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[Collagen synthesis and heart failure].

Manuel F Jiménez-Navarro1, Juan J Gómez-Doblas, Fernando Cabrera-Bueno

  • 1Servicio de Cardiología, Hospital Clínico Universitario Virgen de la Victoria, Málaga, Spain. jimeneznavarro@secardiologia.es

Revista Espanola De Cardiologia
|August 2, 2005
PubMed
Summary

Heart failure patients show increased collagen type I synthesis (PIP) but not degradation (ICTP). Left ventricular systolic function did not significantly impact these collagen markers in heart failure.

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Area of Science:

  • Cardiology
  • Biochemistry
  • Pathophysiology

Background:

  • Collagen metabolism's role in heart failure is poorly understood.
  • Assessing collagen synthesis and degradation markers is crucial for understanding cardiac remodeling.

Purpose of the Study:

  • To investigate collagen type I metabolism in patients with heart failure.
  • To compare collagen markers between heart failure patients and controls.
  • To evaluate the influence of left ventricular systolic function on collagen markers.

Main Methods:

  • Serum concentrations of carboxy-terminal propeptide of procollagen type I (PIP) and carboxy-terminal telopeptide of collagen type I (ICTP) were measured.
  • 70 heart failure patients (with and without systolic dysfunction) and 30 controls were studied.

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  • Exclusion criteria included kidney/liver disease, bone/rheumatic disease, trauma, surgery, or wounds.

    • Main Results:

    • PIP, a collagen synthesis marker, was significantly higher in heart failure patients (140±56.38 mg/L) versus controls (113.66±36.6 μg/L; P=.01).
    • ICTP, a collagen degradation marker, showed no significant difference between heart failure patients (2.89±2.37 mg/L) and controls (2.26±1.7 μg/L).
    • Left ventricular systolic function did not significantly affect PIP or ICTP levels in heart failure patients.

    Conclusions:

    • Heart failure is associated with increased collagen type I synthesis.
    • Collagen type I degradation does not appear altered in heart failure.
    • Collagen metabolism markers warrant further investigation in heart failure pathophysiology.