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1. Sex-specific relevance of diabetes to occlusive vascular and other mortality: a collaborative meta-analysis of individual data from 980 793 adults from 68 prospective studies

Author

Gnatiuc, L, Herrington, WG, Halsey, J, Tuomilehto, J, Fang, X, Kim, HC, De Bacquer, D, Dobson, AJ, Criqui, MH, Jacobs, DR, Jr, Leon, DA, Peters, SAE, Ueshima, H, Sherliker, P, Peto, R, Collins, R, Huxley, RR, Emberson, JR, Woodward, M, Lewington, S, Aoki, N, Arima, H, Arnesen, E, Aromaa, A, Assmann, G, Bachman, DL, Baigent, C, Bartholomew, H, Benetos, A, Bengtsson, C, Bennett, D, Björkelund, C, Blackburn, H, Bonaa, K, Boyle, E, Broadhurst, R, Carstensen, J, Chambless, L, Chen, Z, Chew, SK, Clarke, R, Cox, C, Curb, JD, D'Agostino, R, Date, C, Davey Smith, G, De Backer, G, Dhaliwal, SS, Duan, XF, Ducimetiere, P, Duffy, S, Eliassen, H, Elwood, P, Empana, J, Garcia-Palmieri, MH, Gazes, P, Giles, GG, Gillis, C, Goldbourt, U, Gu, DF, Guasch-Ferre, M, Guize, L, Haheim, L, Hart, C, Hashimoto, S, Hashimoto, T, Heng, D, Hjermann, I, Ho, SC, Hobbs, M, Hole, D, Holme, I, Horibe, H, Hozawa, A, Hu, F, Hughes, K, Iida, M, Imai, K, Imai, Y, Iso, H, Jackson, R, Jamrozik, K, Jee, SH, Jensen, G, Jiang, CQ, Johansen, NB, Jorgensen, T, Jousilahti, P, Kagaya, M, Keil, J, Keller, J, Kim, IS, Kita, Y, Kitamura, A, Kiyohara, Y, Knekt, P, Knuiman, M, Kornitzer, M, Kromhout, D, Kronmal, R, Lam, TH, Law, M, Lee, J, Leren, P, Levy, D, Li, YH, Lissner, L, Luepker, R, Luszcz, M, MacMahon, S, Maegawa, H, Marmot, M, Matsutani, Y, Meade, T, Morris, J, Morris, R, Murayama, T, Naito, Y, Nakachi, K, Nakamura, M, Nakayama, T, Neaton, J, Nietert, PJ, Nishimoto, Y, Norton, R, Nozaki, A, Ohkubo, T, Okayama, A, Pan, WH, Puska, P, Qizilbash, N, Reunanen, A, Rimm, E, Rodgers, A, Saitoh, S, Sakata, K, Sato, S, Schnohr, P, Schulte, H, Selmer, R, Sharp, D, Shifu, X, Shimamoto, K, Shipley, M, Silbershatz, H, Sorlie, p, Sritara, P, Suh, I, Sutherland, SE, Sweetnam, P, Tamakoshi, A, Tanaka, H, Thomsen, T, Tominaga, S, Tomita, M, Törnberg, S, Tunstall-Pedoe, H, Tverdal, A, Vartiainen, E, Wald, N, Wannamethee, SG, Welborn, TA, Whincup, P, Whitlock, G, Willett, W, Woo, J, Wu, ZL, Yao, SX, Yarnell, J, Yokoyama, T, Yoshiike, N, and Zhang, XH

Published
2018
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3. Working group on epidemiology & prevention of the european society of cardiology: Proceedings of meeting held at Shannon May 14th–17th, 1998

