257 results on '"Deedwania PC"'
Search Results
2. Primary prevention of atrial fibrillation - the path untread
- Author
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Lardizabal, JA and Deedwania, PC
- Abstract
The prevalence and incidence of atrial fibrillation (AF) is on the rapid rise. To slow down the AF epidemic, effective primary prevention strategies need to be instituted. Unfortunately, this is an area that has not been well-explored. There is a multitude of risk factors that predispose to the development of AF. Of these, the most common from an epidemiologic perspective are advanced age, hypertension, diabetes, ischemic heart disease, and heart failure. The first-line pharmacologic therapies for these predisposing conditions (e.g. beta blockers, renin-Angiotensin system inhibitors, statins, and omega-3 fatty acids) appear to also have potential roles in the primary prevention of AF. Definitive data, however, is lacking as to efficacy of these drugs for this particular purpose. Large-scale, high-quality randomized clinical trials on AF primary preventive strategies are urgently required in order to guide clinical practice. For now, adherence to the guideline-based therapies of each individual risk factor appears to be the most reasonable approach for the primary prevention of AF.
- Published
- 2013
3. Differing predictive relationships between baseline LDL-C, systolic blood pressure, and cardiovascular outcomes
- Author
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Deedwania, PC, Pedersen, TR, DeMicco, DA, Breazna, A, Betteridge, DJ, Hitman, GA, Durrington, P, Neil, A, and TNT, CARDS and IDEAL Steering Committees and Investigators
- Subjects
Male ,medicine.medical_specialty ,Atorvastatin ,Population ,Blood Pressure ,030204 cardiovascular system & hematology ,Cohort Studies ,03 medical and health sciences ,0302 clinical medicine ,Double-Blind Method ,Predictive Value of Tests ,Risk Factors ,Internal medicine ,Diabetes mellitus ,medicine ,Humans ,Prospective Studies ,cardiovascular diseases ,030212 general & internal medicine ,Myocardial infarction ,education ,Stroke ,Aged ,education.field_of_study ,business.industry ,Cholesterol, LDL ,Middle Aged ,medicine.disease ,Treatment Outcome ,Blood pressure ,Cardiovascular Diseases ,Cohort ,Cardiology ,Female ,Cardiology and Cardiovascular Medicine ,business ,Dyslipidemia ,Follow-Up Studies ,medicine.drug - Abstract
Background Traditional cardiovascular risk factors, such as hypertension and dyslipidemia, predispose individuals to cardiovascular disease, particularly patients with diabetes. We investigated the predictive value of baseline systolic blood pressure (SBP) and low-density lipoprotein cholesterol (LDL-C) on the risk of vascular outcomes in a large population of patients at high risk of future cardiovascular events. Methods Data were pooled from the TNT (Treating to New Targets), CARDS (Collaborative Atorvastatin Diabetes Study), and IDEAL (Incremental Decrease in End-Points Through Aggressive Lipid Lowering) trials and included a total of 21,727 patients (TNT: 10,001; CARDS: 2838; IDEAL: 8888). The effect of baseline SBP and LDL-C on cardiovascular events, coronary events, and stroke was evaluated using a multivariate Cox proportional-hazards model. Results Overall, risk of cardiovascular events was significantly higher for patients with higher baseline SBP or LDL-C. Higher baseline SBP was significantly predictive of stroke but not coronary events. Conversely, higher baseline LDL-C was significantly predictive of coronary events but not stroke. Results from the subgroup with diabetes (5408 patients; TNT: 1501; CARDS: 2838; IDEAL: 1069) were broadly consistent with those of the total cohort: baseline SBP and LDL-C were significantly predictive of cardiovascular events overall, with the association to LDL-C predominantly related to an effect on coronary events. However, baseline SBP was not predictive of either coronary or stroke events in the pooled diabetic population. Conclusions In this cohort of high-risk patients, baseline SBP and LDL-C were significantly predictive of cardiovascular outcomes, but this effect may differ between the cerebrovascular and coronary systems. Trial Registration Number : NCT00327691 (TNT); NCT00327418 (CARDS); NCT00159835 (IDEAL).
- Published
- 2019
4. Evolocumab and clinical outcomes in patients with cardiovascular disease
- Author
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Sabatine, MS, Giugliano, RP, Keech, AC, Honarpour, N, Wiviott, SD, Murphy, SA, Kuder, JF, Wang, H, Liu, T, Wasserman, SM, Sever, PS, Pedersen, TR, Fish, MP, Abrahamsen, TE, Im, K, Kanevsky, E, Bonaca, MP, Lira Pineda, A, Hanlon, K, Knusel, B, Somaratne, R, Kurtz, C, Scott, R, Accini Mendoza, JL, Amerena, J, Badariene, J, Burgess, L, Ceska, R, Charng, MJ, Choi, D, Cobos, JL, Dan, GA, De Ferrari, GM, Deedwania, PC, Chopra, VK, Erglis, A, Ezhov, MV, Ferreira, J, Filipová, S, Gaciong, ZA, Pasierski, T, Georgiev, BG, Gonzalez-Galvez, G, Gouni-Berthold, I, Schäufele, T, Hirayama, A, Huber, K, Rammer, M, Kjaerulf Jensen, H, Wermuth, S, Jiang, L, Jukema, JW, Kraydashenko, O, Leiter, LA, Lewis, BS, López-Miranda, J, Lorenzatti, AJ, Mach, F, McAdam, B, Nilsson, L, Olsson, A, Rallidis, L, Rogelio, GG, Kerr Saraiva, JF, Scheen, A, Schiele, F, Connolly, D, Siu, CW, Tay, L, Thorgeirsson, G, Tikkanen, MJ, Tokgozoglu, SL, Toth, K, Viigimaa, M, Wan Ahmad, WA, Hennekens, CH, Andreotti, F, Baigent, C, Brown, WV, Davis, BR, Newcomer, JW, Wood, SK, LaRosa, J, Ansell, B, Lowe, C, Zahn, L, Awtry, E, Berger, C, Croce, K, Desai, A, Gelfand, E, Ho, C, Leeman, D, Link, M, Norden, A, Pande, A, Rost, N, Ruberg, F, Silverman, S, and Singhal, A
- Abstract
© 2017 Massachusetts Medical Society. BACKGROUND Evolocumab is a monoclonal antibody that inhibits proprotein convertase subtilisin-kexin type 9 (PCSK9) and lowers low-density lipoprotein (LDL) cholesterol levels by approximately 60%. Whether it prevents cardiovascular events is uncertain. METHODS We conducted a randomized, double-blind, placebo-controlled trial involving 27,564 patients with atherosclerotic cardiovascular disease and LDL cholesterol levels of 70 mg per deciliter (1.8 mmol per liter) or higher who were receiving statin therapy. Patients were randomly assigned to receive evolocumab (either 140 mg every 2 weeks or 420 mg monthly) or matching placebo as subcutaneous injections. The primary efficacy end point was the composite of cardiovascular death, myocardial infarction, stroke, hospitalization for unstable angina, or coronary revascularization. The key secondary efficacy end point was the composite of cardiovascular death, myocardial infarction, or stroke. The median duration of follow-up was 2.2 years. RESULTS At 48 weeks, the least-squares mean percentage reduction in LDL cholesterol levels with evolocumab, as compared with placebo, was 59%, from a median baseline value of 92 mg per deciliter (2.4 mmol per liter) to 30 mg per deciliter (0.78 mmol per liter) (P
- Published
- 2017
5. Evolocumab and clinical outcomes in patients with cardiovascular disease
- Author
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Sabatine, Marc S., Giugliano, Robert P., Keech, Anthony C., Honarpour, Narimon, Wiviott, Stephen D., Murphy, Sabina A., Kuder, Julia F., Wang, Huei, Liu, Thomas, Wasserman, Scott M., Sever, Peter S., Pedersen, Fish MP, Terje R., Abrahamsen, Te, Im, K, Kanevsky, E, Bonaca, Mp, Lira Pineda, A, Hanlon, K, Knusel, B, Somaratne, R, Kurtz, C, Scott, R, Accini Mendoza JL, Amerena, J, Badariene, J, Burgess, L, Ceska, R, Charng, Mj, Choi, D, Cobos, Jl, Dan, Ga, De Ferrari GM, Deedwania, Pc, Chopra, Vk, Erglis, A, Ezhov, Mv, Ferreira, J, Filipová, S, Gaciong, Za, Pasierski, T, Georgiev, Bg, Gonzalez-Galvez, G, Gouni-Berthold, I, Schäufele, T, Hirayama, A, Huber, K, Rammer, M, Kjaerulf Jensen, H, Wermuth, S, Jiang, L, Jukema, Jw, Kraydashenko, O, Leiter, La, Lewis, Bs, López-Miranda, J, Lorenzatti, Aj, Mach, F, Mcadam, B, Nilsson, L, Olsson, Å, Rallidis, L, Rogelio, Gg, Kerr Saraiva JF, Scheen, A, Schiele, F, Scott, Rs, Connolly, D, Siu, Cw, Tay, L, Thorgeirsson, G, Tikkanen, Mj, Tokgozoglu, Sl, Toth, K, Viigimaa, M, Wan Ahmad WA, Hennekens, Ch, Andreotti, F, Baigent, C, Brown, Wv, Davis, Br, Newcomer, Jw, Wood, Sk, Larosa, J, Ansell, B, Olsson, A, Lowe, C, Zahn, L, Awtry, E, Berger, C, Croce, K, Desai, A, Gelfand, E, Ho, C, Leeman, D, Link, M, Norden, A, Pande, A, Rost, N, Ruberg, F, Silverman, S, Singhal, A, Vita, J, Mackinnon, I, Vogel, Dr, Leon de la Fuente, R, Perna, E, Amuchastegui, M, Pacora, F, Hershson, A, Blumberg, E, Glenny, Ja, Colombo, H, Cuadrado, Ja, Nicolosi, L, Rojas, Cg, Ulla, Mr, Hasbani, Eg, Cuneo, C, Lopez Santi RG, Sanabria, Hd, Hrabar, A, Lozada, A, Begg, A, Lehman, S, Wittert, G, Juergens, C, Kostner, K, Beltrame, J, Simpson, R, Sinhal, A, Adams, M, Kritharides, L, Roberts Thomson, P, Cross, D, Thompson, P, Van Gaal, W, Cox, N, Farshid, A, Hammett, C, Garrahy, P, Prasan, A, Horrigan, M, Ebenbichler, C, Hanusch, U, Prager, R, Schernthaner, G, Luger, A, Siostrzonek, P, Toplak, H, Bergler-Klein, J, Paulweber, B, Sinzinger, H, Buysschaert, I, Thoeng, J, Vandekerckhove, H, Catez, E, Verheye, S, Descamps, O, Hoffer, E, Wollaert, B, Chenu, P, van de Borne, P, De Meulemeester, M, Friart, A, Charlier, F, De Raedt, H, Rietzschel, E, Roelandt, R, Lalmand, J, Tavares Russo LA, Reis, G, Duarte Barbosa EC, Vidotti, Mh, Fernandes Manenti ER, Dutra, O, Leaes, Pe, Rech, Rl, Bertolim Precoma, D, Nicolau, Jc, Amoedo, R, Eliaschewitz, Fg, Pereira, A, Kurtz Lisboa HR, Soares Piegas, L, Cunha Borges JL, Ferreira Rossi PR, Pimentel Filho, P, Bodanese, Lc, de Sa Cunha, R, Moura Jorge JC, Ardito, Wr, Barroso de Souza WK, Hissa, M, Izar, Mc, Manolova, A, Kitova, L, Kinova, E, Tzekova, M, Velchev, V, Tarnovska-Kadreva, R, Gotchev, D, Petrov, I, Raev, D, Trendafilova-Lazarova, D, Yotov, Y, Lazov, P, Rahimi, S, St Amour, E, Constance, C, Pesant, Y, Hess, A, Anderson, T, Sussex, B, Henein, S, Tsoukas, G, Pandey, As, Bergeron, J, Hart, R, Gosselin, G, Chehayeb, R, Hamet, P, Hartleib, M, Mukherjee, A, Halperin, F, Petrella, R, Bhargava, R, Lonn, E, Sabbah, E, Bata, I, Cha, J, Gaudet, D, Chapman, K, Murthy, D, Nigro, F, Rupka, D, Gossard, D, Gupta, M, Dowell, A, Mansour, S, Baass, A, Geadah, C, Huynh, T, Peterson, S, Poirier, P, Sabe-Affaki, G, Vertes, G, Crowley, D, Duchesne, L, Pincetti Jofre CP, Potthoff Cardenas, S, Conejeros Kindel, C, Saavedra Gajardo VA, Lanas Zanetti, F, Sepulveda Varela PA, Stockins Fernandez