Key result
Intravenous metoprolol resulted in rapid myocardial accumulation (peak at 2.67 min) with a marked delay before maximal hemodynamic effects at 5-10 min, including reduced heart rate (p<0.05).
Why the study?
What is the relationship between acute myocardial uptake and the hemodynamic and electrocardiographic effects of intravenous metoprolol in humans?
What is the relationship between acute myocardial uptake and the hemodynamic and electrocardiographic effects of intravenous metoprolol in humans?
Intravenous metoprolol demonstrates rapid myocardial accumulation but delayed peak hemodynamic effects, indicating marked hysteresis in humans.
May inform acute IV metoprolol timing in chest pain; leaves open confirmation of hemodynamic effects in larger studies.
We studied myocardial disposition of metoprolol after a 4-mg intravenous (i.v.) bolus in 12 patients undergoing cardiac catheterization for investigation of chest pain, using a paired transcoronary sampling technique with simultaneous determination of coronary sinus blood flow (CSF). Myocardial metoprolol content (MMC) was then correlated with concomitant effects on hemodynamic and ECG parameters. Peak myocardial metoprolol content (1.89 +/- 0.40% of injected dose) was attained rapidly (2.67 +/- 0.38 min), but time to peak content was significantly delayed in the presence of extensive coronary artery disease. Residual MMC 17.5 min after injection was 49.1 +/- 8.7% of maximal MMC. Extent of coronary artery disease or variability in left ventricular (LV) systolic function did not influence peak MMC. Metoprolol induced slowing of spontaneous heart rate (HR, p < 0.05), reduction in LV +dP/dt (p < 0.0005), and prolongation of PR intervals (p < 0.05) with maximal changes 5-10 min after injection. Thus, time of peak hemodynamic effects of metoprolol was consistently delayed relative to time of peak MMC. We conclude that after i.v. injection, myocardial metoprolol accumulation in humans is rapid, with marked hysteresis between peak MMC and subsequent hemodynamic effects.
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Ritchie et al. (1994) studied Chest pain (n=12). Metoprolol was evaluated on Myocardial metoprolol content and concomitant effects on hemodynamic and ECG parameters. Intravenous metoprolol resulted in rapid myocardial accumulation (peak at 2.67 min) with a marked delay before maximal hemodynamic effects at 5-10 min, including reduced heart rate (p<0.05).
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