Cardiac microinjury measured by troponin T predicts collagen metabolism in adults aged >=65 years with heart failure.
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.


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.
Department of Medicine/Cardiology, University of Maryland, Baltimore, MD, USA. w.j.kop@tilburguniversity.edu
Willem J
WJ
Kop
John S
JS
Gottdiener
Christopher R
CR
deFilippi
Eddy
E
Barasch
Stephen L
SL
Seliger
Nancy S
NS
Jenny
Robert H
RH
Christenson
D000367:Age Factors; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D003094:Collagen / Q000378:metabolism*; D024042:Collagen Type I / Q000097:blood; D005260:Female; D005355:Fibrosis; D006333:Heart Failure / Q000097:blood / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D016014:Linear Models; D008137:Longitudinal Studies; D008297:Male; D015999:Multivariate Analysis; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D010446:Peptide Fragments / Q000097:blood; D010455:Peptides / Q000097:blood; D011237:Predictive Value of Tests; D011347:Procollagen / Q000097:blood; D011446:Prospective Studies; D018570:Risk Assessment; D012307:Risk Factors; D013997:Time Factors; D020107:Troponin T / Q000097:blood*; D015854:Up-Regulation
D015415:Biomarkers; D024042:Collagen Type I; D010446:Peptide Fragments; D010455:Peptides; D011347:Procollagen; C545568:TNNT2 protein, human; D020107:Troponin T; C052929:collagen type I trimeric cross-linked peptide; C041876:procollagen Type III-N-terminal peptide; C042813:procollagen type I carboxy terminal peptide; D003094:Collagen