Evidence map›Paper›PMID 30972341›Full record

ReviewFrontiers in cardiovascular medicine2019

Cardiac Sympathetic Denervation in Channelopathies.

Veronica Dusi, Gaetano Maria De Ferrari, Luigi Pugliese, Peter J Schwartz

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cardiovascular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.1field-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

18 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Autonomic control of ventricular function in health and disease: current state of the art.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2023
    Review
  10. Electrical storm management in structural heart disease.European heart journal supplements : journal of the European Society of Cardiology · 2023
    Article
  11. Review
  12. Catecholaminergic Polymorphic Ventricular Tachycardia.Arrhythmia & electrophysiology review · 2022
    Review
  13. Article
  14. Autonomic modulation of ventricular electrical activity: recent developments and clinical implications.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2021
    Review
  15. Management of Congenital Long-QT Syndrome: Commentary From the Experts.Circulation. Arrhythmia and electrophysiology · 2021
    Review
  16. Article
  17. [Congenital long QT syndrome].Archivos peruanos de cardiologia y cirugia cardiovascular
    Review
  18. Acute hemodynamics of cardiac sympathetic denervation.Indian pacing and electrophysiology journal
    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

4 authors at 2 institutions in 1 country.

Veronica DusiDepartment of Molecular Medicine, Section of Cardiology, University of Pavia, Pavia, Italy.
Gaetano Maria De FerrariDepartment of Molecular Medicine, Section of Cardiology, University of Pavia, Pavia, Italy.
Luigi PuglieseUnit of General Surgery 2, Department of Surgery, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy.
Peter J SchwartzCenter for Cardiac Arrhythmias of Genetic Origin and Laboratory of Cardiovascular Genetics, Istituto Auxologico Italiano, IRCCS, Milan, Italy.
Policlinico San Matteo Fondazione · ITIstituti di Ricovero e Cura a Carattere Scientifico · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Left cardiac sympathetic denervation (LCSD) is a surgical antiadrenergic intervention with a strong antiarrhythmic effect, supported by preclinical as well as clinical data. The mechanism of action of LCSD in structurally normal hearts with increased arrhythmic susceptibility (such as those of patients with channelopathies) is not limited to the antagonism of acute catecholamines release in the heart. LCSD also conveys a strong anti-fibrillatory action that was first demonstrated over 40 years ago and provides the rationale for its use in almost any cardiac condition at increased risk of ventricular fibrillation. The molecular mechanisms involved in the final antiarrhythmic effect of LCSD turned out to be much broader than anticipated. Beside the vagotonic effect at different levels of the neuraxis, other new mechanisms have been recently proposed, such as the antagonism of neuronal remodeling, the antagonism of neuropeptide Y effects, and the correction of neuronal nitric oxide synthase (nNOS) imbalance. The beneficial effects of LCSD have never been associated with a detectable deterioration of cardiac performance. Finally, patients express a high degree of satisfaction with the procedure. In this review, we focus on the rationale, results and our personal approach to LCSD in patients with channelopathies such as long QT syndrome and catecholaminergic polymorphic ventricular tachycardia.

Indexed as

cardiac autonomic nervous systemcardiac sympathetic denervationcatecholaminergic polymorphic ventricular tachycardialong QT syndromesudden cardiac death

Identifiers

PMID30972341
PMCPMC6443634
OpenAlexW2923125399

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.