The contribution of inflammation to the development of hypertension mediated by increased arterial stiffness

Hirofumi Tomiyama, Kazuki Shiina, Chisa Matsumoto-Nakano, Toshiharu Ninomiya, Shunsuke Komatsu, Kazutaka Kimura, Taishiro Chikamori, Akira Yamashina

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Background-The mechanisms underlying the possible contribution of chronic inflammation to the development of hypertension remain unclear. We examined the longitudinal association of inflammation with the progression of vascular and/or renal abnormalities in the development of hypertension. Methods and Results-In 3274 middle-aged Japanese men without hypertension at the study baseline, brachial-ankle pulse wave velocity, blood pressure, estimated glomerular filtration rate, and serum CRP (C reactive protein) levels were measured annually during a 9-year period. During this study period, 474 participants (14.5%) developed hypertension. Analysis of the repeatedmeasures data revealed that sustained elevation of serum CRP levels was associated with a longitudinal increase of the brachialankle pulse wave velocity. A linear mixed model analysis revealed that higher log-transformed serum CRP values (log CRP) at each measurement were associated with a higher annual increase of the brachial-ankle pulse wave velocity (estimate= 32.553±11.635 cm/s per log CRP, P=0.018), and that higher values of the brachial-ankle pulse wave velocity at each measurement were associated with a higher annual elevation of blood pressure (estimate=0.025±0.002 mm Hg per log CRP, P < 0.001). Conclusions-In middle-aged Japanese men without hypertension at study baseline, long-term active inflammation appears to be associated with a longitudinal increase of arterial stiffness. In turn, this longitudinal increase of arterial stiffness appears to be associated with longitudinal elevation of blood pressure to the hypertensive range. Thus, systemic inflammation may play a role in the pathogenesis of hypertension by the progression of arterial stiffness.

Original languageEnglish
Article numbere005729
JournalJournal of the American Heart Association
Volume6
Issue number7
DOIs
Publication statusPublished - Jul 1 2017

Fingerprint

Vascular Stiffness
C-Reactive Protein
Pulse Wave Analysis
Hypertension
Inflammation
Ankle
Blood Proteins
Arm
Blood Pressure
Glomerular Filtration Rate
Blood Vessels
Linear Models
Kidney

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

The contribution of inflammation to the development of hypertension mediated by increased arterial stiffness. / Tomiyama, Hirofumi; Shiina, Kazuki; Matsumoto-Nakano, Chisa; Ninomiya, Toshiharu; Komatsu, Shunsuke; Kimura, Kazutaka; Chikamori, Taishiro; Yamashina, Akira.

In: Journal of the American Heart Association, Vol. 6, No. 7, e005729, 01.07.2017.

Research output: Contribution to journalArticle

Tomiyama, Hirofumi ; Shiina, Kazuki ; Matsumoto-Nakano, Chisa ; Ninomiya, Toshiharu ; Komatsu, Shunsuke ; Kimura, Kazutaka ; Chikamori, Taishiro ; Yamashina, Akira. / The contribution of inflammation to the development of hypertension mediated by increased arterial stiffness. In: Journal of the American Heart Association. 2017 ; Vol. 6, No. 7.
@article{fdfee05da8264ee99dfc5dc941e3d570,
title = "The contribution of inflammation to the development of hypertension mediated by increased arterial stiffness",
abstract = "Background-The mechanisms underlying the possible contribution of chronic inflammation to the development of hypertension remain unclear. We examined the longitudinal association of inflammation with the progression of vascular and/or renal abnormalities in the development of hypertension. Methods and Results-In 3274 middle-aged Japanese men without hypertension at the study baseline, brachial-ankle pulse wave velocity, blood pressure, estimated glomerular filtration rate, and serum CRP (C reactive protein) levels were measured annually during a 9-year period. During this study period, 474 participants (14.5{\%}) developed hypertension. Analysis of the repeatedmeasures data revealed that sustained elevation of serum CRP levels was associated with a longitudinal increase of the brachialankle pulse wave velocity. A linear mixed model analysis revealed that higher log-transformed serum CRP values (log CRP) at each measurement were associated with a higher annual increase of the brachial-ankle pulse wave velocity (estimate= 32.553±11.635 cm/s per log CRP, P=0.018), and that higher values of the brachial-ankle pulse wave velocity at each measurement were associated with a higher annual elevation of blood pressure (estimate=0.025±0.002 mm Hg per log CRP, P < 0.001). Conclusions-In middle-aged Japanese men without hypertension at study baseline, long-term active inflammation appears to be associated with a longitudinal increase of arterial stiffness. In turn, this longitudinal increase of arterial stiffness appears to be associated with longitudinal elevation of blood pressure to the hypertensive range. Thus, systemic inflammation may play a role in the pathogenesis of hypertension by the progression of arterial stiffness.",
author = "Hirofumi Tomiyama and Kazuki Shiina and Chisa Matsumoto-Nakano and Toshiharu Ninomiya and Shunsuke Komatsu and Kazutaka Kimura and Taishiro Chikamori and Akira Yamashina",
year = "2017",
month = "7",
day = "1",
doi = "10.1161/JAHA.117.005729",
language = "English",
volume = "6",
journal = "Journal of the American Heart Association",
issn = "2047-9980",
publisher = "Wiley-Blackwell",
number = "7",

