Introduction: Cardiac biomarker profile is a well-known predictor of myocardial infarct size, left ventricular dysfunction and major cardiovascular adverse events. However, the impact of previous chronic beta-blocker treatment on cardiac biomarker profile determined at presentation and during hospitalization for acute myocardial infarction (AMI) treated by percuta-neous coronary intervention (PCI) is uncertain.
Objective: The purpose was to determine whether previous chronic beta-blocker treatment influences cardiac biomarker profile in patients with AMI treated by PCI.
Methods: Data from consecutive patients admitted for AMI treated by PCI at a tertiary care cardiovascular center was retrospectively reviewed. Cardiac biomarker profile was assessed by analyzing serum cardiac troponin I (cTnI), creatine kinase (CK) and creatine kinase-MB (CK-MB) levels determined at presentati-on at the emergency department and during hospital admission. Cardiac biomarker profile was compared between patients with and without previous chronic beta-blocker treatment.
Results: A total number of 177 patients were inclu-ded, of which 48 (27.11%) had previous chronic beta-blocker treatment. Patients with previous beta-blocker therapy had significantly slower increase in cTnI (176.5 1 vs. 564.5 ± 625 ng/l/hour, p= 0.04) and CK-MB (2.51 ± 3.01 vs. 11.31 ± 20.85 ng/ml/hour, p= 0.02) le-vels, as well as significantly lower peak CK (720 ± 1006 vs. 1815 ± 1983 U/l, p< 0.001) and peak CK-MB levels (101 ± 141 vs. 365 ± 586 U/l, p< 0.01). Patients with previous beta-blocker therapy had slower increase in myoglobin, although not statistically significant (58.9 80 vs. 108.5 ± 147.7 ng/ml/hour, p= 0.10). In mul-tivariate binary logistic regression analysis of peak se-rum CK-MB, beta-blocker therapy was an independent predictor of cardiac biomarker kinetics (OR= 0.30, 95%CI= 0.12-0.75, P= 0.01), along with ST-elevation AMI type (OR= 9.20 95%CI= 3.54-24, P= 0.001).
Conclusions: Previous chronic beta-blocker treatment appears to limit myocardial infarction size as reflected by slower increase and lower peak values of cardiac biomarkers in AMI patients treated by percutaneous coronary intervention.
Funding: This study was funded by the Romanian Academy of Medical Sciences and European Regional Development Fund, MySMIS 107124: Funding Contract 2/Axa 1/31.07.2017/ 107124 SMIS. The funding source had no role in the collection, analysis, and interpretation of data, in the writing of the report, or in the decision to submit the article for publication.