BA, Li, W, Li, D, Zhao, S, Li, Z, Wang, J, Yang, Y, Zhang, L, Yang, P, Zhang, X, Huang, H, Xue, L, Zheng, Z, Huang, W, Dai, H, Su, H, Zeng, X, Zheng, Y, Tang, Y, Yao, Z, Sun, Y, Du, Y, Ge, Z, Yan, J, Chen, X, Liu, F, Pei, H, Yang, X, Cui, H, Gu, Y, Yang, Z, Li, J, Lian, Y, Cui, Y, Wang, D, Jiang, J, Li, X, Chen, J, Mo, Z, Xu, P, He, Y, Zhou, C, Qu, P, Zhu, Y, Liu, Y, Shen, X, Gao, X, Terront Lozano MA, Moncada Corredor MA, Hernandez Triana, E, Botero Lopez, R, Coronel Arroyo JA, Quintero Baiz AE, Sanchez Vallejo, G, Arana Londoño, C, Molina de Salazar DI, Castellanos Bueno, R, Manzur Jattin, F, Cure Cure CA, Sotomayor Herazo, A, Spinar, J, Hala, T, Machkova, M, Klimsa, Z, Polasek, R, Jerabek, O, Kazdera, P, Pozdisek, Z, Vaclavik, J, Frana, P, Elbl, L, Kucera, D, Kryza, R, Malecha, J, Reichert, P, Sochor, K, Ludka, O, Kellnerova, I, Peterka, K, Zidkova, E, Cech, V, Brabec, T, Fiserova, N, Kvasnicka, J, Rosolova, H, Nemecek, E, Adamkova, V, Dunaj, M, Pojsl, S, Cepelak, M, Podpera, I, Kuchar, L, Rysava, D, Burianova, H, Spinarova, L, Skrobakova, J, Charvat, J, Homza, M, Zemanek, J, Koleckar, P, Karen, I, Krupicka, J, Blaha, V, Matuska, J, Brotanek, J, Cifkova, R, Kuchar, R, Vomacka, Z, Kosek, Z, Hulinsky, V, Krejcova, H, Kuchar, J, Jelinek, Z, Jelinek, P, Markdanner Lindgren, L, Saetre Lihn, A, Korsgaard Thomsen, K, Bronnum-Schou, J, Nielsen, H, Nielsen, T, Egstrup, K, Klausen, Ic, Mickley, H, Hove, J, Jeppesen, J, Melchior, T, Schmidt, Eb, Valter, I, Rosenthal, A, Kaik, J, Kork, A, Alt, I, Strand, J, Nieminen, S, Kahri, J, Suomi, J, Nyman, K, Strandberg, Te, Piippo, T, Savolainen, M, Vikman, S, Pucheu, Y, Cariou, B, Henry, P, Ferrari, E, Montalescot, G, Ferrieres, J, Roubille, F, Bonnet, B, Angoulvant, D, Range, G, Bammert, A, Delarche, N, Mariat, C, Cayla, G, Durlach, V, Coisne, D, Paillard, F, Rouzier, R, Goralski, M, Khanoyan, P, Cottin, Y, Ziegler, O, Khalife, K, Le Corvoisier, P, Motreff, P, Spaulding, C, Vanbelle, E, Bourhaial, H, Opitz, C, Kahrmann, G, Contzen, C, Appel, K, Schenkenberger, I, Rinke, A, Trenk, D, Maus, O, Karakas, M, Hanefeld, M, Darius, H, Hetzel, G, Münzel, T, Wöhrle, J, Stawowy, P, Marten, I, Isermann, B, Kast, P, Vorpahl, M, Bosiljanoff, P, Hengstenberg, C, Kassner, U, Salbach, P, Fischer, M, Steiner, S, Wagner, S, Kraatz, U, von Hodenberg, E, Weyland, K, Mantas, I, Tziakas, D, Bousboulas, S, Patsilinakos, S, Mertzanos, G, Panagoulis, C, Bilianou, H, Skoumas, I, Elisaf, M, Manolis, A, Moschos, N, Kochiadakis, G, Ntaios, G, Richter, D, Athyros, V, Kolovou, G, Danias, P, Melidonis, A, Fan, Kyy, Siu, Sc, Hornyik, A, Lakatos, F, Zilahi, Z, Nagy, K, Laszlo, Z, Peterfai, E, Lupkovics, G, Andreka, P, Merkely, B, Herczeg, B, Piros, Ga, Salamon, C, Mark, L, Papp, A, Szakal, I, Edes, I, Mohacsi, A, Tomcsanyi, J, Hajko, E, Nagy, A, Papp, E, Kiss, R, Karadi, I, Sigurdsson, A, Jain, A, Pai, R, Kothiwale, V, Kulkarni, G, Mahajan, A, Aggarwal, S, Mehta, V, Rajadhyaksha, G, Joshi, A, Khandait, V, Parmar, M, Tyagi, S, Airody Govinda, R, Dwivedi, Sk, Parikh, K, Pothineni, Rb, Solanki, B, O’Donnell, M, Crean, P, Barton, J, Shechter, M, Shotan, A, Klutstein, M, Chorin, E, Gavish, D, Kracoff, O, Atar, S, Rigler, S, Hasin, Y, Schiff, E, Merlini, P, Rapezzi, C, Pirro, M, Gonnelli, S, Floresta, Am, Mennuni, M, Ardissino, D, Senni, M, Marenzi, G, Marcucci, R, Sampietro, T, Cosmi, F, Perrone Filardi, P, De Caterina, R, Fedele, Francesco, Moretti, L, Biasucci, Lm, Ferri, C, Go, Y, Kiyosue, A, Higashi, Y, Tokunaga, T, Kawasaki, T, Sakagami, S, Namba, S, Saku, K, Oku, K, Arakawa, T, Iida, H, Nakamura, Y, Yamamoto, K, Hata, Y, Katsuda, Y, Koga, Y, Shimizu, M, Uehara, H, Kajiyama, S, Okamoto, H, Shinozaki, T, Fujino, Y, Funazaki, T, Higa, N, Kaigawa, K, Koike, A, Nakane, H, Sato, K, Satoh, Y, Shirasawa, K, Sugino, H, Tanabe, J, Uemura, O, Yoshimichi, G, Akai, A, Himeno, H, Inage, T, Inoko, M, Kadokami, T, Noguchi, Y, Yamashita, K, Yasumura, Y, Yuge, M, Hosokawa, S, Kawamitsu, K, Kozuma, K, Matsuo, H, Nakashima, E, Okada, M, Wada, A, Yokoya, K, Iwade, K, Kawabata, K, Tanno, H, Ako, J, Fujita, H, Izumiya, Y, Kanno, M, Nunohiro, T, Ohmura, H, Ueno, T, Kakurina, N, Jasinkevica, I, Stukena, I, Veze, I, Eglite, R, Teterovska, D, Sime, I, Strazdiene, V, Venceviciene, L, Gustiene, O, Radzeviciene-Jurgute, R, Kucinskiene, A, Maskon, O, Lee, Cy, Erng, T, Gan, Hw, Mohamed Yusof AK, Ramanathan, Gl, Liew, H, Lopez Alvarado, A, Nevarez Ruiz LA, De los Rios Ibarra MO, Bazzoni Ruiz AE, Ramos Lopez GA, Llamas Esperon GA, De la Peña Topete GDJ, Violante Ortiz RM, Illescas Diaz JJ, Leon Gonzalez, S, Sanchez Diaz CJ, Mendez Machado GF, Venegas Carrillo LA, Aldrete Velasco JA, Cardona Muñoz EG, Leiva Pons JL, Perez Alva JC, van der Zwaan, C, Oomen, A, van de Wal, R, Magro, M, Boswijk, D, Janus, C, Groutars, R, Tonino, W, Cornel, Jh, Oude Ophuis, A, Troquay, R, Liem, A, Westendorp, I, Van Hessen, M, Lok, D, De Nooijer, C, Den Hartog, F, Van Beek, E, Bendermacher, P, Jansen, R, Römer, T, Rensing, B, Hersbach, F, Herrman, J, Ladyjanskaia, G, Karalis, I, Linssen, G, Bokern, M, Visman, A, Kooij, A, Monajemi, H, Lieverse, A, Baker, J, Tie, S, Risberg, K, Hysing, J, Pedersen, T, Hoivik, Ho, Norheim, P, Solnor, L, Hovland, A, Kjaernli, T, Jocson, G, Coching, Rm, Batalla, E, Go, A, Habaluyas, R, Barcinas, R, Sy, Ra, Estepar, Ra, Germar, A, Trebacz, J, Szymkowiak, K, Wnetrzak-Michalska, R, Kopaczewski, J, Przekwas-Jaruchowska, M, Kania, G, Zabowka, M, Mirek-Bryniarska, E, Dabrowska, M, Napora, P, Konieczny, M, Spyra, J, Lysek, R, Pijanowski, Z, Grzegorzewski, B, Bednarkiewicz, Z, Kinasz, L, Antkowiak-Piatyszek, K, Stania, K, Szpajer, M, Staneta, P, Skonieczny, G, Ksiezycka-Majczynska, E, Blicharski, T, Piepiorka, M, Wozakowska-Kaplon, B, Zechowicz, T, Ilkowski, J, Lubiszewska, B, Hiczkiewicz, J, Wierzbicka, K, Kosior, D, Garbocz, P, Kubica, J, Raczak, G, Wozniak, I, Cygler, J, Kramarczuk, E, Bystryk, L, Pentela-Nowicka, J, Dabrowski, M, Podolec, P, Zieba, B, Mosiewicz, J, Dubaniewicz, W, Banach, M, Tyszecka, G, Lepich, T, Rychlewska-Hanczewska, A, Guzik, T, Monteiro, P, Pereira, H, Oliveira, L, Matos, P, Soares Goncalves, S, Leitao, A, Vasco Salgado, A, Timoteo, At, Pintilei, E, Badila, E, Militaru, C, Tudoran, M, Arsenescu-Georgescu, C, Mitu, F, Zdrenghea, D, Lighezan, D, Teodorescu, I, Popescu, Mi, Coman, I, Vintila, Mm, Vishnevsky, A, Lukyanov, Y, Blokhin, A, Kostenko, V, Shvarts, Y, Markov, V, Motylev, I, Dronov, D, Sherenkov, A, Barbarash, O, Shutemova, E, Bolshakova, O, Kobalava, Z, Voevoda, M, Treshkur, T, Zrazhevskiy, K, Pimenov, L, Solovev, O, Tarasov, N, Arkhipov, M, Freidlin, M, Shalaev, S, Yakhontova, P, Shustov, S, Goloshchekin, B, Panov, A, Bart, B, Bubnova, M, Gordeev, I, Osipova, I, Tereshenko, S, Solovieva, E, Meshkov, A, Zateyshchikov, D, Tan, Jl, Subramaniam, T, Pella, D, Fulop, P, Antalik, L, Dzupina, A, Banikova, A, Sosovec, D, Urgeova, L, Mazur, J, Hranai, M, Banik, M, Vinanska, D, Lennerova, J, Kovar, F, Pastrnakova, E, Uhliar, R, Blasko, P, Gonsorcik, J, Lukacova, J, Oriesek, R, Hatalova, K, du Toit, M, Ebrahim, I, Vawda, G, Lipschitz, S, Blignaut, S, Engelbrecht, J, Coetzer, Tf, Pretorius, M, Urbach, D, Badat, A, Pillay, S, Van Zyl, L, Abelson, M, van der Walt, E, Moodley, R, Jacovides, A, Oosthuysen, Wm, Klug, E, Lottering, H, Kok, J, Saaiman, J, Dawood, S, De Jong DM, Kapp, C, Makotoko, E, Bayat, J, Sarvan, M, Vally, T, Stapelberg, A, Kim, M, Bae, J, Cho, Y, Kim, S, Han, Kh, Her, S, Kim, B, Lee, S, Hong, B, Kim, W, Rha, S, Jeong, M, Shin, Gj, Vida Gutierrez, M, Valdes Chavarri, M, Pinto Sala, X, Gonzalez Juanatey JR, Civeira Murillo, F, Zamorano Gomez JL, Lekuona Goya, I, Iñiguez Romo, A, Cordero Fort, A, Ascaso Gimilio JF, Millan Nuñez-Cortes, J, Lindholm, C, Söderberg, S, Suutari, A, Berglund, S, Mooe, T, Kusiak, D, Bandh, S, Dahlén, G, Olsson, S, Witt, N, Tydén, P, Johansson, P, Cizinsky, S, Falck, G, Pettersson, Si, Rasmanis, G, Östergren, J, Moccetti, T, Beer, Hj, Eberli, F, Krähenbühl, S, Linka, A, Ackermann, D, Michel, P, Yeh, H, Tsai, Cf, Wu, C, Hsia, C, Juang, J, Hsieh, I, Lai, W, Huang, C, Hsieh, Y, Sahin, T, Duzenli, M, Yigit, Z, Demir, M, Yilmaz, Mb, Muderrisoglu, Ih, Kirma, C, Ercan, E, Kayikcioglu, L, Balbay, Y, Lymar, I, Kulynych, O, Prokhorov, O, Karpenko, O, Kraіz, I, Vakaliuk, I, Stanislavchuk, M, Korzh, O, Rudyk, I, Zhurba, S, Svishchenko, Y, Tseluyko, V, Gyrina, O, Reshotko, D, Kopytsya, M, Volkov, V, Myshanych, G, Rebrov, B, Rishko, M, Rudenko, L, Shatylo, V, Parkhomenko, O, Yena, L, Golovchenko, O, Sorokina, I, Malynovsky, Y, Ivan, P, Blagden, M, Dear, H, Mathew, A, Lagocki, S, Kondagunta, V, Ahsan, A, Mckinnon, C, Douglas, F, Thom, S, Fiore, G, Caulfield, M, Lynch, M, Thomas, H, Bain, S, Hall, A, Mcnally, D, Fisher, M, Keeling, P, Al-Bahrani, A, Lip, G, Ellery, A, Purohit, J, Travill, C, Cappuccio, F, Davis, G, Gaunt, R, Adlam, D, Asamoah, N, Jaafar, F, Mccormack, T, Jupp, B, Pye, M, Ainsworth, P, Chauhan, A, Paul, N, Fairlie, H, Fox, C, Muzulu, S, Trevelyan, J, Aggarwal, R, Issa, B, Saravanan, P, Cruickshank, K, Gorog, D, Heller, S, Newby, D, Nicolson, A, Hare, Po, Donnelly, P, Rutherfurd, S, de Belder, M, Finlayson, J, Harvey, J, Hoye, A, Kingston, D, Sarkar, D, Negahban, A, Webster, J, Wyatt, N, Muir, S, Cummings, M, Mackenzie, I, Senior, R, Capps, N, Fotherby, K, Mcintyre, H, Aldegather, J, Dixon, L, Saksena, R, Butler, R, Ramstad, D, Pierpont, B, Levinson, D, Mohammed, A, Haddad, T, Goel, A, Dave, K, Haught, Wh, Desire, A, Hershon, K, Napoli, M, Tami, L, Rothschild, R, Khurana, S, Gupta, D, Cheung, D, Hearne, S, Grubb, S, Miller, A, Baird, I, Marcus, A, Srivastava, S, Forgosh, L, Fritz, R, Mays, M, Bertolet, B, Reddy, J, Khan, M, Nakhle, S, Dill, S, Fishbein, G, Khan, B, Marais, H, Reschak, M, Malone, M, Nadar, V, Whitney, R, Reichman, A, Reyes, H, El Shahawy, M, Rabinowitz, A, Weinstein, D, Farhat, N, Onyema, D, Potu, R, Runquist, L, Barnum, O, Crater, T, Fialkow, J, Shah, A, Thompson, C, Wiseman, A, Doyle, T, Henderson, D, Herzog, W, Schnitzler, R, Carr, K, Davis, M, Nagajothi, N, Olsen, S, Rogers, W, Rubino, J, Singh, I, Tarleton, G, Bhagwat, R, Clardy, D, Jardula, M, Robinson, J, Torres, M, Vijay, N, Farris, N, Lillo, J, Moriarty, P, Recknor, C, Berlacher, P, Christensen, T, Gabra, N, Issa, M, Janik, M, Lawless, A, Molter, D, Stout, E, Brezina, B, Claxton, E, Linsky, R, Poock, J, Remler, R, Roseman, H, Schramm, E, Al-Joundi, T, Amin, J, Hitchcock, J, Isserman, S, Kirstein, J, Rider, J, Shalek, M, Sherman, H, Bernstein, M, Chandra, L, Hatharasinghe, R, Ibrahim, H, Iteld, B, Linzmeyer, K, Seaton, B, Zeig, S, Christofides, E, Dunbar, R, Griffin, S, Kohli, N, Koren, M, Pharr, W, Purdy, D, Spencer, R, Yeoman, G, Banerjee, S, Cheek, Hb, Engel, E, Hamroff, G, Huling, R, Kozlowski, L, Levin, P, Makam, S, Meengs, M, Bhushan, R, Erickson, B, Herman, L, Lo, E, Mcdowell, E, Mcgrew, F, Miller, M, Ord, J, Webel, R, Wilhoit, G, Wise, J, Yang, E, Budoff, M, Collins, J, Dauber, I, Dobkin, L, Focil, A, Gandy, W, Pasquini, J, Ramos, M, Rodriguez, D, Rosenson, R, Sanford, K, Schlau, A, Snyder, B, Stonesifer, L, Tang, A, De