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3. Moderated Posters session: advanced echo techniques in congenital heart diseaseP526Systolic function by strain echocardiography is related to cardiac fibrosis and arrhythmias in hypertrophic cardiomyopathyP527Natural history of bicuspid aortic valve valvulo-aortopathy in affected patients followed in a single centerP528Postsystolic thickening as a likely sign of altered deformation due to pressure overload in a Marfan murine model.P529Strain rate echocardiography in patients with hypertrophic cardiomyopathy undergoing surgical myectomy.P530Transthoracic echocardiography is a safe alternative for assessment and guidance of transcatheter closure of secundum atrial septal defect in childrenP531Aortic root dilatation and stiffness assessed by magnetic resonance imaging in adults with repaired tetralogy of FallotP532Assessment of biventricular and vascular function using three-dimensional speckle tracking echocardiography in adult patients with surgical repair of tetralogy of FallotP533A study of functional anatomy of aortic-mitral valve coupling using 3D echocardiography in patients with double orifice mitral valveP534Evaluation of bicuspid aortic valve and its repercussion in the left ventricle with cardiovascular magnetic resonanceP535Echocardiographic assessment of anomalous pulmonary venous connection.

Author

Haland, T, primary, Neglia, L, primary, Mas-Stachurska, A, primary, Malanin, D, primary, Baruteau, A-E, primary, Pontnau, F, primary, Capotosto, L, primary, Hristova, K, primary, Sevilla, T, primary, Wojtkowska, A, primary, Almaas, VM, additional, Hasselberg, NE, additional, Saberniak, J, additional, Leren, IS, additional, Hopp, E, additional, Edvardsen, T, additional, Haugaa, KH, additional, Piazza, R, additional, Doronzo, A, additional, Leonelli, V, additional, Morosin, M, additional, Leiballi, E, additional, Pecoraro, R, additional, Lutman, C, additional, Dragos, A, additional, Cassin, M, additional, Sitges, M, additional, Meirelles, T, additional, Hernandez, V, additional, Egea, G, additional, Bijnens, B, additional, Poggio, D, additional, Ferrazzi, P, additional, Spirito, P, additional, Specchia, G, additional, Grillo, M, additional, Amigoni, P, additional, Bersano, C, additional, Pisani, M, additional, Chioffi, M, additional, Hascoet, S, additional, Piot, D, additional, Lambert, V, additional, Petit, J, additional, Ladouceur, M, additional, Ferreira, A, additional, Iserin, L, additional, Mousseaux, E, additional, D'angeli, I, additional, Conde, Y, additional, Ashurov, R, additional, Miraldi, F, additional, Vitarelli, A, additional, Dasheva, A, additional, Marinov, R, additional, Lasarov, S, additional, Mitev, I, additional, Mitev, P, additional, Konstantinov, G, additional, Kaneva, A, additional, Katova, TZ, additional, Revilla-Orodea, A, additional, Uruena-Martinez, N, additional, Fuertes-Alija, JJ, additional, Rodriguez-Velasco, M, additional, Gomez-Salvador, I, additional, San Roman-Calvar, JA, additional, Tomaszewski, A, additional, Czekajska-Chehab, E, additional, Wysokinski, A, additional, Adamczyk, P, additional, Siek, E, additional, and Zakoscielna, M, additional

Published
2015
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4. Poster session 6

