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2. Rationale, design, implementation, and baseline characteristics of patients in the dig trial: A large, simple, long-term trial to evaluate the effect of digitalis on mortality in heart failure
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Abernathy, GT, Abrams, J, Akhtar, S, Albitar, I, Amidi, M, Anand, IS, Arnold, JMO, Ashton, T, Aubrey, B, Auger, P, Babb, J, Baigrie, R, Baird, MG, Baitz, T, Barber, NC, Barbour, DJ, Barr, DM, Basu, AK, Baughman, KL, Beckham, V, BekheitSaad, S, Berkson, DM, Bertoglio, M, Bessoudo, R, Beaudoin, J, Bhaskar, G, Binder, A, Bloomfield, D, Bodine, K, Boehmer, JP, Borgersen, K, Borts, D, Bouchard, G, Bourassa, MG, Boutros, G, Bozek, B, Brisbin, D, Brophy, J, Brossoit, R, Brown, E, Brown, J, Bruinsma, N, Burton, G, Cameron, A, Campbell, R, Campeau, J, Campos, EE, Cardello, FP, Carter, RP, Chan, YK, Charles, FR, Chaudhry, MA, Chiaramida, A, Chiaramida, S, Chohan, A, Christie, LG, Clemson, BS, Collin, R, Cook, TH, Copen, DL, Cossett, J, Costantino, T, Crawford, MH, Croke, RP, Crowell, R, DAmours, G, Dagenais, GR, Danisa, K, Davidson, S, Davies, ML, Davies, R, Davies, RA, DeLarochelliere, R, DeLeon, AC, Delage, F, Denes, P, Dennish, GW, Denny, DM, DeVilla, MA, DeYoung, JP, Dhurandhar, RW, DibnerDunlap, M, Dodek, A, Doherty, JE, Dominguez, J, Dubbin, J, Dufton, J, Effron, MB, ElSherif, N, Eladasari, B, Fly, D, Ericson, K, Fahrenholtz, D, Fast, A, Fell, DA, Fishman, S, Fitchett, D, Fleg, JL, Flint, E, Folger, JS, Folkins, D, Forker, AD, Fowles, RE, Fraker, TD, Francis, G, Frerking, TR, Friesinger, GC, Fulop, JC, Gagnon, J, Gamble, L, Ganjavi, F, Garrou, BW, Gervais, PB, Gheorghiade, M, Gilbert, L, Gillie, E, Glatter, TR, Godley, ML, Goeres, M, Goldberger, MH, Gollapudi, A, Goode, JE, Goodman, LS, Gordon, R, Gossard, D, Gosselin, G, Goulet, C, Grant, C, Graettinger, WF, Greene, JG, Greenwood, PV, Gregoratos, G, Gregory, JJ, Groden, DL, Grover, J, Gudapati, R, Guess, MA, Gupta, SC, Habib, N, Hack, I, Hamilton, WP, Hankey, TL, Hanna, M, Harper, D, Harris, DE, Hassapoyannes, CA, Hatheway, RJ, Heinsimer, J, Pequignot, MH, Heiselman, DE, Hess, AR, Hickner, J, Hickey, JE, Higgins, T, Higginson, L, Hill, L, Hobbs, RE, Honos, G, Horner, BA, Horwitz, L, Hsieh, A, Hsueh, JT, Hubbard, J, Hughes, DF, Hui, W, Imrie, JR, Jacobs, MH, Jarmukli, N, Johnson, TH, Johnstone, D, Jutila, CK, Kadri, N, Kahl, FR, Kaimal, PK, Karnegis, J, Kay, R, Kelly, KJ, Kenefick, G, Kennelly, BM, Kent, E, Khan, AH, Khanijo, V, Khouri, M, Kinloch, D, Kirlin, PC, Kiwan, GS, Kline, MD, Kohn, RM, Koilpillai, C, Kornder, JM, Kouz, S, Kumar, VA, Kumar, U, Kuntz, A, Kuritzky, RA, Kuruvilla, G, Kwok, KK, Lader, E, Laforest, M, LaForge, D, Lalonde, G, Lalonde, L, Lang, RM, Latour, Y, Lawal, O, LeBlanc, MH, Lee, AB, Lee, RW, Legault, C, Lemay, M, Lenis, JHF, Lepage, S, Letarte, P, Levesque, C, LevinoffRoth, SN, Lewis, BK, Lipshutz, H, Loungani, RR, Lowery, ML, Lubell, DL, Lucariello, R, LugoRodriguez, JE, Lui, C, Lutterodt, AT, Lutz, L, Machel, T, Macina, G, MacLellan, K, Magnan, O, Mansuri, M, Manyari, DE, Mallis, GI, Marr, D, Mast, DJ, Mathew, J, McBarron, FD, McIntyre, KM, McLean, RW, McMahon, DP, Mercier, M, Methe, M, Miller, AB, Minkowitz, J, Milton, JR, Mizgala, HF, Mohanty, PK, Mohiuddin, S, Montero, A, Mookherjee, S, Morris, A, Morris, L, Morrison, J, Moten, M, Nafziger, A, Nair, PH, Nawaz, S, Neiman, JC, Nutting, P, NguyenPho, HT, OBrien, TK, OKelly, RL, OReilly, MV, Okerson, D, Patel, G, Pande, PN, Papa, LA, Patrick, L, Payne, RM, Perry, G, Philbin, EF, Pierpont, G, Pitt, WA, Poirier, C, Pollak, EM, Popio, K, Poulin, JF, Probst, PA, Pruneau, G, Pu, C, Puram, BS, Putatunda, B, Quinn, B, Rabkin, SW, Racine, N, Raco, DL, Radant, L, Radford, MJ, Radwany, S, Rajachar, M, Ramanathan, KB, Rashkow, A, Rausch, DC, Read, L, Reddy, KR, Reid, R, Rich, MW, Ricci, AJ, Richman, HG, Riley, A, Rim, DA, Rinne, C, Roberge, G, Roberts, DK, Robinson, V, Rodeheffer, RT, Rosenstein, R, Roth, DL, Rothbart, R, Rouleau, JL, Ruble, P, Sacco, J, Safford, RE, Salmon, D, Sahay, BM, Sarma, RJ, Sayeed, MAR, Schick, EC, Schroeder, GS, Seifert, M, Senaratne, MPJ, Sestier, F, Shah, A, Shanes, JG, Sheesley, K, Silverman, A, Shiva, T, Shrestha, DD, Silver, MA, Silverberg, L, Simard, L, Singh, BN, Small, RS, Smith, MR, Smith, S, Sochowski, RA, Southern, RF, Sridharan, MR, StHilaire, R, Stein, M, Stewart, JW, Stillabower, ME, Sullivan, BHM, Sturrock, WA, Sussex, BA, Swan, J, Swenson, L, Talbot, P, Talibi, T, Tamilia, M, Tan, A, Tanser, PH, Tarry, L, Teo, KK, Thadani, U, Thagirisa, S, Thompson, B, Thornton, R, Timmis, GC, Tobin, M, Tommaso, C, Toren, M, Tsuyuki, R, Turek, M, Utley, K, Vanderbush, EJ, VanVoorhees, L, Ventura, H, Vertes, G, Vizel, S, Wagner, KR, Wagner, S, Weeks, A, Weingert, ME, Weinstein, C, Weiss, MM, Weiss, R, Wickemeyer, W, Wielgoz, A, Willens, HJ, Williams, WL, Wong, D, Yarows, SA, Yao, L, Shalev, Y, Young, JB, Yousefian, M, Zajac, EJ, Zatuchni, J, Ziperman, DB, Zoble, RG, Zoneraich, S, Gorlin, R, Sleight, P, Cohn, JN, Collins, R, Deykin, D, Hennekens, C, Kjekshus, J, Smith, TW, Tognoni, G, Collins, JF, Williford, WO, Fye, C, Sather, R, Jolly, MK, Held, CP, Verter, J, Yusuf, S, Egan, D, Garg, R, Johnstone, DE, Montague, T, Bristow, D, Engelhardt, HT, Gent, M, Hood, WB, Jones, S, Meier, P, Pitt, B, Waters, D, Baker, A, Barnhill, S, Carew, B, Hagar, S, Liuni, C, Martin, S, Miles, R, Arthur, MM, Feldbush, MW, Highfield, DA, Hobbins, TE, Kurz, R, Leviton, SP, Libonati, JP, Moore, M, Perez, E, Mills, P, Geller, N, Hunsberger, S, Gold, J, Huang, PC, Burns, A, Caleb, H, Cline, DR, Harris, S, Hockenbrock, R, Horney, RA, Jadwin, LM, King, J, Sexton, P, Spence, ME, Chacon, F, Gagne, W, Maple, S, and Martinez, G
- Subjects
Heart Failure ,Male ,Pharmacology ,Digoxin ,Treatment Outcome ,Patient Selection ,Digitalis Glycosides ,Humans ,Multicenter Studies as Topic ,Female ,Middle Aged ,Aged ,Randomized Controlled Trials as Topic - Abstract
This article provides a detailed overview of the rationale for key aspects of the protocol of the Digitalis Investigation Group (DIG) trial. It also highlights unusual aspects of the study implementation and the baseline characteristics. The DIG trial is a large, simple, international placebo-controlled trial whose primary objective is to determine the effect of digoxin on all cause mortality in patients with clinical heart failure who are in sinus rhythm and whose ejection fraction isor = 0.45. An ancillary study examines the effect in those with an ejection fraction0.45. Key aspects of the trial include the simplicity of the design, broad eligibility criteria, essential data collection, and inclusion of various types of centers. A total of 302 centers in the United States and Canada enrolled 7788 patients between February 1991 and September 1993. Follow-up continued until December 1995 with the results available in Spring 1996.
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- 1996
3. Measurement of the bottom-strange meson mixing phase in the full CDF data set
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Aaltonen, T., Alvarez, González, Amerio, B., Amidei, S., Anastassov, D., Annovi, A., Antos, A., Apollinari, J., Appel, G., J. A., Arisawa, Artikov, T., Asaadi, A., Ashmanskas, J., Auerbach, W., Aurisano, B., Azfar, A., Badgett, F., Bae, W., Barbaro, Galtieri, Barnes, A., V. E., Barnett, B. A., Barria, Bartos, P., Bauce, P., Bedeschi, M., Behari, F., Bellettini, S., Bellinger, G., Benjamin, J., Beretvas, D., Bhatti, A., Bisello, A., Bizjak, D., Bland, I., K. R., Blumenfeld, Bocci, B., Bodek, A., Bortoletto, A., Boudreau, D., Boveia, J., Brigliadori, A., Bromberg, L., Brucken, C., Budagov, E., Budd, J., H. S., Burkett, Busetto, K., Bussey, G., Buzatu, P., Calamba, A., Calancha, A., Camarda, C., Campanelli, S., Campbell, M., Canelli, M., Carls, F., Carlsmith, B., Carosi, D., Carrillo, R., Carron, S., Casal, S., Casarsa, B., Castro, M., Catastini, A., Cauz, P., Cavaliere, D., Cavalli, Sforza, Cerri, M., Cerrito, A., Chen, L., Y. C., Chertok, Chiarelli, M., Chlachidze, G., Chlebana, G., Cho, F., Chokheli, K., Chung, D., W. H., Chung, Y. S., Ciocci, M. A., Clark, Clarke, A., Compostella, C., Convery, G., M. E., Conway, Corbo, J., Cordelli, M., Cox, M., C. A., Cox, D. J., Crescioli, Cuevas, F., Culbertson, J., Dagenhart, R., D'Ascenzo, D., Datta, N., Barbaro, De, Dell'Orso, Mauro, Demortier, M., Deninno, L., Devoto, M., D'Errico, F., Canto, Di, Ruzza, Di, Dittmann, B., J. R., D'Onofrio, Donati, Simone, Dong, P., Dorigo, M., Dorigo, T., Ebina, K., Elagin, A., Eppig, A., Erbacher, R., Errede, S., Ershaidat, N., Eusebi, R., Farrington, S., Feindt, M., Fernandez, J. P., Field, R., Flanagan, G., Forrest, R., Frank, M. J., Franklin, M., Freeman, J. C., Funakoshi, Y., Furic, I., Gallinaro, M., Garcia, J. E., Garfinkel, A. F., Garosi, P., Gerberich, H., Gerchtein, E., Giagu, S., Giakoumopoulou, V., Giannetti, P., Gibson, K., Ginsburg, C. M., Giokaris, N., Giromini, P., Giurgiu, G., Glagolev, V., Glenzinski, D., Gold, M., Goldin, D., Goldschmidt, N., Golossanov, A., Gomez, G., Gomez, Ceballos, Goncharov, G., González, M., Gorelov, O., Goshaw, I., A. T., Goulianos, Grillo, K., Grinstein, L., Grosso, Pilcher, Group, C., R. C., Guimaraes Da Costa, Hahn, J., S. R., Halkiadakis, Hamaguchi, E., Han, A., J. Y., Happacher, Hara, F., Hare, K., Hare, D., Harr, M., R. F., Hatakeyama, Hays, K., Heck, C., Heinrich, M., Herndon, J., Hewamanage, M., Hocker, S., Hopkins, A., Horn, W., Hou, D., Hughes, S., R. E., Hurwitz, Husemann, M., Hussain, U., Hussein, N., Huston, M., Introzzi, J., Iori, G., Ivanov, M., James, A., Jang, E., Jayatilaka, D., Jeon, B., E. J., Jindariani, Jones, S., Joo, M., K. K., Jun, S. Y., Junk, T. R., Kamon, Karchin, T., P. E., Kasmi, Kato, A., Ketchum, Y., Keung, W., Khotilovich, J., Kilminster, V., Kim, B., D. H., Kim, H. S., Kim, J. E., Kim, M. J., Kim, S. B., Kim, S. H., Kim, Y. K., Kim, Y. J., Kimura, Kirby, N., Klimenko, M., Knoepfel, S., Kondo, K., Kong, K., D. J., Konigsberg, Kotwal, J., A. V., Kreps, Kroll, M., Krop, J., Kruse, D., Krutelyov, M., Kuhr, V., Kurata, T., Kwang, M., Laasanen, S., A. T., Lami, Lammel, S., Lancaster, S., Lander, M., R. L., Lannon, Lath, K., Latino, A., Lecompte, G., Lee, T., Lee, E., H. S., Lee, J. S., Lee, S. W., Leo, Leone, S., Lewis, S., J. D., Limosani, Lin, A., C. J., Lindgren, Lipeles, M., Lister, E., Litvintsev, A., D. O., Liu, Liu, C., Liu, H., Liu, Q., Lockwitz, T., Loginov, S., Lucchesi, A., Lueck, D., Lujan, J., Lukens, P., Lungu, P., Lys, G., Lysak, J., Madrak, R., Maeshima, R., Maestro, K., Malik, P., Manca, S., Manousakis, Katsikakis, Margaroli, A., Marino, F., Martínez, C., Mastrandrea, M., Matera, P., Mattson, K., M. E., Mazzacane, Mazzanti, A., Mcfarland, P., K. S., Mcintyre, Mcnulty, P., Mehta, R., Mehtala, A., Mesropian, P., Miao, C., Mietlicki, T., Mitra, D., Miyake, A., Moed, H., Moggi, S., Mondragon, N., M. N., Moon, C. S., Moore, Morello, R., M. J., Morlock, Movilla, Fernandez, Mukherjee, P., Muller, A., Murat, T., Mussini, P., Nachtman, M., Nagai, J., Naganoma, Y., Nakano, J., Napier, I., Nett, A., Neu, J., Neubauer, C., M. S., Nielsen, Nodulman, J., Noh, L., S. Y., Norniella, Oakes, O., Oh, L., S. H., Oh, Y. D., Oksuzian, Okusawa, I., Orava, T., Ortolan, R., Pagan, Griso, Pagliarone, S., Palencia, C., Papadimitriou, E., Paramonov, V., A. A., Patrick, Pauletta, J., Paulini, G., Paus, M., Pellett, C., D. E., Penzo, Phillips, A., T. J., Piacentino, Pianori, G., Pilot, E., Pitts, J., Plager, K., Pondrom, C., Poprocki, L., Potamianos, S., Prokoshin, K., Pranko, F., Ptohos, A., Punzi, Giovanni, Rahaman, G., Ramakrishnan, A., Ranjan, V., Redondo, N., Renton, I., Rescigno, P., Riddick, M., Rimondi, T., Ristori, F., Robson, L., Rodrigo, A., Rodriguez, T., Rogers, T., Rolli, E., Roser, S., Ruffini, R., Ruiz, F., Russ, A., Rusu, J., Safonov, V., Sakumoto, A., W. K., Sakurai, Santi, Y., Sato, L., Saveliev, K., Savoy, Navarro, Schlabach, A., Schmidt, P., Schmidt, A., E. E., Schwarz, Scodellaro, T., Scribano, L., Scuri, A., Seidel, F., Seiya, S., Semenov, Y., Sforza, A., Shalhout, F., S. Z., Shears, Shepard, T., P. F., Shimojima, Shochet, M., Shreyber, Tecker, Simonenko, I., Sinervo, A., Sliwa, P., Smith, K., J. R., Snider, F. D., Soha, Sorin, A., Song, V., Squillacioti, H., Stancari, P., Denis, S. t., Stelzer, R., Stelzer, Chilton, Stentz, O., Strologas, D., Strycker, J., G. L., Sudo, Sukhanov, Y., Suslov, A., Takemasa, I., Takeuchi, K., Tang, Y., Tecchio, J., Teng, M., P. K., Thom, Thome, J., Thompson, J., G. A., Thomson, Toback, E., Tokar, D., Tollefson, S., Tomura, K., Tonelli, T., Torre, D., Torretta, S., Totaro, D., Trovato, P., Ukegawa, M., Uozumi, F., Varganov, S., Vázquez, A., Velev, F., Vellidis, G., Vidal, C., Vila, M., Vilar, I., Vizán, R., Vogel, J., Volpi, M., Wagner, G., Wagner, P., R. L., Wakisaka, Wallny, T., Wang, R., S. M., Warburton, Waters, A., Wester, D., W. C., Whiteson, Wicklund, D., A. B., Wicklund, Wilbur, E., Wick, S., Williams, F., H. H., Wilson, J. S., Wilson, Winer, P., B. L., Wittich, Wolbers, P., Wolfe, S., Wright, H., Wu, T., Wu, X., Yamamoto, Z., Yamato, K., Yang, D., Yang, T., U. K., Yang, Y. C., Yao, W. M., Yeh, G. P., Yi, Yoh, K., Yorita, J., Yoshida, K., Yu, T., G. B., Yu, Yu, I., S. S., Yun, J. 