Author

Sullivan, P. A., Murphy, D., Sullivan, P. A., Keogh, S., Sullivan, P. A., Nash, P., Kaarisalo, M. M., Marttila, J., Immonen-Raiha, P., Salomaa, V., Torppa, J., Tuomilehto, J., Siani, A., Racone, R., Ragone, E., Stinga, F., Strazzullol, P., Cappuccio, F. P., Trevisan, M., Farinaro, E., Mellone, C., Fox, K. F., Cowie, M. R., Wood, D. A., Coats, A. J., Poole Wilson, P. A., Sutton, G. C., Yarnell, J., Sweetnam, P., Thomas, H., Piwonski, J., Piotrowski, W., Pytlak, A., Wannamethee, S. G., Shaper, A. G., Walker, M., Sharpe, P. C., Young, I. S., Hasselwander, O., McMaster, D., Mercer, C., McGrath, L. T., Evans, A. E., Thomas, F., Guize, L., Ducimetiere, P., Benetos, A., Rosolova, H., Simon, J., Mayer, O., Sefrna, F., Mayer, O., Šimon, J., Rosolova, H., Racek, J., Trefil, L., Marin-Tarlea, M., Carp, C., Apetrei, E., Ginghina, C., Serban, I., Florica, N., Ceck, C., Patrascoiu, M., Ginghina, C., Carp, C., Apetrei, E., Tarlea, M., Cioranu, R., Florica, N., Ceck, C., Vaduva, M., Mihaescu, D., Lapadat, M., Ashton, W. D., Wood, D., Nanchahahal, K., Kelleher, C. C., Brennan, P. J., Howarth, D., Meade, T. W., Kelleher, C. C., Fallon, U. B., McCarthy, U., O’Donnell, M. M. K., Dineen, B., Jousilahti, P., Vartiainen, E., Tuomilehto, J., Puska, P., Kastarinen, M., Nissinen, A., Salomaa, V., Vartiainen, E., Jousilahti, P., Tuomilehto, J., Puska, P., Rosengren, A., Wedel, H., Wilhelmsen, L., Liese, A. D., Hense, H. W., Keil, U., Keil, U., Liese, A. D., Hense, H. W., Filipiak, B., Döring, A., Stieber, J., Lowel, H., De Laet, C., Brasseur, D., Kahn, A., Wautrecht, J. C., Decuyper, J., Boeynaems, J. M., Jousilahti, P., Vartiainen, E., Tuomilehto, J., Sundvall, J., Puska, P., Marques-Vidal, P., Ferrières, J., Haas, B., Evans, A., Amouyel, P., Luc, G., Ducimetiere, P., Marques-Vidal, P., Ferrieres, J., Arveiler, D., Montaye, M., Evans, A., Ducimetiere, P., Fuentes, R., Notkola, I. -L., Shemeikka, S., Tuomilehto, J., Nissinen, A., Mak, R., De BacquerBacquer, D., De Backer, G., Stam, M., Koyuncu, R., de Smet, P., Kornitzer, M., Braeckman, L., De Backer, G., De Bacquer, D., Claeys, L., Delanghe, J., De Bacquer, D., Kornitzer, M., De Backer, G., Cífkova, R., Pit’ha, J., Červenka, L., Šejda, T., Lanska, V., Škodová, Z., Stavek, P., Poledne, R., Cífková, R., Duskova, A., Hauserová, G., Hejl, Z., Lánská, V., Škodova, Z., Pistulková, H., Poledne, R., Hubáček, J., Pit’ha, J., Stávek, P., Lánská, V., Cífková, R., Faleiro, L. L., Rodrigues, D., Fonseca, A., Martins, M. C., Norris, R. M., Nyyssönen, K., Seppänen, K., Salonen, R., Kantola, M., Salonen, J. T., Parviainen, M. T., De Henauw, S., Myny, K., Doyen, Z., Van Oyen, H., Tafforeau, J., Kornitzer, M., De Backer, G., Benetos, A., Thomas, F., Guize, L., Immonen-Räihä, P., Kaarisalo, M., Marttila, R. J., Torppa, J., Tuomilehto, J., Houterman, S., Hofman, B., Witteman, J. C. M., Verschuren, W. M. M., van de Vijver, L. P. L., Kardinaal, A. F. M., Grobbee, D. E., van Poppel, G., Princen, H. M. G., Kornitzer, M., Doven, M., Koyuncu, R., De Bacquer, D., Myny, K., De Backer, G., Tafforeau, J., Van Oven, H., Doyen, M., Koyuncu, R., Kornitzer, M., De Bacquer, D., Myny, K., De Backer, G., Tafforeau, J., Van Oyen, H., de Bree, A., Verschuren, W. M. M., Blom, H. J., Mulder, I., Smit, H. A., Menotti, A., Kromhout, D., Van den Hoogen, P. C. W., Hofman, A., Witteman, J. C. M., Feskens, E. J. M., Štika, L., Bruthans, J., Wierzbicka, M., Bolinska, H., Voutilainen, S., Nyyssönen, K., Salonen, R., Lakka, T. A., Salonen, J. T., Lakka, H -M., Lakka, T. A., Salonen, J. T., Tuomainen, T-P., Nyyssonen, K., Salonen, J. T., Punnonen, K., Yarnell, J., Patterson, C., Thomas, H., Sweetnam, P., Smith, W. C. S., Campbell, S. E., Cardy, A., Phillips, D. O., Helms, P. J., Squair, J., Smith, W. C. S., Cardy, A., Phillips, D. O., Helms, P. J., Squair, J., Smith, W. C. S., Cardy, A., Phillips, D. O., Helms, P. J., Squair, J., Pytlak, A., Piotrowski, W., Rywik, S., Waskiewicz, A., Sygnowska, E., Szczesniewska, D., Sygnowska, E., Waskiewicz, A., Wagrowska, H., Polakowska, M., Rywik, S., Broda, G., Jasinski, B., Piotrowski, W., Elandt-Johnson, R. C., Wagrowska, H., Kupsé, W., Szczesniewska, D., Platonov, D. Y., Haapanen, N., Miilunpalo, S., Vuori, I., Pasanen, M., Oja, P., Urponen, H., Kopp, M. S., Skrabski, A., Szedmák, S., Boaz, M., Biro, A., Katzir, Z., Matas, T., Smetana, S., Green, M., Whincup, P. H., Morris, R., Walker, M., Lennon, L., Thomson, A., Ebrahim, S. J. B., Refsum, H., Ueland, P. M., Perry, I. J., Boer, J. M. A., Kuivenhoven, J. A., Feskens, E. J. M., Schouten, E. G., Havekes, L. M., Seidell, J. C., Kastelein, J. J. P., Kromhout, D., Oomen, C. M., Feskens, E. J. M., Rasanen, L., Nissinen, A., Fidanza, F., Menotti, A., Kok, F. J., Kromhout, D., Sileikiene, L., Klambienne, J., Milasauskiene, Z., Cappuccio, F. P., Siani, A., Barba, G., Russo, L., Ragone, E., Strazzullo, P., Farinaro, E., Trevisan, M., Schnohr, P., Parner, J., Lange, P., Meleady, R., Graham, I. M., Ueland, P. M., Refsum, H., Blom, H., Whitehead, A. S., Daly, L. E., Stefanovic, B., Boskovic, D., Mitrovic, P., Perunicic, J., Vukcevic, V., Radovanovic, N., Terzic, B., Mrdovic, I., Orilc, D., Matic, G., Vasiljevic, Z., Mitrovic, P., Boskovic, D., Stefanovic, B., Perunicic, J., Vukcevic, V., Mrdovic, I., Radovanovic, N., Orlic, D., Matic, G., Milentijevic, B., Rajic, D., Mitrovic, N., Boskovic, S., Vasiljevic, Z., Marin-Tarlea, M., Carp, C., Apetrei, E., Serban, I., Ceck, C., Patrascsoiu, M., Florica, N., Mihaescu, D., Murphy, C., Meleady, R., Ingram, S., Love, J., Graham, I., Graham, I. M., Meleady, R., van Berkel, T. F. M., Deckers, J. W., and De Bacquer, D.

