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1. Recommendations for lipid modification in patients with ischemic stroke or transient ischemic attack: A clinical guide by the Hellenic Stroke Organization and the Hellenic Atherosclerosis Society

Author

Sagris, D. Ntaios, G. Georgiopoulos, G. Kakaletsis, N. Elisaf, M. Katsiki, N. Korompoki, E. Kypreos, K.E. Boutari, C. Bilianou, H. Makaritsis, K. Nomikos, T. Papavasileiou, V. Pitsavos, C. Plomaritoglou, A. Spengos, K. Tziomalos, K. Tselepis, A. Vemmos, K. Liberopoulos, E. Milionis, H.

Subjects
cardiovascular diseases
Abstract

This document presents the consensus recommendations of the Hellenic Stroke Organization and the Hellenic Atherosclerosis Society for lipid modification in patients with ischemic stroke or transient ischemic attack. This clinical guide summarizes the current literature on lipid management and can be of assistance to the physicians treating stroke patients in clinical practice. © 2020 World Stroke Organization.

Published
2021

4. Postprandial hypertriglyceridaemia revisited in the era of non-fasting lipid profile testing: A 2019 expert panel statement, narrative review

Author

Kolovou, G.D. Watts, G.F. Mikhailidis, D.P. Pérez-Martínez, P. Mora, S. Bilianou, H. Panotopoulos, G. Katsiki, N. Ooi, T.C. Lopez-Miranda, J. Tybjærg-Hansen, A. Tentolouris, N. Nordestgaard, B.G.

Subjects
nutritional and metabolic diseases
Abstract

Postprandial hypertriglyceridaemia, defined as an increase in plasma triglyceride-containing lipoproteins following a fat meal, is a potential risk predictor of atherosclerotic cardiovascular disease and other chronic diseases. Several non-modifiable factors (genetics, age, sex and menopausal status) and lifestyle factors (diet, physical activity, smoking status, obesity, alcohol and medication use) may influence postprandial hypertriglyceridaemia. This narrative review considers the studies published over the last decade that evaluated postprandial hypertriglyceridaemia. Additionally, the genetic determinants of postprandial plasma triglyceride levels, the types of meals for studying postprandial triglyceride response, and underlying conditions (e.g. familial dyslipidaemias, diabetes mellitus, metabolic syndrome, non-alcoholic fatty liver and chronic kidney disease) that are associated with postprandial hypertriglyceridaemia are reviewed; therapeutic aspects are also considered. © 2019 Bentham Science Publishers.

Published
2019

5. Postprandial hypertriglyceridaemia revisited in the era of non-fasting lipid profile testing: A 2019 expert panel statement, main text

Author

Kolovou, G.D. Watts, G.F. Mikhailidis, D.P. Pérez-Martínez, P. Mora, S. Bilianou, H. Panotopoulos, G. Katsiki, N. Ooi, T.C. Lopez-Miranda, J. Tybjærg-Hansen, A. Tentolouris, N. Nordestgaard, B.G.

Abstract

Residual vascular risk exists despite the aggressive lowering of Low-Density Lipoprotein Cholesterol (LDL-C). A contributor to this residual risk may be elevated fasting, or non-fasting, levels of Triglyceride (TG)-rich lipoproteins. Therefore, there is a need to establish whethe a standardised Oral Fat Tolerance Test (OFTT) can improve atherosclerotic Cardiovascular (CV) Disease (ASCVD) risk prediction in addition to a fasting or non-fasting lipid profile. An expert panel considered the role of postprandial hypertriglyceridaemia (as represented by an OFTT) in predicting ASCVD. The panel updated its 2011 statement by considering new studies and various patient categories. The recommendations are based on expert opinion since no strict endpoint trials have been performed. Individuals with fasting TG concentration 2.5 mmol/L (220 mg/dL). Postprandial hypertriglyceridaemia is an emerging factor that may contribute to residual CV risk. This possibility requires further research. A standardised OFTT will allow comparisons between investiga-tional studies. We acknowledge that the OFTT will be mainly used for research to further clarify the role of TG in relation to CV risk. For routine practice, there is a considerable support for the use of a single non-fasting sample. © 2019 Bentham Science Publishers.

Published
2019

6. Hellenic Postprandial Lipemia Study (HPLS): Rationale and design of a prospective, open-label trial to determinate the prevalence of abnormal postprandial lipemia as well as its interaction with statins in patients at high- and very high-risk for cardiovascular disease

Author

Kolovou, G. Giannakopoulou, V. Kalogeropoulos, P. Anagnostopoulou, K. Goumas, G. Kazianis, G. Limberi, S. Perrea, D. Mihas, C. Kolovou, V. Bilianou, H.

Subjects
digestive, oral, and skin physiology, lipids (amino acids, peptides, and proteins)
Abstract

Fasting and postprandial hypertriglyceridemia have been related to cardiovascular (CV) disease. We describe the design and methods of the Hellenic Postprandial Lipemia Study (HPLS, NCT02163044), a prospective, open-label, randomized, multicentre trial. The study will recruit 900 participants from 8 centers, and aims to determinate the prevalence of abnormal postprandial lipemia in patients at high - and very high-risk for CV disease, the efficacy of statin treatment and other medications on postprandial lipemia, and the interaction between postprandial lipemia and CV risk during a treatment period of 3 years. Participants will be screened in an outpatient lipid clinic setting. Methods: High- and very high-risk individuals with fasting triglycerides (TGs)

Published
2019

7. Evolocumab and clinical outcomes in patients with cardiovascular disease

Author

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, 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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

Subjects
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

Published
2017

8. The use of statins alone, or in combination with pioglitazone and other drugs, for the treatment of non-alcoholic fatty liver disease/non-alcoholic steatohepatitis and related cardiovascular risk. An Expert Panel Statement

Author

Athyros, V.G. Alexandrides, T.K. Bilianou, H. Cholongitas, E. Doumas, M. Ganotakis, E.S. Goudevenos, J. Elisaf, M.S. Germanidis, G. Giouleme, O. Karagiannis, A. Karvounis, C. Katsiki, N. Kotsis, V. Kountouras, J. Liberopoulos, E. Pitsavos, C. Polyzos, S. Rallidis, L.S. Richter, D. Tsapas, A.G. Tselepis, A.D. Tsioufis, K. Tziomalos, K. Tzotzas, T. Vasiliadis, T.G. Vlachopoulos, C. Mikhailidis, D.P. Mantzoros, C.

Subjects
nutritional and metabolic diseases, digestive system, digestive system diseases
Abstract

Non-alcoholic fatty liver disease (NAFLD), the most common liver disease, is characterized by accumulation of fat (> 5% of the liver tissue), in the absence of alcohol abuse or other chronic liver diseases. It is closely related to the epidemic of obesity, metabolic syndrome or type 2 diabetes mellitus (T2DM). NAFLD can cause liver inflammation and progress to non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis or hepatocellular cancer (HCC). Nevertheless, cardiovascular disease (CVD) is the most common cause of death in NAFLD/NASH patients. Current guidelines suggest the use of pioglitazone both in patients with T2DM and in those without. The use of statins, though considered safe by the guidelines, have very limited use; only 10% in high CVD risk patients are on statins by tertiary centers in the US. There are data from several animal studies, 5 post hoc analyses of prospective long-term survival studies, and 5 rather small biopsy proven NASH studies, one at baseline and on at the end of the study. All these studies provide data for biochemical and histological improvement of NAFLD/NASH with statins and in the clinical studies large reductions in CVD events in comparison with those also on statins and normal liver. Ezetimibe was also reported to improve NAFLD. Drugs currently in clinical trials seem to have potential for slowing down the evolution of NAFLD and for reducing liver- and CVD-related morbidity and mortality, but it will take time before they are ready to be used in everyday clinical practice. The suggestion of this Expert Panel is that, pending forthcoming randomized clinical trials, physicians should consider using a PPARgamma agonist, such as pioglitazone, or, statin use in those with NAFLD/NASH at high CVD or HCC risk, alone and/or preferably in combination with each other or with ezetimibe, for the primary or secondary prevention of CVD, and the avoidance of cirrhosis, liver transplantation or HCC, bearing in mind that CVD is the main cause of death in NAFLD/NASH patients. © 2017 Elsevier Inc.

