9 ± 3
4, 5 Dual antiplatelet therapy is highly recommended in the treatment of STEMI to
Background: The effect of β-blockers on infarct size when used in conjunction with primary percutaneous coronary intervention is unknown
Administration of 15 mg intravenous (IV) metoprolol before reperfusion in STEMI patients undergoing PPCI was recently shown to reduce cardiac magnetic resonance (CMR)–measured infarct size in the METOCARD-CNIC (effect of METOprolol of CARDioproteCtioN during an acute myocardial InfarCtion) trial (6)
Off-label uses for the drug include treatment for migraine, cardiac arrhythmias, and essential tremors
2014; 63 (22):2356‐2362
The precise mechanism of action of Lopressor in patients with suspected or definite myocardial infarction is not known
2-mediated vasodilating effects of epinephrine
5% for metoprolol and carvedilol, respectively, with an unadjusted HR=0
Patients in the >12
Long-term treatment with metoprolol after myocardial infarction: effect on 3 year mortality and morbidity
Impact of the Timing of Metoprolol Administration during STEMI on Infarct Size and Ventricular Function
et al
The baseline study population characteristics are shown in Table 1, both overall and by treatment group (IV metoprolol vs
The METOCARD- CNIC trial (“Effect of METO-prolol in CARDioproteCtioN during an Acute Myocardial InfarCtion”) trial (NCT01311700)is an ongoing randomized single-blind clinical trial comparing the effect of intravenous vs oral metoprolol initiation in patients with anterior wall acute myocardial infarction on infarct size
The goal of antithrombotic therapy (the combination The long-term treatment with beta-blockers after ST-segment elevation myocardial infarction (STEMI) is well established and the benefit appears to be greatest for patients with myocardial infarction complicated by heart failure, left ventricular (LV) systolic dysfunction, or ventricular arrhythmias 1, 2
We hypothesize that metoprolol reduces infarct size when administered early (intravenously before reperfusion)
The median minimum plasma concentration during steady state averaged around 200 nmol/l and was comparable to The major determinant of myocardial salvage during an acute myocardial infarction (MI) is the time to reperfusion