Published
1998
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12. Sex-specific relevance of diabetes to occlusive vascular and other mortality: a collaborative meta-analysis of individual data from 980793 adults from 68 prospective studies

Author

Gnatiuc, L, Herrington, WG, Halsey, J, Tuomilehto, J, Fang, X, Kim, HC, DeBacquer, D, Dobson, AJ, Criqui, MH, Jr, JDR, Leon, DA, Peters, SAE, Ueshima, H, Sherliker, P, Peto, R, Collins, R, Huxley, RR, Emberson, JR, Woodward, M, Lewington, S, De Backer, G, De Bacquer, D, Kornitzer, M, Morris, R, Wannamethee, SG, Whincup, P, Law, M, Morris, J, Wald, N, Kromhout, D, Benetos, A, Guize, L, Jensen, G, Schnohr, P, Jousilahti, P, Puska, P, Vartiainen, E, Aromaa, A, Knekt, P, Reunanen, A, Johansen, NB, Thomsen, T, Bengtsson, C, Bjorkelund, C, Lissner, L, Goldbourt, U, Selmer, R, Tverdal, A, Meade, T, Haheim, L, Hjermann, I, Holme, I, Leren, P, Ducimetiere, P, Empana, J, Assmann, G, Schulte, H, Smith, GD, Hart, C, Hole, D, Tunstall-Pedoe, H, Sweetnam, P, Yarnell, J, Arnesen, E, Bonaa, K, Marmot, M, Shipley, M, Gillis, C, Chambless, L, Luszcz, M, Dhaliwal, SS, Welborn, TA, Bartholomew, H, Knuiman, MW, Kronmal, R, Nietert, PJ, Sutherland, SE, Bachman, DL, Gazes, P, Boyle, E, Jackson, R, MacMahon, S, Norton, R, Whitlock, G, D'Agostino, R, Levy, D, Silbershatz, H, Curb, JD, Sharp, D, Giles, GG, Hashimoto, S, Sakata, K, Blackburn, H, Jacobs, D, Luepker, R, Dobson, A, Cox, C, Broadhurst, R, Hobbs, M, Jamrozik, K, Garcia-Palmieri, M, Sorlie, P, Keller, J, Guasch-Ferre, M, Hu, F, Willett, W, Eliassen, H, Maegawa, H, Okayama, A, Aoki, N, Nakamura, M, Wu, ZL, Shifu, X, Tamakoshi, A, Sritara, P, Gu, DF, Jiang, CQ, Lam, TH, Ho, SC, Woo, J, Iso, H, Kitamura, A, Sato, S, Murayama, T, Nishimoto, Y, Tomita, M, Jee, SH, Kim, IS, Suh, I, Kita, Y, Niki, I, Naito, Y, Hozawa, A, Imai, Y, Ohkubo, T, Imai, K, Date, C, Nakayama, T, Yokoyama, T, Yoshiike, N, Tanaka, H, Nozaki, A, Horibe, H, Kagaya, M, Matsutani, Y, Hughes, K, Lee, J, Heng, D, Saitoh, S, Shimamoto, K, Pan, WH, Yao, SX, Baigent, C, Carstensen, J, Chen, Z, Clarke, R, Duffy, S, Neaton, J, Qizilbash, N, Rodgers, A, Tominaga, S, Tornberg, S, Bennett, D, Gu, D, Huxley, R, Zhang, XH, Collaboration, PS, and Studies, APC

