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Introduction: 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)., Discussion: 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.

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.

Background: Studies on exercise-induced left ventricular hypertrophy (LVH) in veteran athletes suggest the presence of abnormal diastolic filling and incomplete regression of LVH on cessation of exercise. Hypothesis: Myocardial fibrosis occurs in exercise induced LVH in veteran athletes. Aim: To document non-invasively the presence of fibrosis in veteran athletes Design: Prospective case-control study. Setting: City centre district general hospital. Participants: 45 normotensive elite veteran athletes and 45 normal sedentary subjects. Interventions: Echocardiographic assessment was made of LV mass, LV systolic and LV diastolic function. Plasma carboxyterminal propeptide of collagen type I (PICP), carboxyterminal telopeptide of collagen type I (CITP) and tissue inhibitor of matrix metalloproteinase type I (TIMP-1) were measured as markers of collagen synthesis, degradation and inhibition of degradation, respectively. Results: Veteran athletes had significant elevation in LV dimensions and calculated LV mass index (LVMI). Diastolic and systolic function was normal. Plasma PICP (259 vs 166 μg/l, p<0.001), ClTP (5.4 vs 2.9 μg/I, p<0.001) and TIMP-1 (350 vs 253 ng/ml, p=0.01) were elevated in the cohort of athletes. There was a further elevation of TIMP-1 in athletes with echocardiographic LVH, defined as an LVMI >130 g/m² (417 vs 266 ng/ml, p=0.02). Conclusion: There is biochemical evidence of disruption of the collagen equilibrium favouring fibrosis in veteran athletes with LVH. This may suggest that fibrosis occurs as part of the hypertrophic process in veteran athletes. [ABSTRACT FROM AUTHOR]