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2. A numerical study of the RG equation for the deformed $O(3)$ nonlinear sigma model

Author

Belardinelli, L., Destri, C., and Onofri, E.

Subjects
High Energy Physics - Theory
Abstract

The Renormalization Group equation describing the evolution of the metric of the nonlinear sigma model poses some nice mathematical problems involving functional analysis, differential geometry and numerical analysis. In this article we briefly report some results obtained from the numerical study of the solutions in the case of a two dimensional target space (deformation of the $O(3)$ sigma model). In particular, our analysis shows that the so-called sausages define an attracting manifold in the $U(1)$-symmetric case, at one-loop level. Moreover, data from two-loop evolution are used to test the association put forward in Nucl. Phys., B406 (1993) 521 between the so-called $SSM_{\nu}$ field theory and a certain $U(1)$-symmetric, factorized scattering theory (FST)., Comment: LaTex (RevTex style), 16 pages, 6 uuencoded figures. Minor technical changes.

Published
1995
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3. Alleviation of AF related symptoms following acute conversion of recent-onset, symptomatic atrial fibrillation to sinus rhythm with flecainide acetate oral inhalation solution

Author

Camm, A J, primary, Crijns, H J G M, additional, Elvan, A, additional, Tuininga, Y, additional, Badings, E, additional, Kuijper, A F M, additional, De Jong, J S S G, additional, Lee, M, additional, Schellings, D, additional, Van Gelder, I C, additional, Ruskin, J, additional, Kowey, P, additional, Dufton, C, additional, Maupas, J, additional, and Belardinelli, L, additional

Published
2022
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4. Predictors of successful cardioversion of recent-onset atrial fibrillation to sinus rhythm with orally inhaled flecainide

Author

Ruskin, J, primary, Dufton, C, additional, Maupas, J, additional, Crijns, H, additional, Elvan, A, additional, De Jong, J, additional, Oosterhof, T, additional, Tuininga, Y, additional, Badings, E, additional, Aksoy, I, additional, Nuyens, D, additional, Van Dijk, V, additional, Camm, A J, additional, Kowey, P, additional, and Belardinelli, L, additional

Published
2022
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5. Open-Label, Multicenter Study of Flecainide Acetate Oral Inhalation Solution for Acute Conversion of Recent-Onset, Symptomatic Atrial Fibrillation to Sinus Rhythm

Author

Crijns, HJGM, Elvan, A, Al-Windy, N, Tuininga, YS, Badings, E, Aksoy, I, Van Gelder, IC, Madhavapeddi, P, Camm, AJ, Kowey, PR, Ruskin, JN, Belardinelli, L, and INSTANT Investigators

Abstract

BACKGROUND: Oral and intravenous flecainide is recommended for cardioversion of atrial fibrillation. In this open-label, dose-escalation study, the feasibility of delivering flecainide via oral inhalation (flecainide acetate inhalation solution) for acute conversion was evaluated. We hypothesized that flecainide delivered by oral inhalation would quickly reach plasma concentrations sufficient to restore sinus rhythm in patients with recent-onset atrial fibrillation. METHODS: Patients (n=101) with symptomatic atrial fibrillation (for ≤48 hours) self administered flecainide acetate inhalation solution using a nebulizer (30 mg [n=10], 60 mg [n=22], 90 mg [n=21], 120 mg [n=19], and 120 mg in a formulation containing saccharin [n=29]). Electrocardiograms and flecainide plasma concentrations were obtained, cardiac rhythm using 4-hour Holter was monitored, and adverse events were recorded. RESULTS: Conversion rates increased with dose and with the maximum plasma concentrations of flecainide. At the highest dose, 48% of patients converted to sinus rhythm within 90 minutes from the start of inhalation. Among patients who achieved a maximum plasma concentration >200 ng/mL, the conversion rate within 90 minutes was 50%; for those who achieved a maximum plasma concentration

Published
2022

9. Functional modulation of atrio-ventricular conduction by enhanced late sodium current and calcium-dependent mechanisms in Scn5a1798insD/þ mice

Author

Rivaud, M.R. (Mathilde R.), Marchal, G.A. (Gerard A.), Wolswinkel, R. (Rianne), Jansen, J.A. (John A.), van-der-Made, I. (Ingeborg), Beekman, L. (Leander), Ruiz-Villalba, A. (Adrián), Baartscheer, A. (Antonius), Rajamani, S. (Sridharan), Belardinelli, L. (Luiz), van-Veen, T.A.B. (Toon A.B.), Basso, C. (Cristina), Thiene, G. (Gaetano), Creemers, E.E. (Ester E.), Bezzina, C.R. (Connie R.), and Remme, C.A. (Carol Ann)

Subjects
Late sodium current, Calcium homeostasis, Mutations, NaV1.5, Atrio-ventricular block/conductionSCN5A
Abstract

Aims SCN5A mutations are associated with arrhythmia syndromes, including Brugada syndrome, long QT syndrome type 3 (LQT3), and cardiac conduction disease. Long QT syndrome type 3 patients display atrio-ventricular (AV) conduction slowing which may contribute to arrhythmogenesis. We here investigated the as yet unknown underlying mechanisms. Methods and results We assessed electrophysiological and molecular alterations underlying AV-conduction abnormalities in mice carrying the Scn5a1798insD/þ mutation. Langendorff-perfused Scn5a1798insD/þ hearts showed prolonged AV-conduction compared to wild type (WT) without changes in atrial and His-ventricular (HV) conduction. The late sodium current (INa,L) inhibitor ranolazine (RAN) normalized AV-conduction in Scn5a1798insD/þ mice, likely by preventing the mutation-induced increase in intracellular sodium ([Naþ]i ) and calcium ([Ca2þ]i ) concentrations. Indeed, further enhancement of [Naþ]i and [Ca2þ]i by the Naþ/Kþ-ATPase inhibitor ouabain caused excessive increase in AV-conduction time in Scn5a1798insD/þ hearts. Scn5a1798insD/þ mice from the 129P2 strain displayed more severe AV-conduction abnormalities than FVB/N-Scn5a1798insD/þ mice, in line with their larger mutation-induced INa,L. Transverse aortic constriction (TAC) caused excessive prolongation of AV-conduction in FVB/N-Scn5a1798insD/þ mice (while HV-intervals remained unchanged), which was prevented by chronic RAN treatment. Scn5a1798insD/þTAC hearts showed decreased mRNA levels of conduction genes in the AV-nodal region, but no structural changes in the AV-node or His bundle. In Scn5a1798insD/þ-TAC mice deficient for the transcription factor Nfatc2 (effector of the calcium-calcineurin pathway), AV-conduction and conduction gene expression were restored to WT levels. Conclusions Our findings indicate a detrimental role for enhanced INa,L and consequent calcium dysregulation on AVconduction in Scn5a1798insD/þ mice, providing evidence for a functional mechanism underlying AV-conduction disturbances secondary to gain-of-function SCN5A mutations.