Author

Lofmark, H, Winter, R, Moukarzel, JA, Filipuzzi, JM, Vaisbuj, F, Salmo, F, Guevara, E, Barbier, P, Savioli, G, Keramida, K, Kouris, N, Dawson, D, Olympios, CD, Nihoyannopoulos, P, Meel, R, Peters, F, Libhaber, E, Nel, S, Goncalves, R, Essop, MR, Dinis, P G, Teixeira, R, Madeira, M, Cachulo, MC, Goncalves, L, Jorstig, S, Emilsson, K, Waldenborg, M, Liden, M, Wodecki, M, Thunberg, P, Perez, Valverde, Sotelo, J, Beerbaum, P, Grotenhuis, H, Greil, G, Razavi, R, Uribe, S, Figueroa, A, Zemedkun, M, Wang, Z, Asch, FM, Gizzi, G, Fabiani, D, Lavorgna, A, Napoletano, C, Saha, S K, Muthukumar, L, Englund, E, Toole, R, Gopal, AS, Di Salvo, G, Issa, Z, Moiduddin, N, Siblini, G, Bulbul, Z, Yurdakul, SELEN, Ercan, G, Tekkesin, ILKER, Sahin, ST, Cengiz, B, Celik, G, Demircan, SABRI, Aytekin, SAIDE, Chumarnaya, T, Alueva, Y, Kochmasheva, VV, Solovyova, O, Tuset, L, Maceira Gonzalez, A M, Igual, B, Bruin De- Bon, HACM, Cocchieri, R, Wagner, GS, Eberl, S, Brink Van Den, RBA, Bouma, BJ, Onishi, T, Kawai, H, Tanaka, H, Fujiwara, S, Hirata, K, Marketou, M, Parthenakis, F, Kontaraki, J, Patrianakos, A, Nakou, H, Maragkoudakis, S, Vougia, D, Logakis, J, Roufas, K, Vardas, P, Bayuga, MT, Ramboyong, RE, Johansson, M C, Wallentin Guron, C, Thurin, A, Wessling, N, Almodares, Q, Fu, M, Mandour Ali, M, Mohamed, LA, Abd Al-Rahman, T, Maghraby, HM, Kora, IM, Abdel-Hameed, FR, Ali, MN, King, GJ, Byrne, D, Bennett, K, Norris, K, Daly, C, Murphy, RT, Marti, G, Degiovanni, A, Di Ruocco, MV, Sartori, C, Devecchi, P, Marino, P, Angelis, A, Aggeli, K, Ioakeimidis, N, Felekos, I, Aznaouridis, K, Rokas, K, Abdelrasoul, M, Terentes, D, Vlachopoulos, C, Tousoulis, D, Spinelli, L, Stabile, E, Santoro, M, Morisco, C, Giudice, C A, Esposito, G, Trimarco, B, Dragoi Galrinho, R, Ciobanu, AO, Rimbas, RC, Manole, GC, Marinescu, B, Vinereanu, D, Krljanac, G, Trifunovic, D, Savic, L, Asanin, M, Lasica, R, Aleksandric, S, Zlatic, N, Petrovic, M, Jovanovic, LJ, Mrdovic, I, Zahidova, K, aethiology, Chronic heart failure of ishemic, anemia, Trifunovic, D, Krljanac, G, Sobic Saranovic, D, Asanin, M, Grozdic Milojevic, I, Savic, L, Vasiljevic, Z, Aleksandric, S, Srdic, M, Mrdovic, I, Mateescu, AD, Calin, A, Rosca, M, Beladan, CC, Enache, R, Gurzun, MM, Varga, P, Calin, C, Ginghina, C, Popescu, BA, Melissopoulou, M, Nguyen, V, Mathieu, T, Attias, D, Dreyfus, J, Codogno, I, Vahanian, A, Messika-Zeitoun, D, study, The COFRASA/GENERAC, Stefanidis, A, Komatanou, E, Anagnostou, E, Armatas, G, Samiotou, D, Papaspyropoulos, A, Philippou, P, Korlou, P, Tzerefos, S, Kranidis, A, Kammerer, I, Wiedemann, M, Sack, FU, Koyama, T, Fukuhara, K, Imai, K, Yamada, R, Kume, T, Neishi, Y, Uemura, S, Pergola, V, Di Salvo, G, Fadel, B, Aladmawi, M, Shahid, M, Alamri, M, Bulbul, Z, Issa, Z, Alhalees, Z, Rafael De La Espriella Juan, RDLE, Rafael Paya-Serrano, RPS, Jose-Leando Perez-Bosca, JLPB, Francisco Ridocci-Soriano, FRS, Oscar Fabregat-Andres, OFA, Cristina Albiach-Montanana, CAM, Natalia Chacon-Hernandez, NCH, Laura Higueras-Ortega, LHO, Blanca Trejo-Velasco, BTV, Salvador Morell-Cabedo, SMC, Bech-Hanssen, O, Polte, CL, Johnsson, AA, Cederbom, U, Lagerstrand, K, Gao, SA, Cho, E J, Hwang, J W, Park, S J, Yun, H R, Lee, S C, Park, S W, Poilane, M, Cueff, C, Jaafar, P, Jobbe Duval, A, Guijarro, D, Le