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L., Wagner, T., Wakisaka, R., Wallny, S. M., Wang, A., Warburton, D., Water, W. C., Wester, D., Whiteson, A. B., Wicklund, E., Wicklund, S., Wilbur, F., Wick, H. H., William, J. S., Wilson, P., Wilson, B. L., Winer, P., Wittich, S., Wolber, H., Wolfe, T., Wright, X., Wu, Z., Wu, K., Yamamoto, D., Yamato, T., Yang, U. K., Yang, Y. C., Yang, W. M., Yao, G. P., Yeh, K., Yi, J., Yoh, K., Yorita, T., Yoshida, G. B., Yu, I., Yu, S. S., Yu, J. C., Yun, A., Zanetti, Y., Zeng, C., Zhou, S., Zucchelli, B. c., Alvarez, A. c., Anastassov, J. c., Anto, J., Appel, T. c., Ct, V., Barne, B., Barnett, P. a., Barria, P. c., Barto, M. a., Bauce, G. a., Bellettini, D. a., Bisello, K., Bland, L. g., Brigliadori, H., Budd, G. a., Busetto, A. b., Cx, F. p., Canelli, S. b., Carrillo, B. b., Casal, A. g., Castro, A. b., Cerri, L. c., Cerrito, Y., Chen, K. c., Ct, W., Chung, Y., Chung, M. a., Ciocci, G. a., Compostella, M., Convery, C., Cox, D., Cox, F. a., Crescioli, J. c., Cueva, N. c., D'Ascenzo, M. a., Dell'Orso, M. a., D'Errico, A. a., Di, J., Dittmann, S. a., Donati, Dorigo, Mirco, N. c., Ershaidat, J., Fernandez, G. c., Flanagan, M., Frank, J., Freeman, J., Garcia, A., Garfinkel, P. a., Garosi, C., Ginsburg, O., González, A., Goshaw, R. b., Group, S., Hahn, J., Han, R., Harr, W. b., Hopkin, R., Hughe, N. b., Cx, M. b., Iori, A. c., Ivanov, E. c., Ct, S., Jun, T., Junk, T. b., C, P., Karchin, Y. c., Kato, D. c., Ct, H. c., Ct, J. c., Ct, M., Kim, S. c., Ct, S., Kim, Y., Kim, Y. c., Ct, A., Kotwal, V. b., Krutelyov, A., Laasanen, R., Lander, K. c., Lannon, G. a., Latino, H. c., Lee, S. c., Lee, S. a., Leo, J., Lewi, A. c., Limosani, C., Lin, D., Litvintsev, D. a., Lucchesi, R. b., Cr, P. a., Maestro, G. b., Manca, M., Martínez, M., Mattson, K., Mcfarland, R. b., Mcnulty, M. b., Mondragon, C. c., Ct, M. a., Morello, M. g., Mussini, J. c., Nachtman, M., Neubauer, J. b., Nielsen, S., Oh, S. a., Pagan, E. b., Palencia, A., Paramonov, G. b., Pauletta, D., Pellett, T., Phillip, S. b., Poprocki, F. c., Prokoshin, F. b., Ptoho, G. a., Punzi, F. g., Rimondi, L. a., Ristori, S. b., Rolli, F. a., Ruffini, W., Sakumoto, L. b., Santi, V. c., Saveliev, A. c., Savoy Navarro, E., Schmidt, A. a., Scribano, F. a., Sforza, S., Shalhout, P., Shepard, M. c., Shimojima, P. b., Cx, J., Smith, F., Snider, P. a., Squillacioti, B. b., Cx, O. b., Cx, D. c., Stentz, G., Strycker, P., Teng, J. b., Thom, G., Thompson, S. c., Tokar, M. a., Trovato, F. b., Vázquez, J., Vizán, R., Wagner, S., Wang, W., Wester, D. b., Whiteson, A., Wicklund, H., William, J., Wilson, B., Winer, P. b., Wittich, U. c., Yang, W., Yao, G., Yeh, K. c., Yi, T. b., Yoshida, G., Yu, I. c., Ct, S., Yu, J., Yun, S. g., Zucchelli, T. Aaltonen, B. Álvarez González, S. Amerio, D. Amidei, A. Anastassov, A. Annovi, J. Anto, G. Apollinari, J. Appel, T. Arisawa, A. Artikov, J. Asaadi, W. Ashmanska, B. Auerbach, A. Aurisano, F. Azfar, W. Badgett, T. Bae, A. Barbaro-Galtieri, V. Barne, B. Barnett, P. Barria, P. Barto, M. Bauce, F. Bedeschi, S. Behari, G. Bellettini, J. Bellinger, D. Benjamin, A. Beretva, A. Bhatti, D. Bisello, I. Bizjak, K. Bland, B. Blumenfeld, A. Bocci, A. Bodek, D. Bortoletto, J. Boudreau, A. Boveia, L. Brigliadori, C. Bromberg, E. Brucken, J. Budagov, H. Budd, K. Burkett, G. Busetto, P. Bussey, A. Buzatu, A. Calamba, C. Calancha, S. Camarda, M. Campanelli, M. Campbell, F. Canelli, B. Carl, D. Carlsmith, R. Carosi, S. Carrillo, S. Carron, B. Casal, M. Casarsa, A. Castro, P. Catastini, D. Cauz, V. Cavaliere, M. Cavalli-Sforza, A. Cerri, L. Cerrito, Y. Chen, M. Chertok, G. Chiarelli, G. Chlachidze, F. Chlebana, K. Cho, D. Chokheli, W. Chung, Y. Chung, M. Ciocci, A. Clark, C. Clarke, G. Compostella, M. Convery, J. Conway, M. Corbo, M. Cordelli, C. Cox, D. Cox, F. Crescioli, J. Cueva, R. Culbertson, D. Dagenhart, N. d’Ascenzo, M. Datta, P. de Barbaro, M. Dell’Orso, L. Demortier, M. Deninno, F. Devoto, M. d’Errico, A. Di Canto, B. Di Ruzza, J. Dittmann, M. D’Onofrio, S. Donati, P. Dong, M. Dorigo, T. Dorigo, K. Ebina, A. Elagin, A. Eppig, R. Erbacher, S. Errede, N. Ershaidat, R. Eusebi, S. Farrington, M. Feindt, J. Fernandez, R. Field, G. Flanagan, R. Forrest, M. Frank, M. Franklin, J. Freeman, Y. Funakoshi, I. Furic, M. Gallinaro, J. Garcia, A. Garfinkel, P. Garosi, H. Gerberich, E. Gerchtein, S. Giagu, V. Giakoumopoulou, P. Giannetti, K. Gibson, C. Ginsburg, N. Giokari, P. Giromini, G. Giurgiu, V. Glagolev, D. Glenzinski, M. Gold, D. Goldin, N. Goldschmidt, A. Golossanov, G. Gomez, G. Gomez-Ceballo, M. Goncharov, O. González, I. Gorelov, A. Goshaw, K. Gouliano, L. Grillo, S. Grinstein, C. Grosso-Pilcher, R. Group, J. Guimaraes da Costa, S. Hahn, E. Halkiadaki, A. Hamaguchi, J. Han, F. Happacher, K. Hara, D. Hare, M. Hare, R. Harr, K. Hatakeyama, C. Hay, M. Heck, J. Heinrich, M. Herndon, S. Hewamanage, A. Hocker, W. Hopkin, D. Horn, S. Hou, R. Hughe, M. Hurwitz, U. Husemann, N. Hussain, M. Hussein, J. Huston, G. Introzzi, M. Iori, A. Ivanov, E. Jame, D. Jang, B. Jayatilaka, E. Jeon, S. Jindariani, M. Jone, K. Joo, S. Jun, T. Junk, T. Kamon, P. Karchin, A. Kasmi, Y. Kato, W. Ketchum, J. Keung, V. Khotilovich, B. Kilminster, D. Kim, H. Kim, J. Kim, M. Kim, S. Kim, Y. Kim, N. Kimura, M. Kirby, S. Klimenko, K. Knoepfel, K. Kondo, D. Kong, J. Konigsberg, A. Kotwal, M. Krep, J. Kroll, D. Krop, M. Kruse, V. Krutelyov, T. Kuhr, M. Kurata, S. Kwang, A. Laasanen, S. Lami, S. Lammel, M. Lancaster, R. Lander, K. Lannon, A. Lath, G. Latino, T. LeCompte, E. Lee, H. Lee, J. Lee, S. Lee, S. Leo, S. Leone, J. Lewi, A. Limosani, C.-J. Lin, M. Lindgren, E. Lipele, A. Lister, D. Litvintsev, C. Liu, H. Liu, Q. Liu, T. Liu, S. Lockwitz, A. Loginov, D. Lucchesi, J. Lueck, P. Lujan, P. Luken, G. Lungu, J. Ly, R. Lysak, R. Madrak, K. Maeshima, P. Maestro, S. Malik, G. Manca, A. Manousakis-Katsikaki, F. Margaroli, C. Marino, M. Martínez, P. Mastrandrea, K. Matera, M. Mattson, A. Mazzacane, P. Mazzanti, K. McFarland, P. McIntyre, R. McNulty, A. Mehta, P. Mehtala, C. Mesropian, T. Miao, D. Mietlicki, A. Mitra, H. Miyake, S. Moed, N. Moggi, M. Mondragon, C. Moon, R. Moore, M. Morello, J. Morlock, P. Movilla Fernandez, A. Mukherjee, Th. Muller, P. Murat, M. Mussini, J. Nachtman, Y. Nagai, J. Naganoma, I. Nakano, A. Napier, J. Nett, C. Neu, M. Neubauer, J. Nielsen, L. Nodulman, S. Noh, O. Norniella, L. Oake, S. Oh, Y. Oh, I. Oksuzian, T. Okusawa, R. Orava, L. Ortolan, S. Pagan Griso, C. Pagliarone, E. Palencia, V. Papadimitriou, A. Paramonov, J. Patrick, G. Pauletta, M. Paulini, C. Pau, D. Pellett, A. Penzo, T. Phillip, G. Piacentino, E. Pianori, J. Pilot, K. Pitt, C. Plager, L. Pondrom, S. Poprocki, K. Potamiano, F. Prokoshin, A. Pranko, F. Ptoho, G. Punzi, A. Rahaman, V. Ramakrishnan, N. Ranjan, I. Redondo, P. Renton, M. Rescigno, T. Riddick, F. Rimondi, L. Ristori, A. Robson, T. Rodrigo, T. Rodriguez, E. Roger, S. Rolli, R. Roser, F. Ruffini, A. Ruiz, J. Ru, V. Rusu, A. Safonov, W. Sakumoto, Y. Sakurai, L. Santi, K. Sato, V. Saveliev, A. Savoy-Navarro, P. Schlabach, A. Schmidt, E. Schmidt, T. Schwarz, L. Scodellaro, A. Scribano, F. Scuri, S. Seidel, Y. Seiya, A. Semenov, F. Sforza, S. Shalhout, T. Shear, P. Shepard, M. Shimojima, M. Shochet, I. Shreyber-Tecker, A. Simonenko, P. Sinervo, K. Sliwa, J. Smith, F. Snider, A. Soha, V. Sorin, H. Song, P. Squillacioti, M. Stancari, R. St. Deni, B. Stelzer, O. Stelzer-Chilton, D. Stentz, J. Strologa, G. Strycker, Y. Sudo, A. Sukhanov, I. Suslov, K. Takemasa, Y. Takeuchi, J. Tang, M. Tecchio, P. Teng, J. Thom, J. Thome, G. Thompson, E. Thomson, D. Toback, S. Tokar, K. Tollefson, T. Tomura, D. Tonelli, S. Torre, D. Torretta, P. Totaro, M. Trovato, F. Ukegawa, S. Uozumi, A. Varganov, F. Vázquez, G. Velev, C. Vellidi, M. Vidal, I. Vila, R. Vilar, J. Vizán, M. Vogel, G. Volpi, P. Wagner, R. Wagner, T. Wakisaka, R. Wallny, S. Wang, A. Warburton, D. Water, W. Wester, D. Whiteson, A. Wicklund, E. Wicklund, S. Wilbur, F. Wick, H. William, J. Wilson, P. Wilson, B. Winer, P. Wittich, S. Wolber, H. Wolfe, T. Wright, X. Wu, Z. Wu, K. Yamamoto, D. Yamato, T. Yang, U. Yang, Y. Yang, W.-M. Yao, G. Yeh, K. Yi, J. Yoh, K. Yorita, T. Yoshida, G. Yu, I. Yu, S. Yu, J. Yun, A. Zanetti, Y. Zeng, C. Zhou, S. Zucchelli, and Universidad de Cantabria
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FERMILAB TEVATRON COLLIDER ,Particle physics ,CP-violating asymmetries ,Meson ,B physic ,General Physics and Astronomy ,FOS: Physical sciences ,B physics ,Angle distribution, Branching ratio, CDF experiments, CP violations, CP-violating asymmetries, Data sample, Fermilab Tevatron collider, Integrated luminosity, Longitudinal polarization, Vector meson ,Longitudinal polarization ,7. Clean energy ,01 natural sciences ,High Energy Physics - Experiment ,Vector meson ,Physics and Astronomy (all) ,High Energy Physics - Experiment (hep-ex) ,High Energy Physics - Phenomenology (hep-ph) ,Mixing (mathematics) ,Strange b mesons ,Phase (matter) ,0103 physical sciences ,STRANGE QUARK ,mixing ,Bottom-Strange Meson Mixing Phase ,proton antiproton collisions ,010306 general physics ,TEVATRON ,Nuclear Experiment ,BOTTOM QUARK ,Physics ,Integrated luminosity ,010308 nuclear & particles physics ,Branching ratio ,High Energy Physics - Phenomenology ,CDF experiments ,CP violations ,Full data ,Content (measure theory) ,Angle distribution ,CDF ,Production (computer science) ,High Energy Physics::Experiment ,Data sample - Abstract
We report a measurement of the bottom-strange meson mixing phase βs using the time evolution of Bs0→J/ψ(→μ+μ-)ϕ(→K+K-) decays in which the quark-flavor content of the bottom-strange meson is identified at production. This measurement uses the full data set of proton-antiproton collisions at s=1.96 TeV collected by the Collider Detector experiment at the Fermilab Tevatron, corresponding to 9.6 fb-1 of integrated luminosity. We report confidence regions in the two-dimensional space of βs and the Bs0 decay-width difference ΔΓs and measure βs∈[-π/2,-1.51]∪[-0.06,0.30]∪[1.26,π/2] at the 68% confidence level, in agreement with the standard model expectation. Assuming the standard model value of βs, we also determine ΔΓs=0.068±0.026(stat)±0.009(syst) ps-1 and the mean Bs0 lifetime τs=1.528±0.019(stat)±0.009(syst) ps, which are consistent and competitive with determinations by other experiments., This work was supported by the U.S. Department of Energy and National Science Foundation; the Italian Istituto Nazionale di Fisica Nucleare; the Ministry of Education, Culture, Sports, Science and Technology of Japan; the Natural Sciences and Engineering Research Council of Canada; the National Science Council of the Republic of China; the Swiss National Science Foundation; the A. P. Sloan Foundation; the Bundesministerium für Bildung und Forschung, Germany; the Korean World Class University Program, the National Research Foundation of Korea; the Science and Technology Facilities Council and the Royal Society, UK; the Russian Foundation for Basic Research; the Ministerio de Ciencia e Innovación, and Programa Consolider-Ingenio 2010, Spain; the Slovak R&D Agency; the Academy of Finland; and the Australian Research Council (ARC).
