Evidence map›Paper›PMID 27206576›Full record

ReviewHeart failure reviews2016

Neurohormonal activation and pharmacological inhibition in pulmonary arterial hypertension and related right ventricular failure.

Pietro Ameri, Edoardo Bertero, Giovanni Meliota, Martino Cheli, Marco Canepa, Claudio Brunelli, Manrico Balbi

Abstract readReview
PubMed Publisher
In one paragraph

Review in Heart failure reviews, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
3.3field-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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Mast Cells in Cardiac Remodeling: Focus on the Right Ventricle.Journal of cardiovascular development and disease · 2024
    Review
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  7. Article
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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

7 authors at 2 institutions in 1 country.

Pietro AmeriCardiovascular Disease Unit, IRCCS AOU San Martino-IST Hospital and Department of Internal Medicine, University of Genova, 16132, Genoa, Italy. pietroameri@unige.it.
Edoardo BerteroCardiovascular Disease Unit, IRCCS AOU San Martino-IST Hospital and Department of Internal Medicine, University of Genova, 16132, Genoa, Italy.
Giovanni MeliotaCardiovascular Disease Unit, IRCCS AOU San Martino-IST Hospital and Department of Internal Medicine, University of Genova, 16132, Genoa, Italy.
Martino CheliCardiovascular Disease Unit, IRCCS AOU San Martino-IST Hospital and Department of Internal Medicine, University of Genova, 16132, Genoa, Italy.
Marco CanepaCardiovascular Disease Unit, IRCCS AOU San Martino-IST Hospital and Department of Internal Medicine, University of Genova, 16132, Genoa, Italy.
Claudio BrunelliCardiovascular Disease Unit, IRCCS AOU San Martino-IST Hospital and Department of Internal Medicine, University of Genova, 16132, Genoa, Italy.
Manrico BalbiCardiovascular Disease Unit, IRCCS AOU San Martino-IST Hospital and Department of Internal Medicine, University of Genova, 16132, Genoa, Italy.
Ospedale Policlinico San Martino · ITIstituto Giannina Gaslini · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During the last decade, hyperactivity of the sympathetic nervous and renin-angiotensin-aldosterone systems (SNS and RAAS, respectively) has repeatedly been related to the pathophysiology of pulmonary arterial hypertension (PAH) and PAH-related right ventricular failure (PAH-RVF), raising the question of whether neurohormonal inhibition may be indicated for these conditions. Experimental data indicate that the RAAS may be involved in pulmonary vascular remodeling, which is in fact halted by RAAS antagonism. Favorable actions of β-blockers on the pulmonary vasculature have also been described, even if information about β-adrenergic receptors in PAH is lacking. Furthermore, the available evidence suggests that stimulation of the pressure-overloaded RV by the SNS and RAAS is initially compensatory, but becomes maladaptive over time. Consistently, RV reverse remodeling has been shown in PAH animal models treated with either β-blockers or RAAS inhibitors, although important differences with human PAH may limit the translational value of these findings. Only few observational studies of neurohormonal antagonism in PAH and PAH-RVF have been published. Nonetheless, β-blockers on top of specific therapy appear to be safe and possibly also effective. The combination of mineralocorticoid receptor and endothelin-A receptor antagonists may result in an additive effect because of a positive pharmacodynamic interaction. While neurohormonal inhibitors cannot be recommended at present for treatment of PAH and PAH-RVF, they are worth being further investigated.

Indexed as

Adrenergic beta-AntagonistsAnimalsHumansHypertension, PulmonaryRenin-Angiotensin SystemSympathetic Nervous SystemVentricular Dysfunction, RightAdrenergic beta-AntagonistsACE-inhibitorAldosteroneAngiotensinNeurohormonalPulmonary arterial hypertensionRight ventricleβ-blocker

Identifiers

PMID27206576
OpenAlexW2400480246

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.