Tourneau, T, Vaturi, M, Kotler, T, Shapira, Y, Weisenberg, D, Monakier, D, Kazum, S, Sagie, A, Valuckiene, Z, Ovsianas, J, Jurgaityte, J, Jasiskyte, V, Jurkevicius, R, Jenei, C, Muraru, D, Aruta, P, Miglioranza, M H, Cavalli, G, Romeo, G, Peluso, D, Cucchini, U, Iliceto, S, Badano, L P, Yesin, M, Kalcik, M, Gursoy, MO, Gunduz, S, Astarcioglu, MA, Karakoyun, S, Bayam, E, Cersit, S, Ozkan, M, Galuszka, O M, Reinthaler, M, Rutschow, S, Gross, M, Landmesser, U, Kasner, M, Caggegi, A M, Scandura, S, Capranzano, P, Mangiafico, S, Ronsivalle, G, Cannata, S, Farruggio, S, Giaquinta, S, Grasso, C, Tamburino, C, Merchan Cuenda, M, Fuentes Canamero, M E, Bengla Limpo, B, Chacon Pinero, A, Millan Nunez, M V, Nogales Asensio, JM, Lopez Minguez, J R, Garcia Corrales, C, Aranda Lopez, C, Merchan Herrera, A, Merchan Cuenda, M, Fuentes Canamero, M E, Bengla Limpo, B, Millan Nunez, M V, Nogales Asensio, J M, Lopez Minguez, J R, Chacon Pinero, A, Marquez Lozano, P, Garcia Corrales, C, Merchan Herrera, A, Lo Presti, M, Polizzi, V, Pino, GP, Luzi, G, Fiorilli, R, Pergolini, A, Madeo, A, Malouf, J, Buffa, V, Musumeci, F, Islas, F, Almeria, C, Olmos, C, Garcia, E, Nombela, L, De Agustin, JA, Marcos-Alberca, P, Mahia, P, Macaya, C, Perez De Isla, L, Pontes Dos Santos, R A, Correia, E, Cruz, I, Reis, L, Oliveira, M, Faria, R, Magalhaes, P, Domingues, K, Picarra, B, Marques, N, Nemes, A, Domsik, P, Kalapos, A, Sepp, R, Foldeak, D, Borbenyi, Z, Forster, T, Masiha, S, Reis, L, Teixeira, R, Caetano, F, Almeida, I, Trigo, J, Botelho, A, Silva, J, Nascimento, J, Goncalves, L, Cubero Gallego, H, Dobarro Perez, D, Diez De Las Heras, D, Llerena Butron, S, Tobar Ruiz, J, Martin Morquecho, I, Arnold, R, San Roman Calvar, JA, De Gregorio, C, Ando', G, Dattilo, G, Trio, O, Cusma' Piccione, M, Zito, C, Nicotera, A, D'angelo, M, Carerj, S, Ziolkowska, L, Spiewak, M, Malek, L, Boruc, A, Kawalec, W, Alvarez-Ortega, C A, Gonzalez Fernandez, O, Refoyo Salicio, E, Mori, R, Peinado Peinado, R, Lago, M, Trigo, E, Lopez-Sedon, JL, Yuan, L, Zhang, XX, Xie, MX, Jin, XY, Hospital, Union, College, Tongji Medical, Science, Huazhong University of, Technology, Ultrasonography, Department of, Leao, S, Bento, D, Lourenco, C, Domingues, K, Almeida, AR, Marmelo, B, Picarra, B, Lima, R, Faria, R, Azevedo, O, Accadia, M, Irace, L, Abitabile, M, Iengo, R, Arnese, MR, Cocchia, R, Scotto Di Uccio, F, Spadaro, P, Tuccillo, A, Tuccillo, B, Budnik, M, Piatkowski, R, Kochanowski, J, Gaska, M, Glowacka, P, Karolczak, P, Ochijewicz, D, Opolski, G, Stevanovic, A, Dekleva, M, Tsai, W-C, Yang, L-T, Liu, Y-W, Abusalma, Y, O'connell, E, Kenny, C, Mcdonald, K, Mohamed Fereig Hamed, H, Hafez, EMAN, Habib, SHIMAA, Peluso, D, Pigatto, E, Romeo, G, Cucchini, U, Muraru, D, Aruta, P, Cozzi, F, Punzi, L, Iliceto, S, Badano, LP, Podoleanu, C, Coman, I, Jeremias, ZS, Varga, A, Tarta, C, Grancea, I, Tarusi, M, Frigy, A, Carasca, E, Doronzo, A, Piazza, R, Neglia, L, Cervesato, E, Nicolosi, GL, Cassin, M, Upton, R, Aye, C, Davis, E, Packham, A, Arnold, L, Kenworthy, Y, Lamata, P, Lewandowski, A, Leeson, P, Abuladze, GA, Jinjolia, NJ, Ribeiro, JM, Teixeira, R, Fernandes, A, Cassandra, M, Pinto, H, Marques, MG, Raposo, H, Carreira, A, Campos, M, Goncalves, L, De La Chica, JA, Ortiz Garrido, A, Cuenca, V, Conejo, L, Zabala, I, De Mora, M, Petruzzelli, MF, Vasti, MP, Scali, MC, Tramacere, F, D'errico, MP, Gianicolo, EAL, Andreassi, MG, Picano, E, Portaluri, M, Ferrera