Abstract

Background\ud Several studies have shown that diabetes confers a higher relative risk of vascular mortality among women than among men, but whether this increased relative risk in women exists across age groups and within defined levels of other risk factors is uncertain. We aimed to determine whether differences in established risk factors, such as blood pressure, BMI, smoking, and cholesterol, explain the higher relative risks of vascular mortality among women than among men.\ud \ud Methods\ud In our meta-analysis, we obtained individual participant-level data from studies included in the Prospective Studies Collaboration and the Asia Pacific Cohort Studies Collaboration that had obtained baseline information on age, sex, diabetes, total cholesterol, blood pressure, tobacco use, height, and weight. Data on causes of death were obtained from medical death certificates. We used Cox regression models to assess the relevance of diabetes (any type) to occlusive vascular mortality (ischaemic heart disease, ischaemic stroke, or other atherosclerotic deaths) by age, sex, and other major vascular risk factors, and to assess whether the associations of blood pressure, total cholesterol, and body-mass index (BMI) to occlusive vascular mortality are modified by diabetes.\ud \ud Results\ud Individual participant-level data were analysed from 980 793 adults. During 9·8 million person-years of follow-up, among participants aged between 35 and 89 years, 19 686 (25·6%) of 76 965 deaths were attributed to occlusive vascular disease. After controlling for major vascular risk factors, diabetes roughly doubled occlusive vascular mortality risk among men (death rate ratio [RR] 2·10, 95% CI 1·97–2·24) and tripled risk among women (3·00, 2·71–3·33; χ2 test for heterogeneity p

Published
2018

15. Sex-specific relevance of diabetes to occlusive vascular and other mortality: a collaborative meta-analysis of individual data from 980?793 adults from 68 prospective studies

Author

Gnatiuc, L., Herrington, W., Halsey, J., Tuomilehto, J., Fang, X., Kim, H., De Bacquer, D., Dobson, A., Criqui, M., Jacobs, D., Leon, D., Peters, S., Ueshima, H., Sherliker, P., Peto, R., Collins, R., Huxley, Rachel, Emberson, J., Woodward, M., Lewington, S., Aoki, N., Arima, H., Arnesen, E., Aromaa, A., Assmann, G., Bachman, D., Baigent, C., Bartholomew, H., Benetos, A., Bengtsson, C., Bennett, D., Björkelund, C., Blackburn, H., Bonaa, K., Boyle, E., Broadhurst, R., Carstensen, J., Chambless, L., Chen, Z., Chew, S., Clarke, R., Cox, C., Curb, J., D'Agostino, R., Date, C., Davey Smith, G., De Backer, G., Dhaliwal, S., Duan, X., Ducimetiere, P., Duffy, S., Eliassen, H., Elwood, P., Empana, J., Garcia-Palmieri, M., Gazes, P., Giles, G., Gillis, C., Goldbourt, U., Gu, D., Guasch-Ferre, M., Guize, L., Haheim, L., Hart, C., Hashimoto, S., Hashimoto, T., Heng, D., Hjermann, I., Ho, S., Hobbs, M., Hole, D., Holme, I., Horibe, H., Hozawa, A., Hu, F., Hughes, K., Iida, M., Imai, K., Imai, Y., Iso, H., Jackson, R., Jamrozik, K., Jee, S., Jensen, G., Jiang, C., Johansen, N., Jorgensen, T., Jousilahti, P., Kagaya, M., Keil, J., Keller, J., Kim, I., Kita, Y., Kitamura, A., Kiyohara, Y., Knekt, P., Knuiman, M., Kornitzer, M., Kromhout, D., Kronmal, R., Gnatiuc, L., Herrington, W., Halsey, J., Tuomilehto, J., Fang, X., Kim, H., De Bacquer, D., Dobson, A., Criqui, M., Jacobs, D., Leon, D., Peters, S., Ueshima, H., Sherliker, P., Peto, R., Collins, R., Huxley, Rachel, Emberson, J., Woodward, M., Lewington, S., Aoki, N., Arima, H., Arnesen, E., Aromaa, A., Assmann, G., Bachman, D., Baigent, C., Bartholomew, H., Benetos, A., Bengtsson, C., Bennett, D., Björkelund, C., Blackburn, H., Bonaa, K., Boyle, E., Broadhurst, R., Carstensen, J., Chambless, L., Chen, Z., Chew, S., Clarke, R., Cox, C., Curb, J., D'Agostino, R., Date, C., Davey Smith, G., De Backer, G., Dhaliwal, S., Duan, X., Ducimetiere, P., Duffy, S., Eliassen, H., Elwood, P., Empana, J., Garcia-Palmieri, M., Gazes, P., Giles, G., Gillis, C., Goldbourt, U., Gu, D., Guasch-Ferre, M., Guize, L., Haheim, L., Hart, C., Hashimoto, S., Hashimoto, T., Heng, D., Hjermann, I., Ho, S., Hobbs, M., Hole, D., Holme, I., Horibe, H., Hozawa, A., Hu, F., Hughes, K., Iida, M., Imai, K., Imai, Y., Iso, H., Jackson, R., Jamrozik, K., Jee, S., Jensen, G., Jiang, C., Johansen, N., Jorgensen, T., Jousilahti, P., Kagaya, M., Keil, J., Keller, J., Kim, I., Kita, Y., Kitamura, A., Kiyohara, Y., Knekt, P., Knuiman, M., Kornitzer, M., Kromhout, D., and Kronmal, R.

