Evidence map›Paper›PMID 9922372›Full record

ReviewPhysiological reviews1999

Molecular mechanisms of myocardial remodeling.

B Swynghedauw

2 registry-linked trialsAbstract readReview
PubMed Publisher
In one paragraph

Review in Physiological reviews, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 371 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
371citing papers in PubMed, 4 pooled it
28.1field-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.

NCT00795912 phase4completedstarted 2003, after this paper: background citation

A Study Of The Usage Of Statins In A Community Heart Failure Population: The Impact of HMG Co-Enzyme A Reductase Inhibitors on Heart Structural Parameters, Brain Naturetic Peptide, Markers of Inflammation and Fibrosis

Ran2003Enrolled56Registered outcomes2Posted comparisons0ConditionsHeart FailureArmsAtorvastatin
PMID 11555537PMID 15302013PMID 12020481PMID 11996626PMID 11036910PMID 15926863PMID 15313958PMID 14726474PMID 12034159PMID 12009719PMID 11806812PMID 11094035other papers from this trial
Open the trial in the graph
NCT01182376 phase3completednot on this mapstarted 2010, after this paper: background citation

SOAR: Study Observing Antiarrhythmic Remodelling Using LGE-MRI

TypeinterventionalSponsorUniversity of UtahRan2010 to 2012Enrolled33ConditionsAtrial FibrillationArmsdronedarone, Placebo
3 · Its place in the literature

Who cites it

371 citing papers in PubMed, 4 syntheses or guidelines pooled it, 1,460 citations in OpenAlex.

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  4. [Electrical storm: definition, prevalence, causes and prognostic implications].Herzschrittmachertherapie & Elektrophysiologie · 2014
    Pooled it
  5. Trial
  6. Beneficial effects of renal sympathetic denervation on cardiovascular inflammation and remodeling in essential hypertension.Clinical research in cardiology : official journal of the German Cardiac Society · 2015
    Trial
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311 more citing papers are in PubMed but not listed here.

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.

B SwynghedauwInstitut National de la Sante et de la Recherche Medicale U. 127, Hopital Lariboisiere, Paris, France.
Hôpital Lariboisière · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

"Remodeling" implies changes that result in rearrangement of normally existing structures. This review focuses only on permanent modifications in relation to clinical dysfunction in cardiac remodeling (CR) secondary to myocardial infarction (MI) and/or arterial hypertension and includes a special section on the senescent heart, since CR is mainly a disease of the elderly. From a biological point of view, CR is determined by 1 ) the general process of adaptation which allows both the myocyte and the collagen network to adapt to new working conditions; 2) ventricular fibrosis, i.e., increased collagen concentration, which is multifactorial and caused by senescence, ischemia, various hormones, and/or inflammatory processes; 3) cell death, a parameter linked to fibrosis, which is usually due to necrosis and apoptosis and occurs in nearly all models of CR. The process of adaptation is associated with various changes in genetic expression, including a general activation that causes hypertrophy, isogenic shifts which result in the appearance of a slow isomyosin, and a new Na+-K+-ATPase with a low affinity for sodium, reactivation of genes encoding for atrial natriuretic factor and the renin-angiotensin system, and a diminished concentration of sarcoplasmic reticulum Ca2+-ATPase, beta-adrenergic receptors, and the potassium channel responsible for transient outward current. From a clinical point of view, fibrosis is for the moment a major marker for cardiac failure and a crucial determinant of myocardial heterogeneity, increasing diastolic stiffness, and the propensity for reentry arrhythmias. In addition, systolic dysfunction is facilitated by slowing of the calcium transient and the downregulation of the entire adrenergic system. Modifications of intracellular calcium movements are the main determinants of the triggered activity and automaticity that cause arrhythmias and alterations in relaxation.

Indexed as

AnimalsContractile ProteinsHeart DiseasesHumansMyocardiumVentricular RemodelingContractile Proteins

Identifiers

PMID9922372
OpenAlexW1889002087

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.