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- 2012
4. The 2001 Canadian recommendations for the management of hypertension: Part two--Therapy
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Finlay McAlister, Zarnke, Kb, Campbell, Nrc, Feldman, Rd, Levine, M., Mahon, J., Grover, Sa, Lewanczuk, R., Leenen, F., Tobe, S., Lebel, M., Stone, J., Schiffrin, El, Rabkin, Sw, Ogilvie, Ri, Larochelle, P., Jones, C., Honos, G., Fodor, G., Burgess, E., Hamet, P., Herman, R., Irvine, J., Culleton, B., and Wright, Jm
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Canada ,Cardiovascular Diseases ,Hypertension ,Humans ,Antihypertensive Agents ,Randomized Controlled Trials as Topic - Abstract
To provide updated, evidence-based recommendations for the therapy of hypertension in adults.For patients with hypertension, a number of antihypertensive agents may control blood pressure. Randomized trials evaluating first-line therapy with thiazides, beta-adrenergic antagonists, angiotensin-converting enzyme inhibitors, calcium channel blockers, alpha-blockers, centrally acting agents or angiotensin II receptor antagonists were reviewed.The health outcomes that were considered were changes in blood pressure, cardiovascular morbidity, and cardiovascular and/or all-cause mortality rates. Economic outcomes were not considered due to insufficient evidence.MEDLINE was searched for the period March 1999 to October 2001 to identify studies not included in the 2000 revision of the Canadian Recommendations for the Management of Hypertension. Reference lists were scanned, experts were polled, and the personal files of the subgroup members and authors were used to identify other published studies. All relevant articles were reviewed and appraised, using prespecified levels of evidence, by content experts and methodological experts.A high value was placed on the avoidance of cardiovascular morbidity and mortality.Various antihypertensive agents reduce the blood pressure of patients with sustained hypertension. In certain settings, and for specific classes of drugs, blood-pressure lowering has been associated with reduced cardiovascular morbidity and/or mortality.The present document contains detailed recommendations pertaining to treatment thresholds, target blood pressures, and choice of agents in various settings in patients with hypertension. The main changes from the 2000 Recommendations are the addition of a section on the treatment of hypertension in patients with diabetes mellitus, the amalgamation of the previous sections on treatment of hypertension in the young and old into one section, increased emphasis on the role of combination therapies over repeated trials of single agents and expansion of the section on the treatment of hypertension after stroke. Implicit in the recommendations for therapy is the principle that treatment for an individual patient should take into consideration global cardiovascular risk, the presence and/or absence of target organ damage, and comorbidities.All recommendations were graded according to strength of the evidence and voted on by the Canadian Hypertension Recommendations Working Group. Individuals with potential conflicts of interest relative to any specific recommendation were excluded from voting on that recommendation. Only those recommendations achieving high levels of consensus are reported here. These guidelines will continue to be updated annually.
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- 2002
5. Guidelines for the use and interpretation of assays for monitoring autophagy.
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Rohrer, B, Roninson, Ib, Rosen, K, Rost-Roszkowska, Mm, Rouis, M, Rouschop, Km, Rovetta, F, Rubin, Bp, Rubinsztein, Dc, Ruckdeschel, K, Rucker EB, 3rd, Rudich, A, Rudolf, E, Ruiz-Opazo, N, Russo, R, Rusten, Te, Ryan, Km, Ryter, Sw, Sabatini, Dm, Sadoshima, J, Saha, T, Saitoh, T, Sakagami, H, Sakai, Y, Salekdeh, Gh, Salomoni, P, Salvaterra, Pm, Salvesen, G, Salvioli, R, Sanchez, Am, Sánchez-Alcázar, Ja, Sánchez-Prieto, R, Sandri, M, Sankar, U, Sansanwal, P, Santambrogio, L, Saran, S, Sarkar, S, Sarwal, M, Sasakawa, C, Sasnauskiene, A, Sass, M, Sato, K, Sato, M, Schapira, Ah, Scharl, M, Schätzl, Hm, Scheper, W, Schiaffino, S, Schneider, C, Schneider, Me, Schneider-Stock, R, Schoenlein, Pv, Schorderet, Df, Schüller, C, Schwartz, Gk, Scorrano, L, Sealy, L, Seglen, Po, Segura-Aguilar, J, Seiliez, I, Seleverstov, O, Sell, C, Seo, Jb, Separovic, D, Setaluri, V, Setoguchi, T, Settembre, C, Shacka, Jj, Shanmugam, M, Shapiro, Im, Shaulian, E, Shaw, Rj, Shelhamer, Jh, Shen, Hm, Shen, Wc, Sheng, 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Tettamanti, G, Thevissen, K, Thompson, Cb, Thorburn, A, Thumm, M, Tian, F, Tian, Y, Tocchini-Valentini, G, Tolkovsky, Am, Tomino, Y, Tönges, L, Tooze, Sa, Tournier, C, Tower, J, Towns, R, Trajkovic, V, Travassos, Lh, Tsai, Tf, Tschan, Mp, Tsubata, T, Tsung, A, Turk, B, Turner, L, Tyagi, Sc, Uchiyama, Y, Ueno, T, Umekawa, M, Umemiya-Shirafuji, R, Unni, Vk, Vaccaro, Mi, Valente, Em, Van den Berghe, G, van der Klei, Ij, van Doorn, W, van Dyk, Lf, van Egmond, M, van Grunsven, La, Vandenabeele, P, Vandenberghe, Wp, Vanhorebeek, I, Vaquero, Ec, Velasco, G, Vellai, T, Vicencio, Jm, Vierstra, Rd, Vila, M, Vindis, C, Viola, G, Viscomi, Maria Teresa, Voitsekhovskaja, Ov, von Haefen, C, Votruba, M, Wada, K, Wade-Martins, R, Walker, Cl, Walsh, Cm, Walter, J, Wan, Xb, Wang, A, Wang, C, Wang, D, Wang, F, Wang, G, Wang, H, Wang, Hg, Wang, Hd, Wang, J, Wang, K, Wang, M, Wang, Rc, Wang, X, Wang, Yj, Wang, Y, Wang, Z, Wang, Zc, Wansink, Dg, Ward, Dm, Watada, H, Waters, Sl, Webster, P, Wei, L, Weihl, Cc, Weiss, Wa, Welford, Sm, Wen, Lp, Whitehouse, Ca, Whitton, Jl, Whitworth, Aj, Wileman, T, Wiley, Jw, Wilkinson, S, Willbold, D, Williams, Rl, Williamson, Pr, Wouters, Bg, Wu, C, Wu, Dc, Wu, Wk, Wyttenbach, A, Xavier, Rj, Xi, Z, Xia, P, Xiao, G, Xie, Z, Xu, Dz, Xu, J, Xu, L, Xu, X, Yamamoto, A, Yamashina, S, Yamashita, M, Yan, X, Yanagida, M, Yang, D, Yang, E, Yang, Jm, Yang, Sy, Yang, W, Yang, Wy, Yang, Z, Yao, Mc, Yao, Tp, Yeganeh, B, Yen, Wl, Yin, Jj, Yin, Xm, Yoo, Oj, Yoon, G, Yoon, Sy, Yorimitsu, T, Yoshikawa, Y, Yoshimori, T, Yoshimoto, K, You, Hj, Youle, Rj, Younes, A, Yu, L, Yu, Sw, Yu, Wh, Yuan, Zm, Yue, Z, Yun, Ch, Yuzaki, M, Zabirnyk, O, Silva-Zacarin, E, Zacks, D, Zacksenhaus, E, Zaffaroni, N, Zakeri, Z, Zeh HJ, 3rd, Zeitlin, So, Zhang, H, Zhang, Hl, Zhang, J, Zhang, Jp, Zhang, L, Zhang, My, Zhang, Xd, Zhao, M, Zhao, Yf, Zhao, Y, Zhao, Zj, Zheng, X, Zhivotovsky, B, Zhong, Q, Zhou, Cz, Zhu, C, Zhu, Wg, Zhu, Xf, Zhu, X, Zhu, Y, Zoladek, T, Zong, Wx, Zorzano, A, Zschocke, J, Zuckerbraun, B., and Viscomi M. T. (ORCID:0000-0002-9096-4967)
- Abstract
In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused o
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- 2012
6. Verapamil but not calpain or creatine alters arsenate-induced cardiac cell death
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Luong, MW, primary and Rabkin, SW, additional
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- 2009
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7. Effect of dynorphin A(1-13) on cardiomyocytes in culture: modulation of the response to increased extracellular calcium, but no effect on intrinsic cardiac contractile frequency or the response to isoproterenol or increased extracellular potassium
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Rabkin Sw
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Chronotropic ,medicine.medical_specialty ,Nifedipine ,Physiology ,chemistry.chemical_element ,Dynorphin ,Chick Embryo ,Calcium ,Dynorphins ,chemistry.chemical_compound ,Physiology (medical) ,Internal medicine ,medicine ,Extracellular ,Myocyte ,Animals ,Drug Interactions ,Cells, Cultured ,Endogenous opioid ,Chemistry ,Myocardium ,Isoproterenol ,Dynorphin A ,Myocardial Contraction ,Peptide Fragments ,Endocrinology ,nervous system ,Mechanism of action ,Potassium ,medicine.symptom ,Cardiology and Cardiovascular Medicine - Abstract
The purpose of this study was to determine whether the endogenous opioid peptide dynorphin A(1-13) has a direct effect on the heart or acts to modulate the cardiac chronotropic response to calcium, potassium, or beta-adrenergic receptor stimulation. Spontaneously contracting myocardial cell aggregates were prepared from 7-day-old chick embryos and were maintained in culture for 72 h before study. Dynorphin A(1-13), 10(-8) to 10(-6)M, did not alter spontaneous contractile frequency. Increases in [Ca2+]o spontaneously suppressed cardiac contractile frequency, and dynorphin A(1-13) significantly (p less than 0.05) enhanced this response. Nifedipine, 10(-8) M, antagonized the effect of increased [Ca2+]o on cardiac contractile frequency, but did not block the action of dynorphin A(1-13) to accentuate the effect of increasing [Ca2+]o. Dynorphin A(1-13) did not alter the significant (p less than 0.05) increase in contractile frequency produced by beta-adrenergic receptor stimulation by isoproterenol, or the suppression in contractile frequency produced by increases in extracellular potassium ([K+]o). These data indicate that dynorphin A(1-13) does not act directly on the cardiac myocyte to alter cardiac contractile frequency or alter the response to increases in [K+]o or to isoproterenol, but that dynorphin A(1-13) does modulate the response to increases in extracellular calcium.
