Evidence map›Paper›PMID 28666991›Full record

Observational studyJournal of the American Heart Association2017

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

Abstract readObservational Study
PubMed Full text at PMC Publisher
In one paragraph

Observational study in Journal of the American Heart Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

52 citing papers in PubMed, 1 synthesis or guideline pooled it.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Hirofumi TomiyamaDepartment of Cardiology, Tokyo Medical University, Shinjyuku-ku, Tokyo, Japan tomiyama@tokyo-med.ac.jp.
Kazuki ShiinaDepartment of Cardiology, Tokyo Medical University, Shinjyuku-ku, Tokyo, Japan.
Chisa Matsumoto-NakanoDepartment of Clinical Epidemiology, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan.
Toshiharu NinomiyaDepartment of Environmental Medicine, Graduate School of Medical Sciences, Kyushu University, Higashi-ku, Fukuoka, Japan.
Shunsuke KomatsuDepartment of Cardiology, Tokyo Medical University, Shinjyuku-ku, Tokyo, Japan.
Kazutaka KimuraDepartment of Cardiology, Tokyo Medical University, Shinjyuku-ku, Tokyo, Japan.
Taishiro ChikamoriDepartment of Cardiology, Tokyo Medical University, Shinjyuku-ku, Tokyo, Japan.
Akira YamashinaDepartment of Cardiology, Tokyo Medical University, Shinjyuku-ku, Tokyo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe 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

resultsIn 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 repeated-measures data revealed that sustained elevation of serum CRP levels was associated with a longitudinal increase of the brachial-ankle 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,

conclusionsIn 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.

Indexed as

AdultAnalysis of VarianceAnkle Brachial IndexC-Reactive ProteinHumansHypertensionMiddle AgedProspective StudiesPulse Wave AnalysisRisk FactorsVascular StiffnessVasculitisC-Reactive Proteinarterial stiffnessC‐reactive proteinhypertensioninflammation

Identifiers

PMID28666991
PMCPMC5586296

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.