Procollagen type 1 N-terminal propeptide is associated with adverse outcome in acute chest pain of suspected coronary origin

Front Cardiovasc Med. 2023 Sep 4:10:1191055. doi: 10.3389/fcvm.2023.1191055. eCollection 2023.

Abstract

Background: Extracellular matrix (ECM) is an integral player in the pathophysiology of a variety of cardiac diseases. Cardiac ECM is composed mainly of collagen, of which type 1 is the most abundant with procollagen type 1 N-terminal Propeptide (P1NP) as a formation marker. P1NP is associated with mortality in the general population, however, its role in myocardial infarction (MI) is still uncertain, and P1NP has not been investigated in acute chest pain. The objective of the current study was to assess the role of P1NP in undifferentiated acute chest pain of suspected coronary origin.

Methods and results: 813 patients from the Risk in Acute Coronary Syndromes study were included. This was a single-center study investigating biomarkers in consecutively enrolled patients with acute chest pain of suspected coronary origin, with a follow-up for up to 7 years. Outcome measures were a composite endpoint of all-cause death, new MI or stroke, as well as its individual components at 1, 2, and 7 years, and cardiac death at 1 and 2 years. In multivariable Cox regression analysis, quartiles of P1NP were significantly associated with the composite endpoint at 1 year of follow-up with a hazard ratio for Q4 of 1.82 (95% CI, 1.12-2.98). There was no other significant association with outcomes at any time points.

Conclusion: P1NP was found to be an independent biomarker significantly associated with adverse clinical outcome at one year in patients admitted to hospital for acute chest pain of suspected coronary origin. This is the first report in the literature on the prognostic value of P1NP in this clinical setting.

Clinicaltrialsygov identifier: NCT00521976.

Keywords: acute coronary syndromes; biomarkers; collagen; extracellular matrix; mortality/survival; risk factors.

Associated data

  • ClinicalTrials.gov/NCT00521976

Grants and funding

This study was funded through a personal research grant to TA from Helse Vest, grant number 912294. Laboratory analyses for this study are in part funded through project funding from Stavanger Universitetssjukehus, grant number 501814.