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Elevated serum markers for collagen synthesis in patients with hypertrophic cardiomyopathy and diastolic dysfunction

M Fassbach1, B Schwartzkopff

  • 1Dept. of Cardiology, Angiology and Pneumology, Heinrich-Heine-University Düsseldorf, Moorenstrasse 5, 40225 Düsseldorf, Germany.

Zeitschrift Fur Kardiologie
|May 4, 2005
PubMed

Insights

In hypertrophic cardiomyopathy (HCM), elevated collagen synthesis markers and increased collagenolysis inhibition indicate fibrosis, explaining diastolic dysfunction. This study measured serum markers to understand collagen metabolism in HCM patients.

Area of Science:

  • Cardiovascular Medicine
  • Biochemistry
  • Pathophysiology

Background:

  • Hypertrophic cardiomyopathy (HCM) is a prevalent condition with diverse clinical presentations.
  • Left ventricular hypertrophy and elevated intramyocardial collagen contribute to diastolic dysfunction in HCM.

Purpose of the Study:

  • To investigate the hypothesis of impaired collagenolysis in patients with HCM.
  • To measure serum markers of type-I collagen metabolism.
  • To correlate these markers with echocardiographic parameters of diastolic function.

Main Methods:

  • Serum levels of matrix metalloproteinase-1 (MMP-1), its inhibitor TIMP-1, and collagen type-I markers (PICP, ICTP) were measured in 26 HCM patients and 38 controls.
  • Assays used included ELISA and RIA.
  • Diastolic function was assessed using Doppler echocardiography.

Main Results:

  • Elevated free TIMP-1 and PICP levels were observed in HCM patients compared to controls.
  • Free MMP-1 was significantly lower in HCM patients.
  • The MMP-1/TIMP-1 ratio was reduced in HCM, suggesting inhibited collagenolysis. PICP correlated with diastolic E/A ratio and septal thickness.

Conclusions:

  • Increased serum PICP indicates heightened collagen synthesis in HCM.
  • Elevated TIMP-1 and a reduced MMP-1/TIMP-1 ratio suggest inhibited collagenolysis and collagen accumulation (fibrosis).
  • This collagen accumulation likely explains the passive diastolic dysfunction observed in HCM patients.
Abstract

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