Abstract

© 2018 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license Background: Several studies have shown that diabetes confers a higher relative risk of vascular mortality among women than among men, but whether this increased relative risk in women exists across age groups and within defined levels of other risk factors is uncertain. We aimed to determine whether differences in established risk factors, such as blood pressure, BMI, smoking, and cholesterol, explain the higher relative risks of vascular mortality among women than among men. Methods: In our meta-analysis, we obtained individual participant-level data from studies included in the Prospective Studies Collaboration and the Asia Pacific Cohort Studies Collaboration that had obtained baseline information on age, sex, diabetes, total cholesterol, blood pressure, tobacco use, height, and weight. Data on causes of death were obtained from medical death certificates. We used Cox regression models to assess the relevance of diabetes (any type) to occlusive vascular mortality (ischaemic heart disease, ischaemic stroke, or other atherosclerotic deaths) by age, sex, and other major vascular risk factors, and to assess whether the associations of blood pressure, total cholesterol, and body-mass index (BMI) to occlusive vascular mortality are modified by diabetes. Results: Individual participant-level data were analysed from 980 793 adults. During 9·8 million person-years of follow-up, among participants aged between 35 and 89 years, 19 686 (25·6%) of 76 965 deaths were attributed to occlusive vascular disease. After controlling for major vascular risk factors, diabetes roughly doubled occlusive vascular mortality risk among men (death rate ratio [RR] 2·10, 95% CI 1·97–2·24) and tripled risk among women (3·00, 2·71–3·33; ?2test for heterogeneity p<0·0001). For both sexes combined, the occlusive vascular death RRs were higher in younger individuals (aged 35–59 years: 2·60

