Search

Your search keyword '"Cipresso C"' showing total 15 results
Start Over Author "Cipresso C"
15 results on '"Cipresso C"'

4. Utility of 2D-speckle tracking echocardiography in early identification of left ventricular dysfunction in antineoplastic therapy-induced cardiotoxicity

Author

Coppola C, Piscopo G, Cipresso C, Maurea C, Lombari MC, Rea D, Maiolino P, Tarantini L, Russo G, Cioffi G, Giotta F, Oliva S, Capaso I, Iaffaioli RV, Arra C, Maurea N., TOCCHETTI, CARLO GABRIELE, MONTI, MARIA GAIA, Conference: Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO), Coppola, C, Tocchetti, CARLO GABRIELE, Piscopo, G, Cipresso, C, Maurea, C, Lombari, Mc, Rea, D, Maiolino, P, Monti, MARIA GAIA, Tarantini, L, Russo, G, Cioffi, G, Giotta, F, Oliva, S, Capaso, I, Iaffaioli, Rv, Arra, C, and Maurea, N.

Published
2013

5. The Tyrosine Kinase ErbB2 Inhibitor Lapatinib and the Anti- ErbB2 Antibody Trastuzumab Depress Cardiac Function Without Inducing Left Ventricular Dilation in Mice

Author

TOCCHETTI, CARLO GABRIELE, Coppola C, Rea D, Barbieri A, Palma G, Piscopo G, Gala M, Luciano A, Giudice A, Cipresso C, Iaffaioli RV, Scala S, De Lorenzo C, Arra C, Maurea N., Conference: Basic Cardiovascular Sciences Scientific Session, Tocchetti, CARLO GABRIELE, Coppola, C, Rea, D, Barbieri, A, Palma, G, Piscopo, G, Gala, M, Luciano, A, Giudice, A, Cipresso, C, Iaffaioli, Rv, Scala, S, De Lorenzo, C, Arra, C, and Maurea, N.

Published
2012

6. Ranolazine protects from doxorubicin-induced oxidative stress and cardiac dysfunction

Author

Cg, Tocchetti, Carpi A, Coppola C, Quintavalle C, Rea D, Campesan M, Arcari A, Piscopo G, Cipresso C, Mg, Monti, De Lorenzo C, Arra C, Condorelli G, Fabio Di Lisa, Maurea N, Tocchetti, CARLO GABRIELE, Andrea, Carpi, Carmela, Coppola, Quintavalle, Cristina, Domenica, Rea, Marika, Campesan, Antonella, Arcari, Giovanna, Piscopo, Clemente, Cipresso, Monti, MARIA GAIA, DE LORENZO, Claudia, Claudio, Arra, Condorelli, Gerolama, Fabio Di, Lisa, and Nicola, Maurea

Subjects
Antibiotics, Antineoplastic, Reverse Transcriptase Polymerase Chain Reaction, Blotting, Western, Sodium, Connective Tissue Growth Factor, Real-Time Polymerase Chain Reaction, Cardiotoxicity, Piperazines, Mice, Inbred C57BL, Mice, Oxidative Stress, Ventricular Dysfunction, Left, Doxorubicin, Ranolazine, Natriuretic Peptide, Brain, Animals, Matrix Metalloproteinase 2, Acetanilides, Myocytes, Cardiac, RNA, Messenger, Enzyme Inhibitors, Poly(ADP-ribose) Polymerases, Reactive Oxygen Species, Atrial Natriuretic Factor, Ultrasonography
Abstract

AIMS: Doxorubicin is widely used against cancer; however, it can produce heart failure (HF). Among other hallmarks, oxidative stress is a major contributor to HF pathophysiology. The late INa inhibitor ranolazine has proven effective in treating experimental HF. Since elevated [Na+ ]i is present in failing myocytes, and has been recently linked with reactive oxygen species (ROS) production, our aim was to assess whether ranolazine prevents doxorubicin-induced cardiotoxicity, and whether blunted oxidative stress is a mechanism accounting for such protection. METHODS AND RESULT: In C57BL6 mice, doxorubicin treatment for 7 days produced LV dilation and decreased echo-measured fractional shortening (FS). Ranolazine (305 mg/kg/day) prevented LV dilation and dysfunction when co-administered with doxorubicin. Doxorubicin-induced cardiotoxicity was accompanied instead by elevations in atrial natriuretic peptide (ANP), BNP, connective tissue growth factor (CTGF), and matrix metalloproteinase 2 (MMP2) mRNAs, which were not elevated on co-treatment with ranolazine. Alterations in extracellular matrix remodelling were confirmed by an increase in interstitial collagen, which did not rise in ranolazine-co-treated hearts. Levels of poly(ADP-ribose) polymerase (PARP) and pro-caspase-3 measured by western blotting were lowered with doxorubicin, with increased cleavage of caspase-3, indicating activation of the proapoptotic machinery. Again, ranolazine prevented this activation. Furthermore, in HL-1 cardiomyocytes transfected with HyPer to monitor H2 O2 emission, besides reducing the extent of cell death, ranolazine prevented the occurrence of oxidative stress caused by doxorubicin. Interestingly, similar protective results were obtained with the Na+ /Ca2+ exchanger (NCX) inhibitor KB-R7943. CONCLUSIONS: Ranolazine protects against experimental doxorubicin cardiotoxicity. Such protection is accompanied by a reduction in oxidative stress, suggesting that INa modulates cardiac redox balance, resulting in functional and morphological derangements.

