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BEAT-AMI: Esmolol-induced heart rate control may reduce myocardial injury
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In patients with STEMI, the use of esmolol to suppress sympathetic activity appears to yield beneficial effects, including reduction of troponin T, creatine kinase, creatine kinase-MB and N-terminal brain natriuretic peptide release as surrogate markers for myocardial injury, according to results of the BEAT-AMI trial.
The prospective, randomized, single blind, placebo-controlled trial included 101 patients with acute STEMI and successful PCI. A prespecified timeline of less than 6 hours between symptom onset and PCI was established. Other requirements for patient eligibility included Killip class I or II STEMI, baseline heart rate of more than 60 bpm and a mean arterial BP of more than 65 mm Hg.
Participants were randomly assigned weight-adapted plus additional bolus infusion of esmolol, aimed at achieving a heart rate of 60 beats per minute (n = 50), or placebo treatment of continuous 0.9% sodium-chloride infusion (n = 51).
The primary endpoint was defined as the greatest change in troponin T from baseline to 48 hours (subtracting baseline troponin T from the apex of troponin T). This endpoint was selected as a surrogate marker for myocardial damage and an appropriate indicator of prognosis. Secondary endpoints included concentrations of creatine kinase, creatine kinase-MB and NT-proBNP at 48 hours; ejection fraction measured by echocardiography at 48 hours, 6 weeks and 6 months; the 6-minute walking test at 6 weeks and 6 months; and evaluation of quality of life. Safety endpoints included incidence of cardiogenic shock, symptomatic bradycardia or hypertension, recurrence of angina pectoris, repeated angiography and target vessel revascularization, rehospitalization, cerebral insult and death.
The placebo group had a significantly higher change in maximum troponin T within 48 hours vs. the esmolol group (placebo group, 2.5 ng/mL vs. esmolol group, 1 ng/mL; P = .01). Baseline levels of serum troponin T were comparable between the groups: 0.2 ng/mL (interquartile range, 0.1-0.7 ng/mL) in the esmolol group vs. 0.3 ng/mL (interquartile range, 0.1-1.2 ng/mL) in the placebo group. The peak level of troponin T was 1.3 ng/mL (interquartile range, 0.6-4.7 ng/mL) in the esmolol group vs. 3.2 ng/mL (interquartile range, 1.5-5.3 ng/mL) in the placebo group (P = .009).
Although the two groups demonstrated similar baseline levels of creatine kinase and creatine kinase-MB, total creatine kinase and creatine kinase-MB release were lower in the esmolol group vs. the placebo group (creatine kinase: esmolol group, 619 U/L vs. placebo group, 1,308 U/L; P = .013; creatine kinase-MB: esmolol group, 73.5 U/L vs. placebo group, 158.5 U/L; P = .005). Baseline levels of NT-proBNP were 83.5 pg/mL in the esmolol group vs. 133.5 pg/mL in the placebo group (P = .228). This value increased within 48 hours to 1,048 pg/mL in the esmolol group and 1,497 pg/mL in the placebo group (P = .059).
During index hospitalization, one patient in the placebo group died of cardiogenic shock, and three patients total (three in the placebo group vs. 0 in the esmolol group) developed cardiogenic shock requiring IV catecholaminergic therapy.
“In the BEAT-AMI trial, all four evaluated biomarkers were significantly lowered by esmolol-induced heart rate control, indicating a protective effect of acute intravenous esmolol,” the researchers wrote. “There is need for further studies to identify the effects of suggested esmolol-induced infarct size limitation on clinical endpoints.” – by Jennifer Byrne
Disclosure: The BEAT-AMI trial was funded by Baxter Healthcare Corp. The researchers report no relevant financial disclosures.
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