Published
2018

19. Body-mass index and cause-specific mortality in 900 000 adults: collaborative analyses of 57 prospective studies

Author

Whitlock, Gary, Lewington, Sarah, Sherliker, Paul, Clarke, Robert, Emberson, Jonathan, Halsey, Jim, Qizilbash, Nawab, Collins, Rory, Peto, Richard, Lewington, S, MacMahon, S, Peto, R, Aromaa, A, Baigent, C, Carstensen, J, Chen, Z, Clarke, R, Collins, R, Duffy, S, Kromhout, D, Neaton, J, Qizilbash, N, Rodgers, A, Tominaga, S, Toernberg, S, Tunstall-Pedoe, H, Whitlock, G, Chambless, L, De Backer, G, De Bacquer, D, Kornitzer, M, Whincup, P, Wannamethee, SG, Morris, R, Wald, N, Morris, J, Law, M, Knuiman, M, Bartholomew, H, Smith, G Davey, Sweetnam, P, Elwood, P, Yarnell, J, Kronmal, R, Sutherland, S, Keil, J, Jensen, G, Schnohr, P, Hames, C, Tyroler, A, Knekt, P, Reunanen, A, Tuomilehto, J, Jousilahti, P, VArtiainen, E, Puska, P, Kuznetsova, Tatiana, Richart, Tom, Staessen, Jan A, Thijs, Lutgarde, Jorgensen, T, Thomsen, T, Sharp, D, Curb, JD, Iso, H, Sato, S, Kitamura, A, Naito, Y, Benetos, A, Guize, L, Goldbourt, U, Tomita, M, Nishimoto, Y, Murayama, T, Criqui, M, Davis, C, Hart, C, Hole, D, Gillis, C, Jacobs, D, Blackburn, H, Luepker, R, Eberly, L, Cox, C, Levy, D, D'Agostino, R, Silbershatz, H, Tverdal, A, Selmer, R, Meade, T, Garrow, K, Cooper, J, Speizer, F, Stampfer, M, Menotti, A, Spagnolo, A, Tsuji, I, Imai, Y, Ohkubo, T, Hisamichi, S, Haheim, L, Holme, I, Hjermann, I, Leren, P, Ducimetiere, P, Empana, J, Jamrozik, K, Broadhurst, R, Assmann, G, Schulte, H, Bengtsson, C, Bjoerkelund, C, Lissner, L, Sorlie, P, Garcia-Palmieri, M, Barrett-Conner, E, Langer, R, Nakachi, K, Imai, K, Fang, X, Buzina, R, Nissinen, A, Aravanis, C, Dontas, A, Kafatos, A, Adachi, H, Toshima, H, Imaizumi, T, Nedeljkovic, S, Ostojic, M, CHen, Z, Nakayama, T, Yoshiike, N, Yokoyama, T, Date, C, Tanaka, H, Keller, J, Bonaa, K, Arnesen, E, Rimm, E, Gaziano, M, Buring, JE, Hennekens, C, Tornberg, S, Shipley, M, Leon, D, Marmot, M, Emberson, J, Halsey, J, Palmer, A, Parish, S, and Sherliker, P

Subjects
Male, obesity, Nutrition and Disease, Respiratory Tract Diseases, Myocardial Ischemia, individual data, 030204 cardiovascular system & hematology, Overweight, Body Mass Index, 0302 clinical medicine, blood-pressure, Cause of Death, Voeding en Ziekte, Medicine, Prospective Studies, 030212 general & internal medicine, Prospective cohort study, risk, Cause of death, Aged, 80 and over, Hazard ratio, Articles, General Medicine, Middle Aged, 3. Good health, Stroke, Female, medicine.symptom, Adult, medicine.medical_specialty, Waist, abdominal adiposity, united-states, 03 medical and health sciences, vascular mortality, Internal medicine, Humans, korean men, Mortality, Aged, VLAG, business.industry, Anthropometry, medicine.disease, Obesity, Surgery, randomized-trials, coronary-heart-disease, business, Body mass index
Abstract

Summary Background The main associations of body-mass index (BMI) with overall and cause-specific mortality can best be assessed by long-term prospective follow-up of large numbers of people. The Prospective Studies Collaboration aimed to investigate these associations by sharing data from many studies. Methods Collaborative analyses were undertaken of baseline BMI versus mortality in 57 prospective studies with 894 576 participants, mostly in western Europe and North America (61% [n=541 452] male, mean recruitment age 46 [SD 11] years, median recruitment year 1979 [IQR 1975–85], mean BMI 25 [SD 4] kg/m2). The analyses were adjusted for age, sex, smoking status, and study. To limit reverse causality, the first 5 years of follow-up were excluded, leaving 66 552 deaths of known cause during a mean of 8 (SD 6) further years of follow-up (mean age at death 67 [SD 10] years): 30 416 vascular; 2070 diabetic, renal or hepatic; 22 592 neoplastic; 3770 respiratory; 7704 other. Findings In both sexes, mortality was lowest at about 22·5–25 kg/m2. Above this range, positive associations were recorded for several specific causes and inverse associations for none, the absolute excess risks for higher BMI and smoking were roughly additive, and each 5 kg/m2 higher BMI was on average associated with about 30% higher overall mortality (hazard ratio per 5 kg/m2 [HR] 1·29 [95% CI 1·27–1·32]): 40% for vascular mortality (HR 1·41 [1·37–1·45]); 60–120% for diabetic, renal, and hepatic mortality (HRs 2·16 [1·89–2·46], 1·59 [1·27–1·99], and 1·82 [1·59–2·09], respectively); 10% for neoplastic mortality (HR 1·10 [1·06–1·15]); and 20% for respiratory and for all other mortality (HRs 1·20 [1·07–1·34] and 1·20 [1·16–1·25], respectively). Below the range 22·5–25 kg/m2, BMI was associated inversely with overall mortality, mainly because of strong inverse associations with respiratory disease and lung cancer. These inverse associations were much stronger for smokers than for non-smokers, despite cigarette consumption per smoker varying little with BMI. Interpretation Although other anthropometric measures (eg, waist circumference, waist-to-hip ratio) could well add extra information to BMI, and BMI to them, BMI is in itself a strong predictor of overall mortality both above and below the apparent optimum of about 22·5–25 kg/m2. The progressive excess mortality above this range is due mainly to vascular disease and is probably largely causal. At 30–35 kg/m2, median survival is reduced by 2–4 years; at 40–45 kg/m2, it is reduced by 8–10 years (which is comparable with the effects of smoking). The definite excess mortality below 22·5 kg/m2 is due mainly to smoking-related diseases, and is not fully explained. Funding UK Medical Research Council, British Heart Foundation, Cancer Research UK, EU BIOMED programme, US National Institute on Aging, and Clinical Trial Service Unit (Oxford, UK).