Duran, C, Gomez-Escalonilla, C, De Agustin, JA, Egido, J, Almeria, C, Simal, P, Marcos, P, Rodrigo, JL, Macaya, C, Perez De Isla, L, Tomaszewski, M, Brzozowski, W, Tomaszewski, A, Poterala, M, Diaz-Pelaez, E, Marciniak, A, Gargallo-Fernandez, P, Barrio-Rodriguez, A, Araco, M, Sharma, R, Wierzbowska-Drabik, K, Kasprzak, JD, Wierzbowska-Drabik, K, Kasprzak, JD, Velasco Del Castillo, S, Anton Ladislao, A, Cacicedo Fernandez Bobadilla, A, Onandia Gandarias, JJ, Sainz, S, Gomez Sanchez, V, Rodriguez Sanchez, I, Garcia Cuenca, E, Zugazabeitia Irazabal, G, Generati, G, Bandera, F, Pellegrino, M, Carbone, F, Labate, V, Alfonzetti, E, Villani, S, Gaeta, M, Ferraro, O, Guazzi, M, Zaborska, B, Smarz, K, Pilichowska-Paszkiet, E, Sikora-Frac, M, Budaj, A, De Diego Soler, O, Ferrer Sistach, E, Vallejo Camazon, N, Lopez-Ayerbe, J, Teis Soley, A, Gual Capllonch, F, Serrano Garcia, S, Bernal Labrador, E, Junca Puig, G, Bayes-Genis, A, Merchan-Gomez, S, Garcia-Sanchez, MJ, Barreiro-Perez, MJ, Arribas-Jimenez, A, Sanchez-Corral, E, Cruz-Gonzalez, I, Martin-Leal, LI, Gajate-Herrero, D, Perdiguero-Martin, PL, Sanchez-Fernandez, PL, Lee, M, Jang, YJ, Lee, YJ, Kim, YS, Chun, WJ, Kang, GH, Oh, JH, Aquila, I, Hinojar, R, Fernandez-Golfin, C, Gonzalez, A, Rincon, LM, Casas, E, Ruiz, S, Barrios, V, Jimenez-Nacher, JJ, Zamorano, JL, Necas, J, Kovalova, S, Perea, GO, Lombardero, M, Henquin, R, Tinetti, M, Corneli, M, Sotaquira, Miguel, Cairati, Mattia, Ettorre, Alessandro, Pepi, Mauro, Tamborini, Gloria, Caiani, Enrico, Sanchez-Martinez, S, Duchateau, N, Erdei, T, Fraser, A, Piella, G, Bijnens, B H, Nestaas, E, Stoylen, A, Fugelseth, D, Hinojar, R, Fernandez-Golfin, C, Esteban, A, Gonzalez-Gomez, A, Garcia-Martin, A, Casas Rojo, E, Pascual-Izco, M, Jimenez-Nacher, JJ, Zamorano, JL, Cerne, A, Berden, P, Agelaki, M, Sundar, S, Antonakaki, D, Grapsa, J, Dawson, D, Papadopoulos, C, Katsivas, A, Nihoyannopoulos, P, Sanchis Ruiz, L, Sanz, M, Bijnens, B, Giraldeau, G, Grazioli, G, Marin, M, Montserrat, S, Sitges, M, Cambronero Cortinas, E, Grapsa, J, Dawson, D, Howard, L, Gin-Sing, W, Valle, A, Corbi-Pascual, MJ, Saez-Mendez, L, Gibbs, S, Nihoyannopoulos, P, Grue, J F, Storve, S, Mjoelstad, O C, Samstad, S O, Dalen, H, Torp, H, Haugen, B O, Yim, D, Mertens, L, Friedberg, MK, Grosse-Wortmann, L, Dragulescu, A, Djikic, DDJ, Simic, SD, Peric, VP, Mujovic, NM, Jankovic, NJ, Marinkovic, MM, Martinez Santos, P, Batlle Lopez, E, Vilacosta, I, Sanchez Sauce, B, De La Rosa Riestra, A, Alonso Bello, J, Espana Barrio, E, Jimenez Valtierra, J, Campuzano Ruiz, R, Rios, Martin, Vrsalovic, M, Hummel, SL, Ghanbari, H, Alpert, C, Oral, H, Kolias, TJ, Mghaieth Zghal, F, Jabberi, Z, Rekik, B, Boudiche, S, Aloui, H, Ben Hlima, M, Ouali, S, Larbi, N, Mourali, MS, Nemes, A, Marton, I, Domsik, P, Kalapos, A, Posfai, E, Modok, S, Borbenyi, Z, Forster, T, Maceira Gonzalez, A M, Monmeneu, JV, Igual, B, Lopez Lereu, MP, Garcia, P, Cosin Sales, J, Maceira Gonzalez, A M, Igual, B, Monmeneu, JV, Lopez Lereu, P, Garcia, MP, Cosin Sales, J, Bala, G, Baudhuin, H, Gillis, K, Remory, I, Krasniqi, A, Lahoutte, T, Devoogdt, N, Droogmans, S, Cosyns, B, Hernot, S, Bulugahapitiya, D S, Bebb, O, Moustafa, A, Vilades, D, Colom Comi, C, Perez-Perez, A, Carreras, F, Leta, R, Pons, G, Jinjolia, NJ, and Abuladze, GA

