David Garcia-Dorado1, Bruno García-del-Blanco2, Imanol Otaegui2, José Rodríguez-Palomares2, Victor Pineda3, Federico Gimeno4, Rafael Ruiz-Salmerón5, Jaime Elizaga6, Arturo Evangelista2, Francisco Fernandez-Avilés6, Alberto San-Román4, Ignacio Ferreira-González7. 1. Cardiology Department, Vall d'Hebron Hospital, Universitat Autónoma de Barcelona, Barcelona, Spain. Electronic address: dgdorado@gmail.com. 2. Cardiology Department, Vall d'Hebron Hospital, Universitat Autónoma de Barcelona, Barcelona, Spain. 3. Institute for Diagnostic Imaging (IDI), Vall d'Hebron Hospital, Barcelona, Spain. 4. Institute for Heart Science (ICICOR), Clinic University Hospital of Valladolid, Valladolid, Spain. 5. Cardiology Department, University Hospital Virgen de la Macarena, Seville, Spain. 6. Cardiology Department, University General Hospital Gregorio Marañón , Department of Cardiology, Madrid, Spain. 7. Cardiology Department, Vall d'Hebron Hospital, Universitat Autónoma de Barcelona, Barcelona, Spain; Research Center for Epidemiology and Public Health of the Carlos III Health Institute (CIBERESP), Spain.
Abstract
BACKGROUND: The effect of intracoronary adenosine (ADO) on ST-segment elevation myocardial infarction (STEMI) size and adverse remodeling is not well established. METHODS: In a double-blind trial, 201 patients with STEMI were randomized to receive percutaneous coronary intervention (PCI) within 6 hours of symptom onset, 4.5mg ADO or saline immediately prior to reperfusion. Primary end-point: percentage of total myocardial necrotic mass by cardiac magnetic resonance (CMR) 2-7 days post-reperfusion. Secondary end-points: changes in left ventricular volumes and ejection fraction (LVEF) at baseline and at 6 months. RESULTS: Baseline CMR could not be performed in 20 patients. Overall, no significant differences were observed between ADO and placebo regarding infarct size (20.8% vs. 22.5%; p=0.40). However, infarct size was significantly reduced (19.4% vs. 25.7%; p for interaction=0.031) in those with ischemia duration below the median (200 min). CMR at 6 months, performed in 138 patients, did not show statistically significant differences between groups in the rate of LVEF increase (3.3 units (SD 9.6) in ADO group vs. 1.5 units (SD 9) in placebo group; p=0.25). In the subgroup analysis, among patients with ischemia time below 200 min, the increase in LVEF was slightly higher with ADO (3.59% vs. 0.43%; p for interaction=0.06). CONCLUSIONS: Although our study failed to demonstrate that intracoronary administration of ADO prior to PCI limits infarct size, in patients receiving early PCI ADO might enhance myocardial salvage and has a favorable effect on LVEF evolution, which may help to reconcile apparently contradictory results of previous studies. CLINICAL TRIAL REGISTRATION: http://clinicaltrials.gov (NCT00781404).
RCT Entities:
BACKGROUND: The effect of intracoronary adenosine (ADO) on ST-segment elevation myocardial infarction (STEMI) size and adverse remodeling is not well established. METHODS: In a double-blind trial, 201 patients with STEMI were randomized to receive percutaneous coronary intervention (PCI) within 6 hours of symptom onset, 4.5mg ADO or saline immediately prior to reperfusion. Primary end-point: percentage of total myocardial necrotic mass by cardiac magnetic resonance (CMR) 2-7 days post-reperfusion. Secondary end-points: changes in left ventricular volumes and ejection fraction (LVEF) at baseline and at 6 months. RESULTS: Baseline CMR could not be performed in 20 patients. Overall, no significant differences were observed between ADO and placebo regarding infarct size (20.8% vs. 22.5%; p=0.40). However, infarct size was significantly reduced (19.4% vs. 25.7%; p for interaction=0.031) in those with ischemia duration below the median (200 min). CMR at 6 months, performed in 138 patients, did not show statistically significant differences between groups in the rate of LVEF increase (3.3 units (SD 9.6) in ADO group vs. 1.5 units (SD 9) in placebo group; p=0.25). In the subgroup analysis, among patients with ischemia time below 200 min, the increase in LVEF was slightly higher with ADO (3.59% vs. 0.43%; p for interaction=0.06). CONCLUSIONS: Although our study failed to demonstrate that intracoronary administration of ADO prior to PCI limits infarct size, in patients receiving early PCI ADO might enhance myocardial salvage and has a favorable effect on LVEF evolution, which may help to reconcile apparently contradictory results of previous studies. CLINICAL TRIAL REGISTRATION: http://clinicaltrials.gov (NCT00781404).
Authors: Allison B Reiss; David Grossfeld; Lora J Kasselman; Heather A Renna; Nicholas A Vernice; Wendy Drewes; Justin Konig; Steven E Carsons; Joshua DeLeon Journal: Am J Cardiovasc Drugs Date: 2019-10 Impact factor: 3.571