TY - JOUR
T1 - Ambulatory blood pressure monitoring for risk stratification in obese and non-obese subjects from 10 populations
AU - Hansen, T. W.
AU - Thijs, L.
AU - Li, Y.
AU - Boggia, J.
AU - Liu, Y.
AU - Asayama, K.
AU - Kikuya, M.
AU - Björklund-Bodegard, K.
AU - Ohkubo, T.
AU - Jeppesen, J.
AU - Torp-Pedersen, C.
AU - Dolan, E.
AU - Kuznetsova, T.
AU - Stolarz-Skrzypek, K.
AU - Tikhonoff, V.
AU - Malyutina, S.
AU - Casiglia, E.
AU - Nikitin, Y.
AU - Lind, L.
AU - Sandoya, E.
AU - Kawecka-Jaszcz, K.
AU - Filipovský, J.
AU - Imai, Y.
AU - Wang, J.
AU - O'Brien, E.
AU - Staessen, J. A.
N1 - Funding Information:
The European Union (Grants IC15-CT98-0329-EPOGH, LSHM-CT-2006-037093 InGenious HyperCare, HEALTH-F4-2007-201550 HyperGenes, HEALTH-F7-2011-278249 EU-MASCARA, HEALTH-F7-305507 HOMAGE and the European Research Council Advanced Research Grant 294713 EPLORE) and the Fonds voor Wetenschappelijk Onderzoek Vlaanderen, Ministry of the Flemish Community, Brussels, Belgium (G.0734.09, G.0881.13 and G.088013N) supported the Studies Coordinating Centre (Leuven, Belgium). The European Union (Grants LSHM-CT-2006-037093 and HEALTH-F4-2007-201550) also supported the research groups in Shanghai, Kraków, Padova and Novosibirsk. The Danish Heart Foundation (Grant 01-2-9-9A-22914) and the Lundbeck Fonden (Grant R32-A2740) supported the studies in Copenhagen. The Ohasama study received support via Grant-in-Aid for Scientific Research (22590767, 22790556, 23249036, 23390171 and 23790242) from the Ministry of Education, Culture, Sports, Science and Technology, Japan; Health Labour Sciences Research Grant (H23-Junkankitou (Seishuu)-Ippan-005) from the Ministry of Health, Labour and Welfare, Japan; Japan Arteriosclerosis Prevention Fund; and a Grant from the Central Miso Research Institute, Tokyo, Japan. The National Natural Science Foundation of China (Grants 30871360 and 30871081), Beijing, China and the Shanghai Commissions of Science and Technology (Grant 07JC14047 and the ‘Rising Star’ program 06QA14043) and Education (Grant 07ZZ32 and the ‘Dawn’ project) supported the JingNing study in China. The Comisión Sectorial de Investigación Científica de la Universidad de la República (Grant I+D GEFA-HT-UY) and the Agencia Nacional de Innovación e Investigación supported research in Uruguay. The funding sources have no role in the design and conduct of the study; collection, management, analysis and interpretation of the data; and preparation, review or approval of the manuscript. We gratefully acknowledge the expert assistance of Mrs Sandra Covens, who is an employee of the Studies Coordinating Centre, Leuven, Belgium, and did not receive any compensation for her contribution to this study.
PY - 2014/9
Y1 - 2014/9
N2 - Overweight clusters with high blood pressure (BP), but the independent contribution of both risk factors remains insufficiently documented. In a prospective population study involving 8467 participants (mean age 54.6 years; 47.0% women) randomly recruited from 10 populations, we studied the contribution of body mass index (BMI) to risk over and beyond BP, taking advantage of the superiority of ambulatory over conventional BP. Over 10.6 years (median), 1271 participants (15.0%) died and 1092 (12.9%), 637 (7.5%) and 443 (5.2%) experienced a fatal or nonfatal cardiovascular, cardiac or cerebrovascular event. Adjusted for sex and age, low BMI (<20.7 kg m -2) predicted death (hazard ratio (HR) vs average risk, 1.52; P<0.0001) and high BMI (≥30.9 kg m -2) predicted the cardiovascular end point (HR, 1.27; P=0.006). With adjustments including 24-h systolic BP, these HRs were 1.50 (P<0.001) and 0.98 (P=0.91), respectively. Across quartiles of the BMI distribution, 24-h and nighttime systolic BP predicted every end point (1.13≤standardized HR ≤1.67; 0.046 ≤P<0.0001). The interaction between systolic BP and BMI was nonsignificant (P≥0.22). Excluding smokers removed the contribution of BMI categories to the prediction of mortality. In conclusion, BMI only adds to BP in risk stratification for mortality but not for cardiovascular outcomes. Smoking probably explains the association between increased mortality and low BMI.
AB - Overweight clusters with high blood pressure (BP), but the independent contribution of both risk factors remains insufficiently documented. In a prospective population study involving 8467 participants (mean age 54.6 years; 47.0% women) randomly recruited from 10 populations, we studied the contribution of body mass index (BMI) to risk over and beyond BP, taking advantage of the superiority of ambulatory over conventional BP. Over 10.6 years (median), 1271 participants (15.0%) died and 1092 (12.9%), 637 (7.5%) and 443 (5.2%) experienced a fatal or nonfatal cardiovascular, cardiac or cerebrovascular event. Adjusted for sex and age, low BMI (<20.7 kg m -2) predicted death (hazard ratio (HR) vs average risk, 1.52; P<0.0001) and high BMI (≥30.9 kg m -2) predicted the cardiovascular end point (HR, 1.27; P=0.006). With adjustments including 24-h systolic BP, these HRs were 1.50 (P<0.001) and 0.98 (P=0.91), respectively. Across quartiles of the BMI distribution, 24-h and nighttime systolic BP predicted every end point (1.13≤standardized HR ≤1.67; 0.046 ≤P<0.0001). The interaction between systolic BP and BMI was nonsignificant (P≥0.22). Excluding smokers removed the contribution of BMI categories to the prediction of mortality. In conclusion, BMI only adds to BP in risk stratification for mortality but not for cardiovascular outcomes. Smoking probably explains the association between increased mortality and low BMI.
KW - ambulatory blood pressure
KW - body mass index
KW - epidemiology
KW - population science
KW - risk factors
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U2 - 10.1038/jhh.2013.145
DO - 10.1038/jhh.2013.145
M3 - Article
C2 - 24430701
AN - SCOPUS:84906320363
VL - 28
SP - 535
EP - 542
JO - Journal of Human Hypertension
JF - Journal of Human Hypertension
SN - 0950-9240
IS - 9
ER -