}

TY - JOUR

T1 - The contribution of inflammation to the development of hypertension mediated by increased arterial stiffness

AU - Tomiyama, Hirofumi

AU - Shiina, Kazuki

AU - Matsumoto-Nakano, Chisa

AU - Ninomiya, Toshiharu

AU - Komatsu, Shunsuke

AU - Kimura, Kazutaka

AU - Chikamori, Taishiro

AU - Yamashina, Akira

PY - 2017/7/1

Y1 - 2017/7/1

N2 - Background-The mechanisms underlying the possible contribution of chronic inflammation to the development of hypertension remain unclear. We examined the longitudinal association of inflammation with the progression of vascular and/or renal abnormalities in the development of hypertension. Methods and Results-In 3274 middle-aged Japanese men without hypertension at the study baseline, brachial-ankle pulse wave velocity, blood pressure, estimated glomerular filtration rate, and serum CRP (C reactive protein) levels were measured annually during a 9-year period. During this study period, 474 participants (14.5%) developed hypertension. Analysis of the repeatedmeasures data revealed that sustained elevation of serum CRP levels was associated with a longitudinal increase of the brachialankle pulse wave velocity. A linear mixed model analysis revealed that higher log-transformed serum CRP values (log CRP) at each measurement were associated with a higher annual increase of the brachial-ankle pulse wave velocity (estimate= 32.553±11.635 cm/s per log CRP, P=0.018), and that higher values of the brachial-ankle pulse wave velocity at each measurement were associated with a higher annual elevation of blood pressure (estimate=0.025±0.002 mm Hg per log CRP, P < 0.001). Conclusions-In middle-aged Japanese men without hypertension at study baseline, long-term active inflammation appears to be associated with a longitudinal increase of arterial stiffness. In turn, this longitudinal increase of arterial stiffness appears to be associated with longitudinal elevation of blood pressure to the hypertensive range. Thus, systemic inflammation may play a role in the pathogenesis of hypertension by the progression of arterial stiffness.

AB - Background-The mechanisms underlying the possible contribution of chronic inflammation to the development of hypertension remain unclear. We examined the longitudinal association of inflammation with the progression of vascular and/or renal abnormalities in the development of hypertension. Methods and Results-In 3274 middle-aged Japanese men without hypertension at the study baseline, brachial-ankle pulse wave velocity, blood pressure, estimated glomerular filtration rate, and serum CRP (C reactive protein) levels were measured annually during a 9-year period. During this study period, 474 participants (14.5%) developed hypertension. Analysis of the repeatedmeasures data revealed that sustained elevation of serum CRP levels was associated with a longitudinal increase of the brachialankle pulse wave velocity. A linear mixed model analysis revealed that higher log-transformed serum CRP values (log CRP) at each measurement were associated with a higher annual increase of the brachial-ankle pulse wave velocity (estimate= 32.553±11.635 cm/s per log CRP, P=0.018), and that higher values of the brachial-ankle pulse wave velocity at each measurement were associated with a higher annual elevation of blood pressure (estimate=0.025±0.002 mm Hg per log CRP, P < 0.001). Conclusions-In middle-aged Japanese men without hypertension at study baseline, long-term active inflammation appears to be associated with a longitudinal increase of arterial stiffness. In turn, this longitudinal increase of arterial stiffness appears to be associated with longitudinal elevation of blood pressure to the hypertensive range. Thus, systemic inflammation may play a role in the pathogenesis of hypertension by the progression of arterial stiffness.

UR - http://www.scopus.com/inward/record.url?scp=85025479382&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85025479382&partnerID=8YFLogxK

U2 - 10.1161/JAHA.117.005729

DO - 10.1161/JAHA.117.005729

M3 - Article

C2 - 28666991

AN - SCOPUS:85025479382

VL - 6

JO - Journal of the American Heart Association

JF - Journal of the American Heart Association

SN - 2047-9980

IS - 7

M1 - e005729

ER -