Evidence map›Paper›PMID 32478097›Full record

ReviewFrontiers in cardiovascular medicine2020

Neurohormones in the Pathophysiology of Vasovagal Syncope in Adults.

David G Benditt, J Gert van Dijk, Darshan Krishnappa, Wayne O Adkisson, Scott Sakaguchi

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cardiovascular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

12 citing papers in PubMed, 35 citations in OpenAlex.

  1. Sensor detection and pacing for impending reflex syncope.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Pediatric syncope: pearls and pitfalls in history taking.Clinical and experimental pediatrics · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Timing of Circulatory and Neurological Events in Syncope.Frontiers in cardiovascular medicine · 2020
    Review
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

5 authors at 2 institutions in 2 countries.

David G BendittCardiovascular Division, Department of Medicine, Cardiac Arrhythmia and Syncope Center, University of Minnesota Medical School, Minneapolis, MN, United States.
J Gert van DijkDepartment of Neurology, Leiden University Medical Center, Leiden, Netherlands.
Darshan KrishnappaCardiovascular Division, Department of Medicine, Cardiac Arrhythmia and Syncope Center, University of Minnesota Medical School, Minneapolis, MN, United States.
Wayne O AdkissonCardiovascular Division, Department of Medicine, Cardiac Arrhythmia and Syncope Center, University of Minnesota Medical School, Minneapolis, MN, United States.
Scott SakaguchiCardiovascular Division, Department of Medicine, Cardiac Arrhythmia and Syncope Center, University of Minnesota Medical School, Minneapolis, MN, United States.
University of Minnesota Medical Center · USLeiden University Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vasovagal syncope (VVS) is the most common cause of syncope across all age groups. Nonetheless, despite its clinical importance and considerable research effort over many years, the pathophysiology of VVS remains incompletely understood. In this regard, numerous studies have been undertaken in an attempt to improve insight into the evolution of VVS episodes and many of these studies have examined neurohormonal changes that occur during the progression of VVS events primarily using the head-up tilt table testing model. In this regard, the most consistent finding is a marked increase in epinephrine (Epi) spillover into the circulation beginning at an early stage as VVS evolves. Reported alterations of circulating norepinephrine (NE), on the other hand, have been more variable. Plasma concentrations of other vasoactive agents have been reported to exhibit more variable changes during a VVS event, and for the most part change somewhat later, but in some instances the changes are quite marked. The neurohormones that have drawn the most attention include arginine vasopressin [AVP], adrenomedullin, to a lesser extent brain and atrial natriuretic peptides (BNP, ANP), opioids, endothelin-1 (ET-1) and serotonin. However, whether some or all of these diverse agents contribute directly to VVS pathophysiology or are principally a compensatory response to an evolving hemodynamic crisis is as yet uncertain. The goal of this communication is to summarize key reported neurohumoral findings in VVS, and endeavor to ascertain how they may contribute to observed hemodynamic alterations during VVS.

Indexed as

catecholaminesneuroendocrineneurohormonetilt-table testingvasovagal syncope

Identifiers

PMID32478097
PMCPMC7232538
OpenAlexW3022673427

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.