Increased circulating matrix metalloproteinase-2 in patients with hypertrophic cardiomyopathy with systolic

Yoshihiro Noji1, Masami Shimizu, Hidekazu Ino

  • 1Molecular Genetics of Cardiovascular Disorders, Division of Cardiovascular Medicine, Graduate School of Medical Science, Kanazawa University, Japan.

Insights

Matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of metalloproteinase-2 (TIMP-2) levels are elevated in hypertrophic cardiomyopathy (HCM) patients with systolic dysfunction, indicating their role in cardiac remodeling.

Area of Science:

  • Cardiology
  • Biochemistry
  • Molecular Biology

Background:

  • Hypertrophic cardiomyopathy (HCM) can lead to left ventricular (LV) wall thinning, dilatation, and systolic dysfunction.
  • Matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs) are implicated in ventricular remodeling.
  • Limited information exists on MMPs and TIMPs in HCM patients.

Purpose of the Study:

  • To investigate the plasma concentrations of MMP-2, MMP-3, MMP-9, TIMP-1, and TIMP-2 in HCM patients.
  • To correlate these levels with systolic function and LV dimensions.
  • To explore the potential role of MMPs and TIMPs in HCM-related cardiac remodeling.

Main Methods:

  • Enzyme-linked immunoassays were used to measure plasma concentrations.
  • Study groups included HCM patients with systolic dysfunction (Group A), HCM patients with preserved systolic function (Group B), and healthy controls.
  • Measurements included MMP-2, MMP-3, MMP-9, TIMP-1, and TIMP-2.

Main Results:

  • MMP-2 and TIMP-2 concentrations were significantly higher in Group A (systolic dysfunction) compared to Group B and controls.
  • MMP-2 levels increased with worsening New York Heart Association functional class.
  • MMP-2 and TIMP-2 showed significant negative and positive correlations with fractional shortening (FS), respectively, and with LV dimension.

Conclusions:

  • Elevated MMP-2 and TIMP-2 levels are associated with systolic dysfunction in HCM.
  • These findings suggest MMP-2 and TIMP-2 play a role in the cardiac remodeling process in HCM.
  • Further research into MMP-2 and TIMP-2 mechanisms in HCM is warranted.
Abstract

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