Published
2014

7. Utility of 2D-speckle tracking echocardiography in diagnosis of left ventricular dysfunction in anti-ErbB2 therapy

Author

Maurea, N., Coppola, C., Piscopo, G., Cipresso, C., Rea, D., Maurea, C., Esposito, E., Arra, C., Carlo Gabriele Tocchetti, Capasso, I., Conference: European Cancer Congress 2013 - 17th ECCO / 38th ESMO / 32nd ESTRO, Maurea, N, Coppola, Carmela, Piscopo, G, Cipresso, C, Rea, Domenica, Maurea, C, Esposito, E, Arra, C, Tocchetti, CARLO GABRIELE, Capasso, I., Autori vari, Quintavalle, Cristina, Condorelli, Gerolama, and Maurea, N.

8. Poster session Wednesday 11 December all day display: 11/12/2013, 09:30-16:00 * Location: Poster area

Author

Bertrand, PB, Grieten, L, Smeets, C, Verbrugge, FH, Mullens, W, Vrolix, M, Rivero-Ayerza, M, Verhaert, D, Vandervoort, P, Tong, L, Ramalli, A, Tortoli, P, Dhoge, J, Bajraktari, G, Lindqvist, P, Henein, MY, Obremska, M, Boratynska, MB, Kurcz, JK, Zysko, DZ, Baran, TB, Klinger, MK, Darahim, K, Mueller, H, Carballo, D, Popova, N, Vallee, J-P, Floria, M, Chistol, R, Tinica, G, Grecu, M, Rodriguez Serrano, M, Osa-Saez, A, Rueda-Soriano, J, Buendia-Fuentes, F, Domingo-Valero, D, Igual-Munoz, B, Alonso-Fernandez, P, Quesada-Carmona, A, Miro-Palau, V, Palencia-Perez, M, Bech-Hanssen, O, Polte, CL, Lagerstrand, K, Janulewicz, M, Gao, S, Erdogan, E, Akkaya, M, Bacaksiz, A, Tasal, A, Sonmez, O, Turfan, M, Kul, S, Vatankulu, MA, Uyarel, H, Goktekin, O, Mincu, RI, Magda, LS, Mihaila, S, Florescu, M, Mihalcea, D, Enescu, OE, Chiru, A, Popescu, B, Tiu, C, Vinereanu, D, 112/2011, Research grant, Broch, K, Kunszt, G, Massey, R, De Marchi, SF, Aakhus, S, Gullestad, L, Urheim, S, Yuan, L, Feng, JL, Jin, XY, Bombardini, T, Casartelli, M, Simon, D, Gaspari, MG, Procaccio, F, Hasselberg, NE, Haugaa, KH, Brunet, A, Kongsgaard, E, Donal, E, Edvardsen, T, Sahin, TAYLAN, Yurdakul, S, Cengiz, BETUL, Bozkurt, AYSEN, Aytekin, SAIDE, Cesana, F, Spano, F, Santambrogio, G, Alloni, M, Vallerio, P, Salvetti, M, Carerj, S, Gaibazzi, N, Rigo, F, Moreo, A, Group, APRES Collaborative, Wdowiak-Okrojek, K, Michalski, B, Kasprzak, JD, Shim, A, Lipiec, P, Generati, G, Pellegrino, M, Bandera, F, Donghi, V, Alfonzetti, E, Guazzi, M, Marcun, R, Stankovic, I, Farkas, J, Vlahovic-Stipac, A, Putnikovic, B, Kadivec, S, Kosnik, M, Neskovic, AN, Lainscak, M, Iliuta, L, Szymanski, P, Lipczynska, M, Klisiewicz, A, Sobieszczanska-Malek, M, Zielinski, T, Hoffman, P, Gjerdalen, G F, Hisdal, J, Solberg, EE, Andersen, TE, Radunovic, Z, Steine, K, Svanadze, A, Poteshkina, N, Krylova, N, Mogutova, P, Shim, A, Kasprzak, JD, Szymczyk, E, Wdowiak-Okrojek, K, Michalski, B, Stefanczyk, L, Lipiec, P, Benedek, T, Matei, C, Jako, B, Suciu, ZS, Benedek, I, Yaroshchuk, N A, Kochmasheva, V V, Dityatev, V P, Kerbikov, O B, Przewlocka-Kosmala, M, Orda, A, Karolko, B, Mysiak, A, Kosmala, W, Rechcinski, T, Wierzbowska-Drabik, K, Lipiec, P, Chmiela, M, Kasprzak, JD, Aziz, A, Hooper, J, Rayasamudra, S, Uppal, H, Asghar, O, Potluri, R, Zaroui, A, Mourali, MS, Rezine, Z, Mbarki, S, Jemaa, M, Aloui, H, Mechmeche, R, Farhati, A, Gripari, P, Maffessanti, F, Tamborini, G, Muratori, M, Fusini, L, Vignati, C, Bartorelli, AL, Alamanni, F, Agostoni, PG, Pepi, M, Ruiz Ortiz, M, Mesa, D, Delgado, M, Seoane, T, Carrasco, F, Martin, M, Mazuelos, F, Suarez De Lezo Herreros De Tejada, J, Romero, M, Suarez De Lezo, J, Brili, S, Stamatopoulos, I, Misailidou, M, Chrisochoou, C, Christoforatou, E, Stefanadis, C, Ruiz