Published
2017

9. Gender differences in the lipid profile of dyslipidemic subjects

Author

Kolovou, G. D., Anagnostopoulou, K. K., Damaskos, D. S., Bilianou, H. I., Mihas, C., Milionis, H. J., Kostakou, P. M., and Cokkinos, D. V.

Subjects
Male, Sex Characteristics, Dyslipidemias/*blood/*epidemiology, Atherosclerosis/blood/epidemiology, Cholesterol, HDL/*blood, Middle Aged, Cholesterol, LDL/blood, Risk Factors, Multivariate Analysis, Linear Models, Humans, Female, Triglycerides/*blood, Sex Distribution, Aged
Abstract

OBJECTIVE: We evaluated the gender-associated differences in lipid profile of subjects intended to receive lipid-lowering therapy with emphasis on the associations between triglycerides (TG) and other plasma lipid variables. DESIGN: Lipid profiles of 1385 patients [aged 55+/-11 years, 549 women (40%)] were evaluated. Eligible subjects fulfilled one or more of the following criteria: total cholesterol (TC)>or=6.2 mmol/l, TG>or=1.7 mmol/l, and high-density lipoprotein cholesterol (HDL-C)or=1.7 mmol/l, women had higher TC and HDL-C levels and lower TC/HDL ratio compared with men. In the subgroup with HDL-C>or=1.0 mmol/l women had higher HDL-C, lower TG levels and lower TC/HDL-C ratio compared with men. CONCLUSIONS: Elevated TG levels and low HDL-C in tandem are common lipid abnormalities in the clinical setting of primary and secondary preventions. Gender-associated differences in the lipid profile are evident in subjects presenting with dyslipidemia and might be of potential relevance for diagnostics and therapy for the prevention of atherosclerosis. Eur J Intern Med

Published
2009

19. The Challenges in Moving from Ageing to Successful Longevity

Author

Helen Bilianou, Claudio Franceschi, Peter Avery, George Panotopoulos, Dimitri P. Mikhailidis, Athanase Benetos, Calogero Caruso, Miriam Capri, Niki Katsiki, Genovefa Kolovou, Ewa Sikora, Nir Barzilai, Irene P. Tzanetakou, Kolovou, Genovefa, Barzilai, Nir, Caruso, Calogero, Sikora, Ewa, Capri, Miriam, Tzanetakou, Irene P, Bilianou, Helen, Avery, Peter, Katsiki, Niki, Panotopoulos, George, Franceschi, Claudio, Benetos, Athanase, Mikhailidis, Dimitri P, Kolovou,G, Barzilai, N, Caruso, C, Sikora, E, Capri, M, Tzanetakou, IP, Bilianou, H, Avery, P, Katsiki, N, Panotopoulos, G, Franceschi, C, Benetos, A, and Mikhailidis, DP

Subjects
ageing, longevity, age-related diseases, Gerontology, Aging, Younger age, Hormone Replacement Therapy, media_common.quotation_subject, Longevity, Population, Health care, Animals, Humans, Medicine, education, Life Style, media_common, Settore MED/04 - Patologia Generale, Aged, 80 and over, Pharmacology, education.field_of_study, Animal, business.industry, Cognition, Diet, Nutrigenomics, Ageing, Life expectancy, Cardiology and Cardiovascular Medicine, business, Human
Abstract

During the last decades survival has significantly improved and centenarians are becoming a fast-growing group of the population. Human life span is mainly dependent on environmental and genetic factors. Favourable modifications of lifestyle factors (e.g. physical activity, diet and not smoking) and healthcare (e.g. effective vascular disease prevention) have also increased human life span. Genetic factors contribute to the variation of human life span by around 25%, which is believed to be more profound after 85 years of age. It is likely that multiple factors influence life span and we need answers to questions such as: 1) What does it take to reach 100?, 2) Do centenarians have better health during their lifespan compared with contemporaries who died at a younger age?, 3) Do centenarians have protective modifications of body composition, fat distribution and energy expenditure, maintain high physical and cognitive function, and sustained engagement in social and productive activities?, 4) Do centenarians have genes which contribute to longevity?, 5) Do centenarians benefit from epigenetic phenomena?, 6). Is it possible to influence the transgenerational epigenetic inheritance (epigenetic memory) which leads to longevity?, 7) Is the influence of nutrigenomics important for longevity?, 8) Do centenarians benefit more from drug treatment, particularly in primary prevention?, and, 9) Are there any potential goals for drug research? Many definitions of successful ageing have been proposed, but at present there is no consensus definition. Such definitions may need to differentiate between "Longevity Syndrome" and "Exceptional Longevity"

Published
2013
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20. Ageing, longevity, exceptional longevity and related genetic and non genetics markers: panel statement

Author

Peter Avery, Claudio Franceschi, Calogero Caruso, Dimitri P. Mikhailidis, Genovefa Kolovou, Niki Katsiki, George Panotopoulos, Helen Bilianou, Ewa Sikora, Irene P. Tzanetakou, Nir Barzilai, Miriam Capri, Athanase Benetos, Avery, Peter, Barzilai, Nir, Benetos, Athanase, Bilianou, Helen, Capri, Miriam, Caruso, Calogero, Franceschi, Claudio, Katsiki, Niki, Mikhailidis, Dimitri P, Panotopoulos, George, Sikora, Ewa, Tzanetakou, Irene P, Kolovou, Genovefa, Défaillance Cardiovasculaire Aiguë et Chronique (DCAC), Université de Lorraine (UL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy), CIG - Interdepartmental Center 'L.Galvani', Department of Pathobiology and Medical and Forensic Biotechnologies, Università degli studi di Palermo - University of Palermo, Department of Experimental, Diagnostic and Specialty Medicine, University of Bologna, Nencki Institute of Experimental Biology, Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lorraine (UL), Avery, P, Barzilai, N, Benetos, A, Bilianou, H, Capri, M, Caruso, C, Franceschi, C, Katsiki, N, Mikhailidis, DP, Panotopoulos, G, Sikora, E, Tzanetakou, IP, and Kolovou, G

Subjects
Genetic Markers, Gerontology, Aging, Statement (logic), media_common.quotation_subject, Longevity, MESH: Genetic Markers, Biology, MESH: Phenotype, [SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, Genetic Marker, Animals, Humans, MESH: Aging, MESH: Animals, ComputingMilieux_MISCELLANEOUS, media_common, Pharmacology, MESH: Humans, Animal, Congresses as Topic, Phenotype, Ageing, Longevity, Age-related diseases, MESH: Longevity, Ageing, Biological Marker, MESH: Biomarkers, Cardiology and Cardiovascular Medicine, MESH: Congresses as Topic, Biomarkers, Human
Abstract

In May 2012, a group of scientists and clinicians met in Athens (Greece) to consider the relevance of ageing, longevity, exceptional longevity and related genetic and non genetic markers. During this meeting, we firstly reviewed recent epidemiological and clinical studies on ageing, longevity and exceptional longevity, briefly analysed the ageing theories and discussed successful and unsuccessful ageing also taking into account the evolutionary perspective. Secondly, we considered the three phenotypes based on the definition of ageing, longevity and exceptional longevity and the associated biomarkers. Third, we discussed proposed treatments suitable to counteract or slow down ageing. Finally, this panel produced a consensus statement to highlight the importance of ageing, longevity and exceptional longevity, since this is a rapidly increasing phenotype worldwide. We acknowledge that not all experts in this field may completely agree with this statement.