Abstract

Purpose: To explore the cost effectiveness of expert hand-held echo (HHE) upstream as an alternative to referral for a complete transthoracic echo (TTE) in clinical routine. We hypothized that an upstream HHE approach would prove adequate and cost effective in terms of - Decrease the numbers of required TTE - Fewer revisits to the outpatient unit - Shorten the length of admission - Increase the number of higly specialized echoes, i.e. stress echo, transesophageal echoes - Shorten the time to final diagnosis and decrease the concerns for the patient who is forced to wait for survey and results at complete TTE. Methods: In this study, a HHE scanner (V-scan, GE Health care) was kept available for the senior consultants with level 3 TTE certification, for use in patients where a TTE was indicated. HHE was performed in different clinical scenarios such in the emergency room, during consultation of inpatients or in the clinic of outpatients. The results of HHE was documented in the patient record under a heading and can directly be found upon request. The length of hospital stay during a representative week, is compared between patients who have not undergone HHE with patients undergoing HHE. Results: Out of a total of 94 patients examined with HHE, 71 patients were not in need of a complete TTE. Additional 11 patients received a more rapid investigation i.e stress-echo, transesophageal echocardiography or other investigations that would otherwise have been delayed because of waiting for the complete TTE. 12 patients were in need of a complete TTE for a more precise analysis. In the heart clinic of Danderyds hospital approximately 18 inpatients were examined with a complete TTE every ordinary week and that postpone the day of submission from hospital among approximately 6 patients a week. Every day of care in hospital cost 445 € in an ordinary ward and 981 € in the heart intensive care unit. This means there is a cost benefit of approximately 3741 € every week if it is possible to prevent this postponing of submission. Conclusions: Upstream HHE in clinical routine was in the setting of this study highly cost-effective, decreasing the need of TTE to a great extent, and leading to quicker diagnosis, shorter hospital stays and less anxiety in patients during the waiting time for a complete TTE and before a response is received.

Published
2015
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5. Moderated Posters session: advanced echo techniques in congenital heart disease

Author

Haland, T, Almaas, VM, Hasselberg, NE, Saberniak, J, Leren, IS, Hopp, E, Edvardsen, T, Haugaa, KH, Neglia, L, Piazza, R, Doronzo, A, Leonelli, V, Morosin, M, Leiballi, E, Pecoraro, R, Lutman, C, Dragos, A, Cassin, M, Mas-Stachurska, A, Sitges, M, Meirelles, T, Hernandez, V, Egea, G, Bijnens, B, Malanin, D, Poggio, D, Ferrazzi, P, Spirito, P, Specchia, G, Grillo, M, Amigoni, P, Bersano, C, Pisani, M, Chioffi, M, Baruteau, A-E, Hascoet, S, Piot, D, Lambert, V, Petit, J, Pontnau, F, Ladouceur, M, Ferreira, A, Iserin, L, Mousseaux, E, Capotosto, L, D'angeli, I, Conde, Y, Ashurov, R, Miraldi, F, Vitarelli, A, Hristova, K, Dasheva, A, Marinov, R, Lasarov, S, Mitev, I, Mitev, P, Konstantinov, G, Kaneva, A, Katova, TZ, Sevilla, T, Revilla-Orodea, A, Uruena-Martinez, N, Fuertes-Alija, JJ, Rodriguez-Velasco, M, Gomez-Salvador, I, San Roman-Calvar, JA, Wojtkowska, A, Tomaszewski, A, Czekajska-Chehab, E, Wysokinski, A, Adamczyk, P, Siek, E, and Zakoscielna, M

Abstract

Purpose: Myocardial fibrosis by cardiac magnetic resonance imaging (CMR) has been related to ventricular arrhythmias (VAs) in hypertrophic cardiomyopathy (HCM). We hypothesized that systolic function by strain echocardiography is related to VAs and to the extent of fibrosis by CMR. Methods: We studied 150 HCM patients (age 54 ± 14, 39% female). VAs were defined as ventricular tachycardia or aborted cardiac arrest. By speckle-tracking echocardiography we assessed global longitudinal strain (GLS) and mechanical dispersion defined as standard deviation of time from Q/R on ECG to peak negative longitudinal strain in 16 LV segments. Late gadolinium enhancement (LGE) was assessed by CMR and quantified as proportion of total LV myocardium (%LGE) Results: VAs were identified in 37 (25%) patients. Patients with VAs had worse GLS (-14.1 ± 3.6% vs. -16.3 ± 3.4%, p<0.01), more pronounced mechanical dispersion (79 ± 27 ms vs. 59 ± 16 ms, p<0.001), and higher %LGE (6.1 ± 7.8% vs. 0.5 ± 1.4%, p<0.001) than HCM patients without VAs (Figure). Mechanical dispersion was the only independent risk predictor of VAs (OR 1.6, 95%CI 1.1-2.3, p=0.02, per 10ms increase) in multivariate analysis. Mechanical dispersion correlated with %LGE (R= 0.52, p<0.001), and there was a weak, but significant correlation between GLS and % LGE (R=0.27, p=0.01), while neither EF (R=0.01, p=0.96) nor E/e’ (R=0.05, p=0.74) correlated with %LGE. Conclusion: Myocardial systolic function by strain echocardiography was related to VAs in HCM . Mechanical dispersion was a strong independent predictor of VAs and related to the extent of fibrosis on CMR and may improve risk stratification in HCM patients.

