Relation of high concentrations of plasma carboxy-terminal telopeptide of collagen type I with outcome in acute myocardial infarction.

Acute myocardial infarction (AMI) is associated with matrix metalloproteinase activation. The plasma concentrations of carboxy-terminal telopeptide of collagen type I (CITP) reflect collagen type I degradation due to matrix metalloproteinase activation. We assessed the role of CITP as an early marker of outcome in AMI. Plasma CITP was measured 72 hours after hospital admission in 432 patients presenting with AMI. The 2 composite end points of the study (death, resuscitated cardiac arrest, recurrent AMI or ischemia, and heart failure or stroke; and death, resuscitated cardiac arrest, or heart failure) and mortality were assessed at 1 year in 4 patient groups stratified by the CITP quartiles. Patients with ST-segment elevation MI represented 75.7% of the population. In-hospital percutaneous coronary intervention was performed in 70.4% of the patients. The mean left ventricular ejection fraction was 53.9 +/- 12.5%. At 1 year of follow-up, high levels of CITP were associated with the occurrence of both composite end points and mortality (p <0.01 for all). Stepwise logistic regression analysis identified CITP as an independent predictor of both composite end points (odds ratio 2.14, 95% confidence interval 1.34 to 3.42, p = 0.001; and odds ratio 3.19, 95% confidence interval 1.50 to 6.81, p = 0.003), along with the Killip class and brain natriuretic peptide levels. In conclusion, high hospital levels of CITP, a marker of collagen degradation and ventricular remodeling, are associated with late mortality and other serious clinical events after AMI.