Published
2020

11. Poster display IV experimental and instrumentation

Author

Masoli, O. Osvaldo, Redruello, M., Ogresta, F., Collaud, C., Koslowski, P., Baliño, N. Perez, Eleta, M., Arce, P., Vidal, L., Kardash, O., Maroz-Vadalajskaya, N. Natalia, Vanhove, C. Christian, Lahoutte, T., Defrise, M., Andreyev, A., Bossuyt, A., Franken, P. R., Franken, P. R. Philippe, Lahoutte, T., Maskali, F., Vanhove, C., Nloga, J., Tran, N., Marie, P. Y., Peix, A. Amalia, Garcia-Barreto, D., Ponce, F., Cabrera, L. O., Valiente, J., Tornes, F., Guerrero, I., Heres, F., Garcia, E. J., Cabale, B., Bindslev, L. Lene, Bisgaard, K. B. Kirsten, Haack-Soerensen, M. H. S. Mandana, Mortensen, S. M. Steen, Kragh, L. K. Linda, Kjaer, A. K. Andreas, Kastrup, J. K. Jens, Hesse, B. H. Birger, Aboul-Enein, F. Fatma, Battah, A., Fattah, A. Abdel, Atty, A. Abdel, Allam, A., Riou, L. Laurent, Broisat, A., Ghezzi, C., Lartizien, C., Berthonneche, C., Toufektsian, M. C., Maitrejean, S., Janier, M., Vanzetto, G., Fagret, D., Rouzet, F. Francois, Daou, D., Lebtahi, R., Frank, R., Leenhardt, A., Slama, M., Guludec, D. Le, Sarda-Mantel, L. Laure, Michel, J. B., Rouzet, F., Martet, G., Meulemans, A., Vrigneaud, J. M., Guludec, D. Le, Daou, D. Doumit, Coaguila, C., Benada, A., Razzouk, M., Idy-Peretti, I., Guludec, D. Le, Vilain, D., Lebtahi, R., Guludec, D. Le, Stegger, L. Lars, Schäfers, K., Flögel, U., Schrader, J., Schober, O., Levkau, B., Schäfers, M., Kies, P. Peter, Wichter, T., Schäfers, K. P., Schäfers, M., Wielepp, J. P. Peter, Baller, D., Pulawski, E., Weise, R., Fricke, E., Horstkotte, D., Burchert, W., Eckert, S., Dongas, A., Horstkotte, D., Burchert, W., Nekolla, S. G. Stephan, Martinez, M. J., Howe, W., Kehren, F., Ziegler, S. I., Vassiliadis, I. Ioannis, Souretis, G., Komporozos, C., Fountos, A., Papademetriou, A., Spanos, A., Antoniou, A., Strembelas, P., Moralidis, E. Efstratios, Arsos, G., Boundas, D., Georga, S., Karatzas, N., Karakatsanis, K., Prassopoulos, V. Vassilios, Parthenakis, F., Patrianakos, A., Koukouraki, S., Velidaki, A., Karkavitsas, N., Vardas, P., Velidaki, A. Antigone, Perisinakis, K., Koukouraki, S., Koutsikos, J., Prassopoulos, V., Vardas, P., Karkavitsas, N., Sundaraiya, S. Sumati, Sumati, S., Sambhasivam, KA., David, S., Zakavi, S. R. Seyed Rasoul, Kakhki, V. R. Dabagh, Jabari, H., Zingerman, B., Bendayan, D., Sagie, A., Solodky, A., Mats, I., Shapira, Y., Kremer, M. R., Zafrir, N. Nili, Rimini, M. L. Maria Luisa De, Catalano, M., Bonzani, G., Scalzone, A., Merenda, R., Monteforte, I., Monda, V., Muto, P., Carboni, G. P. Gian Piero, Miglionico, M., Tavolozza, M., Marcassa, C. Claudio, Campini, R., Calza, P., Giannuzzi, P., Eleuteri, E., Marcassa, C. Claudio, Campini, R., Scapellato, F., Temporelli, P. L., Giannuzzi, P., Pellegrino, T., Storto, G., Sorrentino, A. R., Silvestri, A., Filardi, P. Perrone, Brevetti, G., Cuocolo, A. Alberto, Cho, K. Keiichi, Kumita, S., Seino, K., Nakajo, H., Toba, M., Kumazaki, T., Muramatsu, T. Toshihiro, Yamazaki, T., Seki, K., Kawanami, J., Nakajima, T., Yamada, Y., Suga, T., Matsumoto, K., Nishimura, S., Taki, J. Junichi, Higuchi, T., Kawashima, A., Nakajima, K., Muramori, A., Matsunari, I., Tait, J. F., Vanderheyden, J. L., Strauss, H. W., Tonami, N., Adachi, I. Itaru, Shimomura, H., Kintaka, T., Komori, T., Ogura, Y., Kitaura, Y., Narabayashi, I., Iida, H. Hidehiro, Zeniya, T., Kim, K. M., Watabe, H., Teramoto, N., Yamamichi, Y., Alexanderson, E. Erick, Ricalde, A., Vargas, A., Meave, A., Amigo, M. C., Misko, J., Dziuk, M. Miroslaw, Warczynska, A., Skrobowska, E., Vasconcelos, M. Mariana, Martins, E., Faria, T., Oliveira, A., Pardal, N., Macedo, F., Pereira, J., Rocha-Gonçalves, F., Cantinho, G. Guilhermina, Pena, H., Freire, L., Veiga, A., Gonçalves, P., Godinho, F., Chua, T. Terrance, Lee, C. Y., Keng, F., Ding, Z. P., Koh, T. H., Awamleh, P. Paula, Talavera, P., Torres, V., Balsa, M. A., González, O., Alberca, M. T., Miguel, R., Cosío, F. G., Lomsky, M. Milan, Richter, J., Johansson, L., El-Ali, H., Åström, K., Ljungberg, M., Edenbrandt, L., Hung, G. U. Guang-Uei, Lee, K. W., Chen, C. P., Yang, K. T., Pekindil, G., Sarikaya, A. Ali, Ege, T., Salihoglu, S., Entok, E. Emre, Cavusoglu, Y., Ak, I., Vardareli, E., Timuralp, B., Tout, D. Deborah, Loong, C. Y., Naidoo, V. V., Aswegen, A. Van, Underwood, S. R., Thorley, P. J. Penelope, Goris, M. Michael, ZHU, H. J., Clements, I. P. Ian, Mullan, B. P., O’Connor, M. K., Breen, J. F., McGregor, C. G. A., Liu, Y. H. Yi-Hwa, Li, S., Bourke, B., Weyman, C., Sinusas, A. J., Ramakrishna, G. Gautam, Miller, T. D., O’Connor, M. K., Gibbons, R. J., Tsatkin, V., Wackers, F. J. T. H., Liu, Y. H. Yi-Hwa, Tsatkin, V., Prior, J. O. John, Facta, A. D., Schindler, T. H., Oxilia-Estigarribia, M. A., Hernandez-Pampaloni, M., Campisi, R., Zhang, X., Bischof-Delaloye, A., Nathan, L., Schelbert, H. R., Gullberg, G. T. Grant, Huesman, R. H., Reutter, B. W., Sitek, A., Veress, A. I., Weiss, J. A., Qi, J., Yang, Y., Gordi, T. Toufigh, Olmsted, A., Lieu, H., and Belardinelli, L.

Published
2005
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12. Abstracts of original contributions ASNC 2004 9th annual scientific session September 3-–October 3, 2004 New York, New York

