Evidence map›Paper›PMID 35141778›Full record

ArticlePflugers Archiv : European journal of physiology2022

Hypotension in hereditary cardiomyopathy.

Johny Al-Khoury, Danielle Jacques, Ghassan Bkaily

Abstract read
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In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 36% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

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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

3 authors at 1 institution in 1 country.

Johny Al-KhouryDepartment of Immunology and Cell Biology, Faculty of Medicine, University of Sherbrooke, Sherbrooke, Quebec, J1H 5N4, Canada.
Danielle JacquesDepartment of Immunology and Cell Biology, Faculty of Medicine, University of Sherbrooke, Sherbrooke, Quebec, J1H 5N4, Canada.
Ghassan BkailyDepartment of Immunology and Cell Biology, Faculty of Medicine, University of Sherbrooke, Sherbrooke, Quebec, J1H 5N4, Canada. Ghassan.Bkaily@USherbrooke.ca.ORCID 0000-0002-1295-4309
Université de Sherbrooke · CA

Funding

CIHR MOP-119398CIHR MOP-125932
6 · The paper itself

Abstract

It is well accepted that hypertension may lead to the development of heart failure (HF). However, little is known about the development of hypotension that may contribute to the onset of hereditary cardiomyopathy (HCM), thus promoting heart failure and early death. The purpose of this study is to verify whether a decrease in blood pressure takes place during different phases of HCM (asymptomatic, necrosis, hypertrophy, and heart failure). Using the well-known animal model, the UM-X7.1 hamster strain of HCM (HCMH), our results showed the absence of a change in mean arterial pressure (MAP) during the asymptomatic phase preceding the development of necrosis in HCMHs when compared to age-matched normal hamster (NH). However, there was a progressive decrease in MAP that reached its lowest level during the heart failure phase. The MAP during the development of the necrosis phase of HCM was accompanied by a significant increase in the level of the sodium-hydrogen exchanger, NHE1. Treatments with the potent NHE1 inhibitor, EMD 87580 (rimeporide), did not affect MAP of NH. However, treatments with EMD 87580 during the three phases of the development of HCM significantly reversed the hypotension associated with HCM.Our results showed that the development of HCM is associated with hypotension. These results suggest that a decrease in blood pressure could be a biomarker signal for HCM leading to HF and early death. Since the blockade of NHE1 significantly but partially prevented the reduction in MAP, this suggests that other mechanisms can contribute to the development of hypotension in HCM.

Indexed as

CardiomyopathiesCardiomyopathy, HypertrophicHeart FailureHypotensionAnimalsCricetinaeNecrosisSodium-Hydrogen ExchangersSodium-Hydrogen ExchangersBlood pressureHeart failureHereditary cardiomyopathyHypertrophyHypotensionNecrosisNHE1Sodium–hydrogen exchanger

Identifiers

PMID35141778
OpenAlexW4210831821

What OpenQuestion holds

Textmetadata
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.