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- 1992
8. Novel LMNA mutations seen in patients with familial partial lipodystrophy subtype 2 (FPLD2; MIM 151660)
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Lanktree, M, primary, Cao, H, additional, Rabkin, SW, additional, Hanna, A, additional, and Hegele, RA, additional
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- 2007
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9. Factors associated with implementation of preventive care measures in patients with diabetes mellitus.
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Streja DA and Rabkin SW
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- 1999
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10. Angiotensin II induces activation of phosphatidylinositol 3-kinase in cardiomyocytes.
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Rabkin SW, Goutsouliak V, Kong JY, Rabkin, S W, Goutsouliak, V, and Kong, J Y
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- 1997
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11. Increased mortality with cardiotoxic doses of Adriamycin after verapamil pretreatment despite prevention of myocardial calcium accumulation
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Otten M, Rabkin Sw, and Polimeni Pi
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medicine.medical_specialty ,Heart Diseases ,Physiology ,medicine.drug_class ,Cell ,Antibiotics ,chemistry.chemical_element ,Calcium ,Pharmacology ,Electrolytes ,Body Water ,Physiology (medical) ,Internal medicine ,medicine ,Animals ,Distribution (pharmacology) ,Cardiotoxicity ,Lagomorpha ,biology ,business.industry ,Myocardium ,Electroencephalography ,General Medicine ,biology.organism_classification ,medicine.anatomical_structure ,Endocrinology ,Verapamil ,chemistry ,Doxorubicin ,Toxicity ,Female ,Rabbits ,Extracellular Space ,business ,medicine.drug - Abstract
The purpose of this investigation was to determine whether the calcium blocking agent, verapamil, could modify Adriamycin cardiotoxicity, and if so, whether or not such modification is mediated by a mechanism involving myocardial electrolyte distribution. The mean survival time of female New Zealand white rabbits administered Adriamycin was reduced by pretreatment with verapamil. Myocardial cellular calcium concentration, [Ca]i, in animals pretreated with verapamil before receiving Adriamycin was lower than in animals receiving Adriamycin alone (1.49 ± 0.11 vs. 2.22 ± 0.35 mmol/kg cell water, respectively; P = 0.05). Myocardial [Ca]i in control animals was 1.68 ± 0.10 mmol/kg cell water. Myocardial [Mg]i in animals receiving Adriamycin alone was lower than that for animals receiving verapamil alone (15.6 ± 1.4 vs. 19.2 ± 0.8 mmol/kg cell water, respectively). When these drugs were combined, [Mg]i approached the control value of 17.3 ± 0.6 mmol/kg cell water. Cellular concentrations of the monovalent electrolytes were little affected by these drugs, except for a reduction of [Cl]i by verapamil. Neither myocardial water distribution nor plasma concentrations of these electrolytes were altered by either drug. The data indicate that verapamil pretreatment increases the mortality associated with Adriamycin in rabbits despite the continued efficacy of verapamil as a Ca-blocking agent after injection of Adriamycin. Particular caution must be exercised if clinical combination of Ca-blocking agents and anthracyclines is contemplated.
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- 1983
12. The effect of calcium ions and the calcium ionophore A23187 on choline uptake and phosphatidylcholine biosynthesis in chick embryo hearts
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Rabkin Sw
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Cell Membrane Permeability ,Physiology ,Phospholipid ,Ionophore ,chemistry.chemical_element ,Chick Embryo ,Calcium ,Calcium in biology ,Phosphatidylcholine Biosynthesis ,Choline ,chemistry.chemical_compound ,Physiology (medical) ,Extracellular ,Animals ,Calcimycin ,Cells, Cultured ,Phosphocholine ,Dose-Response Relationship, Drug ,Myocardium ,Cell Differentiation ,chemistry ,Biochemistry ,Phosphatidylcholines ,Calcium Channels ,Cardiology and Cardiovascular Medicine - Abstract
The effect of increases in extracellular calcium [Ca]o and the calcium ionophore A23187 on choline uptake and phosphatidylcholine biosynthesis was assessed in isolated cardiac myocytes. The cells were obtained from 7-day old chick embryos and were maintained in culture. Choline uptake was examined using [methyl 3H] choline. A23187 was found to increase choline uptake through the saturable choline uptake process. Pulse chase experiments using [methyl 3H] choline showed that after a 2 h incubation with choline, about 85% of the label was recovered in phosphocholine with most of the rest in phospholipid and a small amount in CDP-choline and glycerol phosphocholine. Increases in [Ca]o up to 10 mM did not affect the amount of label in phosphocholine or phospholipid, the rate of disappearance of label from phosphocholine, or the rate of appearance of labelled choline in phospholipid. In contrast, A23187, at concentrations up to 10(-4) M, was associated with a significant (p less than 0.05) increase in choline in the phosphocholine and phospholipid pool compared to control cells. The time course of the disappearance of choline from the phosphocholine pool and appearance in phospholipid pool was not significantly different between control cells and those treated with A23187. A23187 increased choline uptake via the specific uptake process. The effect on choline uptake may be attributed to the action of A23187 to facilitate the release of calcium from specific intracellular calcium storage sites rather than a nonspecific increase in [Ca]i that may have resulted from the increase in [Ca]o.
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- 1988
13. The 2005 Canadian Hypertension Education Program recommendations for the management of hypertension: Part II - Therapy
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Khan, Na, Finlay McAlister, Lewanczuk, Rz, Touyz, Rm, Padwal, R., Rabkin, Sw, Leiter, La, Lebel, M., Herbert, C., Schiffrin, El, Herman, Rj, Hamet, P., Fodor, C., Carruthers, G., Culleton, B., Dechamplain, J., Pylypchuk, G., Logan, Ac, Gledhill, N., Petrella, R., Campbell, Nrc, Arnold, M., Moe, G., D Hill, M., Ones, C., Larochelle, P., Ogilvie, Ri, Tobe, S., Houlden, R., Burgess, E., and Feldman, Rd
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Canada ,Evidence-Based Medicine ,Patient Education as Topic ,Hypertension ,Weight Loss ,Humans ,Exercise ,Antihypertensive Agents ,Diet - Abstract
To provide updated, evidence-based recommendations for the management of hypertension in adults.For lifestyle and pharmacological interventions, evidence from randomized controlled trials and systematic reviews of trials was preferentially reviewed. While changes in cardiovascular morbidity and mortality were the primary outcomes of interest, for lifestyle interventions, blood pressure lowering was accepted as a primary outcome given the lack of long-term morbidity/mortality data in this field, and for certain comorbid conditions, other relevant outcomes, such as development of proteinuria or worsening of kidney function, were considered.MEDLINE searches were conducted from November 2003 to October 2004 to update the 2004 recommendations. Reference lists were scanned, experts were contacted, and the personal files of the subgroup members and authors were used to identify additional published studies. All relevant articles were reviewed and appraised independently, using prespecified levels of evidence, by content and methodology experts. As per previous years, only studies that had been published in the peer-reviewed literature were included; evidence from abstracts, conference presentations and unpublished personal communications was not included.Lifestyle modifications to prevent and/or treat hypertension include the following: perform 30 min to 60 min of aerobic exercise on four to seven days of the week; maintain a healthy body weight (body mass index of 18.5 kg/m2 to 24.9 kg/m2) and waist circumference (less than 102 cm for men and less than 88 cm for women); limit alcohol consumption to no more than 14 units per week in men or nine units per week in women; follow a reduced fat, low cholesterol diet with an adequate intake of potassium, magnesium and calcium; restrict salt intake; and consider stress management (in selected individuals). Treatment thresholds and targets should take into account each individual's global atherosclerotic risk, target organ damage and any comorbid conditions. Blood pressure should be lowered to 140/90 mmHg or less in all patients, and to 130/80 mmHg or less in those with diabetes mellitus or chronic kidney disease. Most adults with hypertension require more than one agent to achieve target blood pressures. For adults without compelling indications for other agents, initial therapy should include thiazide diuretics. Other agents appropriate for first-line therapy for diastolic hypertension with or without systolic hypertension include beta-blockers (in those younger than 60 years), angiotensin-converting enzyme (ACE) inhibitors (except in black patients), long-acting calcium channel blockers and angiotensin receptor antagonists. Other agents appropriate for first-line therapy for isolated systolic hypertension include long-acting dihydropyridine calcium channel blockers and angiotensin receptor antagonists. Certain comorbid conditions provide compelling indications for first-line use of other agents: in patients with angina, recent myocardial infarction or heart failure, beta-blockers and ACE inhibitors are recommended as first-line therapy; in patients with diabetes mellitus, ACE inhibitors or angiotensin receptor antagonists (or thiazides in patients with diabetes mellitus without albuminuria) are appropriate first-line therapies; and in patients with nondiabetic chronic kidney disease, ACE inhibitors are recommended. All hypertensive patients should have their fasting lipids screened, and those with dyslipidemia should be treated using the thresholds, targets and agents recommended by the Canadian Hypertension Education Program Working Group on the management of dyslipidemia and the prevention of cardiovascular disease. Selected patients with hypertension, but without dyslipidemia, should also receive statin therapy and/or acetylsalicylic acid therapy.All recommendations were graded according to the strength of the evidence and voted on by the 43 members of the Canadian Hypertension Education Program Evidence-Based Recommendations Task Force. All recommendations reported here achieved at least 95% consensus. These guidelines will continue to be updated annually.
14. Mathematical and mechanical modeling of stress-strain relationship of pericardium
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Rabkin, SW, primary and Hsu, PH, additional
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- 1975
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15. 2008 - Benazepril plus amlodipine reduced cardiovascular risk more than benazepril plus hydrochlorothiazide.
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Rabkin SW
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- 2009
16. Epicardial Fat in Heart Failure with Preserved Ejection Fraction Compared with Reduced Ejection Fraction.
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Sidhu GS and Rabkin SW
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Background: The role of epicardial adipose tissue (EAT) in heart failure with preserved ejection fraction (HFpEF) remains to be defined. Methods: A consecutive series of outpatients with chronic heart failure-heart failure with reduced ejection fraction (HFrEF) and HFpEF and/or diastolic dysfunction-had EAT assessed by echocardiographic measurement and related to indices of cardiac structure and function. Results: Epicardial fat thickness was significantly ( p < 0.05) greater in HFpEF ( N = 141) with a mean of 6.7 ± 1.6 mm compared with a mean of 5.1 ± 1.0 mm in HFrEF ( n = 40). After adjusting for the relationship with BMI, in HFpEF, epicardial fat was significantly ( p < 0.05) negatively correlated with left ventricular internal diameter end diastole (LVIDd), left ventricular internal diameter end systole (LVIDs), left ventricular (LV) end-diastolic volume (EDV) index, lateral e', septal e', right atrial (RA) volume index, and hemoglobin (Hgb). The association with Hgb was no longer significant after adjusting for the effect of age. HFpEF was associated with smaller LVIDd, LVIDs, LV EDV indexes, and left atrial (LA) and RA volume indexes. Conclusions: Epicardial fat is significantly ( p < 0.05) greater in HFpEF than HFrEF. Epicardial fat is associated with smaller cardiac chamber sizes in HFpEF suggesting that epicardial fat acts as a constraint to cardiac dilation.
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- 2024
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17. Eicosapentaenoic Acid (EPA) and Docosahexaenoic Acid (DHA) Ameliorate Heart Failure through Reductions in Oxidative Stress: A Systematic Review and Meta-Analysis.
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Seth J, Sharma S, Leong CJ, and Rabkin SW
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The objectives of this study were to explore the role that eicosapentaenoic acid (EPA) and/or docosahexaenoic acid (DHA) plays in heart failure (HF), highlighting the potential connection to oxidative stress pathways. Following PRISMA guidelines, we conducted electronic searches of the literature in MEDLINE and EMBASE focusing on serum EPA and/or DHA and EPA and/or DHA supplementation in adult patients with heart failure or who had heart failure as an outcome of this study. We screened 254 studies, encompassing RCTs, observational studies, and cohort studies that examined HF outcomes in relation to either serum concentrations or dietary supplementation of EPA and/or DHA. The exclusion criteria were pediatric patients, non-HF studies, abstracts, editorials, case reports, and reviews. Eleven studies met our criteria. In meta-analyses, high serum concentrations of DHA were associated with a lower rate of heart failure with a hazard ratio of 0.74 (CI = 0.59-0.94). High serum concentrations of EPA also were associated with an overall reduction in major adverse cardiovascular events with a hazard ratio of 0.60 (CI = 0.46-0.77). EPA and DHA, or n3-PUFA administration, were associated with an increased LVEF with a mean difference of 1.55 (CI = 0.07-3.03)%. A potential explanation for these findings is the ability of EPA and DHA to inhibit pathways by which oxidative stress damages the heart or impairs cardiac systolic or diastolic function producing heart failure. Specifically, EPA may lower oxidative stress within the heart by reducing the concentration of reactive oxygen species (ROS) within cardiac tissue by (i) upregulating nuclear factor erythroid 2-related factor 2 (Nrf2), which increases the expression of antioxidant enzyme activity, including heme oxygenase-1, thioredoxin reductase 1, ferritin light chain, ferritin heavy chain, and manganese superoxide dismutase (SOD), (ii) increasing the expression of copper-zinc superoxide dismutase (MnSOD) and glutathione peroxidase, (iii) targeting Free Fatty Acid Receptor 4 (Ffar4), (iv) upregulating expression of heme-oxygenase-1, (v) lowering arachidonic acid levels, and (vi) inhibiting the RhoA/ROCK signaling pathway. DHA may lower oxidative stress within the heart by (i) reducing levels of mitochondrial-fission-related protein DRP-1(ser-63), (ii) promoting the incorporation of cardiolipin within the mitochondrial membrane, (iii) reducing myocardial fibrosis, which leads to diastolic heart failure, (iv) reducing the expression of genes such as Appa, Myh7, and Agtr1α, and (v) reducing inflammatory cytokines such as IL-6, TNF-α. In conclusion, EPA and/or DHA have the potential to improve heart failure, perhaps mediated by their ability to modulate oxidative stress.
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- 2024
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18. Searching for the Best Machine Learning Algorithm for the Detection of Left Ventricular Hypertrophy from the ECG: A Review.