Souza, J, Elam, M III, French, J, Guyton, J, Hage Korban, E, Kereiakes, D, King, M, Loh, I, Navarro, J, Simons, R, Tobin, T, Younis, L, Aboufakher, R, Baldari, D, Ballantyne, C, Broughton, R, Eaton, C, Johnston, J, Simon, W, Thomson, S, Vora, K, Youngman, D, Alzohaili, O, Auerbach, E, Brown, C, Burrough, B, Chen, Y, Gilpatrick, M, Landzberg, J, Mitchell, C, Rice, L, Rubenfire, M, Sofley, Cw, Strobl, D, Atassi, K, Davila, W, Diogo, J, Fagan, T, Joffe, I, Krishna, J, Osea, E, Penny, W, Rowe, W, Shapiro, M, Welker, J, Benton, R, Dobratz, D, Fortuin, F, Graham, J, Henry, B, Kusnick, B, Lutskiy, M, Mcrae, A, Saway, W, Scott, J, Shah, M, Weinberg, B, Zarich, S, Acheatel, R, Case, C, Earl, J, Fernandez, S, Giugliano, G, Handelsman, Y, Hermany, P, Holder, S, Kashyap, M, Khan, A, Lader, E, Peniston, J, Raoof, T, Sacco, J, Shore, K, Spriggs, D, Stringam, S, Tahirkheli, N, Delgado, E, Derian, W, Greenwald, J, Harris, M, Jackson, R, Marhefka, G, Mcelveen, W, Mooss, A, Morris, P, Murray, J, Pearlstein, P, Raisinghani, A, Rezkalla, S, Sakhrani, L, Schreibman, D, Shaoulian, E, Steinsapir, J, Yataco, A, De La Cruz, A, Fredrick, M, Goldenberg, E, Lee, D, Mccullum, K, Mclellan, B, Stephens, L, Wilson, S, Alfieri, A, Mandviwala, M, Orourke, D, Samal, A, Schmedtje, J, Waxman, F, Carhart, R, Clements, B, Dyke, C, Ghali, J, Gruberg, L, Hack, T, Jehle, A, Pogue, B, Schooley, C, Shifrin, G., National Institute for Health Research, Amgen Inc, University of Zurich, Sabatine, Marc S, Sabatine, M, Giugliano, R, Keech, A, Honarpour, N, Wiviott, S, Murphy, S, Kuder, J, Wang, H, Liu, T, Wasserman, S, Sever, P, Pedersen, T, Fish, M, Abrahamsen, T, Im, K, Kanevsky, E, Bonaca, M, Lira Pineda, A, Hanlon, K, Knusel, B, Somaratne, R, Kurtz, C, Scott, R, Accini Mendoza, J, Amerena, J, Badariene, J, Burgess, L, Ceska, R, Charng, M, Choi, D, Cobos, J, Dan, G, De Ferrari, G, Deedwania, P, Chopra, V, Erglis, A, Ezhov, M, Ferreira, J, Filipova, S, Gaciong, Z, Pasierski, T, Georgiev, B, Gonzalez-Galvez, G, Gouni-Berthold, I, Schaufele, T, Hirayama, A, Huber, K, Rammer, M, Kjaerulf Jensen, H, Wermuth, S, Jiang, L, Jukema, J, Kraydashenko, O, Leiter, L, Lewis, B, Lopez-Miranda, J, Lorenzatti, A, Mach, F, Mcadam, B, Nilsson, L, Olsson, A, Rallidis, L, Rogelio, G, Kerr Saraiva, J, Scheen, A, Schiele, F, Connolly, D, Siu, C, Tay, L, Thorgeirsson, G, Tikkanen, M, Tokgozoglu, S, Toth, K, Viigimaa, M, Wan Ahmad, W, Hennekens, C, Andreotti, F, Baigent, C, Brown, W, Davis, B, Newcomer, J, Wood, S, Larosa, J, Ansell, B, Lowe, C, Zahn, L, Awtry, E, Berger, C, Croce, K, Desai, A, Gelfand, E, Ho, C, Leeman, D, Link, M, Norden, A, Pande, A, Rost, N, Ruberg, F, Silverman, S, Singhal, A, Vita, J, Mackinnon, I, Vogel, D, Leon de la Fuente, R, Perna, E, Amuchastegui, M, Pacora, F, Hershson, A, Blumberg, E, Glenny, J, Colombo, H, Cuadrado, J, Nicolosi, L, Rojas, C, Ulla, M, Hasbani, E, Cuneo, C, Lopez Santi, R, Sanabria, H, Hrabar, A, Lozada, A, Begg, A, Lehman, S, Wittert, G, Juergens, C, Kostner, K, Beltrame, J, Simpson, R, Sinhal, A, Adams, M, Kritharides, L, Roberts Thomson, P, Cross, D, Thompson, P, Van Gaal, W, Cox, N, Farshid, A, Hammett, C, Garrahy, P, Prasan, A, Horrigan, M, Ebenbichler, C, Hanusch, U, Prager, R, Schernthaner, G, Luger, A, Siostrzonek, P, Toplak, H, Bergler-Klein, J, Paulweber, B, Sinzinger, H, Buysschaert, I, Thoeng, J, Vandekerckhove, H, Catez, E, Verheye, S, Descamps, O, Hoffer, E, Wollaert, B, Chenu, P, van de Borne, P, De Meulemeester, M, Friart, A, Charlier, F, De Raedt, H, Rietzschel, E, Roelandt, R, Lalmand, J, Tavares Russo, L, Reis, G, Duarte Barbosa, E, Vidotti, M, Fernandes Manenti, E, Dutra, O, Leaes, P, Rech, R, Bertolim Precoma, D, Nicolau, J, Amoedo, R, Eliaschewitz, F, Pereira, A, Kurtz Lisboa, H, Soares Piegas, L, Cunha Borges, J, Ferreira Rossi, P, Pimentel Filho, P, Bodanese, L, de Sa Cunha, R, Moura Jorge, J, Ardito, W, Barroso de Souza, W, Hissa, M, Izar, M, Manolova, A, Kitova, L, Kinova, E, Tzekova, M, Velchev, V, Tarnovska-Kadreva, R, Gotchev, D, Petrov, I, Raev, D, Trendafilova-Lazarova, D, Yotov, Y, Lazov, P, Rahimi, S, St Amour, E, Constance, C, Pesant, Y, Hess, A, Anderson, T, Sussex, B, Henein, S, Tsoukas, G, Pandey, A, Bergeron, J, Hart, R, Gosselin, G, Chehayeb, R, Hamet, P, Hartleib, M, Mukherjee, A, Halperin, F, Petrella, R, Bhargava, R, Lonn, E, Sabbah, E, Bata, I, Cha, J, Gaudet, D, Chapman, K, Murthy, D, Nigro, F, Rupka, D, Gossard, D, Gupta, M, Dowell, A, Mansour, S, Baass, A, Geadah, C, Huynh, T, Peterson, S, Poirier, P, Sabe-Affaki, G, Vertes, G, Crowley, D, Duchesne, L, Pincetti Jofre, C, Potthoff Cardenas, S, Conejeros Kindel, C, Saavedra Gajardo, V, Lanas Zanetti, F, Sepulveda Varela, P, Stockins Fernandez, B, Li, W, Li, D, Zhao, S, Li, Z, Wang, J, Yang, Y, Zhang, L, Yang, P, Zhang, X, Huang, H, Xue, L, Zheng, Z, Huang, W, Dai, H, Su, H, Zeng, X, Zheng, Y, Tang, Y, Yao, Z, Sun, Y, Du, Y, Ge, Z, Yan, J, Chen, X, Liu, F, Pei, H, Yang, X, Cui, H, Gu, Y, Yang, Z, Li, J, Lian, Y, Cui, Y, Wang, D, Jiang, J, Li, X, Chen, J, Mo, Z, Xu, P, He, Y, Zhou, C, Qu, P, Zhu, Y, Liu, Y, Shen, X, Gao, X, Terront Lozano, M, Moncada Corredor, M, Hernandez Triana, E, Botero Lopez, R, Coronel Arroyo, J, Quintero Baiz, A, Sanchez Vallejo, G, Arana Londono, C, Molina de Salazar, D, Castellanos Bueno, R, Manzur Jattin, F, Cure Cure, C, Sotomayor Herazo, A, Spinar, J, Hala, T, Machkova, M, Klimsa, Z, Polasek, R, Jerabek, O, Kazdera, P, Pozdisek, Z, Vaclavik, J, Frana, P, Elbl, L, Kucera, D, Kryza, R, Malecha, J, Reichert, P, Sochor, K, Ludka, O, Kellnerova, I, Peterka, K, Zidkova, E, Cech, V, Brabec, T, Fiserova, N, Kvasnicka, J, Rosolova, H, Nemecek, E, Adamkova, V, Dunaj, M, Pojsl, S, Cepelak, M, Podpera, I, Kuchar, L, Rysava, D, Burianova, H, Spinarova, L, Skrobakova, J, Charvat, J, Homza, M, Zemanek, J, Koleckar, P, Karen, I, Krupicka, J, Blaha, V, Matuska, J, Brotanek, J, Cifkova, R, Kuchar, R, Vomacka, Z, Kosek, Z, Hulinsky, V, Krejcova, H, Kuchar, J, Jelinek, Z, Jelinek, P, Markdanner Lindgren, L, Saetre Lihn, A, Korsgaard Thomsen, K, Bronnum-Schou, J, Nielsen, H, Nielsen, T, Egstrup, K, Klausen, I, Mickley, H, Hove, J, Jeppesen, J, Melchior, T, Schmidt, E, Valter, I, Rosenthal, A, Kaik, J, Kork, A, Alt, I, Strand, J, Nieminen, S, Kahri, J, Suomi, J, Nyman, K, Strandberg, T, Piippo, T, Savolainen, M, Vikman, S, Pucheu, Y, Cariou, B, Henry, P, Ferrari, E, Montalescot, G, Ferrieres, J, Roubille, F, Bonnet, B, Angoulvant, D, Range, G, Bammert, A, Delarche, N, Mariat, C, Cayla, G, Durlach, V, Coisne, D, Paillard, F, Rouzier, R, Goralski, M, Khanoyan, P, Cottin, Y, Ziegler, O, Khalife, K, Le Corvoisier, P, Motreff, P, Spaulding, C, Vanbelle, E, Bourhaial, H, Opitz, C, Kahrmann, G, Contzen, C, Appel, K, Schenkenberger, I, Rinke, A, Trenk, D, Maus, O, Karakas, M, Hanefeld, M, Darius, H, Hetzel, G, Munzel, T, Wohrle, J, Stawowy, P, Marten, I, Isermann, B, Kast, P, Vorpahl, M, Bosiljanoff, P, Hengstenberg, C, Kassner, U, Salbach, P, Fischer, M, Steiner, S, Wagner, S, Kraatz, U, von Hodenberg, E, Weyland, K, Mantas, I, Tziakas, D, Bousboulas, S, Patsilinakos, S, Mertzanos, G, Panagoulis, C, Bilianou, H, Skoumas, I, Elisaf, M, Manolis, A, Moschos, N, Kochiadakis, G, Ntaios, G, Richter, D, Athyros, V, Kolovou, G, Danias, P, Melidonis, A, Fan, K, Siu, S, Hornyik, A, Lakatos, F, Zilahi, Z, Nagy, K, Laszlo, Z, Peterfai, E, Lupkovics, G, Andreka, P, Merkely, B, Herczeg, B, Piros, G, Salamon, C, Mark, L, Papp, A, Szakal, I, Edes, I, Mohacsi, A, Tomcsanyi, J, Hajko, E, Nagy, A, Papp, E, Kiss, R, Karadi, I, Sigurdsson, A, Jain, A, Pai, R, Kothiwale, V, Kulkarni, G, Mahajan, A, Aggarwal, S, Mehta, V, Rajadhyaksha, G, Joshi, A, Khandait, V, Parmar, M, Tyagi, S, Airody Govinda, R, Dwivedi, S, Parikh, K, Pothineni, R, Solanki, B, O'Donnell, M, Crean, P, Barton, J, Shechter, M, Shotan, A, Klutstein, M, Chorin, E, Gavish, D, Kracoff, O, Atar, S, Rigler, S, Hasin, Y, Schiff, E, Merlini, P, Rapezzi, C, Pirro, M, Gonnelli, S, Floresta, A, Mennuni, M, Ardissino, D, Senni, M, Marenzi, G, Marcucci, R, Sampietro, T, Cosmi, F, Perrone Filardi, P, De Caterina, R, Fedele, F, Moretti, L, Biasucci, L, Ferri, C, Go, Y, Kiyosue, A, Higashi, Y, Tokunaga, T, Kawasaki, T, Sakagami, S, Namba, S, Saku, K, Oku, K, Arakawa, T, Iida, H, Nakamura, Y, Yamamoto, K, Hata, Y, Katsuda, Y, Koga, Y, Shimizu, M, Uehara, H, Kajiyama, S, Okamoto, H, Shinozaki, T, Fujino, Y, Funazaki, T, Higa, N, Kaigawa, K, Koike, A, Nakane, H, Sato, K, Satoh, Y, Shirasawa, K, Sugino, H, Tanabe, J, Uemura, O, Yoshimichi, G, Akai, A, Himeno, H, Inage, T, Inoko, M, Kadokami, T, Noguchi, Y, Yamashita, K, Yasumura, Y, Yuge, M, Hosokawa, S, Kawamitsu, K, Kozuma, K, Matsuo, H, Nakashima, E, Okada, M, Wada, A, Yokoya, K, Iwade, K, Kawabata, K, Tanno, H, Ako, J, Fujita, H, Izumiya, Y, Kanno, M, Nunohiro, T, Ohmura, H, Ueno, T, Kakurina, N, Jasinkevica, I, Stukena, I, Veze, I, Eglite, R, Teterovska, D, Sime, I, Strazdiene, V, Venceviciene, L, Gustiene, O, Radzeviciene-Jurgute, R, Kucinskiene, A, Maskon, O, Lee, C, Erng, T, Gan, H, Mohamed Yusof, A, Ramanathan, G, Liew, H, Lopez Alvarado, A, Nevarez Ruiz, L, De los Rios Ibarra, M, Bazzoni Ruiz, A, Ramos Lopez, G, Llamas Esperon, G, De la Pena Topete, G, Violante Ortiz, R, Illescas Diaz, J, Leon Gonzalez, S, Sanchez Diaz, C, Mendez Machado, G, Venegas Carrillo, L, Aldrete Velasco, J, Cardona Munoz, E, Leiva Pons, J, Perez Alva, J, van der Zwaan, C, Oomen, A, van de Wal, R, Magro, M, Boswijk, D, Janus, C, Groutars, R, Tonino, W, Cornel, J, Oude Ophuis, A, Troquay, R, Liem, A, Westendorp, I, Van Hessen, M, Lok, D, De Nooijer, C, Den Hartog, F, Van