Temporal association between circulating proteolytic, inflammatory and neurohormonal markers in patients with

Ariel Finkelstein1, Yoav Michowitz, Anastasia Abashidze

  • 1The Department of Cardiology, Tel Aviv Sourasky Medical Center, 6 Weizmann Street, Tel Aviv, Israel.

Atherosclerosis
|March 22, 2005
PubMed

Insights

Matrix metalloproteinase (MMP) and tissue inhibitor of metalloproteinase (TIMP) dysregulation may contribute to generalized coronary ectasia (CE). Pro B-type natriuretic peptide (proBNP) might mediate this imbalance in CE patients.

Area of Science:

  • Cardiovascular Biology
  • Biochemistry
  • Pathophysiology

Background:

  • Coronary ectasia (CE) prevalence is increasing, but its underlying mechanisms remain unclear.
  • Dysregulation of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) is hypothesized to contribute to CE.
  • The association of MMPs with inflammatory and neurohormonal markers in CE is also under investigation.

Purpose of the Study:

  • To investigate the role of circulating MMPs and TIMPs in the pathogenesis of coronary ectasia.
  • To evaluate the association between MMPs, TIMPs, and inflammatory/neurohormonal markers in CE patients.

Main Methods:

  • Serum levels of MMP-2, MMP-3, TIMP-1, pro-B-type natriuretic peptide (proBNP), and high-sensitivity C-reactive protein (hsCRP) were measured.
  • Patients with generalized CE, single CE, atherosclerotic coronary disease, and normal coronary arteries were included.
  • Enzyme-linked immunosorbent assay (ELISA) was used for serum level determination.

Main Results:

  • Serum levels of MMP-2, MMP-3, TIMP-1, proBNP, and hsCRP did not significantly differ between the overall groups.
  • MMP-3 levels were significantly lower in patients with generalized CE compared to single CE.
  • A significant correlation was found between proBNP and MMP-2/TIMP-1 specifically in CE patients.

Conclusions:

  • An MMP/TIMP imbalance appears to be present in generalized CE, potentially contributing to its formation.
  • This imbalance may be mediated by pro-B-type natriuretic peptide (BNP).
  • Further research is warranted to elucidate the precise role of MMP/TIMP dysregulation in CE.
Abstract

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