Published
2014
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22. Prevalence and Risk Factors for Atherosclerotic Cardiovascular Disease in 7704 Individuals: An Analysis from the Greek Registry for the Prevalence of Familial Hypercholesterolemia (GRegistry-FH).

Author

Kolovou G, Makrygiannis S, Marvaki C, Pavlatou N, Anagnostopoulou K, Giannakopoulou V, Goumas G, Kalogeropoulos P, Kolovou V, Limberi S, Perrea D, Tzenalis A, Emre Z, Jahaj E, Kasiara Z, Giannakoulis I, Tsolakoglou I, Kadda O, Tsaloukidis N, Koulaxidou R, Marvaki A, Foussas S, Melidonis A, Hoursalas G, Vlachopoulos C, Katsiki N, Milionis H, Liberopoulos E, and Bilianou H

Abstract

The intention of this study was to profile the cohort from the Greek Registry for the prevalence of Familial Hypercholesterolemia (GRegistry-FH) by estimating the prevalence of coronary artery disease (CAD), myocardial infarction (MI), stroke, dyslipidemia, arterial hypertension, diabetes mellitus (DM), pre-DM, smoking, abnormal thyroid function (ATF), and lipid values. The GRegistry-FH is a prospective study involving door-to-door interviews conducted by trained interviewers. Overall, 7704 individuals aged ≥18 years, randomly selected from all the regions of Greece, participated. The prevalence of atherosclerotic cardiovascular disease (ASCVD) was 13.9% (CAD 6%, MI 3.2%, stroke 4.7%). Treated hypercholesterolemia was present in 20.1%, arterial hypertension in 24%, and DM in 11.3% individuals (25.5% had pre-DM). The prevalence of smoking was 37.9% (29% current) and the prevalence of ATF was 13.1% (hypothyroidism 11.3%). A family history of ASCVD was reported by 60.5% (CAD 32.2%, stroke 28.3%). The mean (SD) lipid values in mg/dL were as follows: total cholesterol of 201.8 (41.5), low-density lipoprotein cholesterol of 126.3 (30.1), high-density lipoprotein cholesterol of 51.9 (12.5), and triglycerides of 135.9 (64.7). The GRegistry-FH highlights the significant prevalence of ASCVD and its risk factors among Greek adults, indicating a pressing need for early detection and management strategies to mitigate ASCVD burden. This nationwide registry serves as a crucial tool for guiding public health policies and personalized preventive measures (NCT03140605).

Published
2024
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23. Lipoprotein apheresis: a Hellenic consensus on its clinical use.

Author

Kolovou G, Kolovou V, Bilianou H, Goumas G, Foussas S, Grapsa E, Garoufi A, Karavolias G, Mavrogieni S, Melidonis A, Milionis H, Rallidis L, Richter D, Skoumas I, Tousoulis D, Vlachopoulos C, and Liberopoulos E

Subjects
Biomarkers, Consensus, Humans, Lipoproteins, Treatment Outcome, Blood Component Removal
Abstract

Competing Interests: Declaration of interest GK: participated in research and consulting activities sponsored by healthcare companies, including Amgen, MSD, Sanofi, and Servier; GG: VK: has participated in research studies sponsored by Amgen, Sanofi, and Regeneron; AM: participated in educational, research, and consulting activities sponsored by healthcare companies, including Lybitec, Lilly, Boehringer, Demo, Novo, Glaxo, Astra, and Amgen; HM: participated in educational, research and consulting activities sponsored by healthcare companies, including Amgen, Bayer, Mylan, MSD, Pfizer, Sanofi, and Servier; LR has received research grants, honoraria, and travel grants from Amgen, MSD, ELPEN, Sanofi, Mylan and Servier; DR: has participated in educational, research, and advisory activities sponsored by AstraZeneca, MSD, Lilly, Bayer, Amgen, Sanofi, Boehringer-Ingelheim, Elpen, Mylan, Unipharma, Lavipharm, and Servier; IS: has received research grants and honoraria from Amgen, Sanofi, MSD, and Elpen. LR has received honoraria for lectures, clinical trials, and consultant fees from Amgen, MSD, MYLAN, Servier, AstraZeneca, and Sanofi-Aventis; DT: participated in research and consulting activities sponsored by healthcare companies, including Amgen, MSD, Sanofi, Servier, Pfizer, and Boehringer-Ingelheim; CV has received research grant(s)/support and honoraria from Amgen, MSD, ELPEN, Sanofi, VIANEX; EL: has participated in educational, research, and advisory activities sponsored by AstraZeneca, MSD, Lilly, Bayer, Amgen, Sanofi, Boehringer-Ingelheim, Novartis, Novo Nordisk, and Servier; HB, SF, AG, EG, GK, SM: No conflict of interest to declare.

Published
2021
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24. Recommendations for lipid modification in patients with ischemic stroke or transient ischemic attack: A clinical guide by the Hellenic Stroke Organization and the Hellenic Atherosclerosis Society.

Author

Sagris D, Ntaios G, Georgiopoulos G, Kakaletsis N, Elisaf M, Katsiki N, Korompoki E, Kypreos KE, Boutari C, Bilianou H, Makaritsis K, Nomikos T, Papavasileiou V, Pitsavos C, Plomaritoglou A, Spengos K, Tziomalos K, Tselepis A, Vemmos K, Liberopoulos E, and Milionis H

Subjects
Humans, Atherosclerosis complications, Brain Ischemia complications, Brain Ischemia therapy, Ischemic Attack, Transient complications, Ischemic Attack, Transient therapy, Ischemic Stroke, Stroke therapy
Abstract

This document presents the consensus recommendations of the Hellenic Stroke Organization and the Hellenic Atherosclerosis Society for lipid modification in patients with ischemic stroke or transient ischemic attack. This clinical guide summarizes the current literature on lipid management and can be of assistance to the physicians treating stroke patients in clinical practice.

Published
2021
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26. Rationale and design of the Greek registry for familial hypercholesterolemia (GRegistry-FH) of the hellenic college of treatment of atherosclerosis (HCTA).

Author

Kolovou G, Marvaki C, Makrygiannis S, Kadda O, Giannakopoulou V, Kalogeropoulos P, Anagnostopoulou K, Goumas G, Kazianis G, Limberi S, Perrea D, Kolovou V, and Bilianou H

Subjects
Cholesterol, LDL, Greece epidemiology, Humans, Registries, Atherosclerosis epidemiology, Hyperlipoproteinemia Type II epidemiology, Hyperlipoproteinemia Type II therapy
Published
2020
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27. Non-traumatic and non-drug-induced rhabdomyolysis.

Author

Kolovou G, Cokkinos P, Bilianou H, Kolovou V, Katsiki N, and Mavrogeni S

Abstract

Rhabdomyolysis (RM), a fortunately rare disease of the striated muscle cells, is a complication of non-traumatic (congenital (glycogen storage disease, discrete mitochondrial myopathies and various muscular dystrophies) or acquired (alcoholic myopathy, systemic diseases, arterial occlusion, viral illness or bacterial sepsis)) and traumatic conditions. Additionally, RM can occur in some individuals under specific circumstances such as toxic substance use and illicit drug abuse. Lipid-lowering drugs in particular are capable of causing RM. This comprehensive review will focus on non-traumatic and non-drug-induced RM. Moreover, the pathology of RM, its clinical manifestation and biochemical effects, and finally its management will be discussed., Competing Interests: The authors declare no conflict of interest., (Copyright © 2019 Termedia & Banach.)

