Intracoronary Beta-Blocker During PCI - Intracoronary Beta-Blocker During PCI
The goal of the trial was to evaluate the effect of intracoronary (IC) beta-blocker use versus placebo during percutaneous coronary intervention (PCI) on the incidence of postprocedural myocardial infarction (MI).
IC propranolol protects ischemic myocardium during PCI and reduces MI and early adverse clinical events after PCI.
Patients Enrolled: 150
Mean Follow Up: 30 days
Mean Patient Age: mean 58 years
Coronary artery disease (including those receiving chronic beta-blockade); undergoing PCI
MI <24 hours previously or recent MI with CK or CK-MB elevation at time of randomization; cardiogenic shock; systolic blood pressure <100 mm Hg; heart rate <50 beats per minute; New York Heart Association class III or IV heart failure; severe left ventricular dysfunction (ejection fraction <30%); severe renal insufficiency (creatinine >3.0 mg/dl); allergy to propranolol; or second planned intervention within 30 days
Incidence of postprocedural MI (CK-MB elevated above upper limit of normal)
Incidence of postprocedural total CK and troponin T elevation; median peak values of CK, CK-MB, and troponin T; rescue therapy with GP IIb/IIIa inhibitors; and combination of death of any cause, post-PCI MI, non–Q wave MI, and Q wave MI after PCI hospitalization or severe myocardial ischemia requiring urgent coronary artery surgery or TLR within 30 days of intervention
Following angiography and the confirmed need for PCI, patients were randomized to propranolol (n=75) or placebo (n=75) in a double-blind fashion. Prior to balloon inflation, propranolol (15 µg/kg12) or placebo (0.9% NaCl) was injected into the coronary artery through the dilatation catheter with the distal tip of the catheter positioned across the stenosis. After study drug administration, PCI was performed.
Aspirin and weight-adjusted heparin prior to intervention
Baseline demographic and angiographic characteristics were well balanced between the two arms. Heart rate and blood pressure did not change after IC injection of propranolol or placebo. Postprocedure MI (creatine kinase-myocardial band [CK-MB] elevation) occurred less frequently in the propranolol arm than in the placebo arm (17% vs. 36%, p=0.01). CK-MB elevation ≥3 times the upper limit of normal occurred in seven patients in the propranolol arm and six in the placebo arm (p=NS). Troponin T elevation postprocedure also occurred less frequently in the propranolol arm (13% vs. 33%, p=0.005).
The frequency of the composite endpoint of death, postprocedural MI, non–Q wave MI after PCI hospitalization, or urgent target lesion revascularization (TLR) was lower in the propranolol arm (18% vs. 40%, hazard ratio 2.14, 95% confidence interval 1.24-3.71, p=0.004). However, the difference was driven almost entirely by postprocedure MI.
There were no deaths in either arm, and no differences in non-Q wave MI (2 placebo and 1 propranolol) or urgent TLR (2 placebo and 0 propranolol). Use of glycoprotein (GP) IIb/IIIa inhibitors did not differ between arms (11% for propranolol and 15% for placebo, p=0.46).
Among patients undergoing PCI, use of IC propranolol was associated with a lower rate of postprocedureal MI compared with placebo. The authors speculate that the reduction in postprocedural MI may be driven by an increase in myocardial salvage with propranolol, findings which were observed in dog models. While findings of the study were positive and provocative, larger multicenter studies are required to confirm these findings.
Keywords: Myocardial Infarction, Coronary Artery Disease, Creatine Kinase, Platelet Aggregation Inhibitors, Propranolol, Troponin T, Dilatation, Blood Pressure, Constriction, Pathologic, Heart Rate, Angioplasty, Balloon, Coronary, Confidence Intervals
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