Beek, E, Bendermacher, P, Jansen, R, Romer, T, Rensing, B, Hersbach, F, Herrman, J, Ladyjanskaia, G, Karalis, I, Linssen, G, Bokern, M, Visman, A, Kooij, A, Monajemi, H, Lieverse, A, Baker, J, Tie, S, Risberg, K, Hysing, J, Hoivik, H, Norheim, P, Solnor, L, Hovland, A, Kjaernli, T, Jocson, G, Coching, R, Batalla, E, Go, A, Habaluyas, R, Barcinas, R, Sy, R, Estepar, R, Germar, A, Trebacz, J, Szymkowiak, K, Wnetrzak-Michalska, R, Kopaczewski, J, Przekwas-Jaruchowska, M, Kania, G, Zabowka, M, Mirek-Bryniarska, E, Dabrowska, M, Napora, P, Konieczny, M, Spyra, J, Lysek, R, Pijanowski, Z, Grzegorzewski, B, Bednarkiewicz, Z, Kinasz, L, Antkowiak-Piatyszek, K, Stania, K, Szpajer, M, Staneta, P, Skonieczny, G, Ksiezycka-Majczynska, E, Blicharski, T, Piepiorka, M, Wozakowska-Kaplon, B, Zechowicz, T, Ilkowski, J, Lubiszewska, B, Hiczkiewicz, J, Wierzbicka, K, Kosior, D, Garbocz, P, Kubica, J, Raczak, G, Wozniak, I, Cygler, J, Kramarczuk, E, Bystryk, L, Pentela-Nowicka, J, Dabrowski, M, Podolec, P, Zieba, B, Mosiewicz, J, Dubaniewicz, W, Banach, M, Tyszecka, G, Lepich, T, Rychlewska-Hanczewska, A, Guzik, T, Monteiro, P, Pereira, H, Oliveira, L, Matos, P, Soares Goncalves, S, Leitao, A, Vasco Salgado, A, Timoteo, A, Pintilei, E, Badila, E, Militaru, C, Tudoran, M, Arsenescu-Georgescu, C, Mitu, F, Zdrenghea, D, Lighezan, D, Teodorescu, I, Popescu, M, Coman, I, Vintila, M, Vishnevsky, A, Lukyanov, Y, Blokhin, A, Kostenko, V, Shvarts, Y, Markov, V, Motylev, I, Dronov, D, Sherenkov, A, Barbarash, O, Shutemova, E, Bolshakova, O, Kobalava, Z, Voevoda, M, Treshkur, T, Zrazhevskiy, K, Pimenov, L, Solovev, O, Tarasov, N, Arkhipov, M, Freidlin, M, Shalaev, S, Yakhontova, P, Shustov, S, Goloshchekin, B, Panov, A, Bart, B, Bubnova, M, Gordeev, I, Osipova, I, Tereshenko, S, Solovieva, E, Meshkov, A, Zateyshchikov, D, Tan, J, Subramaniam, T, Pella, D, Fulop, P, Antalik, L, Dzupina, A, Banikova, A, Sosovec, D, Urgeova, L, Mazur, J, Hranai, M, Banik, M, Vinanska, D, Lennerova, J, Kovar, F, Pastrnakova, E, Uhliar, R, Blasko, P, Gonsorcik, J, Lukacova, J, Oriesek, R, Hatalova, K, du Toit, M, Ebrahim, I, Vawda, G, Lipschitz, S, Blignaut, S, Engelbrecht, J, Coetzer, T, Pretorius, M, Urbach, D, Badat, A, Pillay, S, Van Zyl, L, Abelson, M, van der Walt, E, Moodley, R, Jacovides, A, Oosthuysen, W, Klug, E, Lottering, H, Kok, J, Saaiman, J, Dawood, S, De Jong, D, Kapp, C, Makotoko, E, Bayat, J, Sarvan, M, Vally, T, Stapelberg, A, Kim, M, Bae, J, Cho, Y, Kim, S, Han, K, Her, S, Kim, B, Lee, S, Hong, B, Kim, W, Rha, S, Jeong, M, Shin, G, Vida Gutierrez, M, Valdes Chavarri, M, Pinto Sala, X, Gonzalez Juanatey, J, Civeira Murillo, F, Zamorano Gomez, J, Lekuona Goya, I, Iniguez Romo, A, Cordero Fort, A, Ascaso Gimilio, J, Millan Nunez-Cortes, J, Lindholm, C, Soderberg, S, Suutari, A, Berglund, S, Mooe, T, Kusiak, D, Bandh, S, Dahlen, G, Olsson, S, Witt, N, Tyden, P, Johansson, P, Cizinsky, S, Falck, G, Pettersson, S, Rasmanis, G, Ostergren, J, Moccetti, T, Beer, H, Eberli, F, Krahenbuhl, S, Linka, A, Ackermann, D, Michel, P, Yeh, H, Tsai, C, Wu, C, Hsia, C, Juang, J, Hsieh, I, Lai, W, Huang, C, Hsieh, Y, Sahin, T, Duzenli, M, Yigit, Z, Demir, M, Yilmaz, M, Muderrisoglu, I, Kirma, C, Ercan, E, Kayikcioglu, L, Balbay, Y, Lymar, I, Kulynych, O, Prokhorov, O, Karpenko, O, Kraіz, I, Vakaliuk, I, Stanislavchuk, M, Korzh, O, Rudyk, I, Zhurba, S, Svishchenko, Y, Tseluyko, V, Gyrina, O, Reshotko, D, Kopytsya, M, Volkov, V, Myshanych, G, Rebrov, B, Rishko, M, Rudenko, L, Shatylo, V, Parkhomenko, O, Yena, L, Golovchenko, O, Sorokina, I, Malynovsky, Y, Ivan, P, Blagden, M, Dear, H, Mathew, A, Lagocki, S, Kondagunta, V, Ahsan, A, Mckinnon, C, Douglas, F, Thom, S, Fiore, G, Caulfield, M, Lynch, M, Thomas, H, Bain, S, Hall, A, Mcnally, D, Fisher, M, Keeling, P, Al-Bahrani, A, Lip, G, Ellery, A, Purohit, J, Travill, C, Cappuccio, F, Davis, G, Gaunt, R, Adlam, D, Asamoah, N, Jaafar, F, Mccormack, T, Jupp, B, Pye, M, Ainsworth, P, Chauhan, A, Paul, N, Fairlie, H, Fox, C, Muzulu, S, Trevelyan, J, Aggarwal, R, Issa, B, Saravanan, P, Cruickshank, K, Gorog, D, Heller, S, Newby, D, Nicolson, A, Hare, P, Donnelly, P, Rutherfurd, S, de Belder, M, Finlayson, J, Harvey, J, Hoye, A, Kingston, D, Sarkar, D, Negahban, A, Webster, J, Wyatt, N, Muir, S, Cummings, M, Mackenzie, I, Senior, R, Capps, N, Fotherby, K, Mcintyre, H, Aldegather, J, Dixon, L, Saksena, R, Butler, R, Ramstad, D, Pierpont, B, Levinson, D, Mohammed, A, Haddad, T, Goel, A, Dave, K, Haught, W, Desire, A, Hershon, K, Napoli, M, Tami, L, Rothschild, R, Khurana, S, Gupta, D, Cheung, D, Hearne, S, Grubb, S, Miller, A, Baird, I, Marcus, A, Srivastava, S, Forgosh, L, Fritz, R, Mays, M, Bertolet, B, Reddy, J, Khan, M, Nakhle, S, Dill, S, Fishbein, G, Khan, B, Marais, H, Reschak, M, Malone, M, Nadar, V, Whitney, R, Reichman, A, Reyes, H, El Shahawy, M, Rabinowitz, A, Weinstein, D, Farhat, N, Onyema, D, Potu, R, Runquist, L, Barnum, O, Crater, T, Fialkow, J, Shah, A, Thompson, C, Wiseman, A, Doyle, T, Henderson, D, Herzog, W, Schnitzler, R, Carr, K, Davis, M, Nagajothi, N, Olsen, S, Rogers, W, Rubino, J, Singh, I, Tarleton, G, Bhagwat, R, Clardy, D, Jardula, M, Robinson, J, Torres, M, Vijay, N, Farris, N, Lillo, J, Moriarty, P, Recknor, C, Berlacher, P, Christensen, T, Gabra, N, Issa, M, Janik, M, Lawless, A, Molter, D, Stout, E, Brezina, B, Claxton, E, Linsky, R, Poock, J, Remler, R, Roseman, H, Schramm, E, Al-Joundi, T, Amin, J, Hitchcock, J, Isserman, S, Kirstein, J, Rider, J, Shalek, M, Sherman, H, Bernstein, M, Chandra, L, Hatharasinghe, R, Ibrahim, H, Iteld, B, Linzmeyer, K, Seaton, B, Zeig, S, Christofides, E, Dunbar, R, Griffin, S, Kohli, N, Koren, M, Pharr, W, Purdy, D, Spencer, R, Yeoman, G, Banerjee, S, Cheek, H, Engel, E, Hamroff, G, Huling, R, Kozlowski, L, Levin, P, Makam, S, Meengs, M, Bhushan, R, Erickson, B, Herman, L, Lo, E, Mcdowell, E, Mcgrew, F, Miller, M, Ord, J, Webel, R, Wilhoit, G, Wise, J, Yang, E, Budoff, M, Collins, J, Dauber, I, Dobkin, L, Focil, A, Gandy, W, Pasquini, J, Ramos, M, Rodriguez, D, Rosenson, R, Sanford, K, Schlau, A, Snyder, B, Stonesifer, L, Tang, A, De Souza, J, Elam, M, French, J, Guyton, J, Hage Korban, E, Kereiakes, D, King, M, Loh, I, Navarro, J, Simons, R, Tobin, T, Younis, L, Aboufakher, R, Baldari, D, Ballantyne, C, Broughton, R, Eaton, C, Johnston, J, Simon, W, Thomson, S, Vora, K, Youngman, D, Alzohaili, O, Auerbach, E, Brown, C, Burrough, B, Chen, Y, Gilpatrick, M, Landzberg, J, Mitchell, C, Rice, L, Rubenfire, M, Sofley, C, Strobl, D, Atassi, K, Davila, W, Diogo, J, Fagan, T, Joffe, I, Krishna, J, Osea, E, Penny, W, Rowe, W, Shapiro, M, Welker, J, Benton, R, Dobratz, D, Fortuin, F, Graham, J, Henry, B, Kusnick, B, Lutskiy, M, Mcrae, A, Saway, W, Scott, J, Shah, M, Weinberg, B, Zarich, S, Acheatel, R, Case, C, Earl, J, Fernandez, S, Giugliano, G, Handelsman, Y, Hermany, P, Holder, S, Kashyap, M, Khan, A, Lader, E, Peniston, J, Raoof, T, Sacco, J, Shore, K, Spriggs, D, Stringam, S, Tahirkheli, N, Delgado, E, Derian, W, Greenwald, J, Harris, M, Jackson, R, Marhefka, G, Mcelveen, W, Mooss, A, Morris, P, Murray, J, Pearlstein, P, Raisinghani, A, Rezkalla, S, Sakhrani, L, Schreibman, D, Shaoulian, E, Steinsapir, J, Yataco, A, De La Cruz, A, Fredrick, M, Goldenberg, E, Lee, D, Mccullum, K, Mclellan, B, Stephens, L, Wilson, S, Alfieri, A, Mandviwala, M, Orourke, D, Samal, A, Schmedtje, J, Waxman, F, Carhart, R, Clements, B, Dyke, C, Ghali, J, Gruberg, L, Hack, T, Jehle, A, Pogue, B, Schooley, C, and Shifrin, G
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Male ,STATIN THERAPY ,2700 General Medicine ,Disease ,Cardiovascular ,PLACEBO-CONTROLLED TRIAL ,Gastroenterology ,0302 clinical medicine ,Anticholesteremic Agent ,Medicine ,Myocardial infarction ,11 Medical and Health Sciences ,ddc:616 ,Incidence ,Antibodies, Monoclonal ,General Medicine ,Cholesterol ,Cardiovascular Diseases ,Monoclonal ,Drug Therapy, Combination ,Proprotein Convertase 9 ,Antibody ,Aged ,Anticholesteremic Agents ,Atherosclerosis ,Cholesterol, LDL ,Double-Blind Method ,Female ,Follow-Up Studies ,Humans ,Hydroxymethylglutaryl-CoA Reductase Inhibitors ,Hypercholesterolemia ,Least-Squares Analysis ,Middle Aged ,Medicine (all) ,REDUCING LIPIDS ,Human ,medicine.medical_specialty ,Evinacumab ,Clinical Trials and Supportive Activities ,PCSK9 INHIBITION ,Follow-Up Studie ,LDL ,03 medical and health sciences ,Drug Therapy ,Clinical Research ,LDL-C ,Least-Squares Analysi ,Science & Technology ,Unstable angina ,PCSK9 ,medicine.disease ,chemistry ,Clinical Biochemistry ,030204 cardiovascular system & hematology ,Bococizumab ,FOURIER Steering Committee and Investigators ,Medical and Health Sciences ,chemistry.chemical_compound ,Antibodies monoclonal ,Cardiovascular Disease ,030212 general & internal medicine ,Stroke ,Humanized ,RISK ,biology ,PCSK9 Inhibitors ,10051 Rheumatology Clinic and Institute of Physical Medicine ,Heart Disease ,Atherosclerosi ,6.1 Pharmaceuticals ,Combination ,Cardiology ,Life Sciences & Biomedicine ,Antibodies, Monoclonal, Humanized ,EZETIMIBE ,610 Medicine & health ,Antibodies ,Medicine, General & Internal ,General & Internal Medicine ,Internal medicine ,CORONARY-HEART-DISEASE ,In patient ,Heart Disease - Coronary Heart Disease ,Alirocumab ,Ldl cholesterol ,business.industry ,Evaluation of treatments and therapeutic interventions ,Evolocumab ,Good Health and Well Being ,Settore MED/11 - MALATTIE DELL'APPARATO CARDIOVASCOLARE ,biology.protein ,MODERATE ,Hydroxymethylglutaryl-CoA Reductase Inhibitor ,business - Abstract
Background Evolocumab is a monoclonal antibody that inhibits proprotein convertase subtilisin–kexin type 9 (PCSK9) and lowers low-density lipoprotein (LDL) cholesterol levels by approximately 60%. Whether it prevents cardiovascular events is uncertain. Methods We conducted a randomized, double-blind, placebo-controlled trial involving 27,564 patients with atherosclerotic cardiovascular disease and LDL cholesterol levels of 70 mg per deciliter (1.8 mmol per liter) or higher who were receiving statin therapy. Patients were randomly assigned to receive evolocumab (either 140 mg every 2 weeks or 420 mg monthly) or matching placebo as subcutaneous injections. The primary efficacy end point was the composite of cardiovascular death, myocardial infarction, stroke, hospitalization for unstable angina, or coronary revascularization. The key secondary efficacy end point was the composite of cardiovascular death, myocardial infarction, or stroke. The median duration of follow-up was 2.2 years. Results At 48 weeks, the least-squares mean percentage reduction in LDL cholesterol levels with evolocumab, as compared with placebo, was 59%, from a median baseline value of 92 mg per deciliter (2.4 mmol per liter) to 30 mg per deciliter (0.78 mmol per liter) (P
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- 2017
6. Does response of RAS blockade on serum K+ levels influence its glycemic-mitigating response when combined with hydrochlorothiazide?
