Evidence map›Paper›PMID 28424575›Full record

ReviewFrontiers in neuroscience2017

Contribution of Autonomic Reflexes to the Hyperadrenergic State in Heart Failure.

Edgar Toschi-Dias, Maria Urbana P B Rondon, Chiara Cogliati, Nazareno Paolocci, Eleonora Tobaldini, Nicola Montano

Abstract readReview
In one paragraph

Review in Frontiers in neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

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

  1. Pooled it
  2. Autonomic Neuromodulation Acutely Ameliorates Left Ventricular Strain in Humans.Journal of cardiovascular translational research · 2019
    Trial
  3. Review
  4. Review
  5. Article
  6. β-adrenergic regulation of CaBiophysics reports · 2024
    Article
  7. Review
  8. Article
  9. Twenty-four-hour blood pressure and heart rate variability are reduced in patients on left ventricular assist device support.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2022
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
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

6 authors.

Edgar Toschi-DiasHeart Institute (InCor) do Hospital das Clínicas da Faculdade de Medicina da Universidade de São PauloSão Paulo, Brazil.
Maria Urbana P B RondonSchool of Physical Education and Sports, University of São PauloSão Paulo, Brazil.
Chiara CogliatiMedicina ad Indirizzo Fisiopatologico, ASST Fatebenefratelli SaccoMilan, Italy.
Nazareno PaolocciDivision of Cardiology, Department of Medicine, Johns Hopkins Medical InstitutionsBaltimore, MD, USA.
Eleonora TobaldiniDepartment of Internal Medicine, Fondazione IRCCS Ca' Granda Ospedale Maggiore PoliclinicoMilan, Italy.
Nicola MontanoDepartment of Internal Medicine, Fondazione IRCCS Ca' Granda Ospedale Maggiore PoliclinicoMilan, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heart failure (HF) is a complex syndrome representing the clinical endpoint of many cardiovascular diseases of different etiology. Given its prevalence, incidence and social impact, a better understanding of HF pathophysiology is paramount to implement more effective anti-HF therapies. Based on left ventricle (LV) performance, HF is currently classified as follows: (1) with reduced ejection fraction (HFrEF); (2) with mid-range EF (HFmrEF); and (3) with preserved EF (HFpEF). A central tenet of HFrEF pathophysiology is adrenergic hyperactivity, featuring increased sympathetic nerve discharge and a progressive loss of rhythmical sympathetic oscillations. The role of reflex mechanisms in sustaining adrenergic abnormalities during HFrEF is increasingly well appreciated and delineated. However, the same cannot be said for patients affected by HFpEF or HFmrEF, whom also present with autonomic dysfunction. Neural mechanisms of cardiovascular regulation act as "controller units," detecting and adjusting for changes in arterial blood pressure, blood volume, and arterial concentrations of oxygen, carbon dioxide and pH, as well as for humoral factors eventually released after myocardial (or other tissue) ischemia. They do so on a beat-to-beat basis. The central dynamic integration of all these afferent signals ensures homeostasis, at rest and during states of physiological or pathophysiological stress. Thus, the net result of information gathered by each controller unit is transmitted by the autonomic branch using two different codes:

Indexed as

autonomic nervous systemcardiovascular variabilityheart failuresympathetic nerve activity

Identifiers

PMID28424575
PMCPMC5372354

What OpenQuestion holds

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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.