Evidence map›Paper›PMID 12381651›Full record

ArticleHeart (British Cardiac Society)2002

Cardiac remodelling in end stage heart failure: upregulation of matrix metalloproteinase (MMP) irrespective of the underlying disease, and evidence for a direct inhibitory effect of ACE inhibitors on MMP.

D Reinhardt, H H Sigusch, J Hensse, S C Tyagi, R Körfer, H R Figulla

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Heart (British Cardiac Society), 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
5.6field-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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 139 citations in OpenAlex.

  1. Pooled it
  2. Cardioprotective Role of Captopril: From Basic to Applied Investigations.International journal of molecular sciences · 2025
    Review
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  8. Review
  9. Article
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  11. Article
  12. Review
  13. Article
  14. Extracellular Matrix in Ischemic Heart Disease, Part 4/4: JACC Focus Seminar.Journal of the American College of Cardiology · 2020
    Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  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

6 authors at 3 institutions in 2 countries.

D ReinhardtDepartment of Internal Medicine, University of Jena, Germany. dirk.reinhardt@med.uni-jena.de
H H Sigusch
J Hensse
S C Tyagi
R Körfer
H R Figulla
Friedrich Schiller University Jena · DEHeart and Diabetes Center North Rhine-Westphalia · DEUniversity of Mississippi · US

Funding

Mechanism of Vascular Remodeling in HyperhomocysteinemiaR01HL071010 · NHLBI · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · PI TYAGI, SURESH C. · 2002 to 2010
$2.7M
NHLBI NIH HHS R01 HL071010NHLBI NIH HHS R01-HL-71010
6 · The paper itself

Abstract

objectiveTo investigate matrix metalloproteinases (MMP-2 and MMP-9) in heart failure caused by ischaemic and idiopathic dilated cardiomyopathy, and the impact of angiotensin converting enzyme (ACE) inhibition on MMP. DESIGN AND

main outcome measuresMMP were extracted from myocardium of patients with heart failure (coronary artery disease, n = 13; idiopathic dilated cardiomyopathy (IDCM), n = 16) and from controls (n = 6). The active form of MMP-2 and MMP-9 was measured by enzyme linked immunosorbent assay; activity of MMPs by zymography; mRNA expression of MMPs by reverse transcriptase polymerase chain reaction.

resultsActive MMP-9 was significantly increased in coronary artery disease (mean (SD) 1.6 (0.35) ng/ml) and IDCM (2.11 (0.54) ng/ml) in comparison with controls (0.53 (0.15) ng/ml). Increased MMP-2 was only found in IDCM (3.68 (0.41) ng/ml). There were corresponding increases in MMP activity but no upregulation of mRNA expression was found. The ACE inhibitors captopril and ramiprilate inhibited MMP-2 and MMP-9 activity in vitro (inhibitory capacity (IC50), in mmol/l: MMP-2: captopril 2.0 (0.16), ramiprilate 2.1 (0.3); MMP-9: captopril 1.65 (0.18), ramiprilate 2.0 (0.3)). Lisinopril inhibited MMP-9 significantly but did not inhibit MMP-2 in vitro (IC50 MMP-2: 7.4 (0.88); MMP-9: 7.86 (2.23)). Inhibition of MMP activity by ACE inhibitors was blunted by zinc excess.

conclusionsUpregulation of MMP-9 activity is common in the failing myocardium, independent of the underlying disease. Missing upregulation of transcription suggests that activation of latent forms of MMP is the source of increased MMP activity, rather than increased de novo synthesis. Some ACE inhibitors may influence MMP activity by a direct effect.

Indexed as

Matrix Metalloproteinase InhibitorsAdultAgedAngiotensin-Converting Enzyme InhibitorsBlotting, WesternCardiac Output, LowCardiomyopathy, DilatedDNA, ComplementaryEnzyme-Linked Immunosorbent AssayFemaleHumansMaleMatrix Metalloproteinase 2Matrix Metalloproteinase 9Middle AgedMyocardial IschemiaAngiotensin-Converting Enzyme InhibitorsDNA, ComplementaryMatrix Metalloproteinase 2Matrix Metalloproteinase 9Matrix Metalloproteinase InhibitorsRNA, Messenger

Identifiers

PMID12381651
PMCPMC1767416
OpenAlexW2119031278

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.