Key result
Prolonged beta-blocker therapy fails to alter circulating PICP levels following myocardial infarction.
Why the study?
Beta-blockers reduce heart failure progression after MI with reduced ejection fraction, but their use and effects on fibrosis in MI patients with preserved or mildly reduced ejection fraction without heart failure are debated.
Does prolonged beta-blocker treatment affect circulating levels of fibrillar collagen peptides (PICP) in myocardial infarction patients without heart failure (EF >= 40%)?
RCT (n=490)
Randomized
Yes
Does prolonged beta-blocker treatment affect circulating levels of fibrillar collagen peptides (PICP) in myocardial infarction patients without heart failure (EF >= 40%)?
Six months of beta-blocker therapy did not affect circulating PICP levels in post-MI patients with preserved or mildly reduced ejection fraction, providing a mechanistic correlate to the neutral clinical effects of prolonged beta-blocker use in this population.
Beta-blockers do not alter post-MI PICP levels; confirms neutral clinical effects and collagen turnover in preserved EF.
Background Myocardial infarction (MI) is caused by ischemia, leading to irreversible myocardial injury, chronic inflammation and collagenous scarring, i.e., fibrosis. Beta-blockers (BB) reduce the risk of heart failure progression in MI patients with reduced ejection fraction (EF), however their use and effects in patients with preserved (pEF) or mildly reduced (mrEF) EF is debated. Purpose To evaluate circulating levels of fibrillar collagen peptides in MI patients without heart failure, randomized to prolonged use of BB or not. Methods The BETAMI-DANBLOCK trial (beta blockers after myocardial infarction in patients without heart failure) randomized patients with MI and EF≥ 40% to BBs or not. Patients (n= 5574) were followed for 3.5 years for clinical endpoints. The biobank consisted of n=490 participants (median age 61, 19% women) recruited at four sites in Norway within 7 days of the index event, where n=65 had a primary endpoint. Procollagen has peptides at amino and carboxy termini that are cleaved off by proteases prior to fibril incorporation. They can reach the circulation, e.g. type I collagen C-terminal propeptide (PICP), which provides a stoichiometric representation of collagen type I synthesis. PICP was measured by ELISA (Microvue) in serum at baseline (n=436) and after six months (n=343). Cox proportional hazards regression was used to analyze time to primary composite endpoint, i.e., all-cause death and recurrent cardiovascular event. Results Median (IQR) of PICP was 76 (62, 100) ng/mL at baseline and increased to 97 (77, 126) ng/mL after six months (p<0.001). Baseline PICP was higher in those with age>median vs. those Conclusion Circulating levels of PICP were lower 7 days and 6 months post-MI, in EF≥ 40% patients with a primary endpoint, suggestive of an impaired fibrotic response. PICP levels were unaffected by 6 months of BB treatment. A recent meta-analysis incorporating BETAMI-DANBLOCK reported neutral effects of prolonged BB therapy in MI patients with preserved EF, and our data provide a mechanistic correlate to this conclusion.
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Lunde et al. (2026) conducted an RCT in Myocardial infarction without heart failure (EF ≥40%) (n=490). Beta-blocker therapy vs. No beta-blocker therapy was evaluated on Circulating type I collagen C-terminal propeptide (PICP) levels and primary composite endpoint of all-cause death and recurrent cardiovascular event (p=<0.001). Beta-blocker treatment for 6 months did not affect circulating PICP levels post-MI, which rose from 76 to 97 ng/mL overall (p<0.001) and were lower in patients with clinical events.
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