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Deedwania PC, Zappe DH, Egan BM, Purkayastha D, Samuel R, Sowers JR, Deedwania, Prakash C, Zappe, Dion H, Egan, Brent M, Purkayastha, Das, Samuel, Rita, and Sowers, James R
- Abstract
The authors previously reported that addition of valsartan ameliorated the negative metabolic effects of hydrochlorothiazide in obese hypertensive patients through an enhanced postprandial insulin response. In this secondary analysis, the authors tested whether this enhanced insulin response to valsartan/hydrochlorothiazide was influenced by serum potassium levels, which were reduced to a lesser extent, when compared with amlodipine/hydrochlorothiazide. Results showed that the early insulin response with valsartan plus hydrochlorothiazide occurred regardless of serum potassium levels. Heightened insulin response was, however, not significantly different when patients with normal potassium (>3.9 mEq/L) at baseline and low potassium (≤3.9 mEq/L) at the end of the study were compared with the amlodipine/hydrochlorothiazide group. Despite the influence of serum potassium on insulin secretory response to a glucose challenge, the addition of valsartan maintained normoglycemia in patients given hydrochlorothiazide. Thus, the metabolic response to hydrochlorothiazide was improved with addition of valsartan through an enhanced insulin response that was not greatly affected by changes in potassium levels. [ABSTRACT FROM AUTHOR]
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- 2012
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7. Angiotensin receptor blocker/diuretic combination preserves insulin responses in obese hypertensives.
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Sowers JR, Raij L, Jialal I, Egan BM, Ofili EO, Samuel R, Zappe DH, Purkayastha D, Deedwania PC, Sowers, James R, Raij, Leopoldo, Jialal, Ishwaral, Egan, Brent M, Ofili, Elizabeth O, Samuel, Rita, Zappe, Dion H, Purkayastha, Das, and Deedwania, Prakash C
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- 2010
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8. Benefits of statin therapy and compliance in high risk cardiovascular patients.
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Lardizabal JA, Deedwania PC, Lardizabal, Joel A, and Deedwania, Prakash C
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- 2010
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9. Low use of statins and other coronary secondary prevention therapies in primary and secondary care in India.
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Sharma KK, Gupta R, Agrawal A, Roy S, Kasliwal A, Bana A, Tongia RK, Deedwania PC, Sharma, Krishna K, Gupta, Rajeev, Agrawal, Aachu, Roy, Sanjeeb, Kasliwal, Atul, Bana, Ajeet, Tongia, Ravindra K, and Deedwania, Prakash C
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- 2009
10. Metabolic and antihypertensive effects of combined angiotensin receptor blocker and diuretic therapy in prediabetic hypertensive patients with the cardiometabolic syndrome.
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Zappe DH, Sowers JR, Hsueh WA, Haffner SM, Deedwania PC, Fonseca VA, Keeling L, Sica DA, Zappe, Dion H, Sowers, James R, Hsueh, Willa A, Haffner, Steven M, Deedwania, Prakash C, Fonseca, Vivian A, Keeling, Lucy, and Sica, Domenic A
- Abstract
Hypertensive patients with the cardiometabolic syndrome (CMS) are at increased risk for type 2 diabetes and cardiovascular disease. The authors examined effects of valsartan and hydrochlorothiazide (HCTZ) combined and alone on insulin sensitivity (using homeostasis model assessment-insulin resistance [HOMA-IR]), and inflammatory/metabolic biomarkers in prediabetic hypertensive persons with CMS. Eligible patients entered 16-week therapy with valsartan 320 mg/d (n=189), HCTZ 25 mg/d (n=190), or valsartan/HCTZ 320/25 mg/d (n=187). At the end point, there were no statistically significant differences in HOMA-IR among the 3 groups. HCTZ significantly increased hemoglobin A(1c) and triglyceride concentrations and lowered serum potassium levels vs valsartan. HCTZ also increased plasma aldosterone and C-reactive protein levels. Blood pressure reduction and blood pressure control rates were highest with valsartan/HCTZ. There were no differences between combination valsartan/HCTZ or monotherapies on a measure of insulin sensitivity; however, the negative metabolic effects of HCTZ (increase in triglyceride and hemoglobin A(1c) values) were absent with valsartan/HCTZ, indicating an ameliorating effect of valsartan on these measures. [ABSTRACT FROM AUTHOR]
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- 2008
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11. Comparison of rosuvastatin versus atorvastatin in South-Asian patients at risk of coronary heart disease (from the IRIS trial)
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Deedwania PC, Gupta M, Stein M, Ycas J, Gold A, and IRIS Study Group
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- 2007
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12. Effect of high-dose atorvastatin on hospitalizations for heart failure: subgroup analysis of the Treating to New Targets (TNT) study.
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Khush KK, Waters DD, Bittner V, Deedwania PC, Kastelein JJ, Lewis SJ, and Wenger NK
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- 2007
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13. Diabetes and vascular disease: common links in the emerging epidemic of coronary artery disease.
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Deedwania PC and Deedwania, Prakash C
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- 2003
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14. Beta-blockers and adverse effects: dispelling the myths.
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Deedwania PC and D'Epiro P
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Beta-blockers are underutilized in many patients. Barriers include perceived and real contraindications and frequently cited adverse effects. Misperceptions abound about the benefits and risks of these drugs in patients with cardiovascular diseases. [ABSTRACT FROM AUTHOR]
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- 2002
15. Metoprolol CR/XL in female patients with heart failure: analysis of the experience in Metoprolol Extended-Release Randomized Intervention Trial in Heart Failure (MERIT-HF).
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Ghali JK, Piña IL, Gottlieb SS, Deedwania PC, Wikstrand JC, MERIT-HF Study Group, Ghali, Jalal K, Piña, Ileana L, Gottlieb, Stephen S, Deedwania, Prakash C, and Wikstrand, John C
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- 2002
16. What is the role of angiotensin II receptor blockers?
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Miller D, Deedwania PC, Pitt B, and Ram CVS
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Angiotensin II receptor blockers are as effective as ACE inhibitors in reducing BP, but do they offer equal long-term cardiac and renal protection? The results of several new trials are providing some answers. [ABSTRACT FROM AUTHOR]
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- 2001
17. Relation of gemfibrozil treatment and lipid levels with major coronary events: VA-HIT: a randomized controlled trial.
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Robins SJ, Collins D, Wittes JT, Papademetriou V, Deedwania PC, Schaefer EJ, McNamara JR, Kashyap ML, Hershman JM, Wexler LF, Rubins HB, VA-HIT Study Group, Robins, S J, Collins, D, Wittes, J T, Papademetriou, V, Deedwania, P C, Schaefer, E J, McNamara, J R, and Kashyap, M L
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Context: A low plasma level of high-density lipoprotein cholesterol (HDL-C) is a major risk factor for coronary heart disease (CHD). A secondary prevention study, the Veterans Affairs High-Density Lipoprotein Intervention Trial (VA-HIT), demonstrated that CHD events were significantly reduced during a median follow-up of 5.1 years by treating patients with the fibric acid derivative gemfibrozil when the predominant lipid abnormality was low HDL-C.Objective: To determine if the reduction in major CHD events with gemfibrozil in VA-HIT could be attributed to changes in major plasma lipid levels.Design: Multicenter, randomized, double-blind, placebo-controlled trial conducted from September 1991 to August 1998.Setting: The Department of Veterans Affairs Cooperative Studies Program, in which 20 VA medical centers were participating sites.Participants: A total of 2531 men with a history of CHD who had low HDL-C levels (mean, 32 mg/dL [0.83 mmol/L] ) and low low-density lipoprotein cholesterol (LDL-C) levels (mean, 111 mg/dL [2.88 mmol/L]).Intervention: Participants were randomly assigned to receive gemfibrozil, 1200 mg/d (n = 1264), or matching placebo (n = 1267).Main Outcome Measure: Relation of lipid levels at baseline and averaged during the first 18 months of gemfibrozil treatment with the combined incidence of nonfatal myocardial infarction and CHD death.Results: Concentrations of HDL-C were inversely related to CHD events. Multivariable Cox proportional hazards analysis showed that CHD events were reduced by 11% with gemfibrozil for every 5-mg/dL (0.13-mmol/L) increase in HDL-C (P =.02). Events were reduced even further with gemfibrozil beyond that explained by increases in HDL-C values, particularly in the second through fourth quintiles of HDL-C values during treatment. During gemfibrozil treatment, only the increase in HDL-C significantly predicted a lower risk of CHD events; by multivariable analysis, neither triglyceride nor LDL-C levels at baseline or during the trial predicted CHD events.Conclusions: Concentrations of HDL-C achieved with gemfibrozil treatment predicted a significant reduction in CHD events in patients with low HDL-C levels. However, the change in HDL-C levels only partially explained the beneficial effect of gemfibrozil. [ABSTRACT FROM AUTHOR]- Published
- 2001
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18. Hypertension and diabetes: new therapeutic options.
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Deedwania PC
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- 2000
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19. Hypercholesterolemia: is lipid-lowering worthwhile for older patients?
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Deedwania PC
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- 2000
20. Evidence-based, cost-effective risk stratification and management after myocardial infarction. California Cardiology Working Group on Post-MI Management.
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Deedwania PC, Amsterdam EA, and Vagelos RH
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- 1997
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21. Blood Pressure Control in Diabetes Mellitus: Is Lower Always Better, and How Low Should it Go?
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Deedwania PC
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- 2011
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22. Risk of Diabetes and Cardiovascular Disease: Best to Return Back to the Basics: Comment on 'Long-term Effects of a Lifestyle Intervention on Weight and Cardiovascular Risk Factors in Individuals With Type 2 Diabetes Mellitus'.
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Deedwania PC
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- 2010
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23. Angiotensin receptor blockers and cardiovascular protection: are we ONTARGET?
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Ram CVS and Deedwania PC
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- 2008
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24. Use of intensive lipid-lowering therapy in patients hospitalized with acute coronary syndrome: An analysis of 65,396 hospitalizations from 344 hospita participating in Get With The Guidelines (GWTG).
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Javed U, Deedwania PC, Bhatt DL, Cannon CP, Dai D, Hernandez AF, Peterson ED, Fonarow GC, Javed, Usman, Deedwania, Prakash C, Bhatt, Deepak L, Cannon, Christopher P, Dai, David, Hernandez, Adrian F, Peterson, Eric D, and Fonarow, Gregg C
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Objectives: The study aimed to analyze the use of intensive lipid-lowering therapy (I-LLT) at discharge in a broad population of patients hospitalized with acute coronary syndrome (ACS).Background: Early and intensive statin therapy in ACS has been shown to reduce cardiovascular morbidity and mortality. Utilization and predictors of I-LLT among hospitalized ACS patients are not known.Methods: The GWTG database was analyzed for ACS-related hospitalizations from 2005 to 2009. The use of I-LLT (defined as dose of statin or combination therapy likely to produce > 50% reductions in low-density lipoprotein [LDL]) and less intensive lipid-lowering therapy (LI-LLT) at discharge was assessed. Baseline characteristics and temporal trends in LLT were compared in these 2 treatment groups.Results: Of 65,396 patients receiving LLT, only 25,036 (38.3%) were treated with an I-LLT regimen. Mean total cholesterol, LDL, and triglycerides were significantly higher in the I-LLT group. Even among those with LDL > 130 mg/dL, 50% or less received I-LLT. Predictors of I-LLT at discharge included LLT before admission, hyperlipidemia, prior coronary artery disease, increasing body mass index, and in-hospital percutaneous coronary intervention. Although there was some temporal improvement in the rate of I-LLT from 2005 to 2007, a decline in use of I-LLT was noted in 2008 and 2009. This was attributed to a sharp reduction in use of ezetimibe in combination with statin, without corresponding increases in intensive statin monotherapy.Conclusions: In a large cohort of patients admitted with ACS, most of the eligible patients were not discharged on I-LLT. These data suggest the need for better implementation of guideline-recommended intensive statin therapy in patients with ACS. [ABSTRACT FROM AUTHOR]- Published
- 2011
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25. Use of intensive lipid-lowering therapy in patients hospitalized with acute coronary syndrome: An analysis of 65,396 hospitalizations from 344 hospitals participating in Get With The Guidelines (GWTG)
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Javed U, Deedwania PC, Bhatt DL, Cannon CP, Dai D, Hernandez AF, Peterson ED, and Fonarow GC
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- 2010
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26. Getting with the ACC/AHA guidelines for the treatment of chronic angina as a disease state.
