Evidence map›Paper›PMID 22547315›Full record

ReviewMolecules (Basel, Switzerland)2012

The biological effects of ivabradine in cardiovascular disease.

Lorenza Speranza, Sara Franceschelli, Graziano Riccioni

Open access · goldAbstract readReview
In one paragraph

Review in Molecules (Basel, Switzerland), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Frontiers in pharmacology · 2017
    Review
  6. The effects of ivabradine on left atrial electromechanical function in patients with systolic heart failure.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2016
    Article
  7. Article
  8. Article
  9. Article
  10. 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

3 authors at 1 institution in 1 country.

Lorenza SperanzaDepartment of Medicine and Science of Aging, University G. d'Annunzio, 66123 Chieti, Italy. l.speranza@unich.it
Sara Franceschelli
Graziano Riccioni
University of Chieti-Pescara · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A large number of studies in healthy and asymptomatic subjects, as well as patients with already established cardiovascular disease (CAD) have demonstrated that heart rate (HR) is a very important and major independent cardiovascular risk factor for prognosis. Lowering heart rate reduces cardiac work, thereby diminishing myocardial oxygen demand. Several experimental studies in animals, including dogs and pigs, have clarified the beneficial effects of ivabradine associated with HR lowering. Ivabradine is a selective inhibitor of the hyperpolarisation activated cyclic-nucleotide-gated funny current (If) involved in pacemaker generation and responsiveness of the sino-atrial node (SAN), which result in HR reduction with no other apparent direct cardiovascular effects. Several studies show that ivabradine substantially and significantly reduces major risks associated with heart failure when added to guideline-based and evidence-based treatment. However the biological effect of ivabradine have yet to be studied. This effects can appear directly on myocardium or on a systemic level improving endothelial function and modulating immune cell migration. Indeed ivabradine is an 'open-channel' blocker of human hyperpolarization-activated cyclic nucleotide gated channels of type-4 (hHCN4), and a 'closed-channel' blocker of mouse HCN1 channels in a dose-dependent manner. At endothelial level ivabradine decreased monocyte chemotactin protein-1 mRNA expression and exerted a potent anti-oxidative effect through reduction of vascular NADPH oxidase activity. Finally, on an immune level, ivabradine inhibits the chemokine-induced migration of CD4-positive lymphocytes. In this review, we discuss the biological effects of ivabradine and highlight its effects on CAD.

Indexed as

AnimalsBenzazepinesCardiovascular DiseasesCD4-Positive T-LymphocytesCell MovementChemokine CCL2Cyclic Nucleotide-Gated Cation ChannelsGene ExpressionHeart RateHumansIvabradineNADPH OxidasesRisk FactorsSinoatrial NodeBenzazepinesChemokine CCL2Cyclic Nucleotide-Gated Cation ChannelsIvabradineNADPH Oxidases

Identifiers

PMID22547315
PMCPMC6268753
OpenAlexW2106139494

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.