Ortiz, M, Mesa, D, Delgado, M, Martin, M, Seoane, T, Carrasco, F, Ojeda, S, Segura, J, Pan, M, Suarez De Lezo, J, Cammalleri, V, Ussia, GP, Muscoli, S, Marchei, M, Sergi, D, Mazzotta, E, Romeo, F, Igual Munoz, B, Bel Minguez, ABM, Perez Guillen, MPG, Maceira Gonzalez, AMG, Monmeneu Menadas, JVMM, Hernandez Acuna, CHA, Estornell Erill, JEE, Lopez Lereu, PLL, Francisco Jose Valera Martinez, FJVM, Montero Argudo, AMA, Sunbul, M, Akhundova, A, Sari, I, Erdogan, O, Mutlu, B, Cacicedo, A, Velasco Del Castillo, S, Anton Ladislao, A, Aguirre Larracoechea, U, Rodriguez Sanchez, I, Subinas Elorriaga, A, Oria Gonzalez, G, Onaindia Gandarias, J, Laraudogoitia Zaldumbide, E, Lekuona Goya, I, Ding, W, Zhao, Y, Lindqvist, P, Nilson, J, Winter, R, Holmgren, A, Ruck, A, Henein, MY, Attenhofer Jost, C H, Soyka, R, Oxenius, A, Kretschmar, O, Valsangiacomo Buechel, ER, Greutmann, M, Weber, R, Keramida, K, Kouris, N, Kostopoulos, V, Karidas, V, Damaskos, D, Makavos, G, Paraskevopoulos, K, Olympios, CD, Eskesen, K, Olsen, NT, Fritz-Hansen, T, Sogaard, P, Cameli, M, Lisi, M, Righini, FM, Curci, V, Massoni, A, Natali, B, Maccherini, M, Chiavarelli, M, Massetti, M, Mondillo, S, Mabrouk Salem Omar, A, Ahmed Abdel-Rahman, M, Khorshid, H, Rifaie, O, Santoro, C, Santoro, A, Ippolito, R, De Palma, D, De Stefano, F, Muscariiello, R, Galderisi, M, Squeri, A, Censi, S, Baldelli, M, Grattoni, C, Cremonesi, A, Bosi, S, Saura Espin, D, Gonzalez Canovas, C, Gonzalez Carrillo, J, Oliva Sandoval, MJ, Caballero Jimenez, L, Espinosa Garcia, MD, Garcia Navarro, M, Valdes Chavarri, M, De La Morena Valenzuela, G, Ryu, SK, Shin, DG, Son, JW, Choi, JH, Goh, CW, Choi, JW, Park, JY, Hong, GR, Sklyanna, O, Yuan, L, Yuan, L, Planinc, I, Bagadur, G, Ljubas, J, Baricevic, Z, Skoric, B, Velagic, V, Bijnens, B, Milicic, D, Cikes, M, Gospodinova, M, Chamova, T, Guergueltcheva, V, Ivanova, R, Tournev, I, Denchev, S, Ancona, R, Comenale Pinto, S, Caso, P, Arenga, F, Coppola, MG, Calabro, R, Neametalla, H, Boitard, S, Hamdi, H, Planat-Benard, V, Casteilla, L, Li, Z, Hagege, AA, Mericskay, M, Menasche, P, Agbulut, O, Merlo, M, Stolfo, D, Anzini, M, Negri, F, Pinamonti, B, Barbati, G, Di Lenarda, A, Sinagra, G, Stolfo, D, Merlo, M, Pinamonti, B, Gigli, M, Poli, S, Porto, A, Di Nora, C, Barbati, G, Di Lenarda, A, Sinagra, G, Coppola, C, Piscopo, G, Cipresso, C, Rea, D, Maurea, C, Esposito, E, Arra, C, Maurea, N, Nemes, A, Kalapos, A, Domsik, P, Forster, T, Voilliot, D, Huttin, O, Vaugrenard, T, Schwartz, J, Sellal, J-M, Aliot, E, Juilliere, Y, Selton-Suty, C, Sanchez Millan, P J, Cabeza Lainez, P, Castillo Ortiz, J, Chueca Gonzalez, EM, Gheorghe, L, Fernandez Garcia, P, Herruzo Rojas, MS, Del Pozo Contreras, R, Fernandez Garcia, M, Vazquez Garcia, R, Rosca, M, Popescu, BA, Botezatu, D, Calin, A, Beladan, CC, Gurzun, M, Enache, R, Ginghina, C, Farouk, H, Al-Maimoony, T, Alhadad, A, El Serafi, M, Abdel Ghany, M, Poorzand, H, Mirfeizi, SZ, Javanbakht, A, center, Preventive Cardiovascular care research, center, Lupus Research, sciences, Mashhad university of medical, Tellatin, S, Famoso, G, Dassie, F, Martini, C, Osto, E, Maffei, P, Iliceto, S, Tona, F, Radunovic, Z, Steine, KS, Jedrzejewska, I, Braksator, W, Krol, W, Swiatowiec, A, Sawicki, J, Kostarska-Srokosz, E, Dluzniewski, M, Maceira Gonzalez, A M, Cosin-Sales, J, Diago, JL, Aguilar, J, Ruvira, J, Monmeneu, J, Igual, B, Lopez-Lereu, MP, Estornell, J, Olszanecka, A, Dragan, A, Kawecka-Jaszcz, K, Czarnecka, D, Scholz, F, Gaudron, PD, Hu, K, Liu, D, Florescu, C, Herrmann, S, Bijnens, B, Ertl, G, Stoerk, S, Weidemann, F, Krestjyaninov, M, Razin, VA, Gimaev, RH, Bogdanovic, Z, Burazor, I, Deljanin