Published
2019
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28. Long-Term Administration of Proprotein Convertase Subtilisin/Kexin Type 9 Inhibitors Reduces Arterial FDG Uptake.

Author

Vlachopoulos C, Koutagiar I, Skoumas I, Terentes-Printzios D, Zacharis E, Kolovou G, Stamatelopoulos K, Rallidis L, Katsiki N, Bilianou H, Liberopoulos E, Miliou A, Kafouris P, Georgakopoulos A, Gardikioti V, Tousoulis D, and Anagnostopoulos CD

Subjects
Aged, Aorta diagnostic imaging, Aorta metabolism, Aortic Diseases blood, Aortic Diseases diagnostic imaging, Biomarkers blood, Carotid Arteries diagnostic imaging, Carotid Arteries metabolism, Carotid Artery Diseases blood, Carotid Artery Diseases diagnostic imaging, Cholesterol, LDL blood, Drug Administration Schedule, Dyslipidemias blood, Dyslipidemias diagnosis, Female, Fluorodeoxyglucose F18 administration & dosage, Greece, Humans, Inflammation Mediators blood, Male, Middle Aged, Positron Emission Tomography Computed Tomography, Predictive Value of Tests, Prospective Studies, Radiopharmaceuticals administration & dosage, Time Factors, Treatment Outcome, Antibodies, Monoclonal, Humanized administration & dosage, Anticholesteremic Agents administration & dosage, Aorta drug effects, Aortic Diseases drug therapy, Carotid Arteries drug effects, Carotid Artery Diseases drug therapy, Dyslipidemias diagnostic imaging, PCSK9 Inhibitors
Published
2019
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29. Hellenic Postprandial Lipemia Study (HPLS): Rationale and design of a prospective, open-label trial to determinate the prevalence of abnormal postprandial lipemia as well as its interaction with statins in patients at high- and very high-risk for cardiovascular disease.

Author

Kolovou G, Giannakopoulou V, Kalogeropoulos P, Anagnostopoulou K, Goumas G, Kazianis G, Limberi S, Perrea D, Mihas C, Kolovou V, and Bilianou H

Subjects
Female, Genetic Testing, Greece epidemiology, Humans, Hypertriglyceridemia epidemiology, Hypertriglyceridemia genetics, Male, Multicenter Studies as Topic, Postprandial Period drug effects, Postprandial Period physiology, Prevalence, Prospective Studies, Randomized Controlled Trials as Topic, Risk Factors, Triglycerides blood, Cardiovascular Diseases prevention & control, Hydroxymethylglutaryl-CoA Reductase Inhibitors therapeutic use, Hypertriglyceridemia prevention & control
Abstract

Fasting and postprandial hypertriglyceridemia have been related to cardiovascular (CV) disease. We describe the design and methods of the Hellenic Postprandial Lipemia Study (HPLS, NCT02163044), a prospective, open-label, randomized, multicentre trial. The study will recruit 900 participants from 8 centers, and aims to determinate the prevalence of abnormal postprandial lipemia in patients at high- and very high-risk for CV disease, the efficacy of statin treatment and other medications on postprandial lipemia, and the interaction between postprandial lipemia and CV risk during a treatment period of 3 years. Participants will be screened in an outpatient lipid clinic setting. METHODS: High- and very high-risk individuals with fasting triglycerides (TGs) <220 mg/dL (2.5 mmol/L) will be included. At baseline visit demographic and clinical characteristics will be recorded. At the first follow-up visit (within 2-4 weeks from baseline), plasma TG concentrations will be measured, following an overnight 12 h fasting period, before and 4 h after ingestion of a commercially available oral fat tolerance test (OFTT) meal. Then a statin will be prescribed. At the second follow-up visit (within 3-5 month from baseline), plasma TG concentrations will be measured again following an overnight 12 h fasting period, before and 4 h after ingestion of OFTT and then patients will be followed annually for 3 years. CONCLUSION: HPLS is the largest trial assessing the effects of statin therapy on postprandial lipemia. Its results will provide useful insight on the prevalence of postprandial lipemia, the efficacy of statins regarding postprandial lipemia and the clinical significance of this effect. Clinical trial registration information The HPLS trial is registered with clinicaltrials.gov (NCT Identifier: NCT02163044)., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Published
2019
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30. Postprandial Hypertriglyceridaemia Revisited in the Era of Non-Fasting Lipid Profile Testing: A 2019 Expert Panel Statement, Narrative Review.

Author

Kolovou GD, Watts GF, Mikhailidis DP, Pérez-Martínez P, Mora S, Bilianou H, Panotopoulos G, Katsiki N, Ooi TC, Lopez-Miranda J, Tybjærg-Hansen A, Tentolouris N, and Nordestgaard BG

Subjects
Biomarkers blood, Cardiovascular Diseases blood, Cardiovascular Diseases diagnosis, Cardiovascular Diseases genetics, Consensus, Genetic Predisposition to Disease, Humans, Hypertriglyceridemia blood, Hypertriglyceridemia epidemiology, Hypertriglyceridemia genetics, Predictive Value of Tests, Prognosis, Reproducibility of Results, Risk Assessment, Risk Factors, Up-Regulation, Blood Chemical Analysis standards, Cardiovascular Diseases epidemiology, Hypertriglyceridemia diagnosis, Postprandial Period, Triglycerides blood
Abstract

Postprandial hypertriglyceridaemia, defined as an increase in plasma triglyceride-containing lipoproteins following a fat meal, is a potential risk predictor of atherosclerotic cardiovascular disease and other chronic diseases. Several non-modifiable factors (genetics, age, sex and menopausal status) and lifestyle factors (diet, physical activity, smoking status, obesity, alcohol and medication use) may influence postprandial hypertriglyceridaemia. This narrative review considers the studies published over the last decade that evaluated postprandial hypertriglyceridaemia. Additionally, the genetic determinants of postprandial plasma triglyceride levels, the types of meals for studying postprandial triglyceride response, and underlying conditions (e.g. familial dyslipidaemias, diabetes mellitus, metabolic syndrome, non-alcoholic fatty liver and chronic kidney disease) that are associated with postprandial hypertriglyceridaemia are reviewed; therapeutic aspects are also considered., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Published
2019
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31. Postprandial Hypertriglyceridaemia Revisited in the Era of Non-Fasting Lipid Profile Testing: A 2019 Expert Panel Statement, Main Text.