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Deedwania PC, Carbajal EV, Deedwania, Prakash C, and Carbajal, Enrique V
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The primary objective of treatment in patients with chronic coronary artery disease (CAD) and stable angina is relief of symptoms and improvement of clinical outcome. The American College of Cardiology/American Heart Association guidelines have emphasized the role of evidence-based therapies. There have been regular updates of the guidelines, with an effort to include the latest data in the recommendations. Since the 2002 guidelines were published, there have been several pivotal studies that have provided strong support for the role of aggressive and optimal medical therapy in improving clinical outcomes in patients with chronic CAD. Recent data from 2 landmark studies have emphasized that optimal medical therapy is as effective as myocardial revascularization with percutaneous coronary intervention or coronary artery bypass grafting in reducing risk of adverse clinical outcomes. The 2009-2010 guidelines will likely incorporate the findings of these studies and accordingly modify the recommendations for treatment of patients with chronic CAD and stable angina. [ABSTRACT FROM AUTHOR]
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- 2009
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27. Angiotensin receptor blockers: cardiovascular protection in the metabolic syndrome.
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Deedwania PC and Schmieder R
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It is well recognised that the metabolic syndrome, a constellation of risk factors including obesity, hypertension, insulin resistance and dyslipidaemia, is associated with an increased risk of cardiovascular complications and the development of Type 2 diabetes. Consequently, timely identification and management of all components of the metabolic syndrome is warranted. In particular, guidelines have emphasised the importance of targeting elevated blood pressure (BP) and dyslipidaemia as a method of reducing global cardiovascular risk.Findings from the Valsartan Antihypertensive Long-term Use Evaluation (VALUE) trial show that the angiotensin receptor blocker, valsartan, reduces cardiovascular events and the development of Type 2 diabetes in high-risk individuals. This profile is being further explored in the ongoing Nateglinide And Valsartan in Impaired Glucose Tolerance Outcomes Research (NAVIGATOR) trial.Given the potential advantages to patients and physicians of tackling more than one of the components of the metabolic syndrome, antihypertensive agents such as valsartan would appear to be an important addition to the management of vulnerable patients at high risk of cardiovascular events. [ABSTRACT FROM AUTHOR]
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- 2006
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28. Effects of lipid-altering treatment in diabetes mellitus and the metabolic syndrome.
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Deedwania PC, Hunninghake DB, and Bays H
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- 2004
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29. Drug spotlight. Beta-blockers and adverse effects: dispelling the myths.
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Deedwania PC
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Beta-blockers are underutilized in many patients. Barriers include perceived and real contraindications and frequently cited adverse effects. Misperceptions abound about the benefits and risks of these drugs in patients with cardiovascular diseases. [ABSTRACT FROM AUTHOR]
- Published
- 2002
30. Usefulness of heart rate at rest as a predictor of mortality, hospitalization for heart failure, myocardial infarction, and stroke in patients with stable coronary heart disease (Data from the Treating to New Targets [TNT] trial)
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Ho JE, Bittner V, Demicco DA, Breazna A, Deedwania PC, and Waters DD
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- 2010
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31. Intensive lipid lowering with atorvastatin in patients with coronary artery disease, diabetes, and chronic kidney disease.
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Shepherd J, Kastelein JP, Bittner VA, Carmena R, Deedwania PC, Breazna A, Dobson S, Wilson DJ, Zuckerman AL, Wenger NK, Treating to New Targets Steering Committee and Investigators, Shepherd, James, Kastelein, John P, Bittner, Vera A, Carmena, Rafael, Deedwania, Prakash C, Breazna, Andrei, Dobson, Stephen, Wilson, Daniel J, and Zuckerman, Andrea L
- Abstract
Objective: To investigate the effect of intensive lipid lowering with high-dose atorvastatin on the incidence of major cardiovascular events compared with low-dose atorvastatin in patients with coronary artery disease and type 2 diabetes, with and without chronic kidney disease (CKD).Patients and Methods: Following 8 weeks' open-label therapy with atorvastatin (10 mg/d), 10,001 patients with coronary artery disease were randomized to receive double-blind therapy with either 80 mg/d or 10 mg/d of atorvastatin between July 1, 1998, and December 31, 1999. Of 1501 patients with diabetes, renal data were available for 1431. Patients with CKD were defined as having a baseline estimated glomerular filtration rate (eGFR) below 60 mL/min per 1.73 m2, using the Modification of Diet in Renal Disease equation.Results: After a median follow-up of 4.8 years, 95 (17.4%) of 546 patients with diabetes and CKD experienced a major cardiovascular event vs 119 (13.4%) of 885 patients with diabetes and normal eGFRs (hazard ratio [HR], 1.32; 95% confidence interval [CI], 1.00-1.72; P<.05). Compared with 10 mg of atorvastatin, 80 mg of atorvastatin reduced the relative risk of major cardiovascular events by 35% in patients with diabetes and CKD (20.9% [57/273] vs 13.9% [38/273]; HR, 0.65; 95% CI, 0.43-0.98; P=.04) and by 10% in patients with diabetes and normal eGFR (14.1% [62/441] vs 12.8% [57/444]; HR, 0.90; 95% CI, 0.63-1.29; P=.56). The absolute risk reduction in patients with diabetes and CKD was substantial, yielding a number needed to treat of 14 to prevent 1 major cardiovascular event over 4.8 years. Both treatments were well tolerated.Conclusion: Patients with diabetes, stable coronary artery disease, and mild to moderate CKD experience marked reduction in cardiovascular events with intensive lipid lowering, in contrast to previous observations in patients with diabetes and end-stage renal disease.Trial Registration: clinicaltrials.gov identifier: NCT00327691. [ABSTRACT FROM AUTHOR]- Published
- 2008
32. 2007 chronic angina focused update of the ACC/AHA 2002 guidelines for the management of patients with chronic stable angina: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Writing Group to develop the focused update of the 2002 guidelines for the management of patients with chronic stable angina.
- Author
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Fraker TD Jr, Fihn SD, Gibbons RJ, Abrams J, Chatterjee K, Daley J, Deedwania PC, Douglas JS, Ferguson TB Jr, Gardin JM, O'Rourke RA, Pasternak RC, Williams SV, Smith SC Jr, Jacobs AK, Adams CD, Anderson JL, Buller CE, Creager MA, and Ettinger SM
- Published
- 2007
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33. Results of the National Cholesterol Education (NCEP) Program evaluation project utilizing novel e-technology (NEPTUNE) II survey and implications for treatment under the recent NCEP Writing Group recommendations.
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Davidson MH, Maki KC, Pearson TA, Pasternak RC, Deedwania PC, McKenney JM, Fonarow GC, Maron DJ, Ansell BJ, Clark LT, and Ballantyne CM
- Published
- 2005
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34. Comparison of controlled-onset, extended-release verapamil with amlodipine and amlodipine plus atenolol on exercise performance and ambulatory ischemia in patients with chronic stable angina pectoris.
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Frishman WH, Glasser S, Stone P, Deedwania PC, Johnson M, Fakouhi TD, Frishman, W H, Glasser, S, Stone, P, Deedwania, P C, Johnson, M, and Fakouhi, T D
- Abstract
This multicenter, randomized, double-blind, parallel group, placebo lead-in, placebo-controlled study compared the antianginal and anti-ischemic effects of once-daily bedtime dosing of controlled-onset extended-release (COER-24) verapamil to a once-daily morning dosing of amlodipine +/- atenolol in patients with chronic stable angina. A total of 551 patients with exercise-induced myocardial ischemia and evidence of coronary artery disease were randomized to a 4-week, forced-dose titration treatment period with (1) COER-24 verapamil 240 mg titrated to 480 mg at bedtime (n = 173), (2) amlodipine 5 mg titrated to 10 mg/day (n = 149), (3) amlodipine 5 mg (titrated to 10 mg) plus atenolol 50 mg/day in the A.M. (n = 154), or (4) placebo (n = 75). Treadmill exercise tolerance testing (standard Bruce protocol), and 48-hour ambulatory electrocardiographic (Holter) monitoring were performed at the end of placebo lead-in and double-blind treatment. Each active treatment significantly improved symptom-limited exercise duration and time to moderate angina (p < or = 0.01 vs placebo). For patients with baseline ischemia, amlodipine resulted in a statistically significant increase in total duration of ischemic episodes compared with placebo, whereas COER-24 verapamil and amlodipine plus atenolol resulted in statistically significant decreases compared with placebo and amlodipine. Heart rate at onset of ischemic episodes and ST product were also significantly increased with amlodipine (p < 0.05) compared with either COER-24 or amlodipine plus atenolol. COER-24 and amlodipine alone or in combination with atenolol improved exercise capacity in patients with angina pectoris. COER-24 verapamil monotherapy or amlodipine plus atenolol combination therapy were more effective than amlodipine monotherapy in decreasing ambulatory myocardial ischemia, especially during the hours of 6 A.M. to 12 noon. [ABSTRACT FROM AUTHOR]
- Published
- 1999
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35. Outcomes in patients with acute non-Q-wave myocardial infarction randomly assigned to an invasive as compared with a conservative management strategy.
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Boden WE, O'Rourke RA, Crawford MH, Blaustein AS, Deedwania PC, Zoble RG, Wexler LF, Kleiger RE, Pepine CJ, Ferry DR, Chow BK, Lavori PW, and Veterans Affairs Non-Q-Wave Infarction Strategies in Hospital Trial Investigators
- Published
- 1998
36. Randomised trial of losartan versus captopril in patients over 65 with heart failure (Evaluation of Losartan in the Elderly Study, ELITE)
- Author
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Pitt B, Segal R, Martinez FA, Meurers G, Cowley AL, Thomas I, Deedwania PC, Ney DE, Snavely DB, Chang PI, ELITE Study Investigators, Pitt, B, Segal, R, Martinez, F A, Meurers, G, Cowley, A J, Thomas, I, Deedwania, P C, Ney, D E, and Snavely, D B
- Abstract
Background: To determine whether specific angiotensin II receptor blockade with losartan offers safety and efficacy advantages in the treatment of heart failure over angiotensin-converting-enzyme (ACE) inhibition with captopril, the ELITE study compared losartan with captopril in older heart-failure patients.Methods: We randomly assigned 722 ACE inhibitor naive patients (aged 65 years or more) with New York Heart Association (NYHA) class II-IV heart failure and ejection fractions of 40% or less to double-blind losartan (n = 352) titrated to 50 mg once daily or captopril (n = 370) titrated to 50 mg three times daily, for 48 weeks. The primary endpoint was the tolerability measure of a persisting increase in serum creatinine of 26.5 mumol/L or more (> or = 0.3 mg/dL) on therapy; the secondary endpoint was the composite of death and/or hospital admission for heart failure; and other efficacy measures were total mortality, admission for heart failure, NYHA class, and admission for myocardial infarction or unstable angina.Findings: The frequency of persisting increases in serum creatinine was the same in both groups (10.5%). Fewer losartan patients discontinued therapy for adverse experiences (12.2% vs 20.8% for captopril, p = 0.002). No losartan-treated patients discontinued due to cough compared with 14 in the captopril group. Death and/or hospital admission for heart failure was recorded in 9.4% of the losartan and 13.2% of the captopril patients (risk reduction 32% [95% CI -4% to + 55%], p = 0.075). This risk reduction was primarily due to a decrease in all-cause mortality (4.8% vs 8.7%; risk reduction 46% [95% CI 5-69%], p = 0.035). Admissions with heart failure were the same in both groups (5.7%), as was improvement in NYHA functional class from baseline. Admission to hospital for any reason was less frequent with losartan than with captopril treatment (22.2% vs 29.7%).Interpretation: In this study of elderly heart-failure patients, treatment with losartan was associated with an unexpected lower mortality than that found with captopril. Although there was no difference in renal dysfunction, losartan was generally better tolerated than captopril and fewer patients discontinued losartan therapy. A further trial, evaluating the effects of losartan and captopril on mortality and morbidity in a larger number of patients with heart failure, is in progress. [ABSTRACT FROM AUTHOR]- Published
- 1997
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37. Improving outcomes in post-acute myocardial infarction heart failure: incorporation of aldosterone blockade into combination therapy to optimize neurohormonal blockade.
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Pitt B, Fonarow GC, Gheorghiade M, Deedwania PC, and Duprez DA
- Published
- 2006
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38. Epidemiology of Diabetes and Atherosclerotic Cardiovascular Disease Among Asian American Adults: Implications, Management, and Future Directions: A Scientific Statement From the American Heart Association.