Published
2009
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20. Pacing in hypertrophic obstructive cardiomyopathy: A randomized crossover study

Author

Kappenberger, L., Linde, C., Daubert, C., McKenna, W., Meisel, E., Sadoul, N., Chojnowska, L., Guize, L., Gras, D., Jeanrenaud, X., Rydén, L., Kappenberger, L., Linde, C., Daubert, C., McKenna, W., Meisel, E., Sadoul, N., Chojnowska, L., Guize, L., Gras, D., Jeanrenaud, X., and Rydén, L.

Abstract

Background Uncontrolled studies have shown that short atrioventricular delay dual chamber pacing reduces outflow tract obstruction in hypertrophic obstructive cardiomyopathy. Although the exact mechanism of this beneficial effect is unclear, this seems a promising potential new treatment for hypertrophic obstructive cardiomyopathy. Method In order to evaluate the impact of pacing therapy, we performed a randomized multicentre double-blind crossover (pacemaker activated vs non activated) study to investigate modification of echocardiography, exercise tolerance, angina, dyspnoea and quality of life in 83 patients with a mean age of 53 (range 22-87) years with symptoms refractory or intolerant to classical drug treatment. Results After 12 weeks of activated or inactivated pacing, independent of which phase was first, the pressure gradient fell from 59±36 mmHg to 30±25 mmHg (P<0·001) with active pacing. Exercise tolerance improved by 21% in those patients who at baseline tolerated less than 10 min of Bruce protocol; symptoms of dyspnoea and angina also improved significantly from NYHA class 2·4 to 1·4 and 1·0 to 0·4, respectively (P<0·007). Quality of life assessment with a validated questionnaire objectivated the subjective improvement. Conclusion Pacemaker therapy is of clinical and haemodynamic benefit for patients with hypertrophic obstructive cardiomyopathy, left ventricular outflow gradient at rest over 30 mmHg who are symptomatic despite drug treatment

Published
2017

22. Induction of apoptosis using sphingolipids activates a chloride current in Xenopus laevis oocytes

Author

SOUKTANI, R., BERDEAUX, A., GHALEH, B., GIUDICELLI, J. F., GUIZE, L., LE HEUZEY, J. Y., and HENRY, P.

Subjects
Cell death -- Physiological aspects, Sphingolipids -- Physiological aspects, Xenopus -- Physiological aspects, Protein kinases -- Physiological aspects, Chloride channels -- Physiological aspects, DNA -- Research, Biological sciences
Abstract

Induction of apoptosis using sphingolipids activates a chloride current in Xenopus laevis oocytes. Am J Physiol Cell Physiol 279: C158-C165, 2000.--The purpose of this study was to investigate whether the cell shrinkage that occurs during apoptosis could be explained by a change of the activity in ion transport pathways. We tested whether sphingolipids, which are potent pro-apoptotic compounds, can activate ionic currents in Xenopus laevis oocytes. Apoptosis was characterized in our model by a decrease in cell volume, a loss of cell viability, and DNA cleavage. Oocytes were studied using voltage-clamp after injection with N,N-dimethyl-D-erythro-sphingosine (DMS) or D-sphingosine (DS). DMS and DS activated a fast-activating, slowly inactivating, outwardly rectifying current, similar to [I.sub.Cl-swell], a swelling-induced chloride current. Lowering the extracellular chloride dramatically reduced the current, and the channel was more selective for thiocyanate and iodide (thiocyanate [is greater than] iodide) than for chloride. The current was blocked by 5-nitro-2-(3-phenyl-propylamino)-benzoic acid (NPPB) and lanthanum but not by niflumic acid. Oocytes injected with a pseudosubstrate inhibitor of protein kinase C (PKC), PKC-(19-31), exhibited the same current. DMS-activated current was abolished by pre-exposure with phorbol myristate acetate. Our results suggest that induction of apoptosis in X. laevis oocytes, using sphingolipids or PKC inhibitors, activates a current similar to swelling-induced chloride current previously described in oocytes. cell shrinkage; swelling-induced chloride channel; protein kinase C; deoxyribonucleic acid fragmentation

Published
2000

25. Determinants of accelerated progression of arterial stiffness in normotensive subjects and in treated hypertensive subjects over a 6-year period

Author

Benetos, A., Adamopoulos, C., Bean, J., Temmar, M., Labat, C., Bean, K., Thomas, F., Pannier, B., Asmar, R., Zureik, M., Safar, M., and Guize, L.

