Serological evidence of altered collagen homeostasis reflects early ventricular remodeling following acute myocardial infarction

Background Infarct expansion characterises early ventricular remodeling following myocardial infarction (AMI) and is a product of the balance between collagen degradation and synthesis. Serological markers of collagen turnover may help in predicting those at risk of remodeling. C-propeptide for type-I collagen (PICP) and C-telopeptide for type-I collagen (CITP) are markers of collagen synthesis and degradation, respectively. Methods Fifty-one patients with AMI were recruited and dichotomised by echocardiographic wall motion index (WMI). Sequential measurements of plasma PICP and CITP were correlated to this and other echocardiographic variables of remodeling. Results Twenty-three normal WMI, 28 abnormal WMI. Both groups showed increases in PICP and CITP over time. However, mean admission CITP higher in abnormal WMI group, 4.5 vs. 3.1 ng/ml (p < 0.05) as was peak, 6.3 vs. 4.8 ng/ml (p < 0.05). Conversely, admission PICP was lower in abnormal WMI group 114 vs. 143 ng/ml (p < 0.05). Admission CITP correlated with WMI, r = 0.53, p < 0.001. CITP > 3.2 ng/ml (normal mean + 2S.D.) had 74% positive predictive value for abnormal WMI, negative predictive value 65%. Admission CITP negatively correlated with mitral deceleration time (Dt), r = − 0.38, p = 0.01. CITP > 3.2 was associated with lower Dt—183 vs. 221 ms, p < 0.05. Conclusion There is serological evidence of sequential increases in both collagen synthesis and degradation following AMI. However, the balance between these differs in patients who undergo remodeling, manifested by abnormal WMI and reduced Dt, compared to those with no evidence. They have relatively increased degradation and reduced synthesis, favouring net collagen breakdown. These changes occur early with evidence of increased breakdown on admission predicting early remodeling and support the role of serological markers to identify patients at risk of this.