Author

Abidov, A, Hachamovitch, R, Friedman, JD, Hayes, SW, Kang, X, Cohen, I, Germano, G, Berman, DS, Kjaer, A, Cortsen, A, Federspiel, M, Hesse, B, Holm, S, O’Connor, M, Dhalla, AK, Wong, M-Y, Wang, W-Q, Belardinelli, L, Therapeutics, CV, Epps, A, Dave, S, Brewer, K, Chiaramida, S, Gordon, L, Hendrix, GH, Feng, B, Pretorius, PH, Bruyant, PP, Boening, G, Beach, RD, Gifford, HC, King, MA, Fessler, JA, Hsu, B-L, Case, JA, Gegen, LL, Hertenstein, GK, Cullom, SJ, Bateman, TM, Akincioglu, C, Abidov, A, Nishina, H, Kavanagh, P, Kang, X, Aboul-Enein, F, Yang, L, Hayes, S, Friedman, J, Berman, D, Germano, G, Santana, CA, Rivero, A, Folks, RD, Grossman, GB, Cooke, CD, Hunsche, A, Faber, TL, Halkar, R, Garcia, EV, Hansen, CL, Silver, S, Kaplan, A, Rasalingam, R, Awar, M, Shirato, S, Reist, K, Htay, T, Mehta, D, Cho, J-H, Heo, J, Dubovsky, E, Calnon, DA, Grewal, KS, George, PB, Richards, DR, Hsi, DH, Singh, N, Meszaros, Z, Thomas, JL, Reyes, E, Loong, CY, Latus, K, Anagnostopoulos, C, Underwood, SR, Kostacos, EJ, Araujo, LI, Kostacos, EJ, Araujo, LI, Lewin, HC, Hyun, MC, DePuey, EG, Tanaka, H, Chikamori, T, Igarashi, Y, Harafuji, K, Usui, Y, Yanagisawa, H, Hida, S, Yamashina, A, Nasr, HA, Mahmoud, SA, Dalipaj, MM, Golanowski, LN, Kemp, RA de, Chow, BJ, Beanlands, RS, Ruddy, TD, Michelena, HI, Mikolich, BM, McNelis, P, Decker, WA Van, Stathopoulos, I, Duncan, S- A, Isasi, C, Travin, MI, Kritzman, JN, Ficaro, EP, Corbett, JR, Allison, JS, Weinsaft, JW, Wong, FJ, Szulc, M, Okin, PM, Kligfield, P, Harafuji, K, Chikamori, T, Igarashi, Y, Tanaka, H, Usui, Y, Yanagisawa, H, Hida, S, Ishimaru, S, Yamashima, A, Giedd, KN, Bergmann, SR, Shah, S, Emmett, L, Allman, KC, Magee, M, Van Gaal, W, Kritharides, L, Freedman, B, Abidov, A, Gerlach, J, Akincioglu, C, Friedman, J, Kavanagh, P, Miranda, R, Germano, G, Berman, DS, Hayes, SW, Damera, N, Lone, B, Singh, R, Shah, A, Yeturi, S, Prasad, Y, Blum, S, Heller, EN, Bhalodkar, NC, Koutelou, M, Kollaros, N, Theodorakos, A, Manginas, A, Leontiadis, E, Kouzoumi, A, Cokkinos, D, Mazzanti, M, Marini, M, Cianci, G, Perna, GP, Pai, M, Greenberg, MD, Liu, F, Frankenberger, O, Kokkinos, P, Hanumara, D, Goheen, E, Wu, C, Panagiotakos, D, Fletcher, R, Greenberg, MD, Liu, F, Frankenberger, O, Kokkinos, P, Hanumara, D, Goheen, E, Rodriguez, OJ, Iyer, VN, Lue, M, Hickey, KT, Blood, DK, Bergmann, SR, Bokhari, S, Chareonthaitawee, P, Christensen, SD, Allen, JL, Kemp, BJ, Hodge, DO, Ritman, EL, Gibbons, RJ, Smanio, P, Riva, G, Rodriquez, F, Tricoti, A, Nakhlawi, A, Thom, A, Pretorius, PH, King, MA, Dahlberg, S, Leppo, J, Slomka, PJ, Nishina, H, Berman, DS, Akincioglu, C, Abidov, A, Friedman, JD, Hayes, SW, Germano, G, Petrovici, R, Husain, M, Lee, DS, Nanthakumar, K, Iwanochko, RM, Brunken, RC, DiFilippo, F, Neumann, DR, Bybel, B, Herrington, B, Bruckbauer, T, Howe, C, Lohmann, K, Hayden, C, Chatterjee, C, Lathrop, B, Brunken, RC, Chen, MS, Lohmann, KA, Howe, WC, Bruckbauer, T, Kaczur, T, Bybel, B, DiFilippo, FP, Druz, RS, Akinboboye, OA, Grimson, R, Nichols, KJ, Reichek, N, Ngai, K, Dim, R, Ho, K- T, Pary, S, Ahmed, SU, Ahlberg, A, Cyr, G, Vitols, PJ, Mann, A, Alexander, L, Rosenblatt, J, Mieres, J, Heller, GV, Ahmed, SU, Ahlberg, AW, Cyr, G, Navare, S, O’Sullivan, D, Heller, GV, Chiadika, S, Lue, M, Blood, DK, Bergmann, SR, Bokhari, S, Heston, TF, Heller, GV, Cerqueira, MD, Jones, PG, Bryngelson, JR, Moutray, KL, Gegen, LL, Hertenstein, GK, Moser, K, Case, JA, Zellweger, MJ, Burger, PC, Pfisterer, ME, Mueller-Brand, J, Kang, WJ, Lee, BI, Lee, DS, Paeng, JC, Lee, JS, Chung, J-K, Lee, MC, To, BN, O’Connell, WJ, Botvinick, EH, Duvall, WL, Croft, LB, Einstein, AJ, Fisher, JE, Haynes, PS, Rose, RK, Henzlova, MJ, Prasad, Y, Vashist, A, Blum, S, Sagar, P, Heller, EN, Kuwabara, Y, Nakayama, K, Tsuru, Y, Nakaya, J, Shindo, S, Hasegawa, M, Komuro, I, Liu, Y-H, Wackers, F, Natale, D, DePuey, G, Taillefer, R, Araujo, L, Kostacos, E, Allen, S, Delbeke, D, Anstett, F, Kansal, P, Calvin, JE, Hendel, RC, Gulati, M, Pratap, P, Takalkar, A, Kostacos, E, Alavi, A, Araujo, L, Melduni, RM, Duncan, S-A, Travin, MI, Isasi CR, Rivero, A, Santana, C, Esiashvili, S, Grossman, G, Halkar, R, Folks, RD, Garcia, EV, Su, H, Dobrucki, LW, Chow, C, Hu, X, Bourke, BN, Cavaliere, P, Hua, J, Sinusas, AJ, Spinale, FG, Sweterlitsch, S, Azure, M, Edwards, DS, Sudhakar, S, Chyun, DA, Young, LH, Inzucchi, SE, Davey, JA, Wackers, FJ, Noble, GL, Navare, SM, Calvert, J, Hussain, SA, Ahlberg, AM, Katten, DM, Boden, WE, Heller, GV, Shaw, LJ, Yang, Y, Antunes, A, Botelho, MF, Gomes, C, de Lima, JJP, Silva, ML, Moreira, JN, Simões, S, GonÇalves, L, Providência, LA, Elhendy, A, Bax, JJ, Schinkel, AF, Valkema, R, van Domburg, RT, Poldermans, D, Arrighi, J, Lampert, R, Burg, M, Soufer, R, Veress, AI, Weiss, JA, Huesman, RH, Gullberg, GT, Moser, K, Case, JA, Loong, CY, Prvulovich, EM, Reyes, E, Aswegen, A van, Anagnostopoulos, C, Underwood, SR, Htay, T, Mehta, D, Sun, L, Lacy, J, Heo, J, Brunken, RC, Kaczur, T, Jaber, W, Ramakrishna, G, Miller, TD, O’connor, MK, Gibbons, RJ, Bural, GG, Mavi, A, Kumar, R, El-Haddad, G, Srinivas, SM, A Alavi, El-Haddad, G, Alavi, A, Araujo, L, Thomas, GS, Johnson, CM, Miyamoto, MI, Thomas, JJ, Majmundar, H, Ryals, LA, Ip, ZTK, Shaw, LJ, Bishop, HA, Carmody, JP, Greathouse, WG, Yanagisawa, H, Chikamori, T, Tanaka, H, Usui, Y, Igarashi, U, Hida, S, Morishima, T, Tanaka, N, Takazawa, K, Yamashina, A, Diedrichs, H, Weber, M, Koulousakis, A, Voth, E, Schwinger, RHG, Mohan, HK, Livieratos, L, Gallagher, S, Bailey, DL, Chambers, J, Fogelman, I, Sobol, I, Barst, RJ, Nichols, K, Widlitz, A, Horn, E, Bergmann, SR, Chen, J, Galt, JR, Durbin, MK, Ye, J, Shao, L, Garcia, EV, Mahenthiran, J, Elliott, JC, Jacob, S, Stricker, S, Kalaria, VG, Sawada, S, Scott, JA, Aziz, K, Yasuda, T, Gewirtz, H, Hsu, BL, Moutray, K, Udelson, JE, Barrett, RJ, Johnson, JR, Menenghetti, C., Taillefer, R, Ruddy, T, Hachamovitch, R, Jenkins, SA, Massaro, J, Haught, H, Lim, CS, Underwood, R, Rosman, J, Hanon, S, Shapiro, M, Schweitzer, P, VanTosh, A, Jones, S, Harafuji, K, Giedd, K N, Johnson, N P, Berliner, J I, Sciacca, R R, Chou, R L, Hickey, K T, Bokhari, S S, Rodriguez, O, Bokhari, S, Moser, KW, Moutray, KL, Koutelou, M, Theodorakos, A, Kollaros, N, Manginas, A, Leontiadis, E, Cokkinos, D, Mazzanti, M, Marini, M, Cianci, G, Perna, GP, Nanasato, M, Fujita, H, Toba, M, Nishimura, T, Nikpour, M, Urowitz, M, Gladman, D, Ibanez, D, Harvey, P, Floras, J, Rouleau, J, Iwanochko, R, Pai, M, Guglin, ME, Ginsberg, FL, Reinig, M, Parrillo, JE, Cha, R, Merhige, ME, Watson, GM, Oliverio, JG, Shelton, V, Frank, SN, Perna, AF, Ferreira, MJ, Ferrer-Antunes, AI, Rodrigues, V, Santos, F, Lima, J, Cerqueira, MD, Magram, MY, Lodge, MA, Babich, JW, Dilsizian, V, Line, BR, Bhalodkar, NC, Lone, B, Singh, R, Prasad, Y, Yeturi, S, Blum, S, Heller, EN, Rodriguez, OJ, Skerrett, D, Charles, C, Shuster, MD, Itescu, S, Wang, TS, Bruyant, PP, Pretorius, PH, Dahlberg, S, King, MA, Petrovici, R, Iwanochko, RM, Lee, DS, Emmett, L, Husain, M, Hosokawa, R, Ohba, M, Kambara, N, Tadamura, E, Kubo, S, Nohara, R, Kita, T, Thompson, RC, McGhie, AI, O’Keefe, JH, Christenson, SD, Chareonthaitawee, P, Kemp, BJ, Jerome, S, Russell, TJ, Lowry, DR, Coombs, VJ, Moses, A, Gottlieb, SO, Heiba, SI, Yee, G, Coppola, J, Elmquist, T, Braff, R, Youssef, I, Ambrose, JA, Abdel-Dayem, HM, Canto, J, Dubovsky, E, Scott, J, Terndrup, TE, Faber, TL, Folks, RD, Dim, UR, Mclaughlin, J, Pollepalle, D, Schapiro, W, Wang, Y, Akinboboye, O, Ngai, K, Druz, RS, Polepalle, D, Phippen-Nater, B, Leonardis, J, and Druz, R

Published
2004
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18. Poster display IV experimental and instrumentation

