Evidence map›Paper›PMID 26779036›Full record

ReviewFrontiers in physiology2015

Acute Myocardial Response to Stretch: What We (don't) Know.

João S Neves, André M Leite-Moreira, Manuel Neiva-Sousa, João Almeida-Coelho, Ricardo Castro-Ferreira, Adelino F Leite-Moreira

Abstract readReview
In one paragraph

Review in Frontiers in physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–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

23 citing papers in PubMed.

  1. Trial
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  6. Article
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  9. Fibroblasts under pressure: cardiac fibroblast responses to hypertension and antihypertensive therapies.American journal of physiology. Heart and circulatory physiology · 2024
    Review
  10. Prolonged Piezo1 Activation Induces Cardiac Arrhythmia.International journal of molecular sciences · 2023
    Article
  11. TheFrontiers in physiology · 2023
    Article
  12. Article
  13. Article
  14. Article
  15. Review
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  17. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

João S NevesDepartment of Physiology and Cardiothoracic Surgery, Faculty of Medicine of the University of Porto Porto, Portugal.
André M Leite-MoreiraDepartment of Physiology and Cardiothoracic Surgery, Faculty of Medicine of the University of Porto Porto, Portugal.
Manuel Neiva-SousaDepartment of Physiology and Cardiothoracic Surgery, Faculty of Medicine of the University of Porto Porto, Portugal.
João Almeida-CoelhoDepartment of Physiology and Cardiothoracic Surgery, Faculty of Medicine of the University of Porto Porto, Portugal.
Ricardo Castro-FerreiraDepartment of Physiology and Cardiothoracic Surgery, Faculty of Medicine of the University of Porto Porto, Portugal.
Adelino F Leite-MoreiraDepartment of Physiology and Cardiothoracic Surgery, Faculty of Medicine of the University of Porto Porto, Portugal.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial stretch, as result of acute hemodynamic overload, is one of the most frequent challenges to the heart and the ability of the heart to intrinsically adapt to it is essential to prevent circulatory congestion. In this review, we highlight the historical background, the currently known mechanisms, as well as the gaps in the understanding of this physiological response. The systolic adaptation to stretch is well-known for over 100 years, being dependent on an immediate increase in contractility-known as the Frank-Starling mechanism-and a further progressive increase-the slow force response. On the other hand, its diastolic counterpart remains largely unstudied. Mechanosensors are structures capable of perceiving mechanical signals and activating pathways that allow their transduction into biochemical responses. Although the connection between these structures and stretch activated pathways remains elusive, we emphasize those most likely responsible for the initiation of the acute response. Calcium-dependent pathways, including angiotensin- and endothelin-related pathways; and cGMP-dependent pathways, comprising the effects of nitric oxide and cardiac natriuretic hormones, embody downstream signaling. The ischemic setting, a paradigmatic situation of acute hemodynamic overload, is also touched upon. Despite the relevant knowledge accumulated, there is much that we still do not know. The quest for further understanding the myocardial response to acute stretch may provide new insights, not only in its physiological importance, but also in the prevention and treatment of cardiovascular diseases.

Indexed as

cardiac functionfrank starling mechanismmyocardial stretchneurohumoral adaptationslow force response

Identifiers

PMID26779036
PMCPMC4700209

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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.