Related Experiment Video
Updated: Jul 15, 2026

Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
Published on: May 28, 2019
beta-blockers before percutaneous coronary intervention do not attenuate postprocedural creatine kinase isoenzyme
S G Ellis1, S J Brener, A M Lincoff
1Department of Cardiology, The Cleveland Clinic Foundation, Cleveland, Ohio, USA. elliss@ccf.org
Insights
Beta-blocker (BB) use before percutaneous coronary intervention (PCI) did not reduce myocardial injury, as measured by creatine kinase (CK) and CK-MB levels. This large observational study found no significant difference in cardiac enzyme elevation after risk adjustment.
Area of Science:
- Cardiology
- Clinical Research
- Pharmacology
Background:
- Beta-blocker (BB) use is known to reduce infarct size in nonreperfused myocardial infarctions.
- Its effect on infarct size in patients receiving reperfusion therapy, such as percutaneous coronary intervention (PCI), is less clear.
- Previous studies suggested BB use concurrent with PCI might decrease creatine kinase (CK)-MB elevation, but required robust risk adjustment.
Purpose of the Study:
- To evaluate the association between pre-PCI beta-blocker (BB) use and myocardial injury.
- To determine if BB use prior to PCI influences creatine kinase (CK) and CK-MB levels.
- To assess the impact of BBs on myocardial damage in patients undergoing PCI, accounting for baseline differences.
Main Methods:
- A large observational study analyzed 6200 consecutive patients undergoing PCI.
- Propensity score and multivariate regression analyses were employed to adjust for baseline differences between patients with and without BB treatment.
- Per-protocol measurements of creatine kinase (CK) and CK-MB were assessed in relation to BB use.
Main Results:
- Patients on BBs had significantly higher baseline levels of CK and CK-MB compared to those not on BBs.
- Despite higher baseline enzyme levels in the BB group, maximum CK and CK-MB levels were not significantly different between groups after adjustment.
- Statistical analysis showed no significant difference in maximum CK rise (P=0.21) or maximum CK-MB rise (P=0.99) between BB users and non-users.
Conclusions:
- This study's findings do not support the hypothesis that beta-blocker use before PCI reduces myocardial injury.
- The observed higher CK and CK-MB levels in BB users were likely due to baseline differences, not a direct effect of BBs on infarct size.
- Current evidence does not advocate for routine BB use prior to PCI to limit myocardial damage.
Background:
beta-blocker (BB) use reduces infarct size in spontaneously occurring nonreperfused infarcts but probably does not change infarct size in patients treated with reperfusion therapy. A recent observational study suggested that BB use concurrent with percutaneous coronary intervention (PCI) decreased the risk of creatine kinase (CK)-MB elevation. The cogency of such a conclusion is dependent on the ability to risk-adjust for the multiple differences in patients treated with and without BBs.
Methods And Results:
Using propensity score and multivariate regression analyses, 6200 consecutive patients were analyzed to assess the relationship between BB use before PCI and per protocol-measured CK and CK-MB rise. There were several highly significant (P<0.001) differences between patients with and without BB treatment (eg, age, prior infarction, unstable angina). Maximum CK and CK-MB levels were higher in patients taking BBs (CK median, 95 U [interquartile range: 61, 175]; CK-MB, 3 U [2, 5]) than in patients not taking BBs (CK, 91 U [60, 157]; CK-MB, 3 U [2, 4]) (P=0.011 and P=0.021 for CK and CK-MB, respectively). After adjustment for significant differences in baseline characteristics there was no difference in either maximum CK rise (P=0.21) or maximum CK-MB rise (P=0.99).
Conclusions:
The results of this large observation study do not support the contention that BB use before PCI decreases myocardial injury.
Related Concept Videos
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
Antianginal Drugs: Nitrates and β-Blockers
Organic nitrates, such as nitroglycerin, play a pivotal role. Once metabolized, they liberate nitric oxide, a molecular marvel. Nitric oxide triggers guanylyl cyclase and augments cGMP production. This biochemical cascade orchestrates the relaxation of vascular smooth muscles, ushering in vasodilation and enhancing coronary blood flow. Administered...
Antianginal Drugs: Calcium Channel Blockers and Ranolazine
CCBs, a diverse class that includes dihydropyridines (nifedipine) and diphenylalkylamines (verapamil and diltiazem), exert their effect by blocking calcium channels in cardiac and smooth muscle cells. This...
Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers
TKIs, such as imatinib (Gleevec), are particularly effective in tackling the growth and mitogenic factors that become upregulated in PAH patients. These factors contribute to the...
Blood Studies for Cardiovascular System I: Cardiac Biomarkers
The essential diagnostic tools for detecting myocardial necrosis and monitoring individuals suspected of having acute coronary syndrome (ACS) include:
Troponins
Troponins, particularly cardiac troponins I and T, are the most precise and sensitive markers of myocardial injury. They are detectable within 4-6 hours of myocardial injury and remain...
Acute Coronary Syndrome IV: Interprofessional Care