Ilic, M, Peluso, D, Muraru, D, Cucchini, U, Mihaila, S, Casablanca, S, Pigatto, E, Cozzi, F, Punzi, L, Badano, LP, Iliceto, S, Zhdanova, E, Rameev, VV, Safarova, AF, Moisseyev, SV, Kobalava, ZD, Magnino, C, Omede, P, Avenatti, E, Presutti, D, Losano, I, Moretti, C, Bucca, C, Gaita, F, Veglio, F, Milan, A, Bellsham-Revell, H, Bell, AJ, Miller, OI, Simpson, JM, Hwang, YM, Kim, GH, Jung, MH, Woo, GH, Medicine, Department of Internal, Hospital, St.Vincents, Korea, The Catholic University of, Suwon, Division of Cardiology, Repu, Driessen, MMP, Leiner, T, Schoof, PH, Breur, JMPJ, Sieswerda, GT, Meijboom, FJ, Bellsham-Revell, H, Hayes, N, Anderson, D, Austin, BC, Razavi, R, Greil, GF, Simpson, JM, Bell, AJ, Zhao, XX, Xu, XD, Qin, YW, Szmigielski, C A, Styczynski, G, Sobczynska, M, Placha, G, Kuch-Wocial, A, Ikonomidis, I, Voumbourakis, A, Triantafyllidi, H, Pavlidis, G, Varoudi, M, Papadakis, I, Trivilou, P, Paraskevaidis, I, Anastasiou-Nana, M, Lekakis, I, Kong, WILL, Yip, JAMES, Ling, LH, Milan, A, Tosello, F, Leone, D, Bruno, G, Losano, I, Avenatti, E, Sabia, L, Veglio, F, Zaborska, B, Baran, J, Pilichowska-Paszkiet, E, Sikora-Frac, M, Michalowska, I, Kulakowski, P, Budaj, A, Mega, S, Bono, MC, De Francesco, V, Castiglione, I, Ranocchi, F, Casacalenda, A, Goffredo, C, Patti, G, Di Sciascio, G, Musumeci, F, Kennedy, M, Waterhouse, DF, Sheahan, R, Foley, DF, Mcadam, BF, Ancona, R, Comenale Pinto, S, Caso, P, Arenga, F, Coppola, MG, Calabro, R, Remme, E W, Smedsrud, M K, Hasselberg, N E, Smiseth, O A, Edvardsen, T, Halmai, L, Nemes, A, Kardos, A, Neubauer, S, Degiovanni, A, Baduena, L, Dellera, G, Occhetta, E, Marino, P, Hotchi, J, Yamada, H, Nishio, S, Bando, M, Hayashi, S, Hirata, Y, Amano, R, Soeki, T, Wakatsuki, T, Sata, M, Lamia, B, Molano, LC, Viacroze, C, Cuvelier, A, Muir, JF, Lipczynska, M, Piotr Szymanski, PS, Anna Klisiewicz, AK, Lukasz Mazurkiewicz, LM, Piotr Hoffman, PH, Van T Sant, J, Wijers, SC, Ter Horst, IAH, Leenders, GE, Cramer, MJ, Doevendans, PA, Meine, M, Hatam, N, Goetzenich, A, Aljalloud, A, Mischke, K, Hoffmann, R, Autschbach, R, Sikora-Frac, M, Zaborska, B, Maciejewski, P, Bednarz, B, Budaj, A, Evangelista, A, Torromeo, C, Pandian, NG, Nardinocchi, P, Varano, V, Schiariti, M, Teresi, L, Puddu, PE, Storve, S, Dalen, H, Snare, SR, Haugen, BO, Torp, H, Fehri, W, Mahfoudhi, H, Mezni, F, Annabi, MS, Taamallah, K, Dahmani, R, Haggui, A, Hajlaoui, N, Lahidheb, D, Haouala, H, Colombo, A, Carminati, MC, Maffessanti, F, Gripari, P, Pepi, M, Lang, RM, Caiani, EG, Walker, JR, Abadi, S, Agmon, Y, Carasso, S, Aronson, D, Mutlak, D, Lessick, J, Saxena, A, Ramakrishnan, S, Juneja, R, Ljubas, J, Reskovic Luksic, V, Matasic, R, Pezo Nikolic, B, Lovric, D, Separovic Hanzevacki, J, Quattrone, A, Zito, C, Alongi, G, Vizzari, G, Bitto, A, De Caridi, G, Greco, M, Tripodi, R, Pizzino, G, Carerj, S, Ibrahimi, P, Jashari, F, Johansson, E, Gronlund, C, Bajraktari, G, Wester, P, Henein, MY, Kosmala, W, Marwick, TH, Souza, J R M, Zacharias, L G T, Geloneze, B, Pareja, J C, Chaim, A, Nadruz, W JR, Coelho, O R, Apostolovic, S, Stanojevic, D, Jankovic-Tomasevic, R, Salinger-Martinovic, S, Djordjevic-Radojkovic, D, Pavlovic, M, Tahirovic, E, Musial-Bright, L, Lainscak, M, Duengen, HD, group, CIBIS ELD study, Filipiak, D, Kasprzak, JD, and Lipiec, P