Author

Masoli, O., Redruello, M., Ogresta, F., Collaud, C., Koslowski, P., Baliño, N., Eleta, M., Arce, P., Vidal, L., Kardash, O., Maroz-Vadalajskaya, N., Vanhove, C., Lahoutte, T., Defrise, M., Andreyev, A., Bossuyt, A., Franken, P., Maskali, F., Nloga, J., Tran, N., Marie, P., Peix, A., Garcia-Barreto, D., Ponce, F., Cabrera, L., Valiente, J., Tornes, F., Guerrero, I., Heres, F., Garcia, E., Cabale, B., Bindslev, L., Bisgaard, K., Haack-Soerensen, M., Mortensen, S., Kragh, L., Kjaer, A., Kastrup, J., Hesse, B., Aboul-Enein, F., Battah, A., Fattah, A., Atty, A., Allam, A., Riou, L., Broisat, A., Ghezzi, C., Lartizien, C., Berthonneche, C., Toufektsian, M., Maitrejean, S., Janier, M., Vanzetto, G., Fagret, D., Rouzet, F., Daou, D., Lebtahi, R., Frank, R., Leenhardt, A., Slama, M., Guludec, D., Sarda-Mantel, L., Michel, J., Martet, G., Meulemans, A., Vrigneaud, J., Coaguila, C., Benada, A., Razzouk, M., Idy-Peretti, I., Vilain, D., Stegger, L., Schäfers, K., Flögel, U., Schrader, J., Schober, O., Levkau, B., Schäfers, M., Kies, P., Wichter, T., Wielepp, J., Baller, D., Pulawski, E., Weise, R., Fricke, E., Horstkotte, D., Burchert, W., Eckert, S., Dongas, A., Nekolla, S., Martinez, M., Howe, W., Kehren, F., Ziegler, S., Vassiliadis, I., Souretis, G., Komporozos, C., Fountos, A., Papademetriou, A., Spanos, A., Antoniou, A., Strembelas, P., Moralidis, E., Arsos, G., Boundas, D., Georga, S., Karatzas, N., Karakatsanis, K., Prassopoulos, V., Parthenakis, F., Patrianakos, A., Koukouraki, S., Velidaki, A., Karkavitsas, N., Vardas, P., Perisinakis, K., Koutsikos, J., Sundaraiya, S., Sumati, S., Sambhasivam, KA, David, S., Zakavi, S., Kakhki, V., Jabari, H., Zingerman, B., Bendayan, D., Sagie, A., Solodky, A., Mats, I., Shapira, Y., Kremer, M., Zafrir, N., Rimini, M., Catalano, M., Bonzani, G., Scalzone, A., Merenda, R., Monteforte, I., Monda, V., Muto, P., Carboni, G., Miglionico, M., Tavolozza, M., Marcassa, C., Campini, R., Calza, P., Giannuzzi, P., Eleuteri, E., Scapellato, F., Temporelli, P., Pellegrino, T., Storto, G., Sorrentino, A., Silvestri, A., Filardi, P., Brevetti, G., Cuocolo, A., Cho, K., Kumita, S., Seino, K., Nakajo, H., Toba, M., Kumazaki, T., Muramatsu, T., Yamazaki, T., Seki, K., Kawanami, J., Nakajima, T., Yamada, Y., Suga, T., Matsumoto, K., Nishimura, S., Taki, J., Higuchi, T., Kawashima, A., Nakajima, K., Muramori, A., Matsunari, I., Tait, J., Vanderheyden, J., Strauss, H., Tonami, N., Adachi, I., Shimomura, H., Kintaka, T., Komori, T., Ogura, Y., Kitaura, Y., Narabayashi, I., Iida, H., Zeniya, T., Kim, K., Watabe, H., Teramoto, N., Yamamichi, Y., Alexanderson, E., Ricalde, A., Vargas, A., Meave, A., Amigo, M., Misko, J., Dziuk, M., Warczynska, A., Skrobowska, E., Vasconcelos, M., Martins, E., Faria, T., Oliveira, A., Pardal, N., Macedo, F., Pereira, J., Rocha-Gonçalves, F., Cantinho, G., Pena, H., Freire, L., Veiga, A., Gonçalves, P., Godinho, F., Chua, T., Lee, C., Keng, F., Ding, Z., Koh, T., Awamleh, P., Talavera, P., Torres, V., Balsa, M., González, O., Alberca, M., Miguel, R., Cosío, F., Lomsky, M., Richter, J., Johansson, L., El-Ali, H., Åström, K., Ljungberg, M., Edenbrandt, L., Hung, G., Lee, K., Chen, C., Yang, K., Pekindil, G., Sarikaya, A., Ege, T., Salihoglu, S., Entok, E., Cavusoglu, Y., Ak, I., Vardareli, E., Timuralp, B., Tout, D., Loong, C., Naidoo, V., Aswegen, A., Underwood, S., Thorley, P., Goris, M., ZHU, H., Clements, I., Mullan, B., O'Connor, M., Breen, J., McGregor, C., Liu, Y., Li, S., Bourke, B., Weyman, C., Sinusas, A., Ramakrishna, G., Miller, T., Gibbons, R., Tsatkin, V., Wackers, F., Prior, J., Facta, A., Schindler, T., Oxilia-Estigarribia, M., Hernandez-Pampaloni, M., Campisi, R., Zhang, X., Bischof-Delaloye, A., Nathan, L., Schelbert, H., Gullberg, G., Huesman, R., Reutter, B., Sitek, A., Veress, A., Weiss, J., Qi, J., Yang, Y., Gordi, T., Olmsted, A., Lieu, H., Belardinelli, L., Masoli, O., Redruello, M., Ogresta, F., Collaud, C., Koslowski, P., Baliño, N., Eleta, M., Arce, P., Vidal, L., Kardash, O., Maroz-Vadalajskaya, N., Vanhove, C., Lahoutte, T., Defrise, M., Andreyev, A., Bossuyt, A., Franken, P., Maskali, F., Nloga, J., Tran, N., Marie, P., Peix, A., Garcia-Barreto, D., Ponce, F., Cabrera, L., Valiente, J., Tornes, F., Guerrero, I., Heres, F., Garcia, E., Cabale, B., Bindslev, L., Bisgaard, K., Haack-Soerensen, M., Mortensen, S., Kragh, L., Kjaer, A., Kastrup, J., Hesse, B., Aboul-Enein, F., Battah, A., Fattah, A., Atty, A., Allam, A., Riou, L., Broisat, A., Ghezzi, C., Lartizien, C., Berthonneche, C., Toufektsian, M., Maitrejean, S., Janier, M., Vanzetto, G., Fagret, D., Rouzet, F., Daou, D., Lebtahi, R., Frank, R., Leenhardt, A., Slama, M., Guludec, D., Sarda-Mantel, L., Michel, J., Martet, G., Meulemans, A., Vrigneaud, J., Coaguila, C., Benada, A., Razzouk, M., Idy-Peretti, I., Vilain, D., Stegger, L., Schäfers, K., Flögel, U., Schrader, J., Schober, O., Levkau, B., Schäfers, M., Kies, P., Wichter, T., Wielepp, J., Baller, D., Pulawski, E., Weise, R., Fricke, E., Horstkotte, D., Burchert, W., Eckert, S., Dongas, A., Nekolla, S., Martinez, M., Howe, W., Kehren, F., Ziegler, S., Vassiliadis, I., Souretis, G., Komporozos, C., Fountos, A., Papademetriou, A., Spanos, A., Antoniou, A., Strembelas, P., Moralidis, E., Arsos, G., Boundas, D., Georga, S., Karatzas, N., Karakatsanis, K., Prassopoulos, V., Parthenakis, F., Patrianakos, A., Koukouraki, S., Velidaki, A., Karkavitsas, N., Vardas, P., Perisinakis, K., Koutsikos, J., Sundaraiya, S., Sumati, S., Sambhasivam, KA, David, S., Zakavi, S., Kakhki, V., Jabari, H., Zingerman, B., Bendayan, D., Sagie, A., Solodky, A., Mats, I., Shapira, Y., Kremer, M., Zafrir, N., Rimini, M., Catalano, M., Bonzani, G., Scalzone, A., Merenda, R., Monteforte, I., Monda, V., Muto, P., Carboni, G., Miglionico, M., Tavolozza, M., Marcassa, C., Campini, R., Calza, P., Giannuzzi, P., Eleuteri, E., Scapellato, F., Temporelli, P., Pellegrino, T., Storto, G., Sorrentino, A., Silvestri, A., Filardi, P., Brevetti, G., Cuocolo, A., Cho, K., Kumita, S., Seino, K., Nakajo, H., Toba, M., Kumazaki, T., Muramatsu, T., Yamazaki, T., Seki, K., Kawanami, J., Nakajima, T., Yamada, Y., Suga, T., Matsumoto, K., Nishimura, S., Taki, J., Higuchi, T., Kawashima, A., Nakajima, K., Muramori, A., Matsunari, I., Tait, J., Vanderheyden, J., Strauss, H., Tonami, N., Adachi, I., Shimomura, H., Kintaka, T., Komori, T., Ogura, Y., Kitaura, Y., Narabayashi, I., Iida, H., Zeniya, T., Kim, K., Watabe, H., Teramoto, N., Yamamichi, Y., Alexanderson, E., Ricalde, A., Vargas, A., Meave, A., Amigo, M., Misko, J., Dziuk, M., Warczynska, A., Skrobowska, E., Vasconcelos, M., Martins, E., Faria, T., Oliveira, A., Pardal, N., Macedo, F., Pereira, J., Rocha-Gonçalves, F., Cantinho, G., Pena, H., Freire, L., Veiga, A., Gonçalves, P., Godinho, F., Chua, T., Lee, C., Keng, F., Ding, Z., Koh, T., Awamleh, P., Talavera, P., Torres, V., Balsa, M., González, O., Alberca, M., Miguel, R., Cosío, F., Lomsky, M., Richter, J., Johansson, L., El-Ali, H., Åström, K., Ljungberg, M., Edenbrandt, L., Hung, G., Lee, K., Chen, C., Yang, K., Pekindil, G., Sarikaya, A., Ege, T., Salihoglu, S., Entok, E., Cavusoglu, Y., Ak, I., Vardareli, E., Timuralp, B., Tout, D., Loong, C., Naidoo, V., Aswegen, A., Underwood, S., Thorley, P., Goris, M., ZHU, H., Clements, I., Mullan, B., O'Connor, M., Breen, J., McGregor, C., Liu, Y., Li, S., Bourke, B., Weyman, C., Sinusas, A., Ramakrishna, G., Miller, T., Gibbons, R., Tsatkin, V., Wackers, F., Prior, J., Facta, A., Schindler, T., Oxilia-Estigarribia, M., Hernandez-Pampaloni, M., Campisi, R., Zhang, X., Bischof-Delaloye, A., Nathan, L., Schelbert, H., Gullberg, G., Huesman, R., Reutter, B., Sitek, A., Veress, A., Weiss, J., Qi, J., Yang, Y., Gordi, T., Olmsted, A., Lieu, H., and Belardinelli, L.

Published
2018

19. Novel applications of myocardial perfusion imaging oral abstract session

Author

Lautamäki, R. Riikka, Airaksinen, K. E. J., Seppänen, M., Toikka, J., Luotolahti, M., Borra, R., Sundell, J., Knuuti, J., Nuutila, P., Hermann, S. Sven, Levkau, B., Theilmeier, G., Giet, M. Van der, Chun, J., Schober, O., Schäfers, M., Spadafora, M. Marco, Manganelli, F., Ferro, A., Varrella, P., Rizzo, V., Mansi, L., Rosato, G., Miletto, P., Cuocolo, A., Tsukamoto, T. Takahiro, Morita, K., Naya, M., Katoh, C., Kuge, Y., Okamoto, H., Tsutsui, H., Tamaki, N., Morita, K. Koichi, Tsukamoto, T., Naya, M., Noriyasu, K., Mabichi, M., Kageyama, H., Tamaki, N., Varani, K., Shryock, J. C., Belardinelli, L. Luiz, and Borea, P. A.

Published
2005
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21. P791A common co-morbidity modulates disease expression and treatment efficacy in inherited cardiac sodium channelopathy

Author

Remme, C A, primary, Rivaud, M R, additional, Jansen, J A, additional, Postema, P G, additional, Nannenberg, E A, additional, Marchal, G A, additional, Rajamani, S R, additional, Belardinelli, L, additional, Van Tintelen, J P, additional, Tanck, M W, additional, Creemers, E E, additional, Wilde, A A, additional, Van Den Berg, M P, additional, Van Veen, TAB, additional, and Bezzina, C R, additional

Published
2018
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26. Na+channel function, regulation, structure, trafficking and sequestration

Author

Chen-Izu, Y, Shaw, RM, Pitt, GS, Yarov-Yarovoy, V, Sack, JT, Abriel, H, Aldrich, RW, Belardinelli, L, Cannell, MB, Catterall, WA, Chazin, WJ, Chiamvimonvat, N, Deschenes, I, Grandi, E, Hund, TJ, Izu, LT, Maier, LS, Maltsev, VA, Marionneau, C, Mohler, PJ, Rajamani, S, Rasmusson, RL, Sobie, EA, Clancy, CE, and Bers, DM

Abstract

© 2014 The Physiological Society. This paper is the second of a series of three reviews published in this issue resulting from the University of California Davis Cardiovascular Symposium 2014: Systems approach to understanding cardiac excitation-contraction coupling and arrhythmias: Na+channel and Na+transport. The goal of the symposium was to bring together experts in the field to discuss points of consensus and controversy on the topic of sodium in the heart. The present review focuses on Na+channel function and regulation, Na+channel structure and function, and Na+channel trafficking, sequestration and complexing.

Published
2015
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27. The beneficial effects of ranolazine on cardiac function after myocardial infarction are greater in diabetic than in nondiabetic rats

Author

Mourouzis, I. Mantzouratou, P. Galanopoulos, G. Kostakou, E. Dhalla, A.K. Belardinelli, L. Pantos, C.

