The effect of delay in propranolol administration on reduction of myocardial infarct size after experimental coronary artery occlusion in dogs.

Miura, Masao; Thomas, Reuben; Ganz, William; Sokol, Thomas; Shell, William E.; Toshimitsu, Takashi; Kwan, A C; Singh, B N

doi:10.1161/01.cir.59.6.1148

Cited by 112 publications

(34 citation statements)

References 37 publications

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“…Introvenous β-blocker treatment before coronary artery occlusion is capable of reducing myocardial injury. [19] Clinically,administration of introvenous metoprolol could significantly produce heart protective effect in ischemia-referfusion. [9]…”

Section: Discussionmentioning

confidence: 99%

Effect of metoprolol on myocardial apoptosis after coronary microembolization in rats

Su¹,

Li²,

Liu³

et al. 2013

World Journal of Emergency Medicine

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BACKGROUND:Coronary microembolization (CME) is a serious complication following percutaneous coronary intervention (PCI) in patients with acute coronary syndromes. The use of metoprolol before PCI can significantly protect ischemic myocardium from myocardial damage, but the function of metoprolol in the treatment of CME is not entirely clear. This study was to explore the effect and significance of metoprolol on myocardial apoptosis and caspase-3 activation after CME in rats.METHODS:Thirty rats were randomly divided into three groups including sham-operation (control group), CME plus saline (CME group), CME plus metoprolol (metoprolol group), 10 rats for each group. The CME group was induced by injecting 3 000 polyethylene microspheres (42 μm) into the left ventricle during a 10-second occlusion of the ascending aorta; the control group was injected with physiological saline instead of microembolization ball; the metoprolol or saline group was given three intravenous bolus injections before CME. Echocardiography, TUNEL staining, and Western blotting were used to evaluate cardiac function, proportion of apoptotic cells and activation of caspase-3 respectively at 6 hours after operation.RESULTS:Echocardiographic parameters displayed that the metoprolol group improved cardiac function significantly compared with the CME group (P<0.05). The myocardial apoptotic rate of the CME group as well as the contents of activated caspase-3 increased significantly (P<0.05), both of which were ameliorated significantly by metoprolol treatment (P<0.05).CONCLUSIONS:This study demonstrates that metoprolol can protect the myocardium during CME in rats by inhibiting apoptosis and improving cardiac function. These results suggest that the inhibition of apoptosis can be a potential therapeutic strategy for the treatment of CME.

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Section: Discussionmentioning

confidence: 99%

Effect of metoprolol on myocardial apoptosis after coronary microembolization in rats

Su¹,

Li²,

Liu³

et al. 2013

World Journal of Emergency Medicine

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“…Experience with other drugs known to limit infarct size indicates that only small amounts of myocardium can be salvaged in animals if the intervention is given more than 4 hr after coronary artery occlusion. [29][30][31][32][33][34] Although the hemodynamic effects of nifedipine in patients with chronic ischemic heart disease have been well described,35-37 the actions of this drug in patients with AMI have not been studied as extensively. Jaffe et al38 studied 17 patients with AMI given nifedipine a mean of 8.7 hr after onset of pain.…”

Section: Discussionmentioning

confidence: 99%

Nifedipine therapy for patients with threatened and acute myocardial infarction: a randomized, double-blind, placebo-controlled comparison.

Muller¹,

Morrison²,

Stone³

et al. 1984

Circulation

247

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Preliminary clinical and laboratory observations suggest that nifedipine might prevent progression of threatened myocardial infarction by reversing coronary spasm or 57 [75% for nifedipine-treated patients). Furthermore, infarct size index was similar among placebo-and nifedipine-treated patients (16.9 + 1.5 MB-CK-geq/m ,n 65, and 17.0 ± 1l.5 MB-CK-geq/m', n = 68, respectively) with threatened myocardial infarction who exhibited infarction and for those with acute myocardial infarction. Among the 171 eligible patients randomly assigned to drug or placebo, 6 month mortality did not differ significantly (8.5% for placebo vs 10. 1 % for nifedipine, NS), but mortality in the 2 weeks after randomization was significantly higher for nifedipine-treated patients (0% for placebo compared with 7.9% for nifedipine, p = .0 18). There were no significant differences in 2 week and 6 month mortalities in the group of all participating patients, which included 10 patients randomly assigned therapy but retrospectively determined to be ineligible. Two week mortality for this group (n = 181) was 2.3% for placebo-and 7.5% for nifedipine-treated patients and 6 month mortality was 11.4% for placebo-and 10.8% for nifedipine-treated patients. Thus, nifedipine therapy did not prevent progression of threatened myocardial infarction to the acute event or limit infarct size in patients who experienced infarction. There was a statistically significant increase in 2 week mortality with nifedipine in the group of eligible patients randomly assigned to a regimen, but mortality was balanced when results were analyzed for all patients taking part in the randomization protocol.

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“…6 Experimental studies have shown that intravenous administration of the ␤-blocker propranolol before coronary artery occlusion can significantly reduce the electrocardiographic, enzymatic, and histological indices of myocardial infarction (MI). [7][8][9][10] Clinical PCI studies have shown that intracoronary (IC) propranolol delays the development of ischemia during balloon occlusion as determined by the time to and extent of ST-segment elevation on IC and surface ECGs. 11,12 Currently, there are no data evaluating the impact of adjunctive IC ␤-blocker therapy before PCI on postprocedural MI, as reflected by biochemical marker release, and on clinical…”

mentioning

confidence: 99%

Distal Myocardial Protection During Percutaneous Coronary Intervention With an Intracoronary β-Blocker

et al. 2003

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Background-Experimental studies have demonstrated that intravenous ␤-blocker administration before coronary artery occlusion significantly reduces myocardial injury. Clinical studies have shown that intracoronary (IC) propranolol administration before percutaneous coronary intervention (PCI) delays myocardial ischemia. The present study tested the hypothesis that IC propranolol treatment protects ischemic myocardium from myocardial damage and reduces the incidence of myocardial infarction (MI) and short-term adverse outcomes after PCI. Methods and Results-Patients undergoing PCI (nϭ150) were randomly assigned in a double-blind fashion to receive IC propranolol (nϭ75) or placebo (nϭ75). Study drug was delivered before first balloon inflation via an intracoronary catheter with the tip distal to the coronary lesion. Biochemical markers were evaluated through the first 24 hours and clinical outcomes to 30 days. Evidence of MI with creatine kinase-MB elevation after PCI was seen in 36% of placebo and 17% of propranolol patients (Pϭ0.01). Troponin T elevation was seen in 33% of placebo and 13% of propranolol patients (Pϭ0.005). At 30 days, the composite end point of death, postprocedural MI, non-Q-wave MI after PCI hospitalization, or urgent target-lesion revascularization occurred in 40% of placebo versus 18% of propranolol patients (hazard ratio 2.14, 95% CI 1.24 to 3.71, Pϭ0.004). Conclusions-IC

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The effect of delay in propranolol administration on reduction of myocardial infarct size after experimental coronary artery occlusion in dogs.

Cited by 112 publications

References 37 publications

Effect of metoprolol on myocardial apoptosis after coronary microembolization in rats

Effect of metoprolol on myocardial apoptosis after coronary microembolization in rats

Nifedipine therapy for patients with threatened and acute myocardial infarction: a randomized, double-blind, placebo-controlled comparison.

Distal Myocardial Protection During Percutaneous Coronary Intervention With an Intracoronary β-Blocker

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