Abstract

Purpose: With the advent of percutaneous transcatheter device closures in congenital heart defects and the emergence of percutaneous left atrial appendage closure, there is an increasingly important role for echocardiographic guidance and control of device position and function. Disc occluder devices frequently present as an unexplained ‘figure-of-8’ on echocardiography. The aim of this study was to clarify this ‘figure-of-8’ display and to relate its morphology to transducer position and device type. Methods: A mathematical model was developed to resemble disc occluder geometry and to allow a numerical simulation of the echocardiographic appearance. In addition, we developed an in vitro set-up for echocardiographic analysis of various disc occluders and various transducer positions. Results: In the mathematical model of an epitrochoid curve (closely resembling disc occluder geometry) a ‘figure-of-8’ display is obtained when emphasizing points with tangent vector perpendicular to the direction of ultrasound waves. Decreasing imaging depth results in a more asymmetric ‘figure-of-8’, with small upper part and wide lower part. Clinical and in vitro data are in close agreement with these results (Figure 1). Furthermore a ‘figure-of-8’ display is only obtained in a coronal imaging position, and is similar for different commercially available disc occluder types. Conclusions: The ‘figure-of-8’ display in the ultrasound image of a disc occluder is an imaging artifact due to the specific ‘epitrochoidal’ geometry of a deployed device and its interaction with ultrasound waves. The morphology of the ‘figure-of-8’ depends on transducer position, i.e. imaging depth, and is similar for different device types. Figure 1 Impact of imaging depth

Published
2013
Full Text
View/download PDF

9. DOXORUBICIN-INDUCED CARDIOTOXICITY IN MICE IS BLUNTED BY LATE SODIUM CURRENT INHIBITION WITH RANOLAZINE, WITH IMPROVEMENT IN HEART FUNCTION, FIBROSIS AND APOPTOSIS

Author

Carlo G. Tocchetti, Carlo Maurea, Giovanna Piscopo, Claudia De Lorenzo, Nicola Maurea, Claudio Arra, Carmela Coppola, Domenica Rea, Clemente Cipresso, Aldo Giudice, Conference: 62nd Annual Scientific Session of the American-College-of-Cardiology, Maurea, N, Coppola, C, Piscopo, G, Cipresso, C, Rea, D, Giudice, A, Maurea, C, Arra, C, De Lorenzo, C, and Tocchetti, CARLO GABRIELE