Abstract

Ranolazine (RAN) is known to exert both anti-ischemic and antidiabetic actions. Thus, this study has explored the hypothesis that RAN would have greater effect on the recovery of cardiac function in diabetic mellitus (DM) rat hearts following myocardial infarction (MI). Myocardial infarction was induced in nondiabetic (MI, n= 14) and diabetic (streptozotocin induced; DM-MI, n= 13)Wistar rats by permanent ligation of the left coronary artery. Cardiac function was evaluated using echocardiography (left ventricular ejection fraction %) and in isolated heart preparations by measuring left ventricular developed pressure (LVDP), and the positive and negative first derivative of LVDP (+dp/dt). Ranolazine (20 mg/kg, ip once a day) was administered 24 hours after surgical procedure for 4 weeks to nondiabetic (MIRAN, n=17) and diabetic rats (DM-MIRAN, n=15). The RANimproved the recovery of function in both the nondiabetic and the diabetic postinfarcted hearts but this effect was greater and achieved statistical significance only in the diabetic group. The RAN resulted in increased levels of phosphorylated protein kinase B (Akt) and mammalian target of rapamycin (mTOR, a component of Akt signaling) in both nondiabetic and diabetic infarcted heartswithout changes in the activation of mitogen-activated protein kinases (MAPKs; p38MAPK, c-JunN-terminal kinase, and extracellular signal-regulated kinase). In addition, in diabetic hearts, RANresulted in a significant increase in the ratio of sarcoplasmic Ca2-ATPase/phospholamban (a target of Akt signaling, 2.0-fold increase) and increased levels of phosphorylated calcium-regulated adenosine monophosphate-activated protein kinase (AMPK; 2.0-fold increase). In diabetic animals, RANincreased insulin and lowered glucose levels in serum. In conclusion, the beneficial effect of RANon the recovery of cardiac function afterMIwas greater inDMrats. This response was associatedwith activation of Akt/mTOR and AMPK.These findings provide a plausible explanation for the results of the Type 2 Diabetes Evaluation of Ranolazine in Subjects With Chronic Stable Angina (TERISA) trial,which showed a greater antianginal effect of RAN in patients with coronary artery disease and diabetes.

Published
2014

28. Poster session 1Cell growth, differentiation and stem cells - Heart72Understanding the metabolism of cardiac progenitor cells: a first step towards controlling their proliferation and differentiation?73Expression of pw1/peg3 identifies a new cardiac adult stem cell population involved in post-myocardial infarction remodeling74Long-term stimulation of iPS-derived cardiomyocytes using optogenetic techniques to promote phenotypic changes in E-C coupling75Benefits of electrical stimulation on differentiation and maturation of cardiomyocytes from human induced pluripotent stem cells76Constitutive beta-adrenoceptor-mediated cAMP production controls spontaneous automaticity of human induced pluripotent stem cell-derived cardiomyocytes77Formation and stability of T-tubules in cardiomyocytes78Identification of miRNAs promoting human cardiomyocyte proliferation by regulating Hippo pathway79A direct comparison of foetal to adult epicardial cell activation reveals distinct differences relevant for the post-injury response80Role of neuropilins in zebrafish heart regeneration81Highly efficient immunomagnetic purification of cardiomyocytes derived from human pluripotent stem cells82Cardiac progenitor cells posses a molecular circadian clock and display large 24-hour oscillations in proliferation and stress tolerance83Influence of sirolimus and everolimus on bone marrow-derived mesenchymal stem cell biology84Endoglin is important for epicardial behaviour following cardiac injuryCell death and apoptosis - Heart87Ultrastructural alterations reflecting Ca2+ handling and cell-to-cell coupling disorders precede occurrence of severe arrhythmias in intact animal heart88Urocortin-1 promotes cardioprotection through ERK1/2 and EPAC pathways: role in apoptosis and necrosis89Expression p38 MAPK and Cas-3 in myocardium LV of rats with experimental heart failure at melatonin and enalapril introductionTranscriptional control and RNA species - Heart92Accumulation of beta-amyloid 1-40 in HF patients: the role of lncRNA BACE1-AS93Role of miR-182 in zebrafish and mouse models of Holt-Oram syndrome94Mir-27 distinctly regulates muscle-enriched transcription factors and growth factors in cardiac and skeletal muscle cells95AF risk factors impair PITX2 expression leading to Wnt-microRNA-ion channel remodelingCytokines and cellular inflammation - Heart98Post-infarct survival depends on the interplay of monocytes, neutrophils and interferon gamma in a mouse model of myocardial Infarction99Inflammatory cd11b/c cells play a protective role in compensated cardiac hypertrophy by promoting an orai3-related pro-survival signal100Anti-inflammatory effects of endothelin receptor blockade in the atrial tissue of spontaneously hypertensive rats101Mesenchymal stromal cells reduce NLRP3 inflammasome activity in Coxsackievirus B3-induced myocarditis102Mesenchymal stromal cells modulate monocytes trafficking in Coxsackievirus B3-induced myocarditis103The impact of regulatory T lymphocytes on long-term mortality in patients with chronic heart failure104Temporal dynamics of dendritic cells after ST-elevation myocardial infarction relate with improvement of myocardial functionGrowth factors and neurohormones - Heart107Preconditioning of hypertrophied heart: miR-1 and IGF-1 crosstalk108Modulation of catecholamine secretion from human adrenal chromaffin cells by manipulation of G protein-coupled receptor kinase-2 activity109Evaluation of cyclic adenosin-3,5- monophosphate and neurohormones in patients with chronic heart failureNitric oxide and reactive oxygen species - Heart112Hydrogen sulfide donor inhibits oxidative and nitrosative stress, cardiohemodynamics disturbances and restores cNOS coupling in old rats113Role and mechanisms of action of aldehydes produced by monoamine oxidase A in cardiomyocyte death and heart failure114Exercise training has contrasting effects in myocardial infarction and pressure-overload due to different endothelial nitric oxide synthase regulation115S-Nitroso Human Serum Albumin dose-dependently leads to vasodilation and alters reactive hyperaemia in coronary arteries of an isolated mouse heart model116Modulating endothelial nitric oxide synthase with folic acid attenuates doxorubicin-induced cardiomyopathy119Effects of long-term very high intensity exercise on aortic structure and function in an animal model120Electron paramagnetic resonance spectroscopy quantification of nitrosylated hemoglobin (HbNO) as an index of vascular nitric oxide bioavailability in vivo121Deletion of repressor activator protein 1 impairs acetylcholine-induced relaxation due to production of reactive oxygen speciesExtracellular matrix and fibrosis - Heart124MicroRNA-19b is associated with myocardial collagen cross-linking in patients with severe aortic stenosis. Potential usefulness as a circulating biomarker125A new ex vivo model to study cardiac fibrosis126Heterogeneity of fibrosis and fibroblast differentiation in the left ventricle after myocardial infarction127Effect of carbohydrate metabolism degree compensation to the level of galectin-3 changes in hypertensive patients with chronic heart failure and type 2 diabetes mellitus128Statin paradox in association with calcification of bicuspid aortic valve interstitial cells129Cardiac function remains impaired despite reversible cardiac fibrosis after healed experimental viral myocarditisIon channels, ion exchangers and cellular electrophysiology - Heart132Identifying a novel role for PMCA1 (Atp2b1) in heart rhythm instability133Mutations of the caveolin-3 gene as a predisposing factor for cardiac arrhythmias134The human sinoatrial node action potential: time for a computational model135iPSC-derived cardiomyocytes as a model to dissect ion current alterations of genetic atrial fibrillation136Postextrasystolic potentiation in healthy and diseased hearts: effects of the site of origin and coupling interval of the preceding extrasystole137Absence of Nav1.8-based (late) sodium current in rabbit cardiomyocytes and human iPSC-CMs138hiPSC-derived cardiomyocytes from Brugada Syndrome patients without identified mutations do not exhibit cellular electrophysiological abnormalitiesMicrocirculation141Atherogenic indices, collagen type IV turnover and the development of microvascular complications- study in diabetics with arterial hypertension142Changes in the microvasculature and blood viscosity in women with rheumatoid arthritis, hypercholesterolemia and hypertensionAtherosclerosis145Shear stress regulates endothelial autophagy: consequences on endothelial senescence and atherogenesis146Obstructive sleep apnea causes aortic remodeling in a chronic murine model147Aortic perivascular adipose tissue displays an aged phenotype in early and late atherosclerosis in ApoE-/- mice148A systematic evaluation of the cellular innate immune response during the process of human atherosclerosis149Inhibition of Coagulation factor Xa increases plaque stability and attenuates the onset and progression of atherosclerotic plaque in apolipoprotein e-deficient mice150Regulatory CD4+ T cells from patients with atherosclerosis display pro-inflammatory skewing and enhanced suppression function151Hypoxia-inducible factor (HIF)-1alpha regulates macrophage energy metabolism by mediating miRNAs152Extracellular S100A4 is a key player of smooth muscle cell phenotypic transition: implications in atherosclerosis153Microparticles of healthy origins improve atherosclerosis-associated endothelial progenitor cell dysfunction via microRNA transfer154Arterial remodeling and metabolism impairment in early atherosclerosis155Role of pannexin1 in atherosclerotic plaque formationCalcium fluxes and excitation-contraction coupling158Amphiphysin II induces tubule formation in cardiac cells159Interleukin 1 beta regulation of connexin 43 in cardiac fibroblasts and the effects of adult cardiac myocyte:fibroblast co-culture on myocyte contraction160T-tubular electrical defects contribute to blunted beta-adrenergic response in heart failure161Beat-to-beat variability of intracellular Ca2+ dynamics of Purkinje cells in the infarct border zone of the mouse heart revealed by rapid-scanning confocal microscopy162The efficacy of late sodium current blockers in hypertrophic cardiomyopathy is dependent on genotype: a study on transgenic mouse models with different mutations163Synthesis of cADPR and NAADP by intracellular CD38 in heart: role in inotropic and arrhythmogenic effects of beta-adrenoceptor signalingContractile apparatus166Towards an engineered heart tissue model of HCM using hiPSC expressing the ACTC E99K mutation167Diastolic mechanical load delays structural and functional deterioration of ultrathin adult heart slices in culture168Structural investigation of the cardiac troponin complex by molecular dynamics169Exercise training restores myocardial and oxidative skeletal muscle function from myocardial infarction heart failure ratsOxygen sensing, ischaemia and reperfusion172A novel antibody specific to full-length stromal derived factor-1 alpha reveals that remote conditioning induces its cleavage by endothelial dipeptidyl peptidase 4173Attenuation of myocardial and vascular arginase activity by vagal nerve stimulation via a mechanism involving alpha-7 nicotinic receptor during cardiac ischemia and reperfusion174Novel nanoparticle-mediated medicine for myocardial ischemia-reperfusion injury simultaneously targeting mitochondrial injury and myocardial inflammation175Acetylcholine plays a key role in myocardial ischaemic preconditioning via recruitment of intrinsic cardiac ganglia176The role of nitric oxide and VEGFR-2 signaling in post ischemic revascularization and muscle recovery in aged hypercholesterolemic mice177Efficacy of ischemic preconditioning to protect the human myocardium: the role of clinical conditions and treatmentsCardiomyopathies and fibrosis180Plakophilin-2 haploinsufficiency leads to impaired canonical Wnt signaling in ARVC patient181Improved technique for customized, easier, safer and more reliable transverse aortic arch banding and debanding in mice as a model of pressure overload hypertrophy182Late sodium current inhibitors for the treatment of inducible obstruction and diastolic dysfunction in hypertrophic cardiomyopathy: a study on human myocardium183Angiotensin II receptor antagonist fimasartan has protective role of left ventricular fibrosis and remodeling in the rat ischemic heart184Role of High-Mobility Group Box 1 (HMGB1) redox state on cardiac fibroblasts activities and heart function after myocardial infarction185Atrial remodeling in hypertrophic cardiomyopathy: insights from mouse models carrying different mutations in cTnT186Electrophysiological abnormalities in ventricular cardiomyocytes from a Maine Coon cat with hypertrophic cardiomyopathy: effects of ranolazine187ZBTB17 is a novel cardiomyopathy candidate gene and regulates autophagy in the heart188Inhibition of SRSF4 in cardiomyocytes induces left ventricular hypertrophy189Molecular characterization of a novel cardiomyopathy related desmin frame shift mutation190Autonomic characterisation of electro-mechanical remodeling in an in-vitro leporine model of heart failure191Modulation of Ca2+-regulatory function by three novel mutations in TNNI3 associated with severe infant restrictive cardiomyopathyAging194The aging impact on cardiac mesenchymal like stromal cells (S+P+)195Reversal of premature aging markers after bariatric surgery196Sex-associated differences in vascular remodeling during aging: role of renin-angiotensin system197Role of the receptor for advanced glycation end-products (RAGE) in age dependent left ventricle dysfunctionsGenetics and epigenetics200hsa-miR-21-5p as a key factor in aortic remodeling during aneurysm formation201Co-inheritance of mutations associated with arrhythmogenic and hypertrophic cardiomyopathy in two Italian families202Lamin a/c hot spot codon 190: form various amino acid substitutions to clinical effects203Treatment with aspirin and atorvastatin attenuate cardiac injury induced by rat chest irradiation: Implication of myocardial miR-1, miR-21, connexin-43 and PKCGenomics, proteomics, metabolomics, lipidomics and glycomics206Differential phosphorylation of desmin at serines 27 and 31 drives the accumulation of preamyloid oligomers in heart failure207Potential role of kinase Akt2 in the reduced recovery of type 2 diabetic hearts subjected to ischemia / reperfusion injury208A proteomics comparison of extracellular matrix remodelling in porcine coronary arteries upon stent implantationMetabolism, diabetes mellitus and obesity211Targeting grk2 as therapeutic strategy for cancer associated to diabetes212Effects of salbutamol on large arterial stiffness in patients with metabolic syndrome213Circulating microRNA-1 and microRNA-133a: potential biomarkers of myocardial steatosis in type 2 diabetes mellitus214Anti-inflammatory nutrigenomic effects of hydroxytyrosol in human adipocytes - protective mechanisms of mediterranean diets in obesity-related inflammation215Alterations in the metal content of different cardiac regions within a rat model of diabetic cardiomyopathyTissue engineering218A novel conductive patch for application in cardiac tissue engineering219Establishment of a simplified and improved workflow from neonatal heart dissociation to cardiomyocyte purification and characterization220Effects of flexible substrate on cardiomyocytes cell culture221Mechanical stretching on cardiac adipose progenitors upregulates sarcomere-related genes

