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Increased matrix metalloproteinase-8 and -9 activity in patients with infarct rupture after myocardial infarction

Susanne W M van den Borne1, Jack P M Cleutjens, Roeland Hanemaaijer

  • 1Department of Pharmacology and Toxicology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands.

Cardiovascular Pathology : the Official Journal of the Society for Cardiovascular Pathology
|April 12, 2008
PubMed
Abstract

Insights

Matrix metalloproteinase-8 (MMP-8) and MMP-9 activity, driven by inflammatory cells, significantly increases the risk of heart attack rupture in humans. This study identifies key molecular players in this fatal complication.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Pathophysiology

Background:

  • Infarct rupture is a life-threatening complication of myocardial infarction (MI).
  • The molecular mechanisms underlying human infarct rupture remain largely unknown.
  • Mouse models suggest matrix metalloproteinases (MMPs) degrade extracellular matrix, contributing to rupture.

Purpose of the Study:

  • To investigate the specific roles of MMP-2, MMP-8, and MMP-9 in human infarct rupture.
  • To determine the association between MMP activity and inflammatory cell infiltration in ruptured infarcts.

Main Methods:

  • Analysis of heart samples from patients deceased from infarct rupture and control MI patients.
  • Assessing MMP activity using zymography and quantitative immunocapture assays.
  • Measuring TIMP-1 levels and performing immunohistochemistry for MMP-2 and MMP-9.

Main Results:

  • Significantly higher levels of total and active MMP-8 and MMP-9 were found in ruptured infarct tissue compared to controls.
  • No significant differences in MMP-2 activity were observed between the groups.
  • Ruptured infarcts exhibited a greater number of inflammatory cells than control infarcts.

Conclusions:

  • Elevated MMP-8 and MMP-9 activity in the infarct area is implicated in human infarct rupture.
  • Increased infiltration of inflammatory cells appears to drive the heightened MMP activity.
  • These findings highlight MMP-8 and MMP-9 as potential therapeutic targets for preventing infarct rupture.

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