TY - JOUR
T1 - Home blood pressure variability and subclinical atherosclerosis in multiple vascular beds
T2 - A population-based study
AU - SESSA Research Group
AU - Hisamatsu, Takashi
AU - Miura, Katsuyuki
AU - Ohkubo, Takayoshi
AU - Arima, Hisatomi
AU - Fujiyoshi, Akira
AU - Satoh, Atsushi
AU - Kadota, Aya
AU - Zaid, Maryam
AU - Takashima, Naoyuki
AU - Ohno, Seiko
AU - Horie, Minoru
AU - Ueshima, Hirotsugu
N1 - Funding Information:
T.H. receives the Overseas Research Fellowship grant from the Japan Society for the Promotion of Science (JSPS). No other author reported disclosure.
Funding Information:
Sources of funding: This research has been supported by Grants-in-aid for Scientific Research (A) 13307016, (A) 17209023, (A) 21249043, (A) 23249036, (A) 25253046, (A) 15H02528, 17K15827, and 25893097 from the Ministry of Education, Culture, Sports, Science, and Technology, Japan; and by National Institute of Health in USA (R01HL068200).
Publisher Copyright:
Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.
PY - 2018
Y1 - 2018
N2 - Objective: The mechanism by which higher blood pressure (BP) variability causes cardiovascular events remains unclear. Experimental results indicate that alterations in vessel wall tension related to BP variability may initiate atherosclerosis through oscillatory shear stress. We examined associations of home BP variability with subclinical atherosclerosis at four anatomically distinct vascular beds. Methods: In a cross-sectional population-based study of 1033 Japanese (mean age, 64.0 years; men, 88.7%) without known cardiovascular disease, we defined SBP and DBP variability as variability independent of the mean (VIM) across self-measured home BP values during seven consecutive days and quantified coronary and aortic artery calcification (CAC and AAC) by computed tomography, carotid intima-media thickness (CIMT) by ultrasonography, and ankle-brachial index (ABI). Results: In multivariable adjusted models including mean SBP, higher VIM of SBP was associated with CIMT greater than1.0mm [relative risk (95% confidence interval) fourth versus first quartile, 1.71 (1.15-2.54)], AAC score greater than 0 [1.08 (1.02-1.15)], and ABI less than 1.1 [1.49 (1.12-1.97)], and linear trends were also statistically significant. However, there was no significant association between VIM of SBP and CAC score greater than 0. Meanwhile, higher VIM of DBP was associated only with AAC score greater than 0. The associations were similar when modeling subclinical atherosclerosis severity as continuous outcomes and were consistent across subgroups based on demographics, behavioural, and cardiovascular risk factors. Conclusion: Higher variability in home BP, particularly in home SBP, was associated with greater carotid, aortic, and peripheral but not coronary atherosclerosis burdens independent of the mean home BP.
AB - Objective: The mechanism by which higher blood pressure (BP) variability causes cardiovascular events remains unclear. Experimental results indicate that alterations in vessel wall tension related to BP variability may initiate atherosclerosis through oscillatory shear stress. We examined associations of home BP variability with subclinical atherosclerosis at four anatomically distinct vascular beds. Methods: In a cross-sectional population-based study of 1033 Japanese (mean age, 64.0 years; men, 88.7%) without known cardiovascular disease, we defined SBP and DBP variability as variability independent of the mean (VIM) across self-measured home BP values during seven consecutive days and quantified coronary and aortic artery calcification (CAC and AAC) by computed tomography, carotid intima-media thickness (CIMT) by ultrasonography, and ankle-brachial index (ABI). Results: In multivariable adjusted models including mean SBP, higher VIM of SBP was associated with CIMT greater than1.0mm [relative risk (95% confidence interval) fourth versus first quartile, 1.71 (1.15-2.54)], AAC score greater than 0 [1.08 (1.02-1.15)], and ABI less than 1.1 [1.49 (1.12-1.97)], and linear trends were also statistically significant. However, there was no significant association between VIM of SBP and CAC score greater than 0. Meanwhile, higher VIM of DBP was associated only with AAC score greater than 0. The associations were similar when modeling subclinical atherosclerosis severity as continuous outcomes and were consistent across subgroups based on demographics, behavioural, and cardiovascular risk factors. Conclusion: Higher variability in home BP, particularly in home SBP, was associated with greater carotid, aortic, and peripheral but not coronary atherosclerosis burdens independent of the mean home BP.
KW - Ankle-brachial index
KW - Aortic artery calcification
KW - Atherosclerosis
KW - Blood pressure variability
KW - Carotid intima-media thickness
KW - Coronary artery calcification
KW - Home blood pressure
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U2 - 10.1097/HJH.0000000000001810
DO - 10.1097/HJH.0000000000001810
M3 - Article
C2 - 29939942
AN - SCOPUS:85061436693
SN - 0263-6352
VL - 36
SP - 2193
EP - 2203
JO - Journal of Hypertension
JF - Journal of Hypertension
IS - 11
ER -