Author

Andre, E, primary, Yaniz-Galende, E, primary, Hamilton, C, primary, Dusting, G J, primary, Hellen, N, primary, Poulet, CE, primary, Diez Cunado, M, primary, Smits, AM, primary, Lowe, V, primary, Eckardt, D, primary, Du Pre, B, primary, Sanz Ruiz, R, primary, Moerkamp, A T, primary, Tribulova, N, primary, Smani, T, primary, Liskova, Y V, primary, Greco, S, primary, Guzzolino, E, primary, Franco, D, primary, Lozano-Velasco, E, primary, Knorr, M, primary, Pavoine, C, primary, Bukowska, A, primary, Van Linthout, S, primary, Miteva, K, primary, Sulzgruber, P, primary, Latet, S C, primary, Portnychenko, A, primary, Cannavo, A, primary, Kamilova, U, primary, Sagach, VF, primary, Santin, Y, primary, Octavia, Y, primary, Haller, PM, primary, Rubies, C, primary, Dei Zotti, F, primary, Wong, KHK, primary, Gonzalez Miqueo, A, primary, Kruithof, BPT, primary, Kadur Nagaraju, C, primary, Shaposhnikova, Y, primary, Songia, P, primary, Lindner, D, primary, Wilson, C, primary, Benzoni, P, primary, Fabbri, A, primary, Campostrini, G, primary, Jorge, E, primary, Casini, S, primary, Mengarelli, I, primary, Nikolov, A, primary, Bublikov, DS, primary, Kheloufi, M, primary, Walker, R E, primary, Van Dijk, RA, primary, Posthuma, JJ, primary, Dumitriu, I E, primary, Karshovska, E, primary, Sakic, A, primary, Alexandru, N, primary, Martin-Lorenzo, M, primary, Molica, F, primary, Taylor, RF, primary, Mcarthur, L, primary, Crocini, C, primary, Matsuyama, T-A, primary, Mazzoni, L, primary, Lin, W K, primary, Owen, TJ, primary, Scigliano, M, primary, Sheehan, A, primary, Bezerra Gurgel, A R, primary, Bromage, DI, primary, Kiss, A, primary, Ikeda, G, primary, Pickard, J M J, primary, Wirth, G, primary, Casos, K, primary, Khudiakov, A, primary, Nistal, JF, primary, Ferrantini, C, primary, Park, S-J, primary, Di Maggio, S, primary, Gentile, F, primary, Dini, L, primary, Buyandelger, B, primary, Larrasa-Alonso, J, primary, Schirmer, I, primary, Chin, SH, primary, Cimiotti, D, primary, Martini, 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Sacconi, L, additional, Tanaka, H, additional, Ishibashi-Ueda, H, additional, Takamatsu, T, additional, Gentile, F, additional, Pioner, JM, additional, Santini, L, additional, Sartiani, L, additional, Bargelli, V, additional, Mugelli, A, additional, Maciejewska, M, additional, Bolton, E L, additional, Wang, Y, additional, O'brien, F, additional, Ruas, M, additional, Lei, M, additional, Sitsapesan, R, additional, Galione, A, additional, Terrar, D A, additional, Smith, JG, additional, Garcia, D, additional, Barriales-Villa, R, additional, Monserrat, L, additional, Marston, SB, additional, Watson, S, additional, Tkach, S, additional, Faggian, G, additional, Terracciano, C M, additional, Perbellini, F, additional, Eiros Zamora, J, additional, Papadaki, M, additional, Messer, A, additional, Marston, S, additional, Gould, I, additional, Johnston, A, additional, Dunne, M, additional, Smith, G, additional, Kemi, OJ, additional, Pillai, M, additional, Davidson, SM, additional, Yellon, DM, additional, Tratsiakovich, Y, additional, Jang, J, additional, Gonon, AT, additional, Pernow, J, additional, Matoba, T, additional, Koga, J, additional, Egashira, K, additional, Burke, N, additional, Korpisalo, P, additional, Hakkarainen, H, additional, Laidinen, S, additional, Yla-Herttuala, S, additional, Ferrer-Curriu, G, additional, Perez, M, additional, Permanyer, E, additional, Blasco-Lucas, A, additional, Gracia, JM, additional, Castro, MA, additional, Barquinero, J, additional, Galinanes, M, additional, Kostina, D, additional, Kostareva, A, additional, Malashicheva, A, additional, Merino, D, additional, Ruiz, L, additional, Gomez, J, additional, Juarez, C, additional, Gil, A, additional, Garcia, R, additional, Hurle, MA, additional, Mazzoni, L, additional, Rossi, A, additional, Tesi, C, additional, Belardinelli, L, additional, Olivotto, I, additional, Eun-Ji, EJ, additional, Lim, B-K, additional, Choi, D-J, additional, Milano, G, additional, Bertolotti, M, additional, De Marchis, F, additional, Zollo, F, additional, Sommariva, E, additional, Capogrossi, M C, additional, Pompilio, G, additional, Bianchi, M E, additional, Raucci, A, additional, Scellini, B, additional, Tardiff, J, additional, Diolaiuti, L, additional, Ferrari, P, additional, Mansfield, C, additional, Luther, P, additional, Knoell, R, additional, Villalba, M, additional, Sanchez-Cabo, F, additional, Lopez-Olaneta, MM, additional, Ortiz-Sanchez, P, additional, Garcia-Pavia, P, additional, Lara-Pezzi, E, additional, Klauke, B, additional, Gerdes, D, additional, Schulz, U, additional, Gummert, J, additional, Milting, H, additional, Wake, E, additional, Kocsis-Fodor, G, additional, Brack, KE, additional, Ng, GA, additional, Smolina, N, additional, Majchrzak, M, additional, Moehner, D, additional, Wies, A, additional, Stehle, R, additional, Pfitzer, G, additional, Muegge, A, additional, Jaquet, K, additional, Maggiorani, D, additional, Lefevre, L, additional, Cussac, D, additional, 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Published
2016
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29. Deranged sodium to sudden death