Subjects
Cardiotoxicity, medicine.medical_specialty, business.industry, Ischemia, Cardiomyopathy, Ranolazine, Pharmacology, medicine.disease, Sodium current, carbohydrates (lipids), Fibrosis, Apoptosis, Internal medicine, polycyclic compounds, Cardiology, Medicine, Doxorubicin, business, Cardiology and Cardiovascular Medicine, medicine.drug
Abstract

Doxorubicin (DOX) produces a cardiomyopathy through multiple mechanisms as Ca2+ overload. DOX generates Reactive Oxigen and Nitrogen Species, posing the heart at increased demand for oxygen, setting the stage for metabolic ischemia that activates late sodium current, target of ranolazine (RAN). We

Published
2013
Full Text
View/download PDF

10. The emerging issue of cardiac dysfunction induced by antineoplastic angiogenesis inhibitors

Author

Giovanna Piscopo, Carlo G. Tocchetti, Rosario Vincenzo Iaffaioli, Giuseppina Gallucci, Aldo Giudice, Clemente Cipresso, Nicola Maurea, C. Coppola, Claudio Arra, Carlo Maurea, Tocchetti, CARLO GABRIELE, Gallucci, G, Coppola, C, Piscopo, G, Cipresso, C, Maurea, C, Giudice, A, Iaffaioli, Rv, Arra, C, and Maurea, N.

Subjects
Vascular Endothelial Growth Factor A, medicine.medical_specialty, Anthracycline, Angiogenesis, VEGF receptors, Cardiomyopathy, Angiogenesis Inhibitors, Antineoplastic Agents, Bioinformatics, Cardiovascular System, chemistry.chemical_compound, Ventricular Dysfunction, Left, Risk Factors, Internal medicine, medicine, Humans, biology, business.industry, Cancer, medicine.disease, Vascular endothelial growth factor, Endocrinology, chemistry, Heart failure, Toxicity, biology.protein, Cardiology and Cardiovascular Medicine, business
Abstract

Left ventricular dysfunction from anticancer drugs has emerged as a relevant problem in the clinical and scientific communities. Anthracycline toxicity has always been the most relevant, but with the increasing use of biological targeted therapies in treatment protocols, with an increasing number of cancer survivors, new toxicities have been increasing in more recent years. Cardiomyopathy after ErbB2 inhibitors has been intensively studied. Another important class of biological anticancer drugs are vascular endothelial growth factor (VEGF) inhibitors. VEGF signalling is crucial for vascular growth, but it also has a major impact on myocardial function. Also, it is important to note that such angiogenesis inhibitors are multitargeted in most cases, and can produce a broad spectrum of cardiovascular side effects. Here we review the mechanisms and pathophysiology of the most significant cardiotoxic effects of antiangiogenic drugs, and particular attention is drawn to LV dysfunction, discussing the assessment and management on the basis of the most recent cardio-oncological findings and heart failure guidelines.

Published
2013

11. Inhibition of cardiomyocytes late INa with ranolazine to prevent anthracyclines cardiotoxicity in experimental models in vitro and in vivo

Author

Nicola Maurea, Carmela Coppola, Giovanna Piscopo, Clemente Cipresso, Domenica Rea, Carlo G. Tocchetti, Michelino De Laurentiis, Claudio Arra, Rosario Vincenz Iaffaioli, Conference: Breast Cancer Symposium, Maurea, N, Coppola, Carmela, Piscopo, G, Cipresso, C, Rea, Domenica, Tocchetti, CARLO GABRIELE, DE LAURENTIIS, Michelino, Arra, C, and Iaffaioli, ROSARIO VINCENZO

Subjects
Cancer Research, Oncology
Abstract

170 Background: Anthracyclines are first line drugs against cancer, but produce a well-known cardiomyopathy through multiple mechanisms, which also include Ca2+ overload due to reduced SERCA2a activity and inappropriate opening of the RyR2, and impaired myocardial energetics. Anthracyclines generate Reactive Oxigen and Nitrogen Species, posing the heart at increased demand for oxygen, thus setting the stage for a metabolic ischemia that also activates late INa, the target of ranolazine (RAN). Here, we aim at assessing whether RAN, diminishing intracellular Ca2+ through its inhibition of late INa, and enhancing myocardial glucose utilization (and/or reverting impairment of glucose utilization caused by chemotherapy) blunts anthracyclines cardiotoxicity. Methods: To assess for cardiotoxicity in vitro, rat H9C2 cardiomyoblasts were pretreated with RAN (0.1-1µM) for 72 hours and then treated with doxorubicin (DOX, 0.1 µM)for additional 24 hours. Cells counts were assessed by Trypan exclusion test. To evaluate cardiac function in vivo, fractional shortening (FS) and ejection fraction (EF) were measured by echocardiography in C57BL6 mice, 2-4 mo old, pretreated with RAN (370mg/kg/day, a dose comparable to the one used in humans) per os for 3 days. RAN was then administered for additional 7 days, alone and together with DOX (2.17mg/kg/day ip), according to our well established protocol. Results: After DOX, only 68% of the cells were viable. RAN alone did not affected cell survival, but blunted DOX toxicity, rescuing % cell survival to 87% (p=.01 vs DOX alone). In our in vivo studies, after 7 days with DOX, FS decreased to 50±2%, p=.002 vs 60±1% (sham), and EF to 81+2%, p=0.0001 vs 91+1% (sham). RAN alone did not change FS (59±2%) nor EF 89+1%. Interestingly, in mice treated with RAN and DOX, the reduction in cardiac function was milder: FS was 57±1%, EF was 89+1%, p=0.01 and 0.0009, vs DOX alone. Conclusions: RAN blunts DOX cardiotoxic effects in 2 different models, in vitro and in vivo. We plan to test RAN as a cardioprotective agent with other antineoplastic cardiotoxic drugs in our experimental models, and to better characterize the cardioprotective mechanisms of RAN in all these settings.