Published
2015
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6. Bicuspid aortic valve and unruptured sinus of Valsalva aneurysm, a rare association

Author

Ludovico La Grutta, Emanuela Clara Bertolino, Antonino Mignano, Luigi Neglia, Egle Corrado, Patrizia Carità, Gregory Dendramis, Salvatore Novo, Pasquale Assennato, Giuseppe Coppola, Giuseppina Novo, Carità, P., Dendramis, G., Novo, G., Bertolino, E., Neglia, L., Mignano, A., Coppola, G., La Grutta, L., Assennato, P., Novo, S., and Corrado, E.

Subjects
Male, medicine.medical_specialty, Bicuspid aortic valve, 030204 cardiovascular system & hematology, 03 medical and health sciences, 0302 clinical medicine, Aneurysm, Internal medicine, Incidental Finding, medicine, 030212 general & internal medicine, Sinus (anatomy), business.industry, Medicine (all), Middle Aged, Sinus of Valsalva, medicine.disease, Settore MED/11 - Malattie Dell'Apparato Cardiovascolare, Surgery, Aortic Aneurysm, Heart Valve Disease, medicine.anatomical_structure, Aortic Valve, Cardiology, Valsalva Sinus, Valsalva sinu, business, Cardiology and Cardiovascular Medicine, Settore MED/36 - Diagnostica Per Immagini E Radioterapia, Human
Abstract

Bicuspid aortic valve (BAV) is one of the most common forms of congenital heart defect and is associated with other congenital vascular and cardiac defects. The most common comorbidity is dilation of thoracic aorta and clinical manifestations are usually related to function of the aortic valve and to other cardiovascular acquired complications. Sinus of Valsalva aneurysm (SVA) is an uncommon congenital cardiovascular anomaly and the combination of these two anomalies is very rare. Common complications are rupture and obstruction of the termination chamber due to space-occupying effect of large unruptured aneurysms. Early cardiac imaging can help limiting morbidity and mortality in these patients

Published
2016

7. β2 glycoprotein I participates in phagocytosis of apoptotic neurons and in vascular injury in experimental brain stroke.

Author

Grossi C, Artusi C, Meroni P, Borghi MO, Neglia L, Lonati PA, Oggioni M, Tedesco F, De Simoni MG, and Fumagalli S

Subjects
Animals, Brain metabolism, Brain pathology, Brain Ischemia etiology, Complement System Proteins metabolism, Disease Models, Animal, Endothelial Cells cytology, Endothelial Cells metabolism, Humans, Interleukin-6 metabolism, Liver metabolism, Liver pathology, Macrophages cytology, Macrophages immunology, Macrophages metabolism, Male, Mannose-Binding Lectin metabolism, Mice, Mice, Inbred C57BL, Microscopy, Confocal, Neurons cytology, Phagocytosis, Protein Binding, Vascular System Injuries complications, beta 2-Glycoprotein I blood, Brain Ischemia pathology, Neurons metabolism, Vascular System Injuries pathology, beta 2-Glycoprotein I metabolism
Abstract

Beta-2 Glycoprotein I (β2-GPI) is the main target of anti-phospholipid antibodies (aPL) in the autoimmune anti-phospholipid syndrome, characterized by increased risk of stroke. We here investigated the antibody independent role of β2-GPI after ischemia/reperfusion, modeled in vivo by transient middle cerebral artery occlusion (tMCAo) in male C57Bl/6J mice; in vitro by subjecting immortalized human brain microvascular endothelial cells (ihBMEC) to 16 h hypoxia and 4 h re-oxygenation. ApoH (coding for β2-GPI) was upregulated selectively in the liver at 48 h after tMCAo. At the same time β2-GPI circulating levels increased. β2-GPI was detectable in brain parenchyma and endothelium at all time points after tMCAo. Parenchymal β2-GPI recognized apoptotic neurons (positive for annexin V, C3 and TUNEL) cleared by CD68+ brain macrophages. Hypoxic ihBMEC showed increased release of IL-6, over-expression of thrombomodulin and IL-1α after re-oxygenation with β2-GPI alone. β2-GPI interacted with mannose-binding lectin in mouse plasma and ihBMEC medium, potentially involved in formation of thrombi. We show for the first time that brain ischemia triggers the hepatic production of β2-GPI. β2-GPI is present in the ischemic endothelium, enhancing vascular inflammation, and extravasates binding stressed neurons before their clearance by phagocytosis. Thus β2-GPI may be a new mediator of brain injury following ischemic stroke.

Published
2021
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8. Mannose-binding lectin has a direct deleterious effect on ischemic brain microvascular endothelial cells.