Author

Clancy, C, Chen Izu, Y, Bers, D, Belardinelli, L, Boyden, P, Csernoch, L, Despa, S, Fermini, B, Hool, L, Izu, L, Kass, R, Lederer, W, Louch, W, Maack, C, Matiazzi, A, Qu, Z, Rajamani, S, Rippinger, C, Sejersted, O, O'Rourke, B, Weiss, J, Varró, A, Zaza, A, ZAZA, ANTONIO, Clancy, C, Chen Izu, Y, Bers, D, Belardinelli, L, Boyden, P, Csernoch, L, Despa, S, Fermini, B, Hool, L, Izu, L, Kass, R, Lederer, W, Louch, W, Maack, C, Matiazzi, A, Qu, Z, Rajamani, S, Rippinger, C, Sejersted, O, O'Rourke, B, Weiss, J, Varró, A, Zaza, A, and ZAZA, ANTONIO

Abstract

In February 2014, a group of scientists convened as part of the University of California Davis Cardiovascular Symposium to bring together experimental and mathematical modelling perspectives and discuss points of consensus and controversy on the topic of sodium in the heart. This paper summarizes the topics of presentation and discussion from the symposium, with a focus on the role of aberrant sodium channels and abnormal sodium homeostasis in cardiac arrhythmias and pharmacotherapy from the subcellular scale to the whole heart. Two following papers focus on Na+ channel structure, function and regulation, and Na+/Ca2+ exchange and Na+/K+ ATPase. The UC Davis Cardiovascular Symposium is a biannual event that aims to bring together leading experts in subfields of cardiovascular biomedicine to focus on topics of importance to the field. The focus on Na+ in the 2014 symposium stemmed from the multitude of recent studies that point to the importance of maintaining Na+ homeostasis in the heart, as disruption of homeostatic processes are increasingly identified in cardiac disease states. Understanding how disruption in cardiac Na+-based processes leads to derangement in multiple cardiac components at the level of the cell and to then connect these perturbations to emergent behaviour in the heart to cause disease is a critical area of research. The ubiquity of disruption of Na+ channels and Na+ homeostasis in cardiac disorders of excitability and mechanics emphasizes the importance of a fundamental understanding of the associated mechanisms and disease processes to ultimately reveal new targets for human therapy.

Published
2015

30. Ранолазин у пациентов с сахарным диабетом 2 типа и стабильной стенокардией. Результаты рандомизированного клинического исследования Terisa (Type 2 diabetes evaluation of ranolazine in subjects with chronic stable angina исследование ранолазина у больных сахарным диабетом 2 типа и стабильной стенокардией)

Author

Kosiborod, M., Arnold, S., Spertus, J., Mcguire, D., Li, Y., Yue, P., Ben-yehuda, O., Katz, A., Jones, Ph, Olmsted, A., Belardinelli, L., and Chaitman, B.

Subjects
КЛИНИЧЕСКИЕ ИСПЫТАНИЯ,ИШЕМИЧЕСКАЯ БОЛЕЗНЬ СЕРДЦА,САХАРНЫЙ ДИАБЕТ,РАНОЛАЗИН,СТАБИЛЬНАЯ СТЕНОКАРДИЯ
Abstract

Цель. Изучить влияние терапии ранолазином по сравнению с плацебо на еженедельную частоту приступов стенокардии и сублингвальное использование нитроглицерина у больных сахарным диабетом (СД) 2 типа и стабильной стенокардией, которая сохранялась, несмотря на лечение одним или двумя антиангинальными препаратами. Введение. У больных сахарным диабетом отмечается более выраженное поражение коронарных артерий, чем у пациентов без диабета, и часто наблюдается стенокардия. Применение ранолазина не только эффективно для лечения стенокардии, но и может улучшить гликемический контроль у больных СД, обеспечивая тем самым несколько потенциальных преимуществ в этой группе больных высокого риска. Мы провели рандомизированное исследование, чтобы оценить антиангинальный эффект ранолазина у больных СД и стабильной стенокардией. Материал и методы. Проведенное исследование TERISA (Type 2 Diabetes Evaluation of Ranolazine in Subjects With Chronic Stable Angina исследование Ранолазина у больных сахарным диабетом 2 типа и стабильной стенокардией) было международным, рандомизированным, двойным слепым испытанием ранолазина по сравнению с плацебо у пациентов с сахарным диабетом и стабильной стенокардией, которые получали один или два антиангинальных препарата. После 4-нед «вводного» (run-in) периода простого слепого приема плацебо пациенты были рандомизировано распределены в группы двойного слепого лечения ранолазином (с целевой дозой 1000 мг 2 раза в день), либо плацебо в течение 8 нед. Приступы стенокардии и применение нитроглицерина регистрировались в электронном дневнике каждый день. Первичным исходом была средняя частота приступов стенокардии в неделю на протяжении последних 6 нед исследования. Результаты. Всего 949 пациентов в 104 центрах из 14 стран были рандомизировано распределены в группы лечения. Средний возраст больных был 64 года, мужчин было 61%, средняя длительность сахарного диабета у больных составляла 7,5 лет, а средний исходный уровень HbA^bm 7,3%. Полнота регистрации данных в электронных дневниках была 98% в обеих группах. Средняя частота приступов стенокардии в нед при лечении ранолазином была достоверно ниже по сравнению с частотой в группе плацебо (3,8 эпизодов [95% доверительный интервал (95%ДИ) 3,6-4,1 ] против 4,3 эпизодов [95%ДИ 4,0-4,5], р=0,008), так же, как и среднее еженедельное количество принятых сублингвально доз нитроглицерина (1,7 доз [95%ДИ 1,6-1,9] против 2,1 доз [95%ДИ 1,9-2,3], р =0,003). Частота серьезных нежелательных явлений в группах лечения не различалась. Заключение. У пациентов с сахарным диабетом и стабильной стенокардией, сохранявшейся, несмотря на лечение одним или двумя антиангинальными препаратами, ранолазин уменьшал частоту стенокардии и сублингвального применения нитроглицерина и хорошо переносился.

Published
2013

31. Robust anti-arrhythmic efficacy of verapamil and flunarizine against dofetilide-induced TdP arrhythmias is based upon a shared and a different mode of action

Author

Oros, A, Houtman, MJ, Neco, P, Gomez, AM, Rajamani, S, Oosterhoff, P, Attevelt, NJ, Beekman, JD, van der Heyden, MAG, Ver Donck, L, Belardinelli, L, Richard, S, Antoons, G, and Vos, MA

Subjects
Sulfonamides, Lidocaine, Research Papers, Cell Line, Mice, Dogs, Verapamil, Torsades de Pointes, Phenethylamines, Animals, Humans, Myocytes, Cardiac, Calcium Signaling, Anti-Arrhythmia Agents, Flunarizine
Abstract

The high predisposition to Torsade de Pointes (TdP) in dogs with chronic AV-block (CAVB) is well documented. The anti-arrhythmic efficacy and mode of action of Ca(2+) channel antagonists, flunarizine and verapamil against TdP were investigated.Mongrel dogs with CAVB were selected based on the inducibility of TdP with dofetilide. The effects of flunarizine and verapamil were assessed after TdP and in different experiments to prevent dofetilide-induced TdP. Electrocardiogram and ventricular monophasic action potentials were recorded. Electrophysiological parameters and short-term variability of repolarization (STV) were determined. In vitro, flunarizine and verapamil were added to determine their effect on (i) dofetilide-induced early after depolarizations (EADs) in canine ventricular myocytes (VM); (ii) diastolic Ca(2+) sparks in RyR2(R4496+/+) mouse myocytes; and (iii) peak and late I(Na) in SCN5A-HEK 293 cells.Dofetilide increased STV prior to TdP and in VM prior to EADs. Both flunarizine and verapamil completely suppressed TdP and reversed STV to baseline values. Complete prevention of TdP was achieved with both drugs, accompanied by the prevention of an increase in STV. Suppression of EADs was confirmed after flunarizine. Only flunarizine blocked late I(Na). Ca(2+) sparks were reduced with verapamil.Robust anti-arrhythmic efficacy was seen with both Ca(2+) channel antagonists. Their divergent electrophysiological actions may be related to different additional effects of the two drugs.

Published
2010

32. Inhibition of late sodium current to reduce electrical and mechanical dysfunction of ischaemic myocardium

Author

Shryock, J C and Belardinelli, L

Subjects
Myocardial Ischemia, Reviews, Piperazines, Sodium Channels, Electrophysiology, Drug Delivery Systems, Ranolazine, Potassium Channel Blockers, Animals, Humans, Acetanilides, Drug Therapy, Combination, Controlled Clinical Trials as Topic, Enzyme Inhibitors, Sodium Channel Blockers
Abstract

The sodium current in the heart is not a single current with a mono-exponential decay but rather a mixture of currents with different kinetics. It is not clear whether these arise from distinct populations of channels, or from modulation of a single population. A very slowly inactivating component, [(INa(P))] I(Na(P)) is usually about 1% of the size of the peak transient current [I(Na(T))], but is enhanced by hypoxia. It contributes to Na(+) loading and cellular damage in ischaemia and re-perfusion, and perhaps to ischaemic arrhythmias. Class I antiarrhythmic agents such as flecainide, lidocaine and mexiletine generally block I(NA(P)) more potently than block of I(Na(T)) and have been used clinically to treat LQT3 syndrome, which arises because mutations in SCN5A produce defective inactivation of the cardiac sodium channel. The same approach may be useful in some pathological situations, such as ischaemic arrhythmias or diastolic dysfunction, and newer agents are being developed with this goal. For example, ranolazine blocks I(Na(P)) about 10 times more potently than I(Na(T)) and has shown promise in the treatment of angina. Alternatively, the combination of I(Na(P)) block with K(+) channel block may provide protection from the induction of Torsades de Pointe when these agents are used to treat atrial arrhythmias (eg Vernakalant). In all of these scenarios, an understanding of the role of I(Na(P)) in cardiac pathophysiology, the mechanisms by which it may affect cardiac electrophysiology and the potential side effects of blocking I(Na(P)) in the heart and elsewhere will become increasingly important.