Published
2013

12. Utility of 2D-speckle tracking echocardiography in diagnosis of left ventricular dysfunction in anti-ErbB2 therapy

Author

Emanuela Esposito, Giovanna Piscopo, Immacolata Capasso, Domenica Rea, Carlo G. Tocchetti, Claudio Arra, Nicola Maurea, Carmela Coppola, Clemente Cipresso, Conference: Breast Cancer Symposium, Maurea, N, Piscopo, G, Cipresso, C, Rea, Domenica, Esposito, E, Capasso, I, Tocchetti, CARLO GABRIELE, Arra, C, and Coppola, Carmela

Subjects
Cardiac function curve, Cancer Research, medicine.medical_specialty, Ejection fraction, business.industry, Cardiomyopathy, medicine.disease, Asymptomatic, Breast cancer, Oncology, Trastuzumab, Internal medicine, Heart failure, medicine, Cardiology, Doxorubicin, medicine.symptom, business, medicine.drug
Abstract

169 Background: ErbB2 is overexpressed in about 25% of breast cancers; in the heart, it modulates myocardial development and function. Trastuzumab (T), an anti-ErbB2 inhibitor, has improved the prognosis of patients with breast cancer, but is related to an increased risk of asymptomatic left ventricular (LV) dysfunction (3-34%) and heart failure (2-4%). Conventional measures of ventricular function, such as fractional shortening (FS) and ejection fraction (FE) are insensitive in detecting early cardiomyopathy induced by antineoplastic therapy. Here, we aim at assessing whether myocardial strain by 2D-speckle tracking (ST) is able to identify early LV dysfunction in mice treated with doxorubicin (D) and T, alone or in combination (D+T) and to relate data of cardiac function with tissue alterations. Methods: Cardiac function was measured with FS, by M-mode echocardiography, and with radial myocardial strain with ST in sedated C57BL/6 mice (8-10 wk old) at time 0, 2 and 6 days of daily administration of D (2.17 mg/kg/day), T (2.25 mg/kg/day), D+T (2.17 mg/kg/day + 2.25 mg/kg/day) and in a control group. In excised hearts, we evaluated TNFα and CD68 by immunohistochemistry; interstizial fibrosis was analyzed with picrosirius red staining. Results: FS was reduced in group D and D+T at 2 days (52+0.2% and 49+2%), both p2at 6 days in group D (16.46% and 155), in group T+D (12.35% and 74.16) and in group T (5.65% and 72.32) p

Published
2013
Full Text
View/download PDF

13. Ranolazine protects from doxorubicin-induced oxidative stress and cardiac dysfunction.

Author

Tocchetti CG, Carpi A, Coppola C, Quintavalle C, Rea D, Campesan M, Arcari A, Piscopo G, Cipresso C, Monti MG, De Lorenzo C, Arra C, Condorelli G, Di Lisa F, and Maurea N

Subjects
Animals, Atrial Natriuretic Factor genetics, Blotting, Western methods, Cardiotoxicity diagnostic imaging, Cardiotoxicity prevention & control, Connective Tissue Growth Factor genetics, Matrix Metalloproteinase 2 genetics, Mice, Mice, Inbred C57BL, Myocytes, Cardiac cytology, Natriuretic Peptide, Brain genetics, Oxidative Stress genetics, Poly(ADP-ribose) Polymerases metabolism, RNA, Messenger genetics, Ranolazine, Reactive Oxygen Species metabolism, Real-Time Polymerase Chain Reaction, Reverse Transcriptase Polymerase Chain Reaction methods, Sodium blood, Ultrasonography, Ventricular Dysfunction, Left chemically induced, Ventricular Dysfunction, Left metabolism, Acetanilides therapeutic use, Antibiotics, Antineoplastic toxicity, Doxorubicin toxicity, Enzyme Inhibitors therapeutic use, Oxidative Stress drug effects, Piperazines therapeutic use, Ventricular Dysfunction, Left prevention & control
Abstract

