castagnini A, Rizzoli R, Pasini AF, Lavarini E, Brocco G, and Scuro LA

Subjects
Adolescent, Adult, Aged, Bile Acids and Salts analysis, Double-Blind Method, Duodenogastric Reflux metabolism, Duodenogastric Reflux pathology, Female, Gastric Acidity Determination, Gastric Juice chemistry, Gastritis metabolism, Gastritis pathology, Heartburn prevention & control, Humans, Male, Middle Aged, Pain, Pyloric Antrum, Antiemetics therapeutic use, Benzamides therapeutic use, Domperidone therapeutic use, Duodenogastric Reflux drug therapy, Gastritis drug therapy
Abstract

Altered gastro-duodenal motility seems to be a major factor of alkaline gastritis. Therefore prokinetic drugs have been extensively used for the treatment of this disease. Aim of this study has been to compare the effects of domperidone with those of a more recent drug of the orthopramide class, clebopride. Thirty patients affected by reflux gastritis have been randomly allocated to one of the two treatments. Clinical symptoms, endoscopic and histologic appearance of gastric mucosa, gastric pH and bile acid concentration in gastric juice have been evaluated before and after a four week course of therapy. A statistically significant improvement was observed for the clinical symptoms in the subjects treated with clebopride. Even if no statistical difference has been pointed out for the other parameters between and within the two groups, a slight trend in favour of clebopride was observed. It is concluded that clebopride is at least as effective as domperidone for the treatment of reflux gastritis but that more prolonged studies and different administration schedules are requested for a better evaluation.

Published
1990

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