Author

Neglia L, Fumagalli S, Orsini F, Zanetti A, Perego C, and De Simoni MG

Subjects
Brain Ischemia pathology, Cell Hypoxia drug effects, Cell Survival drug effects, Cells, Cultured, Complement Pathway, Mannose-Binding Lectin drug effects, Endothelial Cells metabolism, Endothelial Cells pathology, Endothelium, Vascular metabolism, Endothelium, Vascular pathology, Glucose metabolism, Humans, Mannose-Binding Lectin genetics, Mannose-Binding Lectin pharmacology, Oxygen metabolism, Primary Cell Culture, Serum metabolism, Brain Ischemia metabolism, Endothelial Cells drug effects, Endothelium, Vascular drug effects, Mannose-Binding Lectin metabolism
Abstract

Mannose-binding lectin (MBL), an initiator of the lectin pathway, is detrimental in ischemic stroke. MBL deposition on the ischemic endothelium indicates the beginning of its actions, but downstream mechanisms are not clear yet.We investigated MBL interactions with the ischemic endothelium by exposing human brain microvascular endothelial cells (hBMECs) to protocols of ischemia. Cells were exposed to hypoxia or oxygen-glucose deprivation (OGD), and re-oxygenated with human serum (HS) or recombinant MBL (rhMBL). Hypoxic hBMECs re-oxygenated with HS showed increased complement system activation (C3c deposition, +59%) and MBL deposition (+93%) than normoxic cells. Super-resolution microscopy showed MBL internalization in hypoxic cells and altered cytoskeletal organization, indicating a potential MBL action on the endothelial structure. To isolate MBL effect, hBMECs were re-oxygenated with rhMBL after hypoxia/OGD. In both conditions, MBL reduced viability (hypoxia: -25%, OGD: -34%) compared to conditions without MBL, showing a direct toxic effect. Ischemic cells also showed greater MBL deposition (hypoxia: +143%, OGD: +126%) than normoxic cells. These results were confirmed with primary hBMECs exposed to OGD (increased MBL-induced cell death: +226%, and MBL deposition: +104%). The present findings demonstrate that MBL can exert a direct deleterious effect on ischemic brain endothelial cells in vitro, independently from complement activation.

Published
2020
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9. Specific contribution of mannose-binding lectin murine isoforms to brain ischemia/reperfusion injury.

Author

Neglia L, Oggioni M, Mercurio D, De Simoni MG, and Fumagalli S

Subjects
Animals, Brain pathology, Brain Ischemia genetics, Brain Ischemia pathology, Humans, Male, Mannose-Binding Lectin genetics, Mice, Mice, Knockout, Protein Isoforms genetics, Protein Isoforms immunology, Reperfusion Injury genetics, Reperfusion Injury pathology, Brain immunology, Brain Ischemia immunology, Mannose-Binding Lectin immunology, Reperfusion Injury immunology
Abstract

Mannose-binding lectin (MBL), an initiator of the lectin pathway (LP) of complement activation, is detrimental in ischemic stroke, as shown in clinical studies and rodent models. Whereas humans have one functional MBL protein, rodents have two isoforms, MBL-A and MBL-C, whose functions relative to that of human MBL are unknown. To permit the clinical translation of preclinical data, we aimed to define the specific contributions of MBL-A and MBL-C to brain ischemia. We subjected mice with double (MBL -/- ) or single (MBL-A -/- or MBL-C -/- ) MBL isoform depletion to transient middle cerebral artery occlusion (tMCAo). MBL -/- mice had fewer neurological deficits and smaller ischemic lesions than WT mice. MBL-A -/- mice had smaller lesions than WT mice and exhibited no significant behavioral defects, whereas MBL-C -/- mice did not differ from WT mice. The induction of Mbl1 and Mbl2 (the MBL-A and MBL-C genes) expression 48 h after tMCAo was similar across genotypes. The time course of Mbl1 and Mbl2 expression in WT ischemic mice showed that Mbl1 activation occurred earlier (24 h) than Mbl2 activation (48 h). The plasma levels of MBL-A and MBL-C in MBL-C -/- and MBL-A -/- mice, respectively, were similar to those in WT mice both at baseline and at 48 h after tMCAo. At 48 h, MBL-A -/- ischemic mice showed higher MBL-C levels in the brain than WT mice. WT and MBL-C -/- ischemic mice had higher LP activity in plasma and, accordingly, higher levels of C3 deposition in the brain than MBL-A -/- and MBL -/- mice. In conclusion, mice with depletion of both MBL isoforms exhibited strong protection from ischemia/reperfusion injury. MBL-A was the main contributor to injury, likely owing to its earlier activation after ischemia and more efficient activation of the complement system than MBL-C.

Published
2020
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10. Human brain trauma severity is associated with lectin complement pathway activation.