Published
2007

37. Proliferation, migration, and ERK activation in human retinal endothelial cells through A(2B) adenosine receptor stimulation

Author

Grant, M. B., Margaret Davis, Caballero, S., Feoktistov, I., Biaggioni, I., and Belardinelli, L.

Subjects
Dose-Response Relationship, Drug, Vasodilator Agents, Blotting, Western, Receptors, Purinergic P1, Retinal Vessels, Cell Count, Adenosine-5'-(N-ethylcarboxamide), Receptor, Adenosine A2B, Capillaries, Enzyme Activation, Purinergic P1 Receptor Antagonists, Cell Movement, Humans, Endothelium, Vascular, Enzyme Inhibitors, Mitogen-Activated Protein Kinases, Cyclic AMP Response Element-Binding Protein, Cell Division, Cells, Cultured, Signal Transduction
Abstract

The nucleoside adenosine has been implicated in angiogenesis. A previous study demonstrated that activation of the A(2B) adenosine receptor (AdoR) increases cAMP accumulation, cell proliferation, and VEGF expression in human retinal endothelial cells (HRECs). In the present study, the role of this receptor was further characterized by examination of the effects of the selective A(2B) AdoR antagonists 3-N-propylxanthine (enprofylline) and 3-isobutyl-8-pyrrolidinoxanthine (IPDX) on AdoR-mediated HREC proliferation, capillary tube formation, and signal-transduction pathways.HRECs were exposed to the adenosine analogue 5'-N-ethylcarboxamido-adenosine (NECA) in the absence or presence of AdoR antagonists. Migration was measured using Boyden chambers. Proliferation was assessed by counting cells. Western analysis was used to assess extracellular signal-related kinase (ERK) and cAMP response element-binding protein (CREB) in cell lysates. The effect of AdoR activation on tube formation was studied using cells grown on a synthetic basement membrane matrix.NECA induced proliferation in a concentration-dependent manner that was inhibited by enprofylline and IPDX. NECA stimulated chemotaxis in a concentration-dependent manner that was also blocked by both A(2B) AdoR antagonists. NECA activated ERK and CREB in HRECs. Both A(2B) AdoR antagonists diminished activation of ERK by NECA exposure. ERK activation was also blocked by the ERK-mitogen-activated protein kinase (MAPK) inhibitor PD98059, but not by the protein kinase A (PKA) inhibitor H-89. CREB activation was blocked by H-89, but not by PD98059, suggesting that ERK activation is independent of PKA. NECA enhanced tube formation on the matrix, whereas both A(2B) AdoR antagonists attenuated this effect.The selective A(2B) AdoR antagonists, enprofylline and IPDX, inhibited NECA-stimulated proliferation, ERK activation, cell migration, and capillary tube formation. A(2B) AdoR inhibition may offer a way to inhibit retinal angiogenesis and provide a novel therapeutic approach to treatment of diseases associated with aberrant neovascularization, such as diabetic retinopathy and retinopathy of prematurity.

Published
2001

40. Relationship between nonsustained ventricular tachycardia after non-ST-elevation acute coronary syndrome and sudden cardiac death: observations from the metabolic efficiency with ranolazine for less ischemia in non-ST-elevation acute coronary syndrome-thrombolysis in myocardial infarction 36 (MERLIN-TIMI 36) randomized controlled trial.

Author

Scirica, B.M., Braunwald, E., Belardinelli, L., Hedgepeth, C.M., Spinar, J., Wang, W., Qin, J., Karwatowska-Prokopczuk, E., Verheugt, F.W.A., Morrow, D.A., Scirica, B.M., Braunwald, E., Belardinelli, L., Hedgepeth, C.M., Spinar, J., Wang, W., Qin, J., Karwatowska-Prokopczuk, E., Verheugt, F.W.A., and Morrow, D.A.

Abstract

Contains fulltext : 89426.pdf (publisher's version ) (Closed access), BACKGROUND: Most studies examining the relationship between ventricular tachycardia (VT) after acute coronary syndrome and sudden cardiac death (SCD) were performed before widespread use of reperfusion, revascularization, or contemporary medical therapy and were limited to ST-elevation myocardial infarction. The incidence and prognostic implications of VT in patients with non-ST-elevation acute coronary syndrome receiving contemporary care have not been examined. METHODS AND RESULTS: The Metabolic Efficiency With Ranolazine for Less Ischemia in Non-ST-Elevation Acute Coronary Syndrome-Thrombolysis in Myocardial Infarction 36 (MERLIN-TIMI 36) trial randomized 6560 patients hospitalized with a non-ST-elevation acute coronary syndrome to ranolazine or placebo in addition to standard therapy. Continuous ECG recording was performed for the first 7 days after randomization and evaluated in a blinded core laboratory. SCD (n=121) was assessed over a median follow-up of 1 year. A total of 6345 patients (97%) had continuous ECG recordings evaluable for analysis. Compared with patients with no VT (n=2764), there was no increased risk of SCD in patients with only ventricular triplets (n=1978, 31.2%) (1.4% versus 1.2%); however, the risk of SCD was significantly greater in patients with VT lasting 4 to 7 beats (n=1172, 18.5%) (SCD, 2.9%; adjusted hazard ratio, 2.3; P<0.001) and in patients with VT lasting at least 8 beats (n=431, 6.8%) (SCD, 4.3%; adjusted hazard ratio, 2.8; P=0.001). This effect was independent of baseline characteristics and ejection fraction. VT occurring within the first 48 hours after admission was not associated with SCD. CONCLUSIONS: Nonsustained VT is common after admission for non-ST-elevation acute coronary syndrome, and even short episodes of VT lasting 4 to 7 beats are independently associated with the risk of SCD over the subsequent year. Clinical Trial Registration- URL: http://www.clinicaltrials.gov. Unique identifier: NCT00099788.

Published
2010

41. Pathophysiology and pharmacology of the cardiac 'late sodium current'

Author

Zaza, A, Belardinelli, L, Shryock, J, ZAZA, ANTONIO, Shryock, JC, Zaza, A, Belardinelli, L, Shryock, J, ZAZA, ANTONIO, and Shryock, JC

Abstract

The "late sodium current" (INaL) is a sustained component of the fast Na+ current of cardiac myocytes and neurons. As recently appreciated, common neurological and cardiac conditions are associated with abnormal INaL enhancement, which may contribute to the pathogenesis of both electrical and contractile dysfunction. For this reason, INaL has become an appealing pharmacological target, with a potentially broad range of therapeutic indications. The recent approval by the FDA of an INaL blocker (ranolazine) for clinical use justifies the increased interest in INaL as a pathogenic mechanism and the rapid evolution of the information concerning it. The review focuses on cardiac aspects of INaL enhancement; it deals with the origin of INaL, with its pathophysiological role and with the consequences of its pharmacological modulation. Both basic aspects and clinical evidence are discussed. © 2008 Elsevier Inc. All rights reserved.

Published
2008

49. Effect of ranolazine, an antianginal agent with novel electrophysiological properties, on the incidence of arrhythmias in patients with non ST-segment elevation acute coronary syndrome: results from the Metabolic Efficiency With Ranolazine for Less Ischemia in Non ST-Elevation Acute Coronary Syndrome Thrombolysis in Myocardial Infarction 36 (MERLIN-TIMI 36) randomized controlled trial.

Author

Scirica, B.M., Morrow, D.A., Hod, H., Murphy, S.A., Belardinelli, L., Hedgepeth, C.M., Molhoek, P., Verheugt, F.W.A., Gersh, B.J., McCabe, C.H., Braunwald, E., Scirica, B.M., Morrow, D.A., Hod, H., Murphy, S.A., Belardinelli, L., Hedgepeth, C.M., Molhoek, P., Verheugt, F.W.A., Gersh, B.J., McCabe, C.H., and Braunwald, E.

Abstract

Contains fulltext : 52580.pdf (publisher's version ) (Closed access), BACKGROUND: Ranolazine, a piperazine derivative, reduces ischemia via inhibition of the late phase of the inward sodium current (late I(Na)) during cardiac repolarization, with a consequent reduction in intracellular sodium and calcium overload. Increased intracellular calcium leads to both mechanical dysfunction and electric instability. Ranolazine reduces proarrhythmic substrate and triggers such as early afterdepolarization in experimental models. However, the potential antiarrhythmic actions of ranolazine have yet to be demonstrated in humans. METHODS AND RESULTS: The Metabolic Efficiency With Ranolazine for Less Ischemia in Non-ST-Elevation Acute Coronary Syndrome (MERLIN)-Thrombolysis in Myocardial Infarction (TIMI) 36 (MERLIN-TIMI 36) trial randomized 6560 patients hospitalized with a non-ST-elevation acute coronary syndrome to ranolazine or placebo in addition to standard therapy. Continuous ECG (Holter) recording was performed for the first 7 days after randomization. A prespecified set of arrhythmias were evaluated by a core laboratory blinded to treatment and outcomes. Of the 6560 patients in MERLIN-TIMI 36, 6351 (97%) had continuous ECG recordings that could be evaluated for arrhythmia analysis. Treatment with ranolazine resulted in significantly lower incidences of arrhythmias. Specifically, fewer patients had an episode of ventricular tachycardia lasting > or = 8 beats (166 [5.3%] versus 265 [8.3%]; P<0.001), supraventricular tachycardia (1413 [44.7%] versus 1752 [55.0%]; P<0.001), or new-onset atrial fibrillation (55 [1.7%] versus 75 [2.4%]; P=0.08). In addition, pauses > or = 3 seconds were less frequent with ranolazine (97 [3.1%] versus 136 [4.3%]; P=0.01). CONCLUSIONS: Ranolazine, an inhibitor of late I(Na), appears to have antiarrhythmic effects as assessed by continuous ECG monitoring of patients in the first week after admission for acute coronary syndrome. Studies specifically designed to evaluate the potential role of ranolazine as an antiarrh

Published
2007

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