Evidence map›Paper›PMID 19352332›Full record

ReviewNature reviews. Cardiology2009

Novel pharmacotherapies to abrogate postinfarction ventricular remodeling.

Gerald W Dorn

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cardiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
10.6field-weighted citation impact, top 1% 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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Observational
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Reverse Cardiac Remodeling and ARNI Therapy.Current heart failure reports · 2021
    Review
  12. Article
  13. Observational
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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

1 author at 1 institution in 1 country.

Gerald W DornCenter for Pharmacogenomics, Washington University, 660 S. Euclid Avenue, St. Louis, MO 63110, USA. gdorn@dom.wustl.edu
Washington University in St. Louis · US

Funding

MOLECULAR MECHANISM OF APOPTOTIC CARDIOMYOPATHYR01HL059888 · NHLBI · WASHINGTON UNIVERSITY · PI DORN, GERALD W. · 1999 to 2016
$5.4M
G-Protein Receptor Kinases in Cardiac Stress AdaptationR01HL087871 · NHLBI · WASHINGTON UNIVERSITY · PI DORN, GERALD W. · 2007 to 2016
$4.1M
NHLBI NIH HHS R01 HL059888NHLBI NIH HHS R01 HL087871
6 · The paper itself

Abstract

Ventricular remodeling after myocardial infarction is defined as progressive chamber dilation and wall thinning, which leads to functional compromise. Remodeling is mediated by active processes of inflammation, fibrosis, and cardiomyocyte dropout over the weeks and months after infarction, and, therefore, provides a large temporal therapeutic window. In experimental models, interruption of molecular and physiological pathways that contribute to cardiomyocyte loss, and the resulting unfavorable ventricular geometry, can abrogate remodeling and prevent or improve heart failure. Remodeling is multifactorial and involves several parallel cellular pathways, which means many potential therapeutic targets exist. Of late, much attention has been given to the development of cell-based therapies; however, the abundant, promising pharmacotherapeutic developments should not be overlooked. This Review examines developments in pharmacological treatment of ventricular remodeling in preclinical models of myocardial infarction-specifically, disruption of the renin-angiotensin-aldosterone system through direct renin inhibition and blockade of aldosterone synthesis and/or uptake, enhancement of endothelial nitric oxide synthase synthesis, G-protein receptor kinase inhibition, administration of erythropoietin, and interruption of apoptosis-and highlights the challenge of translating these successes to treatment of human disease. Therapeutic targeting of multiple organ systems involved in recovery after myocardial infarction might prove to be the best approach to improve patients' cardiac outcome.

Indexed as

AnimalsApoptosisCardiovascular AgentsDisease Models, AnimalDrugs, InvestigationalErythropoiesisHumansMyocardial InfarctionMyocardiumNitric Oxide Synthase Type IIIReceptors, Adrenergic, betaRecovery of FunctionRenin-Angiotensin SystemSignal TransductionTreatment OutcomeVentricular RemodelingCardiovascular AgentsDrugs, InvestigationalNitric Oxide Synthase Type IIIReceptors, Adrenergic, beta

Identifiers

PMID19352332
OpenAlexW2004574799

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.