Author

De Blasio D, Fumagalli S, Orsini F, Neglia L, Perego C, Ortolano F, Zanier ER, Picetti E, Locatelli M, Stocchetti N, Longhi L, Garred P, and De Simoni MG

Subjects
Brain Injuries, Traumatic pathology, Complement Activation, Complement C3 analysis, Complement C3 immunology, Female, Humans, Lectins analysis, Lectins immunology, Male, Mannose-Binding Lectin analysis, Mannose-Binding Lectin immunology, Middle Aged, Ficolins, Brain Injuries, Traumatic immunology, Complement Pathway, Mannose-Binding Lectin
Abstract

We explored the involvement of the lectin pathway of complement in post-traumatic brain injury (TBI) pathophysiology in humans. Brain samples were obtained from 28 patients who had undergone therapeutic contusion removal, within 12 h (early) or from >12 h until five days (late) from injury, and from five non-TBI patients. Imaging analysis indicated that lectin pathway initiator molecules (MBL, ficolin-1, ficolin-2 and ficolin-3), the key enzymes MASP-2 and MASP-3, and the downstream complement components (C3 fragments and TCC) were present inside and outside brain vessels in all contusions. Only ficolin-1 was found in the parenchyma of non-TBI tissues. Immunoassays in brain homogenates showed that MBL, ficolin-2 and ficolin-3 increased in TBI compared to non-TBI (2.0, 2.2 and 6.0-times) samples. MASP-2 increased with subarachnoid hemorrhage and abnormal pupil reactivity, two indicators of structural and functional damage. C3 fragments and TCC increased, respectively, by 3.5 - and 4.0-fold in TBI compared to non-TBI tissue and significantly correlated with MBL, ficolin-2, ficolin-3, MASP-2 and MASP-3 levels in the homogenates. In conclusion, we show for the first time the direct presence of lectin pathway components in human cerebral contusions and their association with injury severity, suggesting a central role for the lectin pathway in the post-traumatic pathophysiology of human TBI.

Published
2019
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11. Clinical and echocardiographic predictors of long-term outcome of a large cohort of patients with bicuspid aortic valve.

Author

Morosin M, Leonelli V, Piazza R, Cassin M, Neglia L, Leiballi E, Cervesato E, Barbati G, Sinagra G, and Nicolosi GL

Subjects
Adolescent, Adult, Aortic Valve surgery, Bicuspid Aortic Valve Disease, Child, Echocardiography, Female, Heart Valve Prosthesis, Humans, Italy, Kaplan-Meier Estimate, Male, Middle Aged, Multivariate Analysis, Proportional Hazards Models, Retrospective Studies, Risk Factors, Severity of Illness Index, Treatment Outcome, Young Adult, Aortic Valve abnormalities, Aortic Valve Insufficiency surgery, Aortic Valve Stenosis surgery, Heart Defects, Congenital surgery, Heart Valve Diseases mortality, Heart Valve Diseases surgery, Transcatheter Aortic Valve Replacement
Abstract

Background and Objectives: Bicuspid aortic valve (BAV) disease is the most common congenital cardiac malformation. The aim of the present article is to determine clinical and echocardiographic prognostic factors and provide a predictive model of outcome of a large cohort of patients with BAV., Methods: We retrospectively enrolled 337 patients consecutively assessed for echocardiography at our Cardiology Department from 1993 to 2014. We considered aortic valve replacement, aortic surgery and cardiovascular death as a clinical combined end-point. Predictors of outcome were determined by Cox regression., Results: Mean age was 29.2 ± 19.8 years, median 27.1 years. A total of 38.4% patients presented a history of hypertension. Mean duration of follow-up was 8.4 ± 6.1 years, range 0-21 years. A total of 73 patients underwent aortic valve replacement and/or aortic surgery during follow-up. Age at surgery was 45.2 ± 15.6 years. Seven patients died because of cardiovascular causes. At multivariate analysis, baseline clinical predictors were history of hypertension [hazard ratio (HR) 2.289, 95% confidence interval (CI) 1.350-3.881, P = 0.002], larger ascending aortic diameter (HR 2.537, 95% CI 1.888-3.410, P < 0.001), moderate-to-severe aortic regurgitation (HR 2.266, 95% CI 1.402-3.661, P = 0.001) and moderate-to-severe aortic stenosis (HR 2.807, 95% CI 1.476-5.338, P = 0.002). A predictive model was created by integrating these four independent covariates. It allows the calculation of calculate a risk score for each patient, which helps better tailor appropriate treatment in BAV patients., Conclusion: At enrolment, history of hypertension, a wider aortic diameter, moderate-to-severe aortic regurgitation and aortic stenosis were independently correlated to combined end-point. Long-term follow-up showed low cardiovascular mortality (2.1%) and a high prevalence of cardiac surgery (21.6%).

Published
2017
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12. Bicuspid aortic valve and unruptured sinus of Valsalva aneurysm, a rare association.

Author

Carità P, Dendramis G, Novo G, Bertolino EC, Neglia L, Mignano A, Coppola G, La Grutta L, Assennato P, Novo S, and Corrado E

Subjects
Bicuspid Aortic Valve Disease, Humans, Incidental Findings, Male, Middle Aged, Aortic Aneurysm complications, Aortic Aneurysm diagnosis, Aortic Valve abnormalities, Heart Valve Diseases complications, Heart Valve Diseases diagnosis, Sinus of Valsalva pathology
Published
2016
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