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Rabkin SW
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Background: Left ventricular hypertrophy (LVH) is a powerful predictor of future cardiovascular events. Objectives: The objectives of this study were to conduct a systematic review of machine learning (ML) algorithms for the identification of LVH and compare them with respect to the classical features of test sensitivity, specificity, accuracy, ROC and the traditional ECG criteria for LVH. Methods: A search string was constructed with the operators "left ventricular hypertrophy, electrocardiogram" AND machine learning; then, Medline and PubMed were systematically searched. Results : There were 14 studies that examined the detection of LVH utilizing the ECG and utilized at least one ML approach. ML approaches encompassed support vector machines, logistic regression, Random Forest, GLMNet, Gradient Boosting Machine, XGBoost, AdaBoost, ensemble neural networks, convolutional neural networks, deep neural networks and a back-propagation neural network. Sensitivity ranged from 0.29 to 0.966 and specificity ranged from 0.53 to 0.99. A comparison with the classical ECG criteria for LVH was performed in nine studies. ML algorithms were universally more sensitive than the Cornell voltage, Cornell product, Sokolow-Lyons or Romhilt-Estes criteria. However, none of the ML algorithms had meaningfully better specificity, and four were worse. Many of the ML algorithms included a large number of clinical (age, sex, height, weight), laboratory and detailed ECG waveform data (P, QRS and T wave), making them difficult to utilize in a clinical screening situation. Conclusions : There are over a dozen different ML algorithms for the detection of LVH on a 12-lead ECG that use various ECG signal analyses and/or the inclusion of clinical and laboratory variables. Most improved in terms of sensitivity, but most also failed to outperform specificity compared to the classic ECG criteria. ML algorithms should be compared or tested on the same (standard) database.
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- 2024
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19. Relationship between Alzheimer dementia and QT interval: A meta-analysis.
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Rabkin SW
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While the link between aging and mortality from dementia is widely appreciated, the mechanism is not clear. The objective of this study was to determine whether there is a direct relationship between Alzheimer dementia (AD) and the QT interval, because the latter has been related to cardiac mortality. A systematic review and meta-analysis were conducted after a Medline and EMBASE search using terms "Alzheimer disease or Dementia AND QT interval, QT dispersion or cardiac repolarization." Four studies with control groups were identified. There were significant differences in QT interval between individuals with AD vs individuals without dementia (controls) (odds ratio (OR)1.665 [random effects model] and 1.879 [fixed effect model]) ( p < 0.001). There were significant differences in QT interval between individuals with AD vs individuals with mild cognitive impairment (MCI) (OR 1.760 [random effects] and 1.810 [fixed effect]) ( p < 0.001). A significant ( p <0.001) correlation exists between the QTc and the Mini-Mental State Exam (MMSE), a test of cognitive function. Two studies examined QT variability (the difference between the longest and shortest QT interval on a 12 lead ECG); the OR for QT variability AD vs MCI was 3.858 [random effects model] and 3.712 [fixed effects model] ( p < 0.001). When compared to the control group, the OR for QT dispersion in AD was 6.358 [random effects model] or 5.143 ( P < 0.001) [fixed effects model]. A qualitative analysis of the data raised questions about paucity of data defining the nature of the control groups, the pathophysiologic mechanism, and the uniform use of a poor QT heart rate correction factor. The longer QT in AD, greater QT variability in AD, and the direct relationship between QT interval and AD severity supports a brain-heart connection in AD that might be fundamental to aging-induced AD and mortality. Issues with defining the control group, limited number of studies, conflicting data in population studies, and the lack of a strong electrophysiological basis underscore the need for additional research in this field., Competing Interests: The author declares no conflict of interest., (© 2024 The Authors. Aging Medicine published by Beijing Hospital and John Wiley & Sons Australia, Ltd.)
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- 2024
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20. Myeloperoxidase, carnitine, and derivatives of reactive oxidative metabolites in heart failure with preserved versus reduced ejection fraction: A meta-analysis.
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Wong CN, Gui XY, and Rabkin SW
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- Humans, Carnitine, Stroke Volume physiology, Biomarkers metabolism, Peroxidase, Oxidative Stress, Prognosis, Heart Failure
- Abstract
Background: Understanding the pathophysiology of heart failure (HF) with preserved ejection fraction (HFpEF) continues to be challenging. Several inflammatory and metabolic biomarkers have recently been suggested to be involved in HFpEF., Objectives: The purpose of this review was to synthesize the evidence on non-traditional biomarkers from metabolomic studies that may distinguish HFpEF from heart failure with reduced ejection fraction (HFrEF) and controls without HF., Methods: A systematic search was conducted using Medline and PubMed with search terms such as "HFpEF" and "metabolomics", and a meta-analysis was conducted., Results: Myeloperoxidase (MPO) levels were significantly (p < 0.001) higher in HFpEF than controls without HF, but comparable (p = 0.838) between HFpEF and HFrEF. Carnitine levels were significantly (p < 0.0001) higher in HFrEF than HFpEF, but comparable (p = 0.443) between HFpEF and controls without HF. Derivatives of reactive oxidative metabolites (DROMs) were not significantly (p = 0.575) higher in HFpEF than controls without HF., Conclusion: These data suggest that MPO is operative in HFpEF and HFrEF and may be a biomarker for HF. Furthermore, circulating carnitine levels may distinguish HFrEF from HFpEF., Competing Interests: Declaration of Competing Interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Elsevier B.V. All rights reserved.)
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- 2024
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21. Estimating Left Ventricular Mass from the Electrocardiogram across the Spectrum of LV Mass from Normal to Increased LV Mass in an Older Age Group.
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Rabkin SW and Zhou JCJ
- Abstract
Objectives: To examine the relationship of QRS voltages and left ventricular (LV) mass across the spectrum of individuals with different LV mass., Methods: Twenty QRS voltage measurements or combinations were determined in a consecutive series of 159 adults with an ECG and echocardiogram without previous myocardial infarction, left or right bundle branch block, pre-excitation, or electronic pacemaker., Results: The four strongest and significant correlations between QRS and LV mass were S in V4, deepest S wave in any precordial lead plus S in V4, S in V3, and S in V3 plus R in AVL times QRS duration. For men, the strength of the relationships were S in V3 ( F = 33.8), deepest S wave in any precordial lead plus S V4 ( F = 33.7), S in V3 plus R aVL ( F = 29.9), S in V4 ( F = 29.79), and deepest S in precordial leads ( F = 17.9). The R wave in AVL alone did not correlate with LV mass. Criteria using the R wave in lateral precordial leads did not correlate as strongly with LV mass. For women, only S in V4 significantly correlated with LV mass. Overall, the R wave voltage in limb leads (AVL I or II) did not correlate with precordial S wave amplitudes. Univariate and multivariate analysis showed that some but not all QRS voltages correlated with each other. In multivariate analysis, using only single variables and not combination of QRS variables, the only significant relationship between QRS voltage and left ventricular mass was for men the S in V3 ( p = 0.04) and for women S in V4 ( p = 0.016) and R in V6 ( p = 0.04)., Conclusion: The S wave in V3 and V4 correlate most strongly with LV mass while the R wave in limb leads, including AVL, do not correlate., Competing Interests: The authors declare that they have no conflicts of interest that could have appeared to influence the work reported in this paper., (Copyright © 2024 Simon W. Rabkin and Jeremy C. J. Zhou.)
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- 2024
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22. Differences in circadian variation in QT interval of the ECG in women compared to men.
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Rabkin SW and Singh I
- Abstract
Background: Measurement of the QT interval in the ECG (QT interval) is important in evaluating risk for cardiac death and for assessing the impact of drugs on the heart. The objective of this study is to determine whether the time of day affects the QT interval, QT interval variability and whether these relationships are influenced by an individual's sex., Methods: Twenty-four hour ECGs were analyzed in detail on 50 individuals, 49 years of age, without evidence of coronary artery disease, structural heart disease, or significant arrhythmias. Four different QT-heart rate adjustment formulae were calculated and compared., Results: There were significant (P=0.0014) differences between the QT-heart rate relationship during three different time-periods (night 00:00 to 08:00 h, day 08:00 to 14:00 h and evening 14:00 to 24:00 h). Women, compared to men, had a steeper relation of QT to RR interval indicating that when heart rate slows at night, the QT interval is more prolonged which is consistent with a greater susceptibility to fatal arrhythmias. The variability of the QT interval (the SD) was significantly (P<0.01) greater in men than women at night and in the evening but not during the day. There were differences in the ability of different QT heart rate adjustment formulae to blunt the effect of heart rate changes on the QT interval during the day., Conclusion: The time of the day that the QT interval is assessed should be considered. The QT heart rate relationship is different in women than in men especially at night. QT interval variability is greater at night especially in men. There are differences in the ability of QT heart rate adjustment formulae to blunt the effect of heart rate on the QT interval. Differences in the QTc at night might be the basis for the higher prevalence of sudden death in women at night., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (AJCD Copyright © 2023.)
- Published
- 2023
23. Epigenetics in Heart Failure: Role of DNA Methylation in Potential Pathways Leading to Heart Failure with Preserved Ejection Fraction.
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Rabkin SW and Wong CN
- Abstract
This review will focus on epigenetic modifications utilizing the DNA methylation mechanism, which is potentially involved in the pathogenesis of heart failure with preserved ejection fraction (HFpEF). The putative pathways of HFpEF will be discussed, specifically myocardial fibrosis, myocardial inflammation, sarcoplasmic reticulum Ca
2+ -ATPase, oxidative-nitrosative stress, mitochondrial and metabolic defects, as well as obesity. The relationship of HFpEF to aging and atrial fibrillation will be examined from the perspective of DNA methylation.- Published
- 2023
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24. Collagen type IV as the link between arterial stiffness and dementia.
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Rabkin SW
- Abstract
Arterial stiffness has been linked to impaired cognitive function and dementia but the reason for the association is uncertain. This review proposes that collagen type IV is a critical factor linking arterial stiffness and dementia. Several genome wide association studies have related arterial stiffness to Collagen type IVα. Proteomic studies of arteries, demonstrated higher levels of collagen IVα1 in persons with high arterial stiffness. Collagen type IV defects are associated genetic causes of dementia as well as dementia of a variety of other causes. There are plausible causal roles for collagen type IV in dementia. Disorders of Collagen type IV can produce (I) fibro-hyalinosis and elastosis of small arterioles leading to cerebral ischemia and infarction; (II) dysfunction of the blood brain barrier leading to cerebral hemorrhage; (III) carotid artery stiffness with increase pulse pressure induces cerebral blood vessel damage leading to cerebral atrophy. The mechanisms by which Collagen type IV can lead to vascular stiffness include its degradation by matrix metalloprotease type 2 that (a) stimulates vascular smooth muscle cells to produce more extracellular matrix or (b) liberates peptides that damage the subendothelial space. Factors, such as TGF-β1, and LDL cholesterol especially oxidized LDL can increase collagen type IV and produce vascular stiffness and dementia. Fibroblast growth factor 23, and abnormal NO signaling have been linked to collagen type IV or increased vascular stiffness and an increased risk of dementia. Recognition of the central role of collagen type IV in arterial stiffness and dementia will inspire new research focused on determining whether its modification can benefit arterial and brain health., Competing Interests: None., (AJTR Copyright © 2023.)
- Published
- 2023
25. Identifying Premature Ventricular Complexes from Outflow Tracts Based on PVC Configuration: A Machine Learning Approach.
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Bajaj S, Bennett MT, and Rabkin SW
- Abstract
Background: Current inferences about the site of origin (SOO) of premature ventricular complexes (PVC) from the surface ECG have not been subjected to newer data analytic techniques that identify signals that are not recognized by visual inspection., Aims: The objective of this study was to apply data analytics to PVC characteristics., Methods: PVCs from 12-lead ECGs of a consecutive series of 338 individuals were examined by unsupervised machine learning cluster analysis, and indexes were compared to a composite criterion for SOO., Results: Data analytics found that V1S plus V2S ≤ 9.25 of the PVC had a LVOT origin (sensitivity 95.4%; specificity 97.5%). V1R + V2R + V3R > 15.0 (a RBBB configuration) likely had a LVOT origin. PVCs with V1S plus V2S > 12.75 (LBBB configuration) likely had a RVOT origin. PVC with V1S plus V2S > 14.25 (LBBB configuration) and all inferior leads positive likely had a RVOT origin., Conclusion: Newer data analytic techniques provide a non-invasive approach to identifying PVC SOO, which should be useful for the clinician evaluating a 12-lead ECG.
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- 2023
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26. Assessment of the QT interval in right bundle branch block.
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Rabkin SW
- Subjects
- Male, Humans, Female, Aged, Electrocardiography, Heart Rate physiology, Bundle-Branch Block diagnosis, Long QT Syndrome diagnosis
- Abstract
Background: Identifying prolonged QT interval in RBBB has been problematic., Methods: Four approaches were compared to adjust for the QT prolongation in intermittent RBBB. The implications were assessed in a separate group of 200 persons with established RBBB., Results: In 12 individuals, mean age 74.5 years with intermittent RBBB, the presence of RBBB significantly ( p < 0.05) increased the QT interval in each of six different heart rate correction formulae by an amount ranging from 35.4 ms in the Hodges formula to 50.2 ms in the Bazett formula. Four different equations were tested to adjust the QT interval and one approach QTc
RBBB = 0.945*QTcRBBB - 26 was the best method to adjust for the increased QT in RBBB as it produced a QT value that was not significantly different from the QT interval in the absence of RBBB in intermittent RBBB.Failure to adjust the QT interval in RBBB produces an overestimate of the QT interval which in some heart rate adjustment formulae was marked. For the Bazett heart rate adjustment approach QTc 450 ms was found in 73.9% of men and QTc over 460 ms was found in 60.6% of women., Conclusion: These data suggest the implementation of a new approach to recalculate the QT intervals in RBBB. QTcRBBB = 0.945*QTcRBBB - 26 with an appropriate heart rate adjustment formula (other than the Bazett formula) accurately predicts the QT interval in the absence of RBBB.- Published
- 2023
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27. Assessing Myocardial Strain and Myocardial Work as a Marker for Hypertensive Heart Disease: A Meta-Analysis.
