Evidence map›Paper›PMID 32009970›Full record

ReviewFrontiers in physiology2019

Sympathetic Activation in Hypertensive Chronic Kidney Disease - A Stimulus for Cardiac Arrhythmias and Sudden Cardiac Death?

Márcio Galindo Kiuchi, Jan K Ho, Janis Marc Nolde, Leslie Marisol Lugo Gavidia, Revathy Carnagarin, Vance B Matthews, Markus P Schlaich

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.7field-weighted citation impact, top 8% 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

13 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  4. A New Scoring System for the Evaluation of Ibrutinib-Associated Arrhythmias in Chronic Lymphocytic Leukemia: The ACEF ScoreTurkish journal of haematology : official journal of Turkish Society of Haematology · 2024
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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

7 authors at 2 institutions in 1 country.

Márcio Galindo KiuchiDobney Hypertension Centre, School of Medicine - Royal Perth Hospital Unit/Medical Research Foundation, The University of Western Australia, Perth, WA, Australia.
Jan K HoDobney Hypertension Centre, School of Medicine - Royal Perth Hospital Unit/Medical Research Foundation, The University of Western Australia, Perth, WA, Australia.
Janis Marc NoldeDobney Hypertension Centre, School of Medicine - Royal Perth Hospital Unit/Medical Research Foundation, The University of Western Australia, Perth, WA, Australia.
Leslie Marisol Lugo GavidiaDobney Hypertension Centre, School of Medicine - Royal Perth Hospital Unit/Medical Research Foundation, The University of Western Australia, Perth, WA, Australia.
Revathy CarnagarinDobney Hypertension Centre, School of Medicine - Royal Perth Hospital Unit/Medical Research Foundation, The University of Western Australia, Perth, WA, Australia.
Vance B MatthewsDobney Hypertension Centre, School of Medicine - Royal Perth Hospital Unit/Medical Research Foundation, The University of Western Australia, Perth, WA, Australia.
Markus P SchlaichDobney Hypertension Centre, School of Medicine - Royal Perth Hospital Unit/Medical Research Foundation, The University of Western Australia, Perth, WA, Australia.
Royal Perth Hospital · AUUniversity of Western Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Studies have revealed a robust and independent correlation between chronic kidney disease (CKD) and cardiovascular (CV) events, including death, heart failure, and myocardial infarction. Recent clinical trials extend this range of adverse CV events, including malignant ventricular arrhythmias and sudden cardiac death (SCD). Moreover, other studies point out that cardiac structural and electrophysiological changes are a common occurrence in this population. These processes are likely contributors to the heightened hazard of arrhythmias in CKD population and may be useful indicators to detect patients who are at a higher SCD risk. Sympathetic overactivity is associated with increased CV risk, specifically in the population with CKD, and it is a central feature of the hypertensive state, occurring early in its clinical course. Sympathetic hyperactivity is already evident at the earliest clinical stage of CKD and is directly related to the progression of renal failure, being most pronounced in those with end-stage renal disease. Sympathetic efferent and afferent neural activity in kidney failure is a crucial facilitator for the perpetuation and evolvement of the disease. Here, we will revisit the role of the feedback loop of the sympathetic neural cycle in the context of CKD and how it may aggravate several of the risk factors responsible for causing SCD. Targeting the overactive sympathetic nervous system therapeutically, either pharmacologically or with newly available device-based approaches, may prove to be a pivotal intervention to curb the substantial burden of cardiac arrhythmias and SCD in the high-risk population of patients with CKD.

Indexed as

chronic kidney diseasehypertensionleft ventricular hypertrophyrenal denervationsudden cardiac deathsympathetic nervous systemventricular remodeling

Identifiers

PMID32009970
PMCPMC6974800
OpenAlexW2999666002

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.