Evidence map›Paper›PMID 22493071›Full record

ArticleHypertension (Dallas, Tex. : 1979)2012

Role of heart rate reduction in the prevention of experimental heart failure: comparison between If-channel blockade and β-receptor blockade.

Peter Moritz Becher, Diana Lindner, Kapka Miteva, Konstantinos Savvatis, Christin Zietsch, Bastian Schmack, Sophie Van Linthout, Dirk Westermann, Heinz-Peter Schultheiss, Carsten Tschöpe

Open access · bronzeAbstract readComparative Study
PubMed Publisher
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

31 citing papers in PubMed, 74 citations in OpenAlex.

  1. β-Blockers and ivabradine differentially affect cardiopulmonary function and left ventricular filling index.Clinical research in cardiology : official journal of the German Cardiac Society · 2016
    Trial
  2. Low and High Pressor Doses of Ang II Lead to Two Distinct Phenotypes of Hypertensive Heart Disease in Mice.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2026
    Article
  3. Characterization of a robust mouse model of heart failure with preserved ejection fraction.American journal of physiology. Heart and circulatory physiology · 2023
    Article
  4. Review
  5. Calpains as Potential Therapeutic Targets for Myocardial Hypertrophy.International journal of molecular sciences · 2022
    Review
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  17. Frontiers in pharmacology · 2017
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Peter Moritz BecherDepartment of Cardiology and Pneumology, Charité-Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany.
Diana Lindner
Kapka Miteva
Konstantinos Savvatis
Christin Zietsch
Bastian Schmack
Sophie Van Linthout
Dirk Westermann
Heinz-Peter Schultheiss
Carsten Tschöpe
Heidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To investigate whether heart rate reduction via I(f)-channel blockade and β-receptor blockade prevents left ventricular (LV) dysfunction, we studied ivabradine and metoprolol in angiotensin II-induced heart failure. Cardiac dysfunction in C57BL/6J mice was induced by implantation of osmotic pumps for continuous subcutaneous dosing of angiotensin II (1.8 mg/kg per day SC) over a period of 3 weeks. Ivabradine (10 mg/kg per day) and metoprolol (90 mg/kg per day), which resulted in similar heart rate reduction, or placebo treatments were simultaneously started with infusion of angiotensin II. After 3 weeks, LV function was estimated by conductance catheter technique, cardiac remodeling assessed by estimation of cardiac hypertrophy, fibrosis, and inflammatory stress response by immunohistochemistry or PCR, respectively. Compared with controls, angiotensin II infusion resulted in hypertension in impaired systolic (LV contractility, stroke volume, end systolic elastance, afterload, index of arterial-ventricular coupling, and cardiac output; P<0.05) and diastolic (LV relaxation, LV end diastolic pressure, τ, and stiffness constant β; P<0.05) LV function. This was associated with a significant increase in cardiac hypertrophy and fibrosis. Increased cardiac stress was also indicated by an increase in cardiac inflammation and apoptosis. Both ivabradine and metoprolol led to a similar reduction in heart rate. Metoprolol also reduced systolic blood pressure. Ivabradine led to a significant improvement in systolic and diastolic LV function (P<0.05). This was associated with less cardiac hypertrophy, fibrosis, inflammation, and cardiac apoptosis (P<0.05). Metoprolol treatment did not prevent the reduction in cardiac function and adverse remodeling, despite a reduction of the inflammatory stress response. Behind heart rate reduction, additional beneficial cardiac effects contribute to heart failure prevention with I(f)-channel inhibition.

Indexed as

Adrenergic beta-1 Receptor AntagonistsAngiotensin IIAnimalsApoptosisBenzazepinesCyclic Nucleotide-Gated Cation ChannelsCytokinesDisease Models, AnimalDose-Response Relationship, DrugDrug Administration ScheduleHeart FailureHeart RateImmunohistochemistryIn Situ Nick-End LabelingIvabradineMaleAdrenergic beta-1 Receptor AntagonistsAngiotensin IIBenzazepinesCyclic Nucleotide-Gated Cation ChannelsCytokinesIvabradineMetoprolol

Identifiers

PMID22493071
OpenAlexW2018503358

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.