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Kwan TW, Wong SS, Hong Y, Kanaya AM, Khan SS, Hayman LL, Shah SH, Welty FK, Deedwania PC, Khaliq A, and Palaniappan LP
- Subjects
- Adult, Humans, American Heart Association, Cardiovascular Diseases epidemiology, Cardiovascular Diseases ethnology, Cardiovascular Diseases etiology, Cardiovascular Diseases therapy, United States epidemiology, Asian ethnology, Asian statistics & numerical data, Atherosclerosis epidemiology, Atherosclerosis ethnology, Atherosclerosis etiology, Atherosclerosis therapy, Diabetes Mellitus, Type 2 epidemiology, Diabetes Mellitus, Type 2 ethnology, Diabetes Mellitus, Type 2 etiology, Diabetes Mellitus, Type 2 therapy
- Abstract
Asian American individuals make up the fastest growing racial and ethnic group in the United States. Despite the substantial variability that exists in type 2 diabetes and atherosclerotic cardiovascular disease risk among the different subgroups of Asian Americans, the current literature, when available, often fails to examine these subgroups individually. The purpose of this scientific statement is to summarize the latest disaggregated data, when possible, on Asian American demographics, prevalence, biological mechanisms, genetics, health behaviors, acculturation and lifestyle interventions, pharmacological therapy, complementary alternative interventions, and their impact on type 2 diabetes and atherosclerotic cardiovascular disease. On the basis of available evidence to date, we noted that the prevalences of type 2 diabetes and stroke mortality are higher in all Asian American subgroups compared with non-Hispanic White adults. Data also showed that atherosclerotic cardiovascular disease risk is highest among South Asian and Filipino adults but lowest among Chinese, Japanese, and Korean adults. This scientific statement discusses the biological pathway of type 2 diabetes and the possible role of genetics in type 2 diabetes and atherosclerotic cardiovascular disease among Asian American adults. Challenges to provide evidence-based recommendations included the limited data on Asian American adults in risk prediction models, national surveillance surveys, and clinical trials, leading to significant research disparities in this population. The large disparity within this population is a call for action to the public health and clinical health care community, for whom opportunities for the inclusion of the Asian American subgroups should be a priority. Future studies of atherosclerotic cardiovascular disease risk in Asian American adults need to be adequately powered, to incorporate multiple Asian ancestries, and to include multigenerational cohorts. With advances in epidemiology and data analysis and the availability of larger, representative cohorts, furthering refining the Pooled Cohort Equations, in addition to enhancers, would allow better risk estimation in segments of the population. Last, this scientific statement provides individual- and community-level intervention suggestions for health care professionals who interact with the Asian American population.
- Published
- 2023
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39. GLP-1 receptor agonists and cardiovascular outcomes in patients with type 2 diabetes: Clinical evidence and best practice.
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Coke LA, Deedwania PC, Hinnen D, Magwire M, and Miller NH
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- Glucagon-Like Peptide-1 Receptor, Humans, Hypoglycemic Agents therapeutic use, Liraglutide, Quality of Life, Cardiovascular Diseases drug therapy, Cardiovascular Diseases etiology, Diabetes Mellitus, Type 2 complications, Diabetes Mellitus, Type 2 drug therapy
- Abstract
Abstract: Cardiovascular disease (CVD) is a major cause of death and disability among people with type 2 diabetes (T2D), presenting a significant impact on longevity, patient quality of life, and health care costs. In the United States, attainment of recommended glycemic targets is low and T2D-related cardiovascular complications remain a significant burden. Many glucose-lowering treatment options are available, but glucagon-like peptide-1 receptor agonists (GLP-1RAs) and sodium-glucose cotransporter-2 (SGLT-2) inhibitors are recommended in recent guidelines as the preferred add-on therapy to metformin to improve glycemic control. This is particularly the case for patients with T2D and established atherosclerotic CVD, at high risk of atherosclerotic CVD, and/or with chronic kidney disease. Recommendations were based on GLP-1RA and SGLT-2 inhibitor cardiovascular outcomes trials (CVOTs), which consistently showed that these agents pose no additional cardiovascular risk compared with placebo. Three GLP-1RAs (liraglutide, dulaglutide, and subcutaneous semaglutide) demonstrated significantly lower major adverse cardiovascular events versus placebo and are now approved for this indication. However, to realize improvement in outcomes in the clinical setting, organized, systematic, and coordinated approaches to patient management are also needed. For example, nurse-led diabetes self-management education and support programs have been shown to be effective. This article explores T2D management with emphasis on cardiovascular risk and CVOTs performed to date and reviews the clinical experience with GLP-1RAs for managing hyperglycemia and their impact on cardiovascular risk. In addition, practical guidance is given for key health care providers involved in the care of patients with T2D with cardiovascular risk outside of diabetes clinics/endocrinology centers., Competing Interests: Competing interests: P. C. Deedwania has acted as a consultant for Janssen and has received research grants for their institution from Boehringer Ingelheim, Novartis, and Sanofi. D. Hinnen has attended advisory boards and served on speakers' bureaus for Eli Lilly and Co., Janssen Pharmaceuticals, Novo Nordisk, and Sanofi. M. Magwire has attended advisory boards and acted as a consultant for Boehringer Ingelheim/Lilly and Novo Nordisk. The remaining authors report no conflicts of interest., (Copyright © 2022 American Association of Nurse Practitioners.)
- Published
- 2022
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40. Efficacy and Safety of Long-Term Evolocumab Use Among Asian Subjects - A Subgroup Analysis of the Further Cardiovascular Outcomes Research With PCSK9 Inhibition in Subjects With Elevated Risk (FOURIER) Trial.
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Keech AC, Oyama K, Sever PS, Tang M, Murphy SA, Hirayama A, Lu C, Tay L, Deedwania PC, Siu CW, Lira Pineda A, Choi D, Charng MJ, Amerena J, Wan Ahmad WA, Chopra VK, Pedersen TR, Giugliano RP, and Sabatine MS
- Subjects
- Cholesterol, LDL, Heart Disease Risk Factors, Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors therapeutic use, Proprotein Convertase 9, Treatment Outcome, Antibodies, Monoclonal, Humanized adverse effects, Asian People, Atherosclerosis drug therapy, Atherosclerosis ethnology, PCSK9 Inhibitors adverse effects
- Abstract
Background: There are concerns that Asian patients respond differently to some medications. This study evaluated the efficacy and safety of evolocumab among Asian vs. other subjects in the FOURIER trial, which randomized stable atherosclerosis patients to receive either evolocumab or placebo.Methods and Results:Effects of adding evolocumab vs. placebo to background statin therapy on low-density lipoprotein cholesterol (LDL-C) reductions, cardiovascular outcomes, and adverse events were compared among 27,564 participants with atherosclerotic disease, according to self-reported Asian (n=2,723) vs. other (n=24,841) races followed for a median of 2.2 years in the FOURIER trial. The primary endpoint was a composite of cardiovascular death, myocardial infarction, stroke, hospitalization for unstable angina, or coronary revascularization. At randomization, Asians had slightly lower LDL-C (median 89 [IQR 78-104] mg/dL vs. 92 [80-109] mg/dL; P<0.001) and were much less likely to be on a high-intensity statin (33.3% vs. 73.3%; P<0.001). Evolocumab lowered LDL-C more in Asians than in others (66% vs. 58%; P<0.001). The effect of evolocumab on the primary endpoint was similar in Asians (HR, 0.79; 95% CI, 0.61-1.03) and others (HR, 0.86; 95% CI, 0.79-0.93; P interaction=0.55). There was no excess of serious adverse events with evolocumab among Asians over others., Conclusions: Use of evolocumab robustly lowers LDL-C and is equally efficacious in lowering the risk of cardiovascular events and safe in Asians as it is in others.
- Published
- 2021
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41. Defining the Role of Icosapent Ethyl in Clinical Practice.
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Chatterjee S, Hajra A, Bandyopadhyay D, Ghosh RK, and Deedwania PC
- Subjects
- Drug Dosage Calculations, Eicosapentaenoic Acid administration & dosage, Eicosapentaenoic Acid adverse effects, Eicosapentaenoic Acid therapeutic use, Humans, Randomized Controlled Trials as Topic, Risk Factors, Eicosapentaenoic Acid analogs & derivatives, Hypertriglyceridemia drug therapy
- Abstract
The health benefit of fish oil, i.e. omega-3 fatty acids (ω-3 FA) has a long history of debate. While there are a number of medications to reduce serum triglyceride levels, none have shown unanimous cardiovascular (CV) benefits. The most recent Reduction of Cardiovascular Events with Icosapent Ethyl-Intervention Trial (REDUCE-IT) assessing the CV outcome of one highly purified prescription ω-3 FA has certainly rejuvenated the debate. While this trial has been regarded as one of the most important landmark trials in preventive cardiology, the tolerability issue in a very high dose (4 g/day, as administered in the trial) is still a matter of concern. This article summarizes the current status and future perspective of icosapent ethyl in clinical practice in light of REDUCE-IT.
- Published
- 2020
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42. Association between depression and readmission of heart failure: A national representative database study.
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Patel N, Chakraborty S, Bandyopadhyay D, Amgai B, Hajra A, Atti V, Das A, Ghosh RK, Deedwania PC, Aronow WS, Lavie CJ, Di Tullio MR, Vaduganathan M, and Fonarow GC
- Subjects
- Aged, Aged, 80 and over, Comorbidity, Databases, Factual, Depression diagnosis, Depression psychology, Depression therapy, Female, Heart Disease Risk Factors, Heart Failure diagnosis, Heart Failure physiopathology, Heart Failure therapy, Humans, Male, Middle Aged, Prognosis, Retrospective Studies, Risk Assessment, Time Factors, United States epidemiology, Depression epidemiology, Heart Failure epidemiology, Patient Readmission
- Abstract
Introduction: Depression is a recognized predictor of adverse outcomes in patients with heart failure (HF) and is associated with poor quality of life, functional limitation, increased morbidity and mortality, decreased adherence to treatment, and increased rehospitalization. To understand the impact of depression on HF readmission, we conducted a retrospective cohort study using the Nationwide Readmission Database (NRD) 2010-2014., Methods: We identified all patients with the primary discharge diagnosis of HF by ICD-9-CM codes. The primary outcome of the study was to identify 30-day all-cause readmission and causes of readmission in patients with and without depression. Multivariate Cox regression analysis was used to estimate the adjusted hazard ratio for the primary and secondary outcomes., Results: Among, 3,500,570 patients admitted with HF, 9.7% had concomitant depression. Patients with depression were more likely to be readmitted within 30 days (19.7% vs. 18.5%; P < 0.001). Concomitant depression was associated with higher risk of all-cause readmissions within 30 days and 90 days [P < 0.001] but was not associated with increased readmissions due to cardiovascular (CV) cause at 30 days and 90 days. The hazard of psychiatric causes of readmission was higher in patients with depression, both at 30 days [P < 0.001], and 90 days [P < 0.001]. Most of the readmissions were due to CV causes, with HF being the most common cause., Conclusion: Among patients hospitalized with HF, the presence of depression is associated with increased all-cause readmission driven mainly by psychiatric causes but not CV-related readmission. Standard interventions targeted toward HF are unlikely to modify this portion of all-cause readmission., (Copyright © 2020 Elsevier Inc. All rights reserved.)
- Published
- 2020
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43. Clinical Management of Stable Coronary Artery Disease in Patients With Type 2 Diabetes Mellitus: A Scientific Statement From the American Heart Association.
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Arnold SV, Bhatt DL, Barsness GW, Beatty AL, Deedwania PC, Inzucchi SE, Kosiborod M, Leiter LA, Lipska KJ, Newman JD, and Welty FK
- Subjects
- American Heart Association, Clinical Decision-Making, Comorbidity, Consensus, Coronary Artery Disease diagnosis, Coronary Artery Disease epidemiology, Diabetes Mellitus, Type 2 diagnosis, Diabetes Mellitus, Type 2 epidemiology, Humans, Risk Assessment, Risk Factors, Treatment Outcome, United States, Coronary Artery Disease therapy, Diabetes Mellitus, Type 2 therapy, Hypoglycemic Agents therapeutic use, Myocardial Revascularization standards, Patient-Centered Care standards, Risk Reduction Behavior, Secondary Prevention standards
- Abstract
Although cardiologists have long treated patients with coronary artery disease (CAD) and concomitant type 2 diabetes mellitus (T2DM), T2DM has traditionally been considered just a comorbidity that affected the development and progression of the disease. Over the past decade, a number of factors have shifted that have forced the cardiology community to reconsider the role of T2DM in CAD. First, in addition to being associated with increased cardiovascular risk, T2DM has the potential to affect a number of treatment choices for CAD. In this document, we discuss the role that T2DM has in the selection of testing for CAD, in medical management (both secondary prevention strategies and treatment of stable angina), and in the selection of revascularization strategy. Second, although glycemic control has been recommended as a part of comprehensive risk factor management in patients with CAD, there is mounting evidence that the mechanism by which glucose is managed can have a substantial impact on cardiovascular outcomes. In this document, we discuss the role of glycemic management (both in intensity of control and choice of medications) in cardiovascular outcomes. It is becoming clear that the cardiologist needs both to consider T2DM in cardiovascular treatment decisions and potentially to help guide the selection of glucose-lowering medications. Our statement provides a comprehensive summary of effective, patient-centered management of CAD in patients with T2DM, with emphasis on the emerging evidence. Given the increasing prevalence of T2DM and the accumulating evidence of the need to consider T2DM in treatment decisions, this knowledge will become ever more important to optimize our patients' cardiovascular outcomes.
- Published
- 2020
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44. Therapeutic Inertia in Cardiovascular Disease Prevention: Time to Move the Bar.
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Dixon DL, Sharma G, Sandesara PB, Yang E, Braun LT, Mensah GA, Sperling LS, Deedwania PC, and Virani SS
- Subjects
- Cardiovascular Diseases diagnosis, Humans, Preventive Medicine methods, Cardiovascular Diseases prevention & control, Patient Care Team standards, Physician-Patient Relations, Practice Guidelines as Topic standards, Preventive Medicine standards
- Published
- 2019
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45. 25-Year trends in hypertension prevalence, awareness, treatment, and control in an Indian urban population: Jaipur Heart Watch.