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Rabkin SW
- Abstract
Background: The main objective of this study was to determine whether myocardial strain and myocardial work are altered in hypertension and whether the strain is independent of hypertension-induced left ventricular hypertrophy., Methods: Two systematic literature searches were conducted using Medline and EMBASE through to June 30, 2022. In the first, search terms left ventricular strain or speckle tracking AND hypertension and left ventricular hypertrophy were used in conjunction with Boolean operators to identify articles reporting left ventricular strain in patients with hypertension. In the second, the terms Global cardiac or myocardial work AND hypertension were used to identify articles. Publication bias was assessed by examination of funnel plots and calculation of the Failsafe N and Duval and Tweedie's Trim and fill. The results were presented as Forrest plots., Results: Global longitudinal strain (GLS) was significantly lower in patients with hypertension compared to those without hypertension with a mean difference of 2.0 ± 0.1 (standard error of mean(SEM)) in the fixed effect model. Global circumferential strain (GCS) was significantly lower in hypertension. The mean difference between the hypertensive and non-hypertensive groups was 1.37 ± 0.17. Global radial strain (GRS) was significantly ( p < 0.05) greater in hypertension. However, this difference was significant in only 3 and of borderline significance in 3 of 14 studies where GRS was measured. The mean difference between the hypertensive and non-hypertensive groups was 1.5 ± 0.5 using the fixed effects model. There was a significant relationship between GLS and GCS as well as between GCS and GRS but no significant relationship between GLS and GRS. There was no significant difference in left ventricular ejection fraction (LVEF) between the hypertension and no hypertension groups. There was no significant relationship between LVEF and either GLS or GCS but a significant negative correlation was found between LVEF and GRS. GLS was further reduced in persons with hypertension and left ventricular hypertrophy (LVH) compared to hypertension without LVH. In contrast, there were no or minimal differences in GCS and GRS for individuals with hypertension and LVH compared to those without LVH. Global myocardial work index (GWI) and Global constructive work (GCW) were significantly greater in patients with hypertension compared to controls. Global wasted work (GWW) indicated significantly less wasted work in controls compared to hypertension. In contrast, Global work efficiency (GWE) was significantly lower in hypertension compared to the control., Conclusions: There was a significant reduction in GLS and GCS in hypertension while GRS was increased. The reduction in GLS in hypertension was not dependent on the presence of LVH. GLS was further reduced in persons with hypertension when LVH was present. In contrast, there were no or minimal differences in GCS and GRS for individuals with LVH compared to those without LVH. GLS was independent of left ventricle (LV) ejection fraction. GWI, GCW and GWW were greater in hypertension while GWE was lower in hypertension compared to controls. These data support the contention that GLS and indices of global work are early markers of hypertensive heart disease., Competing Interests: The authors declare no conflict of interest. Simon W. Rabkin is serving as Guest Editor of this journal. We declare that Simon W. Rabkin had no involvement in the peer review of this article and has no access to information regarding its peer review. Full responsibility for the editorial process for this article was delegated to Vincent Figueredo., (Copyright: © 2023 The Author(s). Published by IMR Press.)
- Published
- 2023
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28. C-Reactive Protein, Interleukin-6, Trimethylamine-N-Oxide, Syndecan-1, Nitric Oxide, and Tumor Necrosis Factor Receptor-1 in Heart Failure with Preserved Versus Reduced Ejection Fraction: a Meta-Analysis.
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Gui XY and Rabkin SW
- Subjects
- Humans, Biomarkers metabolism, Interleukin-6, Natriuretic Peptide, Brain metabolism, Nitric Oxide, Prognosis, Proteomics, Stroke Volume physiology, Syndecan-1, C-Reactive Protein metabolism, Heart Failure
- Abstract
Purpose of Review: The purpose of this review was to synthesize the evidence on non-traditional biomarkers from proteomic and metabolomic studies that may distinguish heart failure (HF) with preserved ejection fraction (HFpEF) from heart failure with reduced ejection fraction (HFrEF) and non-HF., Recent Findings: Understanding the pathophysiology of HFpEF continues to be challenging. A number of inflammatory and metabolic biomarkers that have recently been suggested to be involved include C-reactive protein (CRP), interleukin-6 (IL-6), trimethylamine-N-oxide (TMAO), syndecan-1 (SDC-1), nitric oxide (NO), and tumor necrosis factor receptor-1 (TNFR-1). A systematic search was conducted using Medline, EMBASE, and Web of Science with search terms such as "HFpEF," "metabolomics," and "proteomics," and a meta-analysis was conducted. The results demonstrate significantly higher levels of TMAO, CRP, SDC-1, and IL-6 in HFpEF compared to controls without HF and significantly higher levels of TMAO and CRP in HFrEF compared to controls. The results further suggest that HFpEF might be distinguishable from HFrEF based on higher levels of IL-6 and lower levels of SDC-1 and NO. These data may reflect pathophysiological differences between HFpEF and HFrEF., (© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)
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- 2023
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29. Clozapine-induced Myocarditis: Pathophysiologic Mechanisms and Implications for Therapeutic Approaches.
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Rabkin SW and Tang JKK
- Subjects
- Humans, Myocardium, Myocytes, Cardiac, Apoptosis, Myocarditis chemically induced, Clozapine adverse effects
- Abstract
Clozapine, a superior treatment for treatment-resistant schizophrenia can cause potentially life-threatening myocarditis and dilated cardiomyopathy. While the occurrence of this condition is well known, its molecular mechanisms are unclear and may be multifactorial. Putative mechanisms warrant an in-depth review not only from the perspective of toxicity but also for understanding the molecular mechanisms of the adverse cardiac effects of clozapine and the development of novel therapeutic approaches. Clozapine-induced cardiac toxicity encompasses a diverse set of pathways, including (i) immune modulation and proinflammatory processes encompassing an IgEmediated (type I hypersensitivity) response and perhaps a cytokine release syndrome (ii) catecholaminergic activation (iii) induction of free radicals and oxidative stress (iv) activation of cardiomyocyte cell death pathways, including apoptosis, ischemia through impairment in coronary blood flow via changes in endothelial production of NO and vasoconstriction induced by norepinephrine as well as other factors released from cardiac mast cells. (v) In addition, an extensive examination of the effects of clozapine on non-cardiac cellular proteins demonstrates that clozapine can impair enzymes involved in cellular metabolism, such as pyruvate kinase, mitochondrial malate dehydrogenase, and other proteins, including α-enolase, triosephosphate isomerase and cofilin, which might explain clozapine-induced reductions in myocardial energy generation for cell viability as well as contractile function. Pharmacologic antagonism of these cellular protein effects may lead to the development of strategies to antagonize the cardiac damage induced by clozapine., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)
- Published
- 2023
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30. Heart failure with reduced ejection fraction and diastolic dysfunction (HrEFwDD): Time for a new clinical entity.
- Author
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Rabkin SW
- Subjects
- Diastole, Humans, Stroke Volume, Heart Failure diagnosis, Heart Failure, Diastolic diagnosis, Ventricular Dysfunction, Left diagnostic imaging
- Published
- 2022
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31. Comparison of Unsupervised Machine Learning Approaches for Cluster Analysis to Define Subgroups of Heart Failure with Preserved Ejection Fraction with Different Outcomes.
- Author
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Nouraei H, Nouraei H, and Rabkin SW
- Abstract
Heart failure with preserved ejection (HFpEF) is a heterogenous condition affecting nearly half of all patients with heart failure (HF). Artificial intelligence methodologies can be useful to identify patient subclassifications with important clinical implications. We sought a comparison of different machine learning (ML) techniques and clustering capabilities in defining meaningful subsets of patients with HFpEF. Three unsupervised clustering strategies, hierarchical clustering, K-prototype, and partitioning around medoids (PAM), were used to identify distinct clusters in patients with HFpEF, based on a wide range of demographic, laboratory, and clinical parameters. The study population had a median age of 77 years, with a female majority, and moderate diastolic dysfunction. Hierarchical clustering produced six groups but two were too small (two and seven cases) to be clinically meaningful. The K-prototype methods produced clusters in which several clinical and biochemical features did not show statistically significant differences and there was significant overlap between the clusters. The PAM methodology provided the best group separations and identified six mutually exclusive groups (HFpEF1-6) with statistically significant differences in patient characteristics and outcomes. Comparison of three different unsupervised ML clustering strategies, hierarchical clustering, K-prototype, and partitioning around medoids (PAM), was performed on a mixed dataset of patients with HFpEF containing clinical and numerical data. The PAM method identified six distinct subsets of patients with HFpEF with different long-term outcomes or mortality. By comparison, the two other clustering algorithms, the hierarchical clustering and K-prototype, were less optimal.
- Published
- 2022
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32. Evaluating the adverse outcome of subtypes of heart failure with preserved ejection fraction defined by machine learning: A systematic review focused on defining high risk phenogroups.
- Author
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Rabkin SW
- Abstract
The ability to distinguish clinically meaningful subtypes of heart failure with preserved ejection fraction (HFpEF) has recently been examined by machine learning techniques but studies appear to have produced discordant results. The objective of this study is to synthesize the types of HFpEF by examining their features and relating them to phenotypes with adverse prognosis. A systematic search was conducted using the search terms "Diastolic Heart Failure" OR "heart failure with preserved ejection fraction" OR "heart failure with normal ejection fraction" OR "HFpEF" AND "machine learning" OR "artificial intelligence" OR 'computational biology'. Ten studies were identified and they varied in their prevalence of ten clinical variables: age, sex, body mass index (BMI) or obesity, hypertension, diabetes mellitus, coronary artery disease, atrial fibrillation, chronic kidney disease, chronic obstructive pulmonary disease or symptom severity (NYHA class or BNP). The clinical findings associated with the different phenotypes in > 85 % of studies were age, hypertension, atrial fibrillation, chronic kidney disease and worse symptoms severity; an adverse outcome was in 65 % to 85 % of studies identified diabetes mellitus and female sex and in less than 65 % of studies was body mass index or obesity, and coronary artery disease. COPD was a relevant factor in only 33 % of studies. Adverse clinical outcome - death or admission to hospital (for heart failure) defined phenogroups with the worst outcome. Combining the 4 studies that calculated the MAGGIC score showed a significant (p<0.05) linear relationship between MAGGIC score and outcome, using the one-year event rate. A new score based on strength of the evidence of the HFpEF studies analyzed here, using 9 variables (eliminating COPD), showed a significant (p<0.009) linear relationship with one-year event rate. Three studies examined biomarkers in detail and the ones most prominently related to outcome or consistently found in the studies were GDF15, FABP4, FGF23, sST2, renin and TNF. The dominant factors that identified phenotypes of HFpEF with adverse outcome were hypertension, atrial fibrillation, chronic kidney disease and worse symptoms severity. A new simplified score, based on clinical factors, was proposed to assess prognosis in HFpEF. Several biomarkers were consistently elevated in phenogroups with adverse outcomes and may indicate the underlying mechanism or pathophysiology specific for phenotypes with an adverse prognosis., (Copyright © 2022 Rabkin.)
- Published
- 2022
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33. Hypocalcemia-Induced QT Interval Prolongation.
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Tang JKK and Rabkin SW
- Subjects
- Aged, 80 and over, Arrhythmias, Cardiac, Electrocardiography methods, Heart Rate, Humans, Male, Hypocalcemia complications, Long QT Syndrome
- Abstract
An 87-year-old man with a history of transcatheter aortic valve replacement, pulmonary hypertension, diastolic dysfunction with preserved systolic function, and myelofibrosis had a 12-lead ECG showed a prolonged QT interval of 508 ms with heart-rate correction placing it in the 99th percentile of the population. Reduction in the dose of furosemide and calcium supplementation increased serum calcium and shortened the QT interval. This case provides an opportunity to examine newer concepts for the understanding of the mechanisms by which hypocalcemia might induce QT prolongation. Hypocalcemia likely produces corrected QT interval prolongation primarily through a calcium-dependent inactivation (CDI) mechanism on the L-type calcium channel (LTCC). Lower extracellular calcium leads to a decreased ICaL, subsequently causing intracellular calcium to take longer to reach the critical threshold to induce CDI of the LTCC. The resulting prolonged repolarization of the ventricular myocyte can lead to early after-depolarizations and ensuing life-threatening ventricular arrhythmias. Genetic polymorphisms in Ca2+-binding protein calmodulin which can prolong QT, underscore the role for disturbances of intracellular myocardial calcium handling in arrhythmogenesis. Hypocalcemia is an under-recognized cause of QT prolongation and should be taken into careful consideration in patients presenting with incidental findings of a prolonged QT interval., (© 2022 S. Karger AG, Basel.)
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- 2022
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34. The Fundamental Basis of Palpitations: A Neurocardiology Approach.
- Author
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Kandiah JW, Blumberger DM, and Rabkin SW
- Subjects
- Arrhythmias, Cardiac diagnosis, Arrhythmias, Cardiac etiology, Brain, Heart Rate, Humans, Magnetic Resonance Imaging, Interoception physiology
- Abstract
Background and Objective: Palpitations are a common symptom that may indicate cardiac arrhythmias, be a somatic complaint in anxiety disorders, and can be present in patients without either condition. The objective of this review was to explore the pathways and fundamental mechanisms through which individuals appreciate palpitations., Observations: Cardiac afferents provide beat-to-beat sensory information on the heart to the spinal cord, brain stem, and higher brain centers. Cardioception, a subset of interoception ('the physiological sense of the condition of the body'), refers to sensing of the heartbeat. High cardioception is present in persons with lower body mass index, lower percentages of body fat, and anxiety disorders. Low cardioception (lower interoceptive awareness) is associated with psychiatric disorders, such as depression, personality disorders, and schizophrenia. CNS sites associated with heartbeat detection have been identified by functional magnetic resonance imaging studies and heartbeat-evoked electroencephalogram potentials. The right insula, cingulate gyrus, somatomotor and somatosensory cortices nucleus accumbens, left subthalamic nucleus, and left ventral capsule/striatum are implicated in both palpitations and heartbeat detection. Involvement of the brain as a primary modulator of palpitations rests on the data that various areas of the brain are activated in association with cardioception, the ability of focal brain stimulation to induce palpitations, the ability of central alpha receptor agonists and antagonists to modulate palpitations, and suppression of palpitations by transcranial repetitive magnetic stimulation (rTMS)., Conclusions: Palpitations should be viewed as a pathway extending from the heart to the brain. Palpitations are, in part, a reflection of an individual's cardioception awareness, which is modulated by body size, percentage of body fat, and psychological or psychiatric conditions. Palpitations can originate in the brain and involve central neurotransmitters. Treatment of palpitations unrelated to cardiac arrhythmias or anxiety disorders should consider the use of central alpha-2 agonists and possibly rTMS., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)
- Published
- 2022
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35. Overcoming Obstacles to Develop High-Performance Teams Involving Physician in Health Care Organizations.
- Author
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Rabkin SW and Frein M
- Abstract
Many health care organizations struggle and often do not succeed to be high-performance organizations that are not only efficient and effective but also enjoyable places to work. This review focuses on the physician and organizational roles in limiting achievement of a high-performance team in health care organizations. Ten dimensions were constructed and a number of competencies and metrics were highlighted to overcome the failures to: (i) Ensure that the goals, purpose, mission and vision are clearly defined; (ii) establish a supportive organizational structure that encourages high performance of teams; (iii) ensure outstanding physician leadership, performance, goal attainment; and (iv) recognize that medical team leaders are vulnerable to the abuses of personal power or may create a culture of intimidation/fear and a toxic work culture; (v) select a good team and team members-team members who like to work in teams or are willing and able to learn how to work in a team and ensure a well-balanced team composition; (vi) establish optimal team composition, individual roles and dynamics, and clear roles for members of the team; (vii) establish psychological safe environment for team members; (viii) address and resolve interpersonal conflicts in teams; (xi) ensure good health and well-being of the medical staff; (x) ensure physician engagement with the organization. Addressing each of these dimensions with the specific solutions outlined should overcome the constraints to achieving high-performance teams for physicians in health care organizations.
- Published
- 2021
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36. The association of polymorphism in PHACTR1 rs9349379 and rs12526453 with coronary artery atherosclerosis or coronary artery calcification. A systematic review.