Author

Kolovou GD, Watts GF, Mikhailidis DP, Pérez-Martínez P, Mora S, Bilianou H, Panotopoulos G, Katsiki N, Ooi TC, Lopez-Miranda J, Tybjærg-Hansen A, Tentolouris N, and Nordestgaard BG

Subjects
Biomarkers blood, Cardiovascular Diseases blood, Cardiovascular Diseases diagnosis, Consensus, Humans, Hypertriglyceridemia blood, Hypertriglyceridemia epidemiology, Predictive Value of Tests, Prognosis, Reproducibility of Results, Risk Assessment, Risk Factors, Up-Regulation, Blood Chemical Analysis standards, Cardiovascular Diseases epidemiology, Hypertriglyceridemia diagnosis, Postprandial Period, Triglycerides blood
Abstract

Residual vascular risk exists despite the aggressive lowering of Low-Density Lipoprotein Cholesterol (LDL-C). A contributor to this residual risk may be elevated fasting, or non-fasting, levels of Triglyceride (TG)-rich lipoproteins. Therefore, there is a need to establish whethe a standardised Oral Fat Tolerance Test (OFTT) can improve atherosclerotic Cardiovascular (CV) Disease (ASCVD) risk prediction in addition to a fasting or non-fasting lipid profile. An expert panel considered the role of postprandial hypertriglyceridaemia (as represented by an OFTT) in predicting ASCVD. The panel updated its 2011 statement by considering new studies and various patient categories. The recommendations are based on expert opinion since no strict endpoint trials have been performed. Individuals with fasting TG concentration <1 mmol/L (89 mg/dL) commonly do not have an abnormal response to an OFTT. In contrast, those with fasting TG concentration ≥2 mmol/L (175 mg/dL) or nonfasting ≥2.3 mmol/L (200 mg/dL) will usually have an abnormal response. We recommend considering postprandial hypertriglyceridaemia testing when fasting TG concentrations and non-fasting TG concentrations are 1-2 mmol/L (89-175 mg/dL) and 1.3-2.3 mmol/L (115-200 mg/dL), respectively as an additional investigation for metabolic risk prediction along with other risk factors (obesity, current tobacco abuse, metabolic syndrome, hypertension, and diabetes mellitus). The panel proposes that an abnormal TG response to an OFTT (consisting of 75 g fat, 25 g carbohydrate and 10 g proteins) is >2.5 mmol/L (220 mg/dL). Postprandial hypertriglyceridaemia is an emerging factor that may contribute to residual CV risk. This possibility requires further research. A standardised OFTT will allow comparisons between investigational studies. We acknowledge that the OFTT will be mainly used for research to further clarify the role of TG in relation to CV risk. For routine practice, there is a considerable support for the use of a single non-fasting sample., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Published
2019
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32. Postprandial Hypertriglyceridaemia Revisited in the Era of Non-fasting Lipid Profiles: Executive Summary of a 2019 Expert Panel Statement.

Author

Kolovou GD, Watts GF, Mikhailidis DP, Pérez-Martínez P, Mora S, Bilianou H, Panotopoulos G, Katsiki N, Ooi TC, Lopez-Miranda J, Tybjærg-Hansen A, Tentolouris N, and Nordestgaard BG

Subjects
Biomarkers blood, Cardiovascular Diseases blood, Cardiovascular Diseases diagnosis, Consensus, Humans, Hypertriglyceridemia blood, Hypertriglyceridemia epidemiology, Predictive Value of Tests, Prognosis, Reproducibility of Results, Risk Assessment, Risk Factors, Up-Regulation, Blood Chemical Analysis standards, Cardiovascular Diseases epidemiology, Hypertriglyceridemia diagnosis, Postprandial Period, Triglycerides blood
Published
2019
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33. Five gene variants in nonagenarians, centenarians and average individuals.

Author

Kolovou V, Bilianou H, Giannakopoulou V, Kalogeropoulos P, Mihas C, Kouris M, Cokkinos DV, Boutsikou M, Hoursalas I, Mavrogeni S, Katsiki N, and Kolovou G

Abstract

Introduction: Genetic factors contribute to the variation of human life span which is believed to be more profound after 85 years of age. The aim of the present study was to evaluate the frequency of 5 gene polymorphisms between nonagenarians, centenarians and average individuals., Material and Methods: Single nucleotide polymorphisms (SNPs) of telomerase reverse transcriptase ( TERT ; rs2736098), insulin-like growth factor-1 binding protein-3 ( IGFBP3 ; A-202C, rs2857744), fork-head box O3A ( FOXO3A ; rs13217795 and rs2764264) factor and adiponectin ( ADIPOQ ; rs2241766) were evaluated in 405 individuals: n = 256 nonagenarians and centenarians (study group) and n = 149 average lifespan individuals (control group aged 18 - < 80 years)., Results: The frequency of women was significantly higher in the study group than the control group (64.5 vs. 49.7%, p = 0.004). Genotypic and allele frequencies did not differ between groups according to gender. However, in men, the frequency of TT genotype of FOXO3A ; rs2764264 was higher in the study group than the control group (45.6 vs. 28.0%, p = 0.05). Overall, the frequency of the C allele of FOXO3A ; rs2764264 was significantly lower in the study group than the control group (3.9 vs. 9.5%, respectively, p = 0.023). Furthermore, in the study group, the T allele was significantly more frequent in the nonagenarians ( n = 239) than the centenarians ( n = 17) in both FOXO3A ; rs13217795 and rs2764264 (64.4 vs. 44.1%, p = 0.018 and 69.7 vs. 50.0%, p = 0.017, respectively)., Conclusions: According to survival status, there is differentiation in the prevalence of both studied FOXO3A gene polymorphisms. The study group had half of the C alleles compared with the control group and centenarians less frequently had the T allele of both FOXO3A gene polymorphisms compared with nonagenarians. No difference was found between groups according to TERT , IGFBP3 and ADIPOQ gene polymorphisms. It seems that some polymorphisms may be significant in prolonging our lifespan. Nevertheless, confirmation in additional study populations is needed.

Published
2017
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34. The use of statins alone, or in combination with pioglitazone and other drugs, for the treatment of non-alcoholic fatty liver disease/non-alcoholic steatohepatitis and related cardiovascular risk. An Expert Panel Statement.

Author

Athyros VG, Alexandrides TK, Bilianou H, Cholongitas E, Doumas M, Ganotakis ES, Goudevenos J, Elisaf MS, Germanidis G, Giouleme O, Karagiannis A, Karvounis C, Katsiki N, Kotsis V, Kountouras J, Liberopoulos E, Pitsavos C, Polyzos S, Rallidis LS, Richter D, Tsapas AG, Tselepis AD, Tsioufis K, Tziomalos K, Tzotzas T, Vasiliadis TG, Vlachopoulos C, Mikhailidis DP, and Mantzoros C

Subjects
Animals, Drug Therapy, Combination, Fatty Liver complications, Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors adverse effects, Hypoglycemic Agents adverse effects, Non-alcoholic Fatty Liver Disease complications, Pioglitazone, Thiazolidinediones adverse effects, Cardiovascular Diseases etiology, Cardiovascular Diseases prevention & control, Fatty Liver drug therapy, Hydroxymethylglutaryl-CoA Reductase Inhibitors therapeutic use, Hypoglycemic Agents therapeutic use, Non-alcoholic Fatty Liver Disease drug therapy, Thiazolidinediones therapeutic use
Abstract

Non-alcoholic fatty liver disease (NAFLD), the most common liver disease, is characterized by accumulation of fat (>5% of the liver tissue), in the absence of alcohol abuse or other chronic liver diseases. It is closely related to the epidemic of obesity, metabolic syndrome or type 2 diabetes mellitus (T2DM). NAFLD can cause liver inflammation and progress to non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis or hepatocellular cancer (HCC). Nevertheless, cardiovascular disease (CVD) is the most common cause of death in NAFLD/NASH patients. Current guidelines suggest the use of pioglitazone both in patients with T2DM and in those without. The use of statins, though considered safe by the guidelines, have very limited use; only 10% in high CVD risk patients are on statins by tertiary centers in the US. There are data from several animal studies, 5 post hoc analyses of prospective long-term survival studies, and 5 rather small biopsy proven NASH studies, one at baseline and on at the end of the study. All these studies provide data for biochemical and histological improvement of NAFLD/NASH with statins and in the clinical studies large reductions in CVD events in comparison with those also on statins and normal liver. Ezetimibe was also reported to improve NAFLD. Drugs currently in clinical trials seem to have potential for slowing down the evolution of NAFLD and for reducing liver- and CVD-related morbidity and mortality, but it will take time before they are ready to be used in everyday clinical practice. The suggestion of this Expert Panel is that, pending forthcoming randomized clinical trials, physicians should consider using a PPARgamma agonist, such as pioglitazone, or, statin use in those with NAFLD/NASH at high CVD or HCC risk, alone and/or preferably in combination with each other or with ezetimibe, for the primary or secondary prevention of CVD, and the avoidance of cirrhosis, liver transplantation or HCC, bearing in mind that CVD is the main cause of death in NAFLD/NASH patients., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Published
2017
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35. The frequency of 4 common gene polymorphisms in nonagenarians, centenarians, and average life span individuals.

