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Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
Published on: May 28, 2019
The cardioprotection granted by metoprolol is restricted to its administration prior to coronary reperfusion
Borja Ibanez1, Giovanni Cimmino, Susanna Prat-González
1Atherothrombosis Research Unit, Mount Sinai School of Medicine, New York, NY, USA.
Insights
Intravenous metoprolol before reperfusion significantly increased myocardial salvage compared to oral metoprolol after reperfusion. This finding suggests optimizing beta-blocker timing and route may improve outcomes in myocardial infarction.
Area of Science:
- Cardiology
- Pharmacology
- Biomedical Engineering
Background:
- Myocardial infarct size predicts cardiovascular events.
- Intravenous metoprolol before reperfusion reduces infarct size.
- The cardioprotective effect of early oral metoprolol post-reperfusion is unclear.
Purpose of the Study:
- Compare myocardial salvage with pre-reperfusion intravenous metoprolol versus post-reperfusion oral metoprolol or placebo.
- Investigate the impact on reperfusion injury markers.
Main Methods:
- Thirty Yorkshire pigs with reperfused myocardial infarction were randomized.
- Groups received pre-reperfusion intravenous metoprolol, post-reperfusion oral metoprolol, or placebo.
- Cardiac MRI quantified salvaged myocardium; post-mortem analysis assessed reperfusion injury.
Main Results:
- Pre-reperfusion metoprolol yielded significantly larger myocardial salvage (31%) compared to post-reperfusion metoprolol (13%) or placebo (7%).
- Pre-reperfusion metoprolol showed reduced reperfusion injury markers (neutrophil infiltration, apoptosis) and increased phospho-Akt.
- Significant differences were observed between the pre-reperfusion group and the other two groups.
Conclusions:
- Intravenous metoprolol before reperfusion is more effective for myocardial salvage than oral metoprolol initiated early after reperfusion.
- Clinical guidelines on beta-blocker timing and route may need revision.
- Further clinical studies are warranted to confirm these findings.
Background:
Myocardial infarct size is a strong predictor of cardiovascular events. Intravenous metoprolol before coronary reperfusion has been shown to reduce infarct size; however, it is unknown whether oral metoprolol initiated early after reperfusion, as clinical guidelines recommend, is similarly cardioprotective. We compared the extent of myocardial salvage associated with intravenous pre-reperfusion-metoprolol administration in comparison with oral post-reperfusion-metoprolol or placebo. We also studied the effect on suspected markers of reperfusion injury.
Methods:
Thirty Yorkshire-pigs underwent a reperfused myocardial infarction, being randomized to pre-reperfusion-metoprolol, post-reperfusion-metoprolol or placebo. Cardiac magnetic resonance imaging was performed in eighteen pigs at day 3 for the quantification of salvaged myocardium. The amounts of at-risk and infarcted myocardium were quantified using T2-weighted and post-contrast delayed enhancement imaging, respectively. Twelve animals were sacrificed after 24h for reperfusion injury analysis.
Results:
The pre-reperfusion-metoprolol group had significantly larger salvaged myocardium than the post-reperfusion-metoprolol or the placebo groups (31 ± 4%, 13 ± 6%, and 7 ± 3% of myocardium at-risk respectively). Post-mortem analyses suggest lesser myocardial reperfusion injury in the pre-reperfusion-metoprolol in comparison with the other 2 groups (lower neutrophil infiltration, decreased myocardial apoptosis, and higher activation of the salvage-kinase phospho-Akt). Salvaged myocardium and reperfusion injury pair wise comparisons proved there were significant differences between the pre-reperfusion-metoprolol and the other 2 groups, but not among the latter two.
Conclusions:
The intravenous administration of metoprolol before coronary reperfusion results in larger myocardial salvage than its oral administration initiated early after reperfusion. If confirmed in the clinical setting, the timing and route of β-blocker initiation could be revisited.
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