Key result
Increases in cTnT over 3 years were associated with higher levels of carboxyterminal telopeptide of type I collagen (β=0.22, P<0.001) and aminoterminal propeptide of procollagen III (β=0.12, P=0.035).
Why the study?
Do increases in highly sensitive cardiac troponin T (cTnT) over 3 years predict higher levels of collagen metabolism biomarkers in older adults?
Cohort (n=353)
Do increases in highly sensitive cardiac troponin T (cTnT) over 3 years predict higher levels of collagen metabolism biomarkers in older adults?
Effect estimate: β=0.22 and β=0.12
p-value: p=<0.001 and 0.035
Increases in myocardial microinjury, as measured by rising cTnT over 3 years, are associated with elevated markers of collagen metabolism, highlighting a potential mechanism for myocardial fibrosis and heart failure progression.
Rising cTnT may mark collagen turnover in older adults; hypothesis-generating and should not yet change practice.
BACKGROUND: Repeated myocardial microinjuries lead to collagen deposition and fibrosis, thereby increasing the risk of clinical heart failure. Little is known about the longitudinal association between increases in myocardial injury and the biology of collagen synthesis and deposition. METHODS AND RESULTS: Repeated measures of highly sensitive cardiac troponin T (cTnT) were obtained in participants of the Cardiovascular Health Study (N=353; mean age, 74±6 years; 52% women) at baseline and at 3 years follow-up. Biomarkers of collagen metabolism were obtained at follow-up and included carboxyterminal propeptide of procollagen type I, carboxyterminal telopeptide of type I collagen, and aminoterminal propeptide of procollagen III. Multivariable linear regression analyses were used to examine the association between baseline cTnT and changes in cTnT with collagen metabolism markers at follow-up adjusting for demographics, heart failure status, and cardiovascular risk factors. Results indicated that cTnT increases over 3-years were significantly associated with higher levels of carboxyterminal telopeptide of type I collagen (β=0.22, P<0.001) and aminoterminal propeptide of procollagen III (β=0.12, P=0.035) at follow-up when adjusting for demographic, clinical, and biochemical covariates including baseline cTnT. These associations were stronger in patients with heart failure than in control subjects. Conclusions- Increases in myocardial microinjury measured by changes in cTnT adversely affect markers of collagen metabolism. These findings are important to the biology of myocardial fibrosis and tissue repair. Serial evaluation of cTnT combined with collagen metabolism markers may further elucidate the pathophysiology of heart failure.
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Kop et al. (2012) conducted a cohort in Heart failure (n=353). Increases in highly sensitive cardiac troponin T (cTnT) was evaluated on Levels of carboxyterminal telopeptide of type I collagen and aminoterminal propeptide of procollagen III at follow-up (β=0.22 and β=0.12, p=<0.001 and 0.035). Increases in cTnT over 3 years were associated with higher levels of carboxyterminal telopeptide of type I collagen (β=0.22, P<0.001) and aminoterminal propeptide of procollagen III (β=0.12, P=0.035).
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