title: Serological evidence of early remodeling in high-risk non-ST elevation acute coronary syndromes.
abstract: BACKGROUND
  Non-ST elevation acute coronary syndrome (ACS) represents a spectrum of risk, with electrocardiographic (ECG) changes and a positive troponin being associated with higher morbidity and mortality. Ischaemia produces alterations in the collagenous component of the heart, even in the absence of myocyte necrosis. Collagen turnover can be assessed biochemically with C-propeptide for type I collagen (PICP) and C-telopeptide for type I collagen (CITP) being markers of collagen synthesis and degradation respectively. Tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) is a marker of inhibition of degradation.
  
  
  METHODS
  Fifty-two patients with non-ST elevation acute ACS were recruited and dichotomised into high- and low-risk groups based on ECG and troponin level. Sequential measurements of plasma PICP, CITP and TIMP-1 were performed over a 48 hour period.
  
  
  RESULTS
  Twenty were classified as low-risk (negative troponin and normal ECG) and 32 as high-risk. PICP was within the normal range at all time points in both groups. However, admission CITP was higher in the high-risk group (3.7 vs. 2.6 ng/ml, p<0.001) and, unlike the low-risk group, demonstrated a further rise over 48 h. Similarly, mean TIMP-1 displayed a sequential change over time in the high-risk group only, and admission level was higher compared to the low-risk group (302 vs. 221 ng/ml, p<0.01).
  
  
  CONCLUSIONS
  There is serological evidence of time-dependent altered collagen metabolism in high-risk ACS, which is not present in the low-risk group. This may reflect a degree of remodeling and may aid risk stratification of patients presenting with non-ST elevation ACS.
authors: Department of Cardiology, Glasgow Royal Infirmary, Glasgow G4 0SF, United Kingdom. amcgav@hotmail.com
authors: Andrew D
authors: AD
authors: McGavigan
authors: Paul R
authors: PR
authors: Maxwell
authors: Francis G
authors: FG
authors: Dunn
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood / Q000175:diagnosis* / Q000378:metabolism* / Q000503:physiopathology; D000208:Acute Disease; D015415:Biomarkers / Q000097:blood; D003094:Collagen / Q000378:metabolism*; D024042:Collagen Type I / Q000097:blood; D004562:Electrocardiography; D005260:Female; D006329:Heart Conduction System / Q000503:physiopathology*; D006801:Humans; D008297:Male; D020781:Matrix Metalloproteinase 1 / Q000097:blood*; D008875:Middle Aged; D010446:Peptide Fragments / Q000097:blood; D010455:Peptides / Q000097:blood; D011347:Procollagen / Q000097:blood; D011446:Prospective Studies; D018570:Risk Assessment; D013997:Time Factors; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000097:blood; D014336:Troponin / Q000097:blood*
chemical_list: D015415:Biomarkers; D024042:Collagen Type I; D010446:Peptide Fragments; D010455:Peptides; D011347:Procollagen; D019715:Tissue Inhibitor of Metalloproteinase-1; D014336:Troponin; C052929:collagen type I trimeric cross-linked peptide; C042813:procollagen type I carboxy terminal peptide; D003094:Collagen; D020781:Matrix Metalloproteinase 1