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Gupta R, Gupta VP, Prakash H, Agrawal A, Sharma KK, and Deedwania PC
- Subjects
- Adult, Aged, Cardiovascular Diseases diagnosis, Female, Humans, India epidemiology, Male, Middle Aged, Prevalence, Retrospective Studies, Risk Factors, Awareness, Cardiovascular Diseases epidemiology, Forecasting, Risk Assessment, Urban Population statistics & numerical data
- Abstract
Objectives: We evaluated trends in hypertension prevalence, awareness, treatment and control in an Indian urban population over 25 years. Trends were projected to year 2030 to determine attainment of World Health Organization (WHO) Global Monitoring Framework targets., Methods: Adult participants (n=7440, men 4237, women 3203) enrolled in successive population based studies in Jaipur, India from years 1991 to 2015 were evaluated for hypertension prevalence, awareness, treatment and control. The studies were performed in years 1991-93 (n=2212), 1999-01 (n=1123), 2003-04 (n=458), 2006-07 (n=1127), 2009-10 (n=739) and 2012-15 (n=1781). Descriptive statistics are reported. We used logarithmic forecasting to year 2030 and compared outcomes to WHO target of 25% lower prevalence and >50% control., Results: The age-adjusted hypertension prevalence (%) among adults in successive studies increased from 29.5, 30.2, 36.5, 42.1, 34.4 to 36.1 (R
2 =0.41). Increasing trends were observed for hypertension awareness (13, 44, 49, 44, 49, 56; R2 =0.63); treatment in all (9, 22, 38, 34, 41, 36; R2 =0.68) and aware hypertensives (61, 66, 77, 79, 70, 64; R2 =0.46); and control in all (2, 14, 13, 18, 21, 21; R2 =0.82), aware (12, 33, 27, 46, 37, 37; R2 =0.54) and treated (9, 20, 21, 48, 36, 49; R2 =0.80) hypertensive participants. Projections to year 2030 show increases in prevalence to 44% (95% CI 43-45), awareness to 82% (81-83), treatment to 62% (61-63), and control to 36% (35-37)., Conclusion: Hypertension prevalence, awareness, treatment and control rates are increasing among urban populations in India. Better awareness is associated with greater control. The rates of increase are off-target for WHO Global Monitoring Framework and UN Sustainable Development Goals., (Copyright © 2017. Published by Elsevier B.V.)- Published
- 2018
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46. Low Prevalence of AHA-Defined Ideal Cardiovascular Health Factors: A Study of Urban Indian Men and Women.
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Gupta B, Gupta R, Sharma KK, Gupta A, Mahanta TG, and Deedwania PC
- Subjects
- Adult, Aged, American Heart Association, Cardiovascular Diseases classification, Female, Humans, India epidemiology, Life Style, Male, Middle Aged, Prevalence, Risk Factors, Socioeconomic Factors, United States, Young Adult, Cardiovascular Diseases epidemiology, Health Status, Risk Assessment, Urban Population
- Abstract
Background: Coronary heart disease risk factors are widely prevalent among urban subjects in India but the prevalence of good cardiovascular health is unknown., Objectives: This multisite study sought to determine the prevalence of American Heart Association-defined ideal cardiovascular health factors., Methods: The study was performed in 11 cities using cluster sampling. Middle-class urban subjects ages 20 to 75 years (N = 6,198; men: 3,426; women: 2,772, response: 62%) were evaluated for socioeconomic, biophysical, and biochemical factors. Prevalence of ideal cardiovascular health using 7-factor American Heart Association metric (nonsmoking, moderate or greater physical activity, low-fat, high-fruit/vegetable diet, body mass index <25 kg/m
2 , untreated blood pressure <120/<80 mm Hg, cholesterol <200 mg/dl, and fasting glucose <100 mg/dl) was determined. Descriptive statistics are reported., Results: Age-adjusted prevalences of ideal health factors in men and women, respectively, were non-tobacco use in 72.0% and 89.6%, moderate physical activity in 20.1% and 20.6%, healthy diet in 10.6% and 10.6%, normal body mass index in 57.7% and 52.8%, normotension in 17.1% and 22.4%, normocholesterolemia in 72.4% and 72.7%, and normoglycemia in 57.4% and 59.5%. Prevalence of all the 7 health factors was in <1.0% in both men and women, any 6 in 3.4% and 3.5%, any 5 in 12.7% and 17.8%, any 4 in 36.9% and 44.7%, any 3 in 67.2% and 70.8%, any 2 in 89.1% and 92.4%, and 1 in 98.2% and 99.1%. Cardiovascular health was poor (1 to 3 factors) in 62.4% of men and 54.9% of women, average (4 to 5 factors) in 34.1% and 41.5%, and good (≥6 factors) in 3.5% and 3.6%. With increasing age, the behavioral health factors (tobacco use, physical activity, healthy diet) did not change, whereas others declined (ptrend < 0.01). Clustering of average and good health factors also declined with age (ptrend < 0.01). There were no socioeconomic status-related differences in prevalence of good cardiovascular health., Conclusions: Good cardiovascular health factors-physical activity, healthy diet, and desirable body mass index, blood pressure, and glucose levels-are low in urban Asian Indians., (Copyright © 2015 World Heart Federation (Geneva). Published by Elsevier B.V. All rights reserved.)- Published
- 2017
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47. Benefits of Heart Rate Slowing With Ivabradine in Patients With Systolic Heart Failure and Coronary Artery Disease.
- Author
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Borer JS, Deedwania PC, Kim JB, and Böhm M
- Subjects
- Chronic Disease, Coronary Artery Disease physiopathology, Heart Failure, Systolic physiopathology, Heart Rate, Hospitalization, Humans, Ivabradine, Mortality, Quality of Life, Treatment Outcome, Ventricular Function, Left, Benzazepines therapeutic use, Cardiovascular Agents therapeutic use, Coronary Artery Disease drug therapy, Heart Failure, Systolic drug therapy
- Abstract
Heart rate (HR) is a risk factor in patients with chronic systolic heart failure (HF) that, when reduced, provides outcome benefits. It is also a target for angina pectoris prevention and a risk marker in chronic coronary artery disease without HF. HR can be reduced by drugs; however, among those used clinically, only ivabradine reduces HR directly in the sinoatrial nodal cells without other known effects on the cardiovascular system. This review provides current information regarding the safety and efficacy of HR reduction with ivabradine in clinical studies involving >36,000 patients with chronic stable coronary artery disease and >6,500 patients with systolic HF. The largest trials, Morbidity-Mortality Evaluation of the I
f Inhibitor Ivabradine in Patients With Coronary Disease and Left Ventricular Dysfunction and Study Assessing the Morbidity-Mortality Benefits of the If Inhibitor Ivabradine in Patients With Coronary Artery Disease, showed no effect on outcomes. The Systolic Heart Failure Treatment With the If Inhibitor Ivabradine Trial, a randomized controlled trial in >6,500 patients with HF, revealed marked and significant HR-mediated reduction in cardiovascular mortality or HF hospitalizations while improving quality of life and left ventricular mechanical function after treatment with ivabradine. The adverse effects of ivabradine predominantly included bradycardia and atrial fibrillation (both uncommon) and ocular flashing scotomata (phosphenes) but otherwise were similar to placebo. In conclusion, ivabradine improves outcomes in patients with systolic HF; rates of overall adverse events are similar to placebo., (Copyright © 2016 Elsevier Inc. All rights reserved.)- Published
- 2016
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48. Differing predictive relationships between baseline LDL-C, systolic blood pressure, and cardiovascular outcomes.
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Deedwania PC, Pedersen TR, DeMicco DA, Breazna A, Betteridge DJ, Hitman GA, Durrington P, and Neil A
- Subjects
- Aged, Cardiovascular Diseases physiopathology, Cohort Studies, Double-Blind Method, Female, Follow-Up Studies, Humans, Male, Middle Aged, Predictive Value of Tests, Prospective Studies, Risk Factors, Treatment Outcome, Blood Pressure physiology, Cardiovascular Diseases blood, Cardiovascular Diseases diagnosis, Cholesterol, LDL blood
- Abstract
Background: Traditional cardiovascular risk factors, such as hypertension and dyslipidemia, predispose individuals to cardiovascular disease, particularly patients with diabetes. We investigated the predictive value of baseline systolic blood pressure (SBP) and low-density lipoprotein cholesterol (LDL-C) on the risk of vascular outcomes in a large population of patients at high risk of future cardiovascular events., Methods: Data were pooled from the TNT (Treating to New Targets), CARDS (Collaborative Atorvastatin Diabetes Study), and IDEAL (Incremental Decrease in End-Points Through Aggressive Lipid Lowering) trials and included a total of 21,727 patients (TNT: 10,001; CARDS: 2838; IDEAL: 8888). The effect of baseline SBP and LDL-C on cardiovascular events, coronary events, and stroke was evaluated using a multivariate Cox proportional-hazards model., Results: Overall, risk of cardiovascular events was significantly higher for patients with higher baseline SBP or LDL-C. Higher baseline SBP was significantly predictive of stroke but not coronary events. Conversely, higher baseline LDL-C was significantly predictive of coronary events but not stroke. Results from the subgroup with diabetes (5408 patients; TNT: 1501; CARDS: 2838; IDEAL: 1069) were broadly consistent with those of the total cohort: baseline SBP and LDL-C were significantly predictive of cardiovascular events overall, with the association to LDL-C predominantly related to an effect on coronary events. However, baseline SBP was not predictive of either coronary or stroke events in the pooled diabetic population., Conclusions: In this cohort of high-risk patients, baseline SBP and LDL-C were significantly predictive of cardiovascular outcomes, but this effect may differ between the cerebrovascular and coronary systems., Trial Registration Number: NCT00327691 (TNT); NCT00327418 (CARDS); NCT00159835 (IDEAL)., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)
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- 2016
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49. Relation Between Change in Renal Function and Cardiovascular Outcomes in Atorvastatin-Treated Patients (from the Treating to New Targets [TNT] Study).
- Author
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Shepherd J, Breazna A, Deedwania PC, LaRosa JC, Wenger NK, Messig M, and Wilson DJ
- Subjects
- Adult, Aged, Cause of Death trends, Coronary Artery Disease complications, Coronary Artery Disease mortality, Creatinine blood, Dose-Response Relationship, Drug, Double-Blind Method, Female, Follow-Up Studies, Glomerular Filtration Rate drug effects, Humans, Kidney Function Tests, Male, Middle Aged, Prospective Studies, Renal Insufficiency, Chronic etiology, Renal Insufficiency, Chronic physiopathology, Risk Factors, Survival Rate trends, United States epidemiology, Atorvastatin administration & dosage, Coronary Artery Disease drug therapy, Glomerular Filtration Rate physiology, Hydroxymethylglutaryl-CoA Reductase Inhibitors administration & dosage, Renal Insufficiency, Chronic prevention & control
- Abstract
Statins may have nephroprotective as well as cardioprotective effects in patients with cardiovascular disease. In the Treating to New Targets (TNT) study (NCT00327691), patients with coronary heart disease (CHD) were randomized to atorvastatin 10 or 80 mg/day and followed for 4.9 years. The relation between intrastudy change in estimated glomerular filtration rate (eGFR) from baseline and the risk of major cardiovascular events (MCVEs, defined as CHD death, nonfatal non-procedure-related myocardial infarction, resuscitated cardiac arrest, or fatal or nonfatal stroke) was assessed among 9,500 patients stratified by renal function: improving (change in eGFR more than +2 ml/min/1.73 m(2)), stable (-2 to +2 ml/min/1.73 m(2)), and worsening (less than -2 ml/min/1.73 m(2)). Compared with patients with worsening renal function (1,479 patients, 15.6%), the rate of MCVEs was 28% lower in patients with stable renal function (2,241 patients, 23.6%) (hazard ratio [HR] 0.72; 95% confidence interval [CI] 0.60 to 0.87; p = 0.0005) and 64% lower in patients with improving renal function (5,780 patients, 60.8%; HR 0.36; 95% CI 0.30 to 0.43; p <0.0001). For each 1 ml/min/1.73 m(2) increase in eGFR, the absolute reduction in the rate of MCVEs was 2.7% (HR 0.973; 95% CI 0.967 to 0.980; p <0.0001). An absolute MCVE rate reduction per 1 ml/min/1.73 m(2) increase in eGFR of 2.0% was reported with atorvastatin 10 mg and 3.3% with atorvastatin 80 mg. In conclusion, intrastudy stabilization or increase in eGFR in atorvastatin-treated patients with CHD from the TNT study was associated with a reduced rate of MCVEs. Statin-treated CHD patients with progressive renal impairment are at high risk for future cardiovascular events., (Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.)
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- 2016
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50. Effect of high-dose atorvastatin on the cardiovascular risk associated with individual components of metabolic syndrome: a subanalysis of the Treating to New Targets (TNT) study.
- Author
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Deedwania PC, Shepherd J, Breazna A, and DeMicco DA
- Subjects
- Adult, Aged, Anticholesteremic Agents administration & dosage, Atorvastatin administration & dosage, Blood Glucose analysis, Body Mass Index, Cardiovascular Diseases etiology, Cholesterol, HDL blood, Cholesterol, LDL blood, Dose-Response Relationship, Drug, Double-Blind Method, Fasting blood, Female, Humans, Hypertension complications, Male, Metabolic Syndrome blood, Metabolic Syndrome complications, Middle Aged, Predictive Value of Tests, Risk Factors, Triglycerides blood, Anticholesteremic Agents pharmacology, Atorvastatin pharmacology, Cardiovascular Diseases prevention & control, Cholesterol, LDL drug effects, Metabolic Syndrome drug therapy
- Abstract
Aims: To investigate the impact of intensive lipid-lowering with high-dose atorvastatin on the cardiovascular risk associated with individual metabolic syndrome components [high body mass index (BMI), elevated triglycerides, low high-density lipoprotein (HDL) cholesterol, hypertension and elevated fasting glucose] in patients with coronary heart disease (CHD)., Methods: Patients with clinically evident, stable CHD and low-density lipoprotein (LDL) cholesterol <3.4 mmol/l (130 mg/dl) were randomized to double-blind therapy with atorvastatin 10 mg/day (n = 5006) or 80 mg/day (n = 4995) after an 8-week open-label run-in with atorvastatin 10 mg. The median follow-up was 4.9 years. The impact of individual metabolic syndrome risk factors was tested on the primary endpoint, which was the occurrence of a first major cardiovascular event., Results: On-treatment LDL cholesterol was 2.6 mmol/l (101 mg/dl) with atorvastatin 10 mg and 2.0 mmol/l (77 mg/dl) with atorvastatin 80 mg. Among patients receiving atorvastatin 10 mg, the presence of each individual metabolic syndrome component significantly increased the risk of major cardiovascular events compared with the absence of each (BMI, p = 0.014; triglycerides, p = 0.006; HDL cholesterol, p = 0.0006; hypertension, p < 0.0001; and fasting glucose p < 0.0001). In patients receiving atorvastatin 80 mg, elevated triglycerides and fasting glucose were no longer significant predictors of major cardiovascular events. The predictive power of hypertension on the risk of major cardiovascular events was reduced in patients treated with atorvastatin 80 mg, although it remained a significant predictor., Conclusions: Treatment with high-dose atorvastatin to a mean LDL cholesterol level of 2.0 mmol/l (77 mg/dl) considerably attenuated the predictive power associated with three metabolic syndrome components., (© 2015 John Wiley & Sons Ltd.)
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- 2016
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