- Author
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Koitsopoulos PG and Rabkin SW
- Subjects
- Coronary Artery Disease pathology, Coronary Artery Disease physiopathology, Genetic Predisposition to Disease, Humans, Polymorphism, Single Nucleotide, Atherosclerosis genetics, Coronary Artery Disease genetics, Coronary Stenosis genetics, Microfilament Proteins genetics, Vascular Calcification genetics
- Abstract
Objective: There is a need to identify genetic factors that may produce coronary artery atherosclerotic disease (CAD) that are not involved in the usual risk factors leading to CAD. Previous studies have often equated coronary artery calcification (CAC) with CAD with coronary stenosis or its sequelae. The objective of this study was to examine the relationship between phosphatase and actin regulator 1 (PHACTR1) single nucleotide polymorphisms (SNPs) and the type of coronary artery disease CAD versus CAC., Method: A systematic review of the literature was conducted to answer the question of whether PHACTR1 gene polymorphisms are associated with coronary artery disease expressed as coronary artery atherosclerosis or CAC., Results: Eighteen studies spanning seven PHACTR1 SNPs were identified and evaluated for the relationship between PHACTR1 and coronary artery disease. There were significant relationships between rs9349379, rs12526453, and CAD with odds ratios (ORs) (confidence interval) of, respectively, 1.15 (1.13-1.17), 1.13 (1.09-1.17) but not for rs2026458, 1.03 (0.88-1.19). The OR for CAC was 1.22 (1.18-1.26) for rs9349379 and 1.28 (1.21-1.38) for rs12526453., Conclusions: Several PHACTR1 specifically rs9349379 and rs12526453 polymorphisms but not rs2026458, are associated with CAD. There are differences in the association of PHACTR1 SNPs with CAC. PHACTR1 warrants more attention and study for the prevention and treatment of CAD., (Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.)
- Published
- 2021
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37. The utility of growth differentiation factor-15, galectin-3, and sST2 as biomarkers for the diagnosis of heart failure with preserved ejection fraction and compared to heart failure with reduced ejection fraction: a systematic review.
- Author
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Rabkin SW and Tang JKK
- Subjects
- Blood Proteins, Galectin 3 blood, Galectins, Growth Differentiation Factor 15 blood, Humans, Interleukin-1 Receptor-Like 1 Protein blood, Stroke Volume, Biomarkers blood, Heart Failure diagnosis
- Abstract
The objective was to evaluate the diagnosis of heart failure with preserved ejection fraction (HFpEF) using the biomarkers, growth differentiation factor-15 (GDF-15), galectin-3 (Gal-3), and soluble ST2 (sST2), and to determine whether they can differentiate HFpEF from heart failure with reduced ejection fraction (HFrEF). Medline and Embase databases were searched with the terms diastolic heart failure or HFpEF, biomarkers, and diagnosis, limited to years 2000 to 2019. There were significantly and consistently higher levels of GDF-15, Gal-3, and sST2 in HFpEF compared to no heart failure. Importantly, the magnitude of the increase in GDF-15 or Gal-3 and possibly sST2,correlated with a greater degree of diastolic dysfunction. There were no significant differences between GDF-15, Gal-3, and sST2 in patients with HFpEF vs HFrEF. In the studies assessing these three biomarkers, BNP was significantly greater in heart failure than controls. Furthermore, BNP was significantly higher in HFrEF compared to HFpEF. The diagnostic utility of GDF-15, Gal-3, and sST2 compared to BNP was evaluated by comparing ROC curves. The data supports the contention that to distinguish HFpEF from HFrEF, an index is needed that incorporates GDF-15, Gal-3, or sST2 as well as BNP. The three biomarkers GDF-15, Gal-3, or sST2 can identify patients with HFpEF compared to individuals without heart failure but cannot differentiate HFpEF from HFrEF. BNP is higher in and is better at differentiating HFrEF from HFpEF. Indices that incorporate GDF-15, Gal-3, or sST2 as well as BNP show promise in differentiating HFpEF from HFrEF.
- Published
- 2021
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38. A new approach to the clinical subclassification of heart failure with preserved ejection fraction.
- Author
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Nouraei H and Rabkin SW
- Subjects
- Female, Humans, Male, Prognosis, Risk Factors, Stroke Volume, Atrial Fibrillation, Coronary Artery Disease, Heart Failure diagnosis
- Abstract
Objective: Heart failure with preserved ejection (HFpEF) represents nearly half of all patients with heart failure (HF). The objective of this study was to determine whether patient characteristics identify discrete kinds of HFpEF., Methods: Data were collected on 196 patients with HFpEF in a non-hospitalized setting. Clinical and laboratory variables were collected, and 47 candidate variables were examined by the unsupervised clustering strategy partitioning around medoids. The Meta-analysis Global Group in Chronic Heart Failure (MAGGIC) risk score was calculated. Follow-up data on all-cause mortality, cardiovascular mortality, and HF exacerbation, were collected and were not part of the data used to identify subgroups., Results: Six significantly different groups or clusters were found. There were three groups of women (i) individuals with a low proportion of vascular risk factors (HFpEF
1 ) (ii) individuals with a high proportion of hypertension and diabetes, but lower proportion of kidney disease and diastolic dysfunction (HFpEF3) (iii) older individuals with high rates of atrial fibrillation (AF), chronic kidney disease. They had the worst long-term outcomes (HFpEF4 ). There were three groups of men (i) individuals with a high proportion of coronary artery disease (CAD), dyslipidemia, higher serum creatinine, and diastolic dysfunction (HFpEF2 )(ii) individuals with highest BMI, and high proportion of CAD, obstructive sleep apnea, and poorly controlled diabetes (HFpEF5 ) (iii) individuals with high rates of AF, elevated BNP, biventricular remodeling (HFpEF6 ). They had a high cardiovascular mortality., Conclusions: HFpEF consists of a heterogenous group of individuals with six distinct clinical subsets that have different long-term outcomes., Competing Interests: Declaration of Competing Interest There were no conflicts of interest., (Copyright © 2021 Elsevier B.V. All rights reserved.)- Published
- 2021
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39. Circadian variation of the QT interval and heart rate variability and their interrelationship.
- Author
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Singh I and Rabkin SW
- Subjects
- Adrenergic beta-Antagonists, Heart, Heart Rate, Humans, Circadian Rhythm, Electrocardiography
- Abstract
Background: Whether the QT interval displays circadian rhythm after heart rate correction is unresolved and the relationship of QT interval to heart rate variability (HRV) is uncertain., Objectives: To test the hypothesis that there is a circadian rhythm to QT interval and HRV and determine the relationship between QTc and HRV., Methods: The hourly average ECG data from 24-h ECGs were examined in individuals (50 without medications and 9 on beta blockers only) with no evidence of coronary artery disease or structural heart disease. The QT duration of normal QRS complexes from a series of 30-s windows was measured. The presence of circadian rhythm was tested by the data analytic approach of goodness of fit to a cosine function., Results: QT interval with and without heart rate correction showed a circadian rhythm for five heart rate adjustment formulae except for the Bazett formula. HRV also showed circadian rhythm but with different acrophages and nadirs depending on the HRV component. There were significant (p < 0.05) positive correlations of QTc with pNN50 rms-SD and SDNN and significant (p < 0.05) negative correlations with SDANN and Tri. The beta blocker group did not generally show circadian rhythm for QT interval or HRV., Conclusion: QT, after heart rate adjustment, and HRV have circadian rhythmicity. There are significant correlations between QT interval and HRV indices. Circadian rhythm was blunted with beta blockers. The data are consistent with the concept of a predominance of parasympathetic activity to increase QTc and sympathetic activity to shorten QTc, even after 'correction' of the QT interval for heart rate., (Copyright © 2021 Elsevier Inc. All rights reserved.)
- Published
- 2021
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40. The Short QTc Is a Marker for the Development of Atrial Flutter and Atrial Fibrillation.
- Author
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Rabkin SW and Tang JKK
- Abstract
A short QT interval has been difficult to define, and there is debate whether it exists outside of an extremely small group of individuals with inherited channelopathies and whether it predicts cardiac arrhythmias. The objective was to identify cases with short QT and their consequences. Our hospital ECG database was screened for cases with a QTc based on the Bazett formula (QTcBZT) of less than 340 ms. The QTc was recalculated using the spline (QTcRBK) formula, which more accurately adjusts for the heart rate and identifies cases based on percentile distribution of the QT interval. The exclusion criteria were presence of bundle branch block, arrhythmias, or electronic pacemakers. An age- and sex-matched cohort was obtained from individuals with normal QT intervals with the same exclusion criteria. There were 28 cases with a short QTc (QTcRBK < 380 ms). The age was 69.6 ± 14.6 years (mean ± SD) (50% males). The QT interval was 305.7 ± 61.1 ms with QTcRBK 308.4 ± 31.4 ms. Subsequent ECGs showed atrial flutter in 21%, atrial fibrillation in 18%, and atrial tachycardia in 4% of cases. Thus, atrial arrhythmias occurred in 43% of cases. This incidence was significantly ( p < 0.0001) greater than the incidence of atrial arrhythmias in age- and sex-matched controls. In conclusion, a short QT interval can be readily identified based on the first percentile of the new QTc formula. A short QTc is an important marker for the development of atrial arrhythmias, including atrial flutter and atrial fibrillation, with the former predominating. It should be part of patient assessment and warrants consideration to develop strategies for detection and prevention of atrial arrhythmias., Competing Interests: The authors declare no conflicts of interest., (Copyright © 2020 Simon W. Rabkin and Jacky K. K. Tang.)
- Published
- 2020
- Full Text
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41. Blood Pressure Variability: The Implications of Home Versus Automated Office Measurement.
- Author
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Rabkin SW
- Subjects
- Blood Pressure, Blood Pressure Determination, Blood Pressure Monitoring, Ambulatory
- Published
- 2020
- Full Text
- View/download PDF
42. Hypertension Canada's 2020 Comprehensive Guidelines for the Prevention, Diagnosis, Risk Assessment, and Treatment of Hypertension in Adults and Children.
- Author
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Rabi DM, McBrien KA, Sapir-Pichhadze R, Nakhla M, Ahmed SB, Dumanski SM, Butalia S, Leung AA, Harris KC, Cloutier L, Zarnke KB, Ruzicka M, Hiremath S, Feldman RD, Tobe SW, Campbell TS, Bacon SL, Nerenberg KA, Dresser GK, Fournier A, Burgess E, Lindsay P, Rabkin SW, Prebtani APH, Grover S, Honos G, Alfonsi JE, Arcand J, Audibert F, Benoit G, Bittman J, Bolli P, Côté AM, Dionne J, Don-Wauchope A, Edwards C, Firoz T, Gabor JY, Gilbert RE, Grégoire JC, Gryn SE, Gupta M, Hannah-Shmouni F, Hegele RA, Herman RJ, Hill MD, Howlett JG, Hundemer GL, Jones C, Kaczorowski J, Khan NA, Kuyper LM, Lamarre-Cliche M, Lavoie KL, Leiter LA, Lewanczuk R, Logan AG, Magee LA, Mangat BK, McFarlane PA, McLean D, Michaud A, Milot A, Moe GW, Penner SB, Pipe A, Poppe AY, Rey E, Roerecke M, Schiffrin EL, Selby P, Sharma M, Shoamanesh A, Sivapalan P, Townsend RR, Tran K, Trudeau L, Tsuyuki RT, Vallée M, Woo V, Bell AD, and Daskalopoulou SS
- Subjects
- Adult, Algorithms, Antihypertensive Agents therapeutic use, Blood Pressure Monitoring, Ambulatory, Canada, Cardiovascular Diseases complications, Cardiovascular Diseases prevention & control, Child, Diabetes Complications, Drug Resistance, Female, Health Promotion, Heart Failure complications, Humans, Hypertension complications, Hypertension etiology, Hypertrophy, Left Ventricular complications, Medication Adherence, Preconception Care, Pregnancy, Pregnancy Complications, Cardiovascular therapy, Renal Insufficiency, Chronic complications, Risk Assessment, Stroke complications, Telemedicine, Hypertension diagnosis, Hypertension therapy
- Abstract
Hypertension Canada's 2020 guidelines for the prevention, diagnosis, risk assessment, and treatment of hypertension in adults and children provide comprehensive, evidence-based guidance for health care professionals and patients. Hypertension Canada develops the guidelines using rigourous methodology, carefully mitigating the risk of bias in our process. All draft recommendations undergo critical review by expert methodologists without conflict to ensure quality. Our guideline panel is diverse, including multiple health professional groups (nurses, pharmacy, academics, and physicians), and worked in concert with experts in primary care and implementation to ensure optimal usability. The 2020 guidelines include new guidance on the management of resistant hypertension and the management of hypertension in women planning pregnancy., (Copyright © 2020 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.)
- Published
- 2020
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43. Assessment of QT interval in ventricular paced rhythm: Derivation of a novel formula.
- Author
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Tang JKK, Bennett MT, and Rabkin SW
- Subjects
- Cardiac Pacing, Artificial, Electrocardiography, Heart Rate, Heart Ventricles, Humans, Long QT Syndrome, Pacemaker, Artificial
- Abstract
Objective: The objective of the study was to determine the optimal formula to estimate QT interval adjusting for QRS prolongation during right ventricular (RV) pacing., Methods: This observational study included individuals (n = 43) with a newly implanted permanent ventricular pacemaker, who had a narrow QRS complex before pacemaker insertion. QT interval with RV pacing was related to QT interval before pacemaker implantation. The validation cohort (n = 442) had permanent RV pacing in DDD mode., Results: A new QTc formula was derived utilizing the constants from the relationship between the spline heart rate QT correction (QTcRBK) before and after pacing; specifically, QTcRBK
PACED = QTcRBK × 0.86. The JT interval from paced complexes was highly heart rate (HR) dependent and was not accurate for QT assessment. Previous, QTc formula for paced complexes were not highly correlated with QT before pacing unless a robust HR correction is added. Formulae subtracting a fixed amount from QTcPACED markedly overestimated QTc before pacing., Conclusion: We proposed a new, simple formula for QT estimation in RV pacing. JT interval in paced complexes is highly HR dependent and is not accurate for QT assessment. The new spline approach for HR correction for the QT, once incorporated into some previously proposed formulae, blunts HR dependency and improves prediction of QT before pacing. QTcRBKPACED *0.86 and QTcRBKPACED - (QRS*0.5) demonstrated the best balance of relatively strong correlation to QTc before pacing and accurate QTc prolongation identification. Abnormal QT for QTcRBKPACED *0.86 as defined by the 97.5th and 99th percentile are 469 and 479 ms respectively., (Copyright © 2019 Elsevier Inc. All rights reserved.)- Published
- 2019
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44. Physician engagement: the Vancouver Medical Staff Association engagement charter.
