Fikret Er1, Kristina M Dahlem2, Amir M Nia3, Erland Erdmann2, Johannes Waltenberger4, Martin Hellmich5, Kathrin Kuhr5, Minh Tam Le2, Tina Herrfurth2, Zulfugar Taghiyev6, Esther Biesenbach7, Dilek Yüksel8, Aslihan Eran-Ergöknil8, Maria Vanezi2, Evren Caglayan2, Natig Gassanov8. 1. Klinikum Gütersloh, Department of Cardiology and Electrophysiology I, University Hospital Münster, Gütersloh, Germany. Electronic address: fikret.er@klinikum-guetersloh.de. 2. Department of Internal Medicine III, University of Cologne, Cologne, Germany. 3. Division of Cardiology, Pulmonology, and Vascular Medicine, Heinrich Heine University Medical Center Düsseldorf, Düsseldorf, Germany. 4. Department of Cardiovascular Medicine, University Hospital Münster, Münster, Germany. 5. Institute of Medical Statistics, Informatics and Epidemiology, University of Cologne, Cologne, Germany. 6. Department of Cardiac and Thoracic Surgery, BG University Hospital Bergmannsheil, Bochum, Germany. 7. Department of Cardiology and Electrophysiology, University of Witten/Herdecke, Medical Center Porz am Rhein, Cologne, Germany. 8. Klinikum Gütersloh, Department of Cardiology and Electrophysiology I, University Hospital Münster, Gütersloh, Germany.
Abstract
OBJECTIVES: 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).
RCT Entities:
OBJECTIVES: 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).
Authors: Niels Pg Hoedemaker; Vincent Roolvink; Robbert J de Winter; Niels van Royen; Valentin Fuster; José M García-Ruiz; Fikret Er; Natig Gassanov; Kenji Hanada; Ken Okumura; Borja Ibáñez; Arnoud W van 't Hof; Peter Damman Journal: Eur Heart J Acute Cardiovasc Care Date: 2019-02-14