Evidence map›Paper›PMID 28217927›Full record

ReviewThe Journal of physiology2017

Hypertension-induced remodelling: on the interactions of cardiac risk factors.

Jakub Tomek, Gil Bub

Open access · hybridAbstract readReview
In one paragraph

Review in The Journal of physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.7field-weighted citation impact, top 6% of its field
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

46 citing papers in PubMed, 80 citations in OpenAlex.

  1. Understanding the Mortality Trends in Patients With Ventricular Arrhythmias and Cardiomyopathy: A 25-Year Retrospective Analysis From 1999-2024.Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc · 2026
    Observational
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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

2 authors at 2 institutions in 2 countries.

Jakub TomekDepartment of Physiology Anatomy and Genetics, University of Oxford, Oxford, UK.
Gil BubDepartment of Physiology, McGill University, Canada.ORCID 0000-0002-5304-0036
McGill University · CAUniversity of Oxford · GB

Funding

Medical Research Council MR/K015877/1
6 · The paper itself

Abstract

Hypertension induces considerable cardiac remodelling, such as hypertrophy, interstitial fibrosis, and abnormal activity of the cardiac sympathetic nervous system, which are established risk factors in several highly dangerous heart diseases, such as ventricular fibrillation and congestive heart failure. All these risk factors and heart diseases are studied extensively in isolation, but to our knowledge, there is no comprehensive review of their interactions. At the same time, there is growing evidence suggesting that such interactions are numerous and that a successful therapy against a particular condition may have unexpectedly weak effects on mortality, as treated patients may die of a different cause exacerbated by the therapy. In this article, we present a multiscale review of the literature focusing on the relationships between the above-mentioned risk factors and heart diseases, and introduce a framework that gives insight into their possible interactions. We use this framework to demonstrate that conditions such as fibrosis and elevated activity of the sympathetic nervous system may be compensatory, rather than purely pathological, mechanisms in certain contexts. Finally, we show why the described mechanisms are relevant not only in hypertension, but also in the case of healed myocardial infarction.

Indexed as

AnimalsHeartHeart FailureHumansHypertensionMyocardial InfarctionRisk FactorsSympathetic Nervous SystemVentricular Remodelingarrhythmiaextracellular matrixheart failurehypertension

Identifiers

PMID28217927
PMCPMC5471416
OpenAlexW2588357562

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.