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Residual stress ischaemia is associated with blood markers of myocardial structural remodelling

Anca Radauceanu1, Frédéric Moulin, Wassila Djaballah

  • 1Centre d'Investigation Clinique (CIC) CHU-INSERM, Nancy, France.

European Journal of Heart Failure
|December 5, 2006
PubMed

Insights

Persistent stress ischemia in coronary artery disease (CAD) patients is linked to increased collagen-III turnover, even with normal heart function. This may indicate future adverse cardiac remodeling.

Area of Science:

  • Cardiology
  • Biochemistry
  • Medical Diagnostics

Background:

  • Long-term prognosis for coronary artery disease (CAD) patients is negatively impacted by persistent stress ischemia.
  • The association between persistent stress ischemia and adverse cardiac remodeling has not been previously investigated.

Purpose of the Study:

  • To investigate changes in blood markers of fibrosis in patients with chronic CAD who exhibit exercise-induced ischemia.
  • To explore the relationship between collagen turnover and cardiac remodeling markers in CAD patients.

Main Methods:

  • Blood samples were collected from 139 CAD patients undergoing exercise 201Tl-SPECT.
  • Circulating markers of collagen turnover (amino-terminal propeptide of collagen-III [PIIINP]) and degradation (matrix metalloproteinase 1 [MMP-1]) were measured.

Main Results:

  • Patients with SPECT-identified ischemia showed higher PIIINP and lower MMP-1 levels compared to those without ischemia.
  • PIIINP levels were independently associated with left ventricular (LV) volume, ischemia, and age.
  • In patients with normal LV ejection fraction, PIIINP remained significantly related to SPECT-ischaemia.

Conclusions:

  • Exercise-induced ischemia in chronic CAD patients is associated with elevated collagen-III turnover.
  • This collagen turnover is independent of medications and normal LV ejection fraction.
  • Increased collagen turnover may predict future adverse cardiac remodeling, even before overt cardiac dysfunction is apparent.
Abstract

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