Author

Kolovou G, Kolovou V, Vasiliadis I, Giannakopoulou V, Mihas C, Bilianou H, Kollia A, Papadopoulou E, Marvaki A, Goumas G, Kalogeropoulos P, Limperi S, Katsiki N, and Mavrogeni S

Subjects
Adolescent, Adult, Aged, Aged, 80 and over, Aging physiology, Alleles, Genotype, Humans, Middle Aged, Cholesterol Ester Transfer Proteins genetics, Gene Frequency, NF-kappa B genetics, Peptidyl-Dipeptidase A genetics, Polymorphism, Single Nucleotide
Abstract

Single nucleotide polymorphisms of angiotensin-converting enzyme (ACE) such as rs1799752, nuclear factor kappa B (NFkB) such as rs28362491 and cholesteryl ester transport protein (CETP) such as rs708272 (TaqB1) and rs5882 (I405V) were evaluated in nonagenarians, centenarians, and average life span individuals (controls). The study population (n = 307; 190 nonagenarians, 12 centenarians and 105 middle-aged controls) was genotyped for ACE, NFkB, and CETP genetic variants. The age of nonagenarian and centenarian group ranged between 90 and 111 years; centenarians and controls age ranged from 99 to 111, and from 18 to 80 years, respectively. The I carriers of ACE I/D gene were fewer in nonagenarians compared to centenarians (37.6% vs 62.5%, P = .016). The I carriers of ACE gene were more frequent in centenarians compared to controls (62% vs 41%, P = .045). No differences in frequency of common NFkB and CETP genotypes between patients with exceptional longevity and middle-aged patients were observed.

Published
2014
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36. Ageing mechanisms and associated lipid changes.

Author

Kolovou G, Katsiki N, Pavlidis A, Bilianou H, Goumas G, and Mikhailidis DP

Subjects
Aging drug effects, Animals, Humans, Hypercholesterolemia blood, Hypercholesterolemia drug therapy, Lipid Metabolism drug effects, Simvastatin pharmacology, Simvastatin therapeutic use, Aging blood, Lipid Metabolism physiology, Lipids blood
Abstract

Ageing is related to slowdown/breakdown of the somatotropic axis (i.e. the somatopause) leading to many physiological changes. The somatopause is accompanied by DNA and other macromolecule damage, and is characterized by a progressive decline in vitality and tissue function. We still do not have a definitive understanding of the mechanism( s) of ageing. Several overlapping theories have been proposed such as: 1) The free radical theory, 2) Mitochondrial Ageing, 3) The Glycation Theory, 4) Protein Damage and Maintenance in Ageing, and, 5) DNA Damage and Repair. Furthermore, several models of ageing were introduced such as genetically programmed senescence, telomere shortening, genomic instability, heterochromatin loss, altered epigenetic patterns and long lived cells. There are certain lipid modifications associated with the somatopause, characterized mainly by an increase in total cholesterol and triglyceride levels in both genders. In this review we consider the mechanisms of ageing and the associated changes in lipid metabolism according to gender.

Published
2014
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37. Ageing, longevity, exceptional longevity and related genetic and non genetics markers: panel statement.

Author

Avery P, Barzilai N, Benetos A, Bilianou H, Capri M, Caruso C, Franceschi C, Katsiki N, Mikhailidis DP, Panotopoulos G, Sikora E, Tzanetakou IP, and Kolovou G

Subjects
Aging metabolism, Animals, Biomarkers metabolism, Congresses as Topic trends, Humans, Aging genetics, Genetic Markers genetics, Longevity genetics, Phenotype
Abstract

In May 2012, a group of scientists and clinicians met in Athens (Greece) to consider the relevance of ageing, longevity, exceptional longevity and related genetic and non genetic markers. During this meeting, we firstly reviewed recent epidemiological and clinical studies on ageing, longevity and exceptional longevity, briefly analyzed the ageing theories and discussed successful and unsuccessful ageing also taking into account the evolutionary perspective. Secondly, we considered the three phenotypes based on the definition of ageing, longevity and exceptional longevity and the associated biomarkers. Third, we discussed proposed treatments suitable to counteract or slow down ageing. Finally, this panel produced a consensus statement to highlight the importance of ageing, longevity and exceptional longevity, since this is a rapidly increasing phenotype worldwide. We acknowledge that not all experts in this field may completely agree with this statement.

Published
2014
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38. Changes in Lipids and Lipoproteins after Selective LDL Apheresis (7-Year Experience).

Author

Kolovou G, Hatzigeorgiou G, Mihas C, Gontoras N, Litras P, Devekousos D, Kontodima P, Sorontila C, Bilianou H, and Mavrogeni S

Abstract

Background. The aim of the study was to investigate the changes in plasma lipids and lipoproteins and the cardiovascular events after selective LDL apheresis. Methods and Results. Two pediatric patients with familial hypercholesterolemia aged 11 and 13 years and 19 dyslipidemic adults aged 41 ± 14 years underwent direct adsorption of lipoproteins (DALI) sessions. The mean follow-up period was 47 ± 23 months. The total cholesterol (TC) values before and after treatment were 8.2 ± 2.2 and 3.1 ± 1.6 mmol/l (318 ± 86 and 122 ± 62 mg/dL), respectively. The interval mean of TC was 6.9 ± 1.9 mmol/l (268 ± 75 mg/dL). The LDL cholesterol concentrations before and after treatment were 6.6 ± 2.1 and 1.7 ± 1.1 mmol/l, (256 ± 82 mg/dL and 65 ± 41 mg/dL), respectively. The percentage of acute LDL cholesterol reduction was 75 ± 11%. Cardiovascular events were observed in seven patients. The average annual event rate was 5.51%. Conclusion. LDL apheresis is a very important therapeutic tool in managing patients at high risk for premature CAD or with aggressive CAD, despite adequate medical treatment.

Published
2012
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39. One more look at guidelines for primary and secondary prevention of cardiovascular disease in women.

Author

Kolovou G, Marvaki A, and Bilianou H

Abstract

The most common cause of death in menopausal women is due to complications from cardiovascular disease. However, many physicians feel that the prevention in women may be delayed, because women present the clinical manifestations of cardiovascular disease 10 years later than men. Another matter emerged following the results of the Women's Health Initiative study and of the Heart Estrogen/Progestin Replacement Study. Thus the proper interpretation and implementation of science should be included in a strict procedure of appreciation and clear communication for both the qualitative and quantitative evaluation of evidence, used for the clinical guidelines. Based on objective scientific collaboration among various specialities, guidelines for the prevention of cardiovascular disease of adult women with a broad range of cardiovascular risk have been formed. In this review, the guidelines or recommendations which have been reported in the last 2 decades by various scientific societies for prevention of cardiovascular disease in women will be analysed.

Published
2011
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40. The role of common variants of the cholesteryl ester transfer protein gene in left main coronary artery disease.