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Rabkin SW, Dahl M, Patterson R, Mallek N, Straatman L, Pinfold A, Charles MK, van Gaal S, Wong S, and Vaghadia H
- Subjects
- British Columbia, Burnout, Professional prevention & control, Humans, Leadership, Medical Staff organization & administration, Patient Care standards, Physicians organization & administration, Work Engagement
- Abstract
Engagement of physicians with their healthcare community or institution should be a central issue in healthcare because it can be translated into improved patient care, enhanced well-being for physicians as well as safer, more effective and less costly healthcare. To accomplish the mission/goal of meaningful physician engagement, we set about to establish a 'charter' for physician engagement. We defined our concept of meaningful physician engagement and customised the engagement spectrum construct for physician relationship with their healthcare community or institution. While recognising the importance of physician leaders within the hierarchical system for efficacy of organisational management, relying only on physicians in formal executive positions is insufficient for developing physician engagement. There is a need for widespread physician engagement across the organisation. The objective is both an improvement in patient care and in physician well-being., (© Royal College of Physicians 2019. All rights reserved.)
- Published
- 2019
- Full Text
- View/download PDF
45. The effect of exercise on the ECG criteria for early repolarization pattern.
- Author
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Nouraei H and Rabkin SW
- Subjects
- Exercise, Heart Rate, Humans, Arrhythmias, Cardiac, Electrocardiography
- Abstract
Objective: To determine the effect of exercise and heart rate on the early repolarization (ER) pattern; focusing on the new criteria for identification of ER., Methods: The ECG measurements on the terminal QRS notch or slur found in early repolarization were quantitated before, during and after exercise; specifically: (i) the amplitude at the onset of the notch (J
o ) (ii) the amplitude at the peak of the notch (Jp ), (iii) the amplitude at the end of the notch (Jt ), (iv) the duration from Jo to Jp (D1 ) and (v) the duration from Jo to Jt (D2 )., Results: All individuals (N = 21) fulfilling the criteria for ER showed complete disappearance of ER after 3 min of exercise. After 5 min of recovery, 29% of subjects showed return of the ER. The return of ER was dynamic with QRS notching of varying extent, without ST elevation, being evident first. The relationship between heart rate and ER was significant and nonlinear, best fit by a second-order polynomial, suggesting that changes in heart rate with exercise was a factor influencing the presence of the ER pattern and the parameters that define ER., Conclusion: Each of the newly defined characteristics of the ER are modified and eventually disappear with exercise. The return of ER was dynamic with QRS notching of varying extent being evident first. The changes correlated with variations in heart rate, during both exercise and recovery, suggesting, in part, a role in the underlying mechanism of ER., (Copyright © 2019 Elsevier Inc. All rights reserved.)- Published
- 2019
- Full Text
- View/download PDF
46. Determination of the QT Interval in Left Bundle Branch Block: Development of a Novel Formula.
- Author
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Tang JKK and Rabkin SW
- Subjects
- Aged, Female, Heart Rate physiology, Humans, Male, Bundle-Branch Block physiopathology, Electrocardiography, Models, Cardiovascular
- Abstract
Background: Determination of the prolonged QT interval in left bundle branch block (LBBB), which should be of special concern to identify individuals at high risk of potentially fatal cardiac arrhythmia risk, has been problematic., Methods: Electrocardiograms (ECGs) (n = 17) in intermittent LBBB were used to develop a new formula for the calculation of QTc in LBBB. This formula and 5 others were compared in a population with LBBB (n = 2610). The QT was corrected for heart rate (HR) using the Bazett formula (QTcBZT) and the spline QT formula (QTcRBK), which is relatively independent of HR. The JT interval was significantly related to HR., Results: The new approach (QTc
LBBB NEW = 0.945*QTcRBKLBBB - 26) in LBBB showed the highest correlation with intrinsic QTc (without LBBB) and had minimal HR dependency. Previous formulae to determine the QT interval in LBBB showed significant HR dependency except for one proposed by Rautaharju et al. Inclusion of an HR correction factor in existing formulae blunted HR dependency but not if the QT interval was adjusted by the QTcBZT. In men and women, use of the QTcBZT markedly increases the proportion of individuals with prolonged QTc, which was more evident with increasing HR. The 99th and 97.5th percentiles for QTcLBBB NEW for men and women identified abnormal QT prolongation in LBBB., Conclusions: A new formula that modifies the QT and JT intervals in LBBB predicts the QT interval in the absence of LBBB. Abnormal QT intervals in the 99th and 97.5th percentiles can identify patients with LBBB who have QT interval prolongation., (Copyright © 2019 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.)- Published
- 2019
- Full Text
- View/download PDF
47. Hypoxia-inducible factor 1-alpha (HIF-1α) as a factor mediating the relationship between obesity and heart failure with preserved ejection fraction.
- Author
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Warbrick I and Rabkin SW
- Subjects
- Animals, Fibrosis metabolism, Heart Failure complications, Humans, Macrophages metabolism, Obesity complications, Adipose Tissue metabolism, Heart Failure metabolism, Hypoxia-Inducible Factor 1, alpha Subunit metabolism, Obesity metabolism, Stroke Volume physiology
- Abstract
Heart failure with preserved ejection fraction (HFpEF), a common condition with an increased mortality, is strongly associated with obesity and the metabolic syndrome. The latter two conditions are associated with increased epicardial fat that can extend into the heart. This review advances the proposition that hypoxia-inhibitory factor-1α (HIF-1α) maybe a key factor producing HFpEF. HIF-1α, a highly conserved transcription factor that plays a key role in tissue response to hypoxia, is increased in adipose tissue in obesity. Increased HIF-1α expression leads to expression of a potent profibrotic transcriptional programme involving collagen I, III, IV, TIMP, and lysyl oxidase. The net effect is the formation of collagen fibres leading to fibrosis. HIF-1α is also responsible for recruiting M1 macrophages that mediate obesity-associated inflammation, releasing IL-6, MCP-1, TNF-α, and IL-1β with increased expression of thrombospondin, pro α2 (I) collagen, transforming growth factor β, NADPH oxidase, and connective tissue growth factor. These factors can accelerate cardiac fibrosis and impair cardiac diastolic function. Inhibition of HIF-1α expression in adipose tissue of mice fed a high-fat diet suppressed fibrosis and reduces inflammation in adipose tissue. Delineation of the role played by HIF-1α in obesity-associated HFpEF may lead to new potential therapies., (© 2019 World Obesity Federation.)
- Published
- 2019
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48. Effect of the peptides Relaxin, Neuregulin, Ghrelin and Glucagon-like peptide-1, on cardiomyocyte factors involved in the molecular mechanisms leading to diastolic dysfunction and/or heart failure with preserved ejection fraction.
- Author
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Warbrick I and Rabkin SW
- Subjects
- Animals, Humans, Myocytes, Cardiac metabolism, Sarcoplasmic Reticulum Calcium-Transporting ATPases metabolism, Ghrelin metabolism, Glucagon-Like Peptide 1 metabolism, Heart Failure metabolism, Neuregulins metabolism, Relaxin metabolism
- Abstract
Heart failure with preserved ejection fraction (HFpEF) represents an important cardiac condition because of its increasing prevalence, resistance to treatment and high associated morbidity and mortality. Two of the major mechanisms responsible for HFpEF are impaired cardiomyocyte sarcoplasmic reticulum (SR) Ca
2+ ATPase (SERCA2a), which is responsible for calcium reuptake into the SR, and cardiac fibroblasts/myofibroblasts that produce collagen or myocardial fibrosis. Phospholamban (PLB), in the SR and endoplasmic reticulum, is the primary regulator of SERCA2a in the heart and acts as a reversible inhibitor of SERCA2a. Glucagon-like peptide-1, a 30 amino acid peptide, improves diastolic function through increasing SERCA2a expression and activity as well as by decreasing phosphorylation of Ryanodine receptors. It also enhances collagen production through enhanced procollagen IalphaI/IIIalphaI, connective tissue growth factor, fibronectin, TGF-β3 as well as Interleukin -10, -1beta, and -6 gene expression. Relaxin-2, a two chain, 53 amino acid peptide, increases Ser16- and Thr17-phosphorylation levels of PLB, thereby relieving SERCA2a of its inhibition. H3 Relaxin inhibits TGF-β1-stimulated collagen deposition through H3 relaxin-induced increases in pSmad2. Neuregulin-1, an epidermal growth factor, induces nitric oxide and PI-3 kinase activation that enhance SERCA2 activity. Neuregulin-1 was associated with less myocardial macrophage infiltration and cytokine expression reducing collagen deposition. Ghrelin, a 28 amino acid peptide, improves SERCA2a function by inducing PLB phosphorylation. Ghrelin also reduces cardiac fibrosis. In summary, Glucagon-like peptide-1, Relaxin-2, Neuregulin-1, and Ghrelin each modify calcium dynamics, collagen expression, and myocardial fibrosis through attenuation of deleterious signaling cascades, and induction of adaptive pathways, representing potential therapeutic targets for HFpEF., (Copyright © 2018 Elsevier Inc. All rights reserved.)- Published
- 2019
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49. Hypertension Canada's 2018 Guidelines for Diagnosis, Risk Assessment, Prevention, and Treatment of Hypertension in Adults and Children.
- Author
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Nerenberg KA, Zarnke KB, Leung AA, Dasgupta K, Butalia S, McBrien K, Harris KC, Nakhla M, Cloutier L, Gelfer M, Lamarre-Cliche M, Milot A, Bolli P, Tremblay G, McLean D, Padwal RS, Tran KC, Grover S, Rabkin SW, Moe GW, Howlett JG, Lindsay P, Hill MD, Sharma M, Field T, Wein TH, Shoamanesh A, Dresser GK, Hamet P, Herman RJ, Burgess E, Gryn SE, Grégoire JC, Lewanczuk R, Poirier L, Campbell TS, Feldman RD, Lavoie KL, Tsuyuki RT, Honos G, Prebtani APH, Kline G, Schiffrin EL, Don-Wauchope A, Tobe SW, Gilbert RE, Leiter LA, Jones C, Woo V, Hegele RA, Selby P, Pipe A, McFarlane PA, Oh P, Gupta M, Bacon SL, Kaczorowski J, Trudeau L, Campbell NRC, Hiremath S, Roerecke M, Arcand J, Ruzicka M, Prasad GVR, Vallée M, Edwards C, Sivapalan P, Penner SB, Fournier A, Benoit G, Feber J, Dionne J, Magee LA, Logan AG, Côté AM, Rey E, Firoz T, Kuyper LM, Gabor JY, Townsend RR, Rabi DM, and Daskalopoulou SS
- Subjects
- Adult, Antihypertensive Agents administration & dosage, Antihypertensive Agents classification, Canada, Cardiovascular Diseases etiology, Child, Evidence-Based Practice, Female, Health Promotion methods, Humans, Male, Risk Assessment methods, Blood Pressure Determination instrumentation, Blood Pressure Determination methods, Blood Pressure Determination standards, Blood Pressure Monitoring, Ambulatory instrumentation, Blood Pressure Monitoring, Ambulatory methods, Cardiovascular Diseases prevention & control, Hypertension complications, Hypertension diagnosis, Hypertension therapy, Preventive Health Services methods
- Abstract
Hypertension Canada provides annually updated, evidence-based guidelines for the diagnosis, assessment, prevention, and treatment of hypertension in adults and children. This year, the adult and pediatric guidelines are combined in one document. The new 2018 pregnancy-specific hypertension guidelines are published separately. For 2018, 5 new guidelines are introduced, and 1 existing guideline on the blood pressure thresholds and targets in the setting of thrombolysis for acute ischemic stroke is revised. The use of validated wrist devices for the estimation of blood pressure in individuals with large arm circumference is now included. Guidance is provided for the follow-up measurements of blood pressure, with the use of standardized methods and electronic (oscillometric) upper arm devices in individuals with hypertension, and either ambulatory blood pressure monitoring or home blood pressure monitoring in individuals with white coat effect. We specify that all individuals with hypertension should have an assessment of global cardiovascular risk to promote health behaviours that lower blood pressure. Finally, an angiotensin receptor-neprilysin inhibitor combination should be used in place of either an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker in individuals with heart failure (with ejection fraction < 40%) who are symptomatic despite appropriate doses of guideline-directed heart failure therapies. The specific evidence and rationale underlying each of these guidelines are discussed., (Copyright © 2018 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.)
- Published
- 2018
- Full Text
- View/download PDF
50. Effect of Lowering Diastolic Pressure in Patients With and Without Cardiovascular Disease: Analysis of the SPRINT (Systolic Blood Pressure Intervention Trial).
- Author
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Khan NA, Rabkin SW, Zhao Y, McAlister FA, Park JE, Guan M, Chan S, and Humphries KH
- Subjects
- Aged, Blood Pressure drug effects, Cardiovascular Diseases complications, Cardiovascular Diseases mortality, Comorbidity, Dose-Response Relationship, Drug, Drug Administration Schedule, Female, Follow-Up Studies, Humans, Hypertension complications, Hypertension mortality, Male, Middle Aged, Reference Values, Risk Assessment, Severity of Illness Index, Survival Analysis, Systole drug effects, Treatment Outcome, Antihypertensive Agents therapeutic use, Blood Pressure Determination methods, Cardiovascular Diseases diagnosis, Diastole drug effects, Hypertension diagnosis, Hypertension drug therapy
- Abstract
Systolic and diastolic blood pressure thresholds, below which cardiovascular events increase, are widely debated. Using data from the SPRINT (Systolic Blood Pressure Intervention Trial), we evaluated the relation between systolic and diastolic pressure and cardiovascular events among 1519 participants with or 7574 without prior cardiovascular disease. Using Cox regression, we examined the composite risk of myocardial infarction, other acute coronary syndrome, stroke, heart failure, or cardiovascular death, and follow-up systolic and diastolic pressure were analyzed as time-dependent covariates for a median of 3.1 years. Models were adjusted for age, sex, baseline systolic pressure, body mass index, 10-year Framingham risk score, and estimated glomerular filtration rate. A J-shaped relationship with diastolic pressure was observed in both treatment arms in patients with or without cardiovascular disease ( P nonlinearity≤0.002). When diastolic pressure fell <55 mm Hg, the hazards were at least 25% higher relative to 70 mm Hg ( P =0.29). The hazard ratios (95% CI) of diastolic pressure <55 mm Hg versus 55 to 90 mm Hg were 1.68 (1.16-2.43), P value 0.006 and 1.52 (0.99-2.34), P value 0.06 in patients without and with prior cardiovascular disease, respectively. After adjusting for follow-up diastolic pressure, follow-up systolic pressure was not associated with the outcome in those without prior cardiovascular disease ( P =0.64). In those with cardiovascular disease, adjusting for diastolic pressure, follow-up systolic pressure was associated with the risk in the intensive arm (hazard ratio per 10 mm Hg decrease, 0.86; 95% CI, 0.75-0.99; P interaction=0.02). Although the observed J-shaped relationship may be because of reverse causality in the SPRINT population, we advise caution in aggressively lowering diastolic pressure., (© 2018 American Heart Association, Inc.)
- Published
- 2018
- Full Text
- View/download PDF
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