Subjects
Health, Seniors
Abstract

Background: Elastic artery stiffness, a result of arterial aging, is an independent indicator of cardiovascular risk. The aim of the present longitudinal study was to compare the progression of aortic stiffness over a 6-year period in treated hypertensive subjects and normotensive subjects, and to evaluate the determinants of this progression. Methods and Results: Data for the present analysis were gathered from 483 subjects who had two health check-ups at the IPC Center, the first one in 1992-93 and the second one in 1998-99. Carotid-femoral pulse wave velocity (PWV) was used to evaluate aortic stiffness in 187 hypertensive subjects who were under treatment at the time of the first visit and throughout the follow-up period, and in 296 subjects who were classified as normotensive during the first visit and who remained treatment-free throughout the follow-up period. In both populations, PWV progression was higher in older subjects. Annual rates of progression in PWV in treated hypertensives were significantly higher than in normotensives. Only treated hypertensive patients with well controlled blood pressure levels at the time of both visits had a PWV progression similar to that of normotensive subjects. In treated hypertensives, high heart rate and high creatinine during the first visit, were associated with an accelerated progression in PWV. Conclusions: The presence of high blood pressure, high heart rate and high serum creatinine were the major determinants of accelerated progression of aortic stiffness in treated hypertensives. This is the first longitudinal study to evaluate the determinants of arterial aging over an extended period of time.

Published
2002

27. Plasma 17beta estradiol is inversely correlated with circulating vascular cell adhesion molecule

Author

Oger, Emmanuel, Alhenc-Gelas, Martine, Plu-Bureau, Geneviève, Guize, L., Scarabin, Pierre-Yves, Groupe d'Etude de la Thrombose de Bretagne Occidentale (GETBO), Institut Brestois Santé Agro Matière (IBSAM), Université de Brest (UBO)-Université de Brest (UBO)-Université de Brest (UBO), Centre de recherche en épidémiologie et santé des populations (CESP), and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris-Sud - Paris 11 (UP11)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)

Subjects
MESH: Humans, Estradiol, MESH: Vascular Cell Adhesion Molecule-1, MESH: Blood Circulation, Down-Regulation, Vascular Cell Adhesion Molecule-1, MESH: Down-Regulation, MESH: Linear Models, Blood Circulation, Linear Models, Humans, MESH: Estradiol, ComputingMilieux_MISCELLANEOUS, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract

International audience

Published
2001

28. Pacing in hypertrophic obstructive cardiomyopathy. A randomized crossover study. PIC Study Group

Author

Kappenberger, L., Linde, C., Daubert, C., McKenna, W., Meisel, E., Sadoul, N., Chojnowska, L., Guize, L., Gras, D., Jeanrenaud, X., and Ryden, L.

Subjects
Adult Aged Aged, 80 and over *Cardiac Pacing, Artificial Cardiomyopathy, Hypertrophic/*therapy Cross-Over Studies Double-Blind Method Exercise Tolerance Humans Middle Aged Prospective Studies Statistics, Nonparametric
Abstract

BACKGROUND: Uncontrolled studies have shown that short atrioventricular delay dual chamber pacing reduces outflow tract obstruction in hypertrophic obstructive cardiomyopathy. Although the exact mechanism of this beneficial effect is unclear, this seems a promising potential new treatment for hypertrophic obstructive cardiomyopathy. METHOD: In order to evaluate the impact of pacing therapy, were performed a randomized multicentre double-blind cross-over (pacemaker activated vs non activated) study to investigate modification of echocardiography, exercise tolerance, angina, dyspnoea and quality of life in 83 patients with a mean age of 53 (range 22-87) years with symptoms refractory or intolerant to classical drug treatment. RESULTS: After 12 weeks of activated or inactivated pacing, independent of which phase was first, the pressure gradient fell from 59 +/- 36 mmHg to 30 +/- 25 mmHg (P < 0.001) with active pacing. Exercise tolerance improved by 21% in those patients who at baseline tolerated less than 10 min of Bruce protocol; symptoms of dyspnoea and angina also improved significantly from NYHA class 2.4 to 1.4 and 1.0 to 0.4, respectively (P < 0.007). Quality of life assessment with a validated questionnaire objectivated the subjective improvement. CONCLUSION: Pacemaker therapy is of clinical and haemodynamic benefit for patients with hypertrophic obstructive cardiomyopathy, left ventricular outflow gradient at rest over 30 mmHg who are symptomatic despite drug treatment.

Published
1997

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