Author

Kolovou G, Vasiliadis I, Kolovou V, Karakosta A, Mavrogeni S, Papadopoulou E, Papamentzelopoulos S, Giannakopoulou V, Marvaki A, Degiannis D, and Bilianou H

Subjects
Aged, Alleles, Amino Acid Substitution, Coronary Angiography, Coronary Artery Disease blood, Coronary Artery Disease diagnostic imaging, Coronary Artery Disease pathology, Exons, Female, Gene Frequency, Genetic Association Studies, Greece, Humans, Introns, Lipids blood, Male, Middle Aged, Polymerase Chain Reaction, Polymorphism, Restriction Fragment Length, Cholesterol Ester Transfer Proteins genetics, Coronary Artery Disease genetics, Coronary Vessels pathology, Polymorphism, Genetic
Abstract

Background: The cholesteryl ester transfer protein (CETP) has a central role in the lipid metabolism and therefore may alter the susceptibility to atherosclerosis., Methods: The DNA of 471 subjects [133 subjects with angiographically documented left main coronary artery disease (LMCAD), 241 subjects with more peripheral coronary artery disease (MPCAD) and 97 subjects self reported healthy (Controls)] was analyzed for the frequency of TaqIB and I405V polymorphisms in the gene coding CETP., Results: There is no significant difference in CETP allele frequency or genotype distribution among LMCAD and MPCAD patients although there is statistical difference between LMCAD and Controls (p = 0.001). Specifically, patients with LMCAD and B1B1 genotype of TaqIB polymorphism were more frequent present compared to Controls (33.8% vs 22.9%, respectively). The frequency of B2B2 genotype was 3 times lower in the LMCAD group compared to Controls (10.5% vs 30.2%, respectively). In the LMCAD group the frequency of B1 allele compared to Controls was higher (62% vs 46%, respectively, p = 0.001). The relationship between TaqIB gene polymorphism and the LMCAD was independent of lipid profile, with the exception of apolipoprotein A., Conclusions: These findings indicate that the TaqIB polymorphism may have potential importance in screening individuals at high risk for developing CAD. However, this polymorphism cannot distinguish between LMCAD and MPCAD. Further prospective investigations in larger populations are required to confirm these findings.

Published
2011
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41. Assessment and clinical relevance of non-fasting and postprandial triglycerides: an expert panel statement.

Author

Kolovou GD, Mikhailidis DP, Kovar J, Lairon D, Nordestgaard BG, Ooi TC, Perez-Martinez P, Bilianou H, Anagnostopoulou K, and Panotopoulos G

Subjects
Animals, Cardiovascular Diseases etiology, Humans, Hyperlipidemias complications, Hyperlipidemias diagnosis, Hyperlipidemias therapy, Hypertriglyceridemia diagnosis, Hypertriglyceridemia therapy, Hypolipidemic Agents pharmacology, Life Style, Postprandial Period, Risk Factors, Dietary Fats administration & dosage, Hypertriglyceridemia complications, Triglycerides blood
Abstract

An Expert Panel group of scientists and clinicians met to consider several aspects related to non-fasting and postprandial triglycerides (TGs) and their role as risk factors for cardiovascular disease (CVD). In this context, we review recent epidemiological studies relevant to elevated non-fasting TGs as a risk factor for CVD and provide a suggested classification of non-fasting TG concentration. Secondly, we sought to describe methodologies to evaluate postprandial TG using a fat tolerance test (FTT) in the clinic. Thirdly, we discuss the role of non-fasting lipids in the treatment of postprandial hyperlipemia. Finally, we provide a series of clinical recommendations relating to non-fasting TGs based on the consensus of the Expert Panel: 1). Elevated non-fasting TGs are a risk factor for CVD. 2). The desirable non-fasting TG concentration is <2 mmol/l (<180 mg/dl). 3). For standardized postprandial testing, a single FTT meal should be given after an 8 h fast and should consist of 75 g of fat, 25 g of carbohydrates and 10 g of protein. 4). A single TG measurement 4 h after a FTT meal provides a good evaluation of the postprandial TG response. 5). Preferably, subjects with non-fasting TG levels of 1-2 mmol/l (89-180 mg/dl) should be tested with a FTT. 6). TG concentration ≤ 2.5 mmol/l (220 mg/dl) at any time after a FTT meal should be considered as a desirable postprandial TG response. 7). A higher and undesirable postprandial TG response could be treated by aggressive lifestyle modification (including nutritional supplementation) and/or TG lowering drugs like statins, fibrates and nicotinic acid.

Published
2011
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42. Definition of postprandial lipaemia.

Author

Kolovou GD, Mikhailidis DP, Nordestgaard BG, Bilianou H, and Panotopoulos G

Subjects
Humans, Hyperlipidemias complications, Hyperlipidemias therapy, Hypertriglyceridemia complications, Hypertriglyceridemia therapy, Postprandial Period, Risk Factors, Terminology as Topic, Cardiovascular Diseases etiology, Hyperlipidemias physiopathology, Hypertriglyceridemia physiopathology, Triglycerides blood
Abstract

At the present time, there is no widely agreed definition of postprandial lipaemia (PPL). This lack of a shared definition limits the identification and treatment of patients with exaggerated PPL as well as the evaluation of potential therapeutic agents. PPL is a complex syndrome characterized by non-fasting hypertriglyceridaemia that is associated with an increased risk of vascular events. This review considers the definition of PPL and the methodology for assessing this process.

Published
2011
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43. Diagnostic value of postprandial triglyceride testing in healthy subjects: a meta-analysis.

Author

Mihas C, Kolovou GD, Mikhailidis DP, Kovar J, Lairon D, Nordestgaard BG, Ooi TC, Perez-Martinez P, Bilianou H, Anagnostopoulou K, and Panotopoulos G

Subjects
Adult, Female, Humans, Male, Middle Aged, Postprandial Period, Time Factors, White People, Dietary Fats administration & dosage, Hyperlipidemias diagnosis, Triglycerides blood
Abstract

Background/aim: Triglycerides (TGs) are measured in studies evaluating changes in non-fasting lipid profiles after a fat tolerance test (FTT); however, the optimal timing for TG measurements after the oral fat load is unclear. The aim of this study was to evaluate how non-fasting TG levels vary after an oral FTT in healthy subjects., Methods: This meta-analysis included 113 studies with >5 participants of Caucasian race that were indexed in PubMed from its inception through March 2010, using the search term "postprandial lipemia". We only included studies that provided mean values and standard deviation (SD) (or standard error of the mean) for TG measurements at baseline (=fasting) and for at least one other time-point. Exclusion criteria included uncommon sampling time-points after the FTT, baseline TGs≥2.0 mmol/L (≥177mg/dl), and a body mass index ≥30kg/m(2)., Results: All studies combined, weighted mean±SD TG values in mmol/L were 1.25±0.32 fasting, 1.82±0.40 at 2 h, 2.31±0.62 at 4 h, 1.87±0.63 at 6 h, and 1.69±0.80 at 8 h. After stratifying studies based on fat quantity in the test meal (<40, ≥40-<50, ≥50-<60, ≥60-<70, ≥70-<80, ≥80-<90, ≥90-<100, ≥100-<110, ≥110-120, ≥120 g), the highest standardized mean difference in TG levels from fasting levels was found in those having an oral fat load of ≥70 g and <80 g, and at 4 h (difference=1.74 mmol/L; p<0.001)., Conclusion: The 4 h time-point after an oral fat load during a FTT was the most representative measurement of TGs. The highest standardized mean difference of TGs was found after a meal containing 70-79g of fat. The relevance of these two key parameters determined in healthy subjects should be considered for further developments of an oral FFT for clinical purposes.

Published
2011
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44. Postprandial lipemia in children and adolescents.

