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1 Department of Internal Medicine, Kuopio University Hospital, Kuopio, Finland
2 Department of Clinical Chemistry, Kuopio University Hospital, Kuopio, Finland
3 Department of Internal Medicine, Oulu University Hospital, Oulu, Finland
4 Department of Clinical Chemistry, Kuopio University Hospital, Kuopio, Finland; Department of Clinical Chemistry, Oulu University Hospital, Oulu, Finland
5 Department of Physiology, University of Oulu, Oulu, Finland
6 Department of Pharmacology and Toxicology, University of Oulu, Oulu, Finland
* To whom correspondence should be addressed. E-mail: Keijo.Peuhkurinen{at}kuh.fi.
Experimental data suggests that atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) act locally as antifibrotic factors in heart. We investigated the interrelationships of natriuretic peptides and collagen markers in 93 patients receiving thrombolytic treatment for their first acute myocardial infarction (AMI). Collagen formation following AMI, evaluated as serum levels of aminoterminal propeptide of type III procollagen (PIIINP), correlated with N-terminal proANP (r = 0.45, p < 0.001), BNP (r = 0.55, p < 0.001) and N-terminal proBNP (NT-proBNP) (r = 0.50, p < 0.001) on day four following thrombolysis. Levels of intact aminoterminal propeptide of type I procollagen decreased by 34 % (p<0.001) and levels of carboxyterminal cross-linked telopeptide of type I collagen (ICTP) increased by 65 % (p<0.001). ICTP levels correlated with NT-proBNP (r=0.26, p<0.05) and BNP (r=0.28, p<0.05) on day four. Our results suggest that ANP and BNP may act as regulators of collagen scar formation and left ventricular remodeling after AMI in humans. Furthermore, degradation of type I collagen is increased after AMI and may be regulated by BNP.
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