Evidence map›Paper›PMID 31375968›Full record

ReviewHeart failure reviews2020

Angiotensin II and angiotensin 1-7: which is their role in atrial fibrillation?

Annamaria Mascolo, Konrad Urbanek, Antonella De Angelis, Maurizio Sessa, Cristina Scavone, Liberato Berrino, Giuseppe Massimo Claudio Rosano, Annalisa Capuano, Francesco Rossi

Abstract readReview
PubMed Publisher
In one paragraph

Review in Heart failure reviews, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 2 pooled it
4.3field-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

29 citing papers in PubMed, 2 syntheses or guidelines pooled it, 53 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

9 authors at 2 institutions in 2 countries.

Annamaria MascoloDepartment of Experimental Medicine, Section of Pharmacology L. Donatelli, University of Campania "Luigi Vanvitelli", Via Santa Maria di Costantinopoli 16, 80138, Naples, Italy. annamaria.mascolo@unicampania.it.
Konrad UrbanekDepartment of Experimental Medicine, Section of Pharmacology L. Donatelli, University of Campania "Luigi Vanvitelli", Via Santa Maria di Costantinopoli 16, 80138, Naples, Italy.
Antonella De AngelisDepartment of Experimental Medicine, Section of Pharmacology L. Donatelli, University of Campania "Luigi Vanvitelli", Via Santa Maria di Costantinopoli 16, 80138, Naples, Italy.
Maurizio SessaDepartment of Experimental Medicine, Section of Pharmacology L. Donatelli, University of Campania "Luigi Vanvitelli", Via Santa Maria di Costantinopoli 16, 80138, Naples, Italy.
Cristina ScavoneDepartment of Experimental Medicine, Section of Pharmacology L. Donatelli, University of Campania "Luigi Vanvitelli", Via Santa Maria di Costantinopoli 16, 80138, Naples, Italy.
Liberato BerrinoDepartment of Experimental Medicine, Section of Pharmacology L. Donatelli, University of Campania "Luigi Vanvitelli", Via Santa Maria di Costantinopoli 16, 80138, Naples, Italy.
Giuseppe Massimo Claudio RosanoIRCCS San Raffaele Pisana, Rome, Italy.
Annalisa CapuanoDepartment of Experimental Medicine, Section of Pharmacology L. Donatelli, University of Campania "Luigi Vanvitelli", Via Santa Maria di Costantinopoli 16, 80138, Naples, Italy.
Francesco RossiDepartment of Experimental Medicine, Section of Pharmacology L. Donatelli, University of Campania "Luigi Vanvitelli", Via Santa Maria di Costantinopoli 16, 80138, Naples, Italy.
University of Campania "Luigi Vanvitelli" · ITIstituto di Ricovero e Cura a Carattere Scientifico San Raffaele

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atrial fibrillation (AF) is a significant cause of morbidity and mortality as well as a public health burden considering the high costs of AF-related hospitalizations. Pre-clinical and clinical evidence showed a potential role of the renin angiotensin system (RAS) in the etiopathogenesis of AF. Among RAS mediators, angiotensin II (AII) and angiotensin 1-7 (A1-7) have been mostly investigated in AF. Specifically, the stimulation of the pathway mediated by AII or the inhibition of the pathway mediated by A1-7 may participate in inducing and sustaining AF. In this review, we summarize the evidence showing that both RAS pathways may balance the onset of AF through different biological mechanisms involving inflammation, epicardial adipose tissue (EAT) accumulation, and electrical cardiac remodeling. EAT is a predictor for AF as it may induce its onset through direct (infiltration of epicardial adipocytes into the underlying atrial myocardium) and indirect (release of inflammatory adipokines, the stimulation of oxidative stress, macrophage phenotype switching, and AF triggers) mechanisms. Classic RAS blockers such as angiotensin converting enzyme inhibitors (ACE-I) and angiotensin receptor blockers (ARB) may prevent AF by affecting the accumulation of the EAT, representing a useful therapeutic strategy for preventing AF especially in patients with heart failure and known left ventricular dysfunction. Further studies are necessary to prove this benefit in patients with other cardiovascular diseases. Finally, the possibility of using the A1-7 or ACE2 analogues, to enlarge current therapeutic options for AF, may represent an important field of research.

Indexed as

Atrial RemodelingAngiotensin IAngiotensin IIAtrial FibrillationHumansPeptide FragmentsAngiotensin Iangiotensin I (1-7)Angiotensin IIPeptide FragmentsAngiotensinAtrial fibrillationEpicardial adipose tissueRenin angiotensin system inhibitors

Identifiers

PMID31375968
OpenAlexW2965141422

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.