Author

Kolovou GD, Bilianou H, and Mikhailidis DP

Subjects
Adolescent, Age Factors, Atherosclerosis epidemiology, Child, Cholesterol, HDL blood, Dietary Fats adverse effects, Disease Progression, Humans, Hyperlipidemias diagnosis, Hypertriglyceridemia complications, Lipoproteins blood, Postprandial Period, Atherosclerosis etiology, Hyperlipidemias complications, Triglycerides blood
Abstract

Atherosclerosis is a result of a lifelong process that has its origins in childhood. Data in adults suggest that impaired postprandial lipoprotein metabolism may contribute to, or be a marker of, the development and progression of atherosclerosis. After an 8-year follow up period, the Bogalusa Heart Study showed that children with low high density lipoprotein cholesterol, high triglyceride levels and high body mass index had a notably increased occurrence of dyslipidemia as adults. A significantly greater postprandial response of triglycerides in children with elevated fasting triglyceride levels was reported. It is well known that dietary fat is associated with higher plasma triglyceride levels. It is not clear if postprandial lipemia should be evaluated in children and adolescents. However, in special situations this may help determine the underlying lipid disorder. This review discusses the current status in this field.

Published
2011
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45. Effects of estrogens on atherogenesis.

Author

Kolovou G, Giannakopoulou V, Vasiliadis Y, and Bilianou H

Subjects
Animals, Atherosclerosis etiology, Atherosclerosis genetics, Atherosclerosis physiopathology, Estrogen Replacement Therapy, Estrogens pharmacology, Female, Humans, Male, Risk Factors, Atherosclerosis drug therapy, Estrogens therapeutic use
Abstract

Cardiovascular disease, in spite of the significant interventions that have been made for primary and secondary preventions, is still the main cause of death in men and women in the western world. The prevalence of myocardial infarction in women with normal level of estrogens is very rare and 3-5 times lower than in men. However, this favorable relationship disappears in older women. Thus, the results from several clinical trials regarding the hormone status of women and the occurrence of cardiovascular events have led to the conclusions that estrogens exert a protective effect on atherogenesis, on formation of the atherosclerotic plaque, and, subsequently, on clinical manifestations of atherogenesis. In the last years, after the development of models for studying atherogenesis significant progress has been made, concerning the understanding of evolutionary biological and cellular events, leading to atherogenesis. In this review, atherogenesis (the formation of atherosclerotic plaque and its stages), the factors which advance atherogenesis (environmental and genetic), the effect of estrogens on the stages of atherogenesis, and the effect of estrogens on the factors which promote atherosclerosis will be discussed. Finally, hormone replacement therapy will be briefly described.

Published
2011
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46. Aging men and lipids.

Author

Kolovou G, Bilianou H, Marvaki A, and Mikhailidis DP

Subjects
Age Factors, Body Composition, Body Mass Index, Cholesterol, HDL blood, Cholesterol, HDL metabolism, Cholesterol, LDL blood, Cholesterol, LDL metabolism, Dyslipidemias blood, Dyslipidemias pathology, Estrogens, Genotype, Health Status, Humans, Life Style, Lipids blood, Male, Receptors, Androgen blood, Testosterone blood, Testosterone metabolism, United States epidemiology, Aging blood, Andropause, Dyslipidemias epidemiology, Lipid Metabolism, Receptors, Androgen metabolism
Abstract

Many theories aim at explaining the mechanisms of aging and death in humans. Decreased levels of androgens, growth hormone, and insulin-like growth factor accompany natural aging in men. Androgens influence the growth and maturation of men in various stages of their life. The action of androgens is performed by binding or not binding to androgen receptors. However, various actions of androgens were clarified after the discovery and genotyping of the androgen receptor. The influence of androgens on the lipid profile was reported by several researchers. This negative influence of androgens in men and the positive influence of estrogens in women are responsible for the higher impact of atherogenesis in men compared with women. In aging men, this negative influence of androgens on the lipid profile is more pronounced. This review considers the influence of age on lipid metabolism in men., (© The Author(s) 2011)

Published
2011
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47. Primary and secondary hypertriglyceridaemia.

Author

Kolovou GD, Anagnostopoulou KK, Kostakou PM, Bilianou H, and Mikhailidis DP

Subjects
Animals, Humans, Hypertriglyceridemia genetics, Hypertriglyceridemia blood, Hypertriglyceridemia diagnosis, Triglycerides blood
Abstract

Familial hypertriglyceridaemia is inherited in an autosomal dominant manner. The responsible genetic abnormality is unknown but recently, a novel gene encoding apolipoprotein AV has been linked to familial hypertriglyceridaemia. All patients develop the same phenotype with elevated levels of very low density lipoproteins (VLDL) in plasma. The main disorder of this dyslipidaemia is decreased intestinal absorption of biliary acids, leading to a compensatory increase of VLDL production. In familial hypertriglyceridaemia, a marked increase in plasma triglyceride (TG) levels can cause acute pancreatitis. Moreover, patients with other genetic factors, like familial chylomicronaemia, familial combined hyperlipidaemia, familial dysbetalipoproteinaemia and other rare disorders (e.g. Tangier disease and fish eye disease) may present increase of TG levels or cholesterol levels or both. Secondary hypertriglyceridaemias include hypothyroidism, kidney abnormalities (e.g. nephrotic syndrome or chronic kidney failure), diabetes mellitus, heavy alcohol consumption and obesity. In men and postmenopausal women, it seems that estrogen deficiency is responsible for higher TG levels compared with premenopausal women postprandially. In every state -fasting or postprandial-, women demonstrate lower plasma TG levels compared with men. This fact is due not only to increased muscular TG uptake and storage but also to higher TG clearance. Many studies demonstrated an age impact on plasma TG increase and larger variation of fasting TG levels caused by age. Also, hypertriglyceridaemia (TG >150 mg/dl; 1.7 mmol/l) is one of the diagnostic criteria of metabolic syndrome. Finally, several drugs may increase TG levels (e.g. chlorthalidone or beta-blockers).

Published
2009
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48. The effect of nicotinic acid and alcohol co-administration in Wistar rats.

Author

Kolovou GD, Mikhailidis DP, Adamopoulou EN, Salpea KD, Kafaltis N, Bilianou HG, Malakos J, Pilatis ND, Mykoniatis M, and Cokkinos DV

Subjects
Animals, Drug Interactions, Ethanol administration & dosage, Liver enzymology, Liver metabolism, Liver Function Tests, Male, Niacin administration & dosage, Rats, Rats, Wistar, Triglycerides blood, Central Nervous System Depressants pharmacology, Ethanol pharmacology, Hypolipidemic Agents pharmacology, Liver drug effects, Niacin pharmacology
Abstract

The effects of co-administration of nicotinic acid (NA) and alcohol (Alc) on liver function in male Wistar rats were evaluated. The rats were randomized into five groups: (i) Olive oil (Oil), (ii) Alc+Oil, (iii) NA+Oil, (iv) NA+Alc+Oil, and (v) Controls (fed only normal rat chow). Alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (AP), total cholesterol and triglycerides (TG) were measured. Liver histopathology was also assessed. The Alc+Oil group had higher TG levels compared with the NA+Alc+Oil group and all other groups, as well. NA+Oil group had higher levels of AP compared with Alc+Oil and Oil groups. The NA+Oil group had higher ALT levels compared with the Oil group. The Oil group had lower ALT levels compared with the control group. The Alc+Oil group had higher AST levels compared with the NA+Alc+Oil group, as well as with all other groups. Liver histopathology was within the normal range. A moderate amount of Alc daily together with NA is safe in rats. The NA and Alc co-administration reduces the TG and AST levels in rats, compared with the administration of Alc alone., (Copyright (c) 2005 Prous Science. All rights reserved.)

Published
2005
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