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Published on: January 28, 2020
Serological evidence of early remodeling in high-risk non-ST elevation acute coronary syndromes
Andrew D McGavigan1, Paul R Maxwell, Francis G Dunn
1Department of Cardiology, Glasgow Royal Infirmary, Glasgow G4 0SF, United Kingdom. amcgav@hotmail.com
Insights
High-risk acute coronary syndrome (ACS) shows altered collagen metabolism, unlike low-risk ACS. These findings suggest collagen markers may aid in risk stratification for non-ST elevation ACS patients.
Area of Science:
- Cardiology
- Biochemistry
- Pathology
Background:
- Non-ST elevation acute coronary syndrome (ACS) presents a risk spectrum, with ECG changes and elevated troponin indicating higher morbidity and mortality.
- Ischemia can alter cardiac collagen, even without myocyte necrosis.
- Collagen turnover markers include C-propeptide for type I collagen (PICP) for synthesis and C-telopeptide for type I collagen (CITP) for degradation; tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) indicates degradation inhibition.
Purpose of the Study:
- To investigate collagen metabolism alterations in patients with non-ST elevation ACS.
- To assess if collagen turnover markers can differentiate between high- and low-risk ACS patients.
- To explore the potential of these markers in risk stratification for ACS.
Main Methods:
- Fifty-two patients with non-ST elevation ACS were divided into high- and low-risk groups based on ECG and troponin levels.
- Sequential plasma measurements of PICP, CITP, and TIMP-1 were taken over 48 hours.
- Statistical analysis compared marker levels between risk groups and over time.
Main Results:
- High-risk patients (32) had higher admission CITP (3.7 vs. 2.6 ng/ml, p<0.001) and a further rise over 48 hours, unlike low-risk patients (20).
- Admission TIMP-1 was higher in the high-risk group (302 vs. 221 ng/ml, p<0.01) and showed sequential changes over time only in this group.
- PICP levels remained within the normal range in both groups throughout the study period.
Conclusions:
- Serological evidence indicates time-dependent altered collagen metabolism in high-risk ACS patients, absent in the low-risk group.
- These collagen alterations may reflect cardiac remodeling processes.
- Biochemical markers of collagen metabolism could potentially aid in the risk stratification of non-ST elevation ACS.
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.
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