Randomized Control of Sympathetic Drive With Continuous Intravenous Esmolol in Patients With Acute ST-Segment Elevation Myocardial Infarction: The BEtA-Blocker Therapy in Acute Myocardial Infarction (BEAT-AMI) Trial

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• 作者：Fikret Er ; MD^a ; ^{fikret.er@klinikum-guetersloh.de" class="auth_mail" title="E-mail the corresponding author} ; Kristina M. Dahlem ; MD^b ; Amir M. Nia ; MD^c ; Erland Erdmann ; MD ; PhD^b ; Johannes Waltenberger ; MD^d ; Martin Hellmich ; PhD^e ; Kathrin Kuhr^e ; Minh Tam Le^b ; Tina Herrfurth^b ; Zulfugar Taghiyev ; MD^f ; Esther Biesenbach ; MD^g ; Dilek Yü ; ksel ; MD^a ; Aslihan Eran-Ergö ; knil ; MD^a ; Maria Vanezi ; MD^b ; Evren Caglayan ; MD^b ; Natig Gassanov ; MD^a
• 关键词：beta-blocker ; clinical trial ; heart rate ; sympathetic nervous system ; STEMI
• 刊名：JACC: Cardiovascular Interventions
• 出版年：2016
• 出版时间：8 February 2016
• 年：2016
• 卷：9
• 期：3
• 页码：231-240
• 全文大小：950 K

文摘

This study sought to evaluate the role of esmolol-induced tight sympathetic control in patients with ST-segment elevation myocardial infarction (STEMI).

Background

Elevated sympathetic drive has a detrimental effect on patients with acute STEMI. The effect of beta-blocker-induced heart rate mediated sympathetic control on myocardial damage is unknown.

Methods

The authors conducted a prospective, randomized, single-blind trial involving patients with STEMI and successful percutaneous intervention (Killip class I and II). Patients were randomly allocated to heart rate control with intravenous esmolol for 24 h or placebo. The primary outcome was the maximum change in troponin T release as a prognostic surrogate marker for myocardial damage. A total of 101 patients were enrolled in the study.

Results

There was a significant difference between patients allocated to placebo and those who received sympathetic control with esmolol in terms of maximum change in troponin T release: the median serum troponin T concentration increased from 0.2 ng/ml (interquartile range [IQR] 0.1 to 0.7 ng/ml) to 1.3 ng/ml (IQR: 0.6 to 4.7 ng/ml) in the esmolol group and from 0.3 ng/ml (IQR: 0.1 to 1.2 ng/ml) to 3.2 ng/ml (IQR: 1.5 to 5.3 ng/ml) in the placebo group (p = 0.010). The levels of peak creatine kinase (CK), CK subunit MB (CK-MB), and n-terminal brain natriuretic peptide (NT-proBNP) were lower in the esmolol group compared with placebo (CK 619 U/l [IQR: 250–1,701 U/l] vs. 1,308 U/l [IQR: 610 to 2,324 U/l]; p = 0.013; CKMB: 73.5 U/l [IQR: 30 to 192 U/l] vs. 158.5 U/l [IQR: 74 to 281 U/l]; p = 0.005; NT-proBNP: 1,048 pg/ml (IQR: 623 to 2,062 pg/ml] vs. 1,497 pg/ml [IQR: 739 to 3,318 pg/ml]; p = 0.059). Cardiogenic shock occurred in three patients in the placebo group and in none in the esmolol group.

Conclusions

Esmolol treatment statistically significantly decreased troponin T, CK, CK-MB and NT-proBNP release as surrogate markers for myocardial injury in patients with STEMI. (Heart Rate Control After Acute Myocardial Infarction; DRKS00000766)