title: Residual stress ischaemia is associated with blood markers of myocardial structural remodelling.
abstract: BACKGROUND
  Long-term prognosis of coronary artery disease (CAD) patients is worsened when stress ischemia persists on treatment, but the relationship with adverse cardiac remodelling had never been investigated.
  
  
  OBJECTIVE
  To analyze changes in blood markers of fibrosis in patients with chronic CAD exhibiting exercise ischaemia.
  
  
  METHODS
  Circulating markers of collagen: (i) turnover (amino-terminal propeptide of collagen-III [PIIINP]) and (ii) degradation (matrix metalloproteinase 1 [MMP-1]), were obtained in 139 CAD patients referred for exercise 201Tl-SPECT.
  
  
  RESULTS
  In the 57 patients who had SPECT-ischaemia, PIIINP was higher (4.3+/-2.9 microg L-1 vs. 3.1+/-1.5 microg L-1, p=0.002) and MMP-1 lower (3.8+/-2.1 microg L-1 vs. 4.7+/-2.8 microg L-1, p=0.04) than in the 82 patients without SPECT-ischaemia. PIIINP was independently related to LV volume, SPECT-ischaemia and age, whereas MMP-1 was related to current treatment with ACEI and beta-blockers (p<0.05). In the 104 patients with a normal LV ejection fraction, only PIIINP was related to SPECT-ischaemia (4.1+/-2.2 microg L-1 vs. 3.1+/-1.5 microg L-1, p=0.01).
  
  
  CONCLUSIONS
  In patients with chronic CAD, exercise ischaemia is associated with increased collagen-III turnover, independently of concomitant medications and even when LV ejection fraction is normal. Long-term, this increase might relate to adverse cardiac remodelling even when cardiac function is not clearly affected at baseline.
authors.affiliation: Centre d'Investigation Clinique (CIC) CHU-INSERM, Nancy, France.
authors.forename: Anca
authors.initials: A
authors.lastname: Radauceanu
authors.forename: Frédéric
authors.initials: F
authors.lastname: Moulin
authors.forename: Wassila
authors.initials: W
authors.lastname: Djaballah
authors.forename: Pierre Y
authors.initials: PY
authors.lastname: Marie
authors.forename: François
authors.initials: F
authors.lastname: Alla
authors.forename: Brigitte
authors.initials: B
authors.lastname: Dousset
authors.forename: Jean M
authors.initials: JM
authors.lastname: Virion
authors.forename: Josette
authors.initials: J
authors.lastname: Capiaumont
authors.forename: Gilles
authors.initials: G
authors.lastname: Karcher
authors.forename: Etienne
authors.initials: E
authors.lastname: Aliot
authors.forename: Faïez
authors.initials: F
authors.lastname: Zannad
mesh_terms: D000222:Adaptation, Physiological; D015415:Biomarkers; D024061:Collagen Type III / Q000097:blood; D003324:Coronary Artery Disease / Q000097:blood / Q000150:complications*; D015444:Exercise / Q000502:physiology*; D005260:Female; D005355:Fibrosis / Q000503:physiopathology; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000097:blood / Q000209:etiology*; D009206:Myocardium; D018384:Oxidative Stress; D013318:Stroke Volume; D015899:Tomography, Emission-Computed, Single-Photon
chemical_list: D015415:Biomarkers; D024061:Collagen Type III