Aims: Doxorubicin is widely used against cancer; however, it can produce heart failure (HF). Among other hallmarks, oxidative stress is a major contributor to HF pathophysiology. The late INa inhibitor ranolazine has proven effective in treating experimental HF. Since elevated [Na+]i is present in failing myocytes, and has been recently linked with reactive oxygen species (ROS) production, our aim was to assess whether ranolazine prevents doxorubicin-induced cardiotoxicity, and whether blunted oxidative stress is a mechanism accounting for such protection., Methods and Result: In C57BL6 mice, doxorubicin treatment for 7 days produced LV dilation and decreased echo-measured fractional shortening (FS). Ranolazine (305 mg/kg/day) prevented LV dilation and dysfunction when co-administered with doxorubicin. Doxorubicin-induced cardiotoxicity was accompanied instead by elevations in atrial natriuretic peptide (ANP), BNP, connective tissue growth factor (CTGF), and matrix metalloproteinase 2 (MMP2) mRNAs, which were not elevated on co-treatment with ranolazine. Alterations in extracellular matrix remodelling were confirmed by an increase in interstitial collagen, which did not rise in ranolazine-co-treated hearts. Levels of poly(ADP-ribose) polymerase (PARP) and pro-caspase-3 measured by western blotting were lowered with doxorubicin, with increased cleavage of caspase-3, indicating activation of the proapoptotic machinery. Again, ranolazine prevented this activation. Furthermore, in HL-1 cardiomyocytes transfected with HyPer to monitor H2O2 emission, besides reducing the extent of cell death, ranolazine prevented the occurrence of oxidative stress caused by doxorubicin. Interestingly, similar protective results were obtained with the Na+/Ca2+ exchanger (NCX) inhibitor KB-R7943., Conclusions: Ranolazine protects against experimental doxorubicin cardiotoxicity. Such protection is accompanied by a reduction in oxidative stress, suggesting that INa modulates cardiac redox balance, resulting in functional and morphological derangements., (© 2014 The Authors. European Journal of Heart Failure © 2013 European Society of Cardiology.)

Published
2014
Full Text
View/download PDF

14. The pursuit of happiness measurement: a psychometric model based on psychophysiological correlates.

Author

Pietro C, Silvia S, and Giuseppe R

Subjects
Emotions physiology, Humans, Happiness, Psychometrics methods
Abstract

Everyone is interested in the pursuit of happiness, but the real problem for the researchers is how to measure it. Our aim was to deeply investigate happiness measurement through biomedical signals, using psychophysiological methods to objectify the happiness experiences measurements. The classic valence-arousal model of affective states to study happiness has been extensively used in psychophysiology. However, really few studies considered a real combination of these two dimensions and no study further investigated multidimensional models. More, most studies focused mainly on self-report to measure happiness and a deeper psychophysiological investigation on the dimensions of such an experience is still missing. A multidimensional model of happiness is presented and both the dimensions and the measures extracted within each dimension are comprehensively explained. This multidimensional model aims at being a milestone for future systematic study on psychophysiology of happiness and affective states.

Published
2014
Full Text
View/download PDF

15. The emerging issue of cardiac dysfunction induced by antineoplastic angiogenesis inhibitors.

Author

Tocchetti CG, Gallucci G, Coppola C, Piscopo G, Cipresso C, Maurea C, Giudice A, Iaffaioli RV, Arra C, and Maurea N

Subjects
Cardiovascular System drug effects, Humans, Risk Factors, Vascular Endothelial Growth Factor A antagonists & inhibitors, Ventricular Dysfunction, Left physiopathology, Angiogenesis Inhibitors adverse effects, Antineoplastic Agents adverse effects, Cardiovascular System physiopathology, Ventricular Dysfunction, Left chemically induced
Abstract

Left ventricular dysfunction from anticancer drugs has emerged as a relevant problem in the clinical and scientific communities. Anthracycline toxicity has always been the most relevant, but with the increasing use of biological targeted therapies in treatment protocols, with an increasing number of cancer survivors, new toxicities have been increasing in more recent years. Cardiomyopathy after ErbB2 inhibitors has been intensively studied. Another important class of biological anticancer drugs are vascular endothelial growth factor (VEGF) inhibitors. VEGF signalling is crucial for vascular growth, but it also has a major impact on myocardial function. Also, it is important to note that such angiogenesis inhibitors are multitargeted in most cases, and can produce a broad spectrum of cardiovascular side effects. Here we review the mechanisms and pathophysiology of the most significant cardiotoxic effects of antiangiogenic drugs, and particular attention is drawn to LV dysfunction, discussing the assessment and management on the basis of the most recent cardio-oncological findings and heart failure guidelines.

Published
2013
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results