Diana A Gorog1,2,3, Mohamed Farag2,4, Nikolaos Spinthakis2,3, Derek M Yellon5, Hans Erik Bøtker6, Rajesh K Kharbanda7,8, Derek J Hausenloy9,10,11,12,13,14. 1. National Heart and Lung Institute, Faculty of Medicine, Imperial College, Dovehouse Street, London SW3 6LR, UK. 2. Postgraduate Medical School, University of Hertfordshire, Hertfordshire, UK. 3. Department of Cardiology, East and North Hertfordshire NHS Trust, Hertfordshire, UK. 4. Cardiology Department, Royal Papworth Hospital NHS Foundation Trust, Papworth Everard, Cambridge, UK. 5. The Hatter Cardiovascular Institute, University College London, London, UK. 6. Department of Cardiology, Aarhus University Hospital, Aarhus N, Denmark. 7. Cardiology Department, Oxford Heart Centre, Oxford University Hospitals NHS Trust, Oxford, UK. 8. Department of Cardiovascular Medicine, University of Oxford, Oxford, UK. 9. The Hatter Cardiovascular Institute, University College London, London, UK. 10. Cardiovascular & Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore, Singapore. 11. Department of Cardiology, National Heart Research Institute Singapore, National Heart Centre, Singapore, Singapore. 12. Yong Loo Lin School of Medicine, National University Singapore, Singapore, Singapore. 13. Cardiovascular Research Center, College of Medical and Health Sciences, Asia University, Taichung City, Taiwan. 14. Tecnologico de Monterrey, Centro de Biotecnologia-FEMSA, Nuevo Leon, Mexico.
Abstract
AIMS: Remote ischaemic conditioning (RIC) has been shown to reduce myocardial infarct size in animal models of myocardial infarction. Platelet thrombus formation is a critical determinant of outcome in ST-segment elevation myocardial infarction (STEMI). Whether the beneficial effects of RIC are related to thrombotic parameters is unclear. METHODS AND RESULTS: In a substudy of the Effect of Remote Ischaemic Conditioning on clinical outcomes in STEMI patients undergoing Primary Percutaneous Coronary Intervention (ERIC-PPCI) trial, we assessed the effect of RIC on thrombotic status. Patients presenting with STEMI were randomized to immediate RIC consisting of an automated autoRIC™ cuff on the upper arm inflated to 200 mmHg for 5 min and deflated for 5 min for four cycles (n = 53) or sham (n = 47). Venous blood was tested at presentation, discharge (48 h) and 6-8 weeks, to assess platelet reactivity, coagulation, and endogenous fibrinolysis using the Global Thrombosis Test and thromboelastography. Baseline thrombotic status was similar in the two groups. At discharge, there was some evidence that the time to in vitro thrombotic occlusion under high shear stress was longer with RIC compared to sham (454 ± 105 s vs. 403 ± 105 s; mean difference 50.1 s; 95% confidence interval 93.7-6.4, P = 0.025), but this was no longer apparent at 6-8 weeks. There was no difference in clot formation or endogenous fibrinolysis between the study arms at any time point. CONCLUSION: RIC may reduce platelet reactivity in the first 48 h post-STEMI. Further research is needed to delineate mechanisms through which RIC may reduce platelet reactivity, and whether it may improve outcomes in patients with persistent high on-treatment platelet reactivity. Published on behalf of the European Society of Cardiology. All rights reserved.
AIMS: Remote ischaemic conditioning (RIC) has been shown to reduce myocardial infarct size in animal models of myocardial infarction. Platelet thrombus formation is a critical determinant of outcome in ST-segment elevation myocardial infarction (STEMI). Whether the beneficial effects of RIC are related to thrombotic parameters is unclear. METHODS AND RESULTS: In a substudy of the Effect of Remote Ischaemic Conditioning on clinical outcomes in STEMI patients undergoing Primary Percutaneous Coronary Intervention (ERIC-PPCI) trial, we assessed the effect of RIC on thrombotic status. Patients presenting with STEMI were randomized to immediate RIC consisting of an automated autoRIC™ cuff on the upper arm inflated to 200 mmHg for 5 min and deflated for 5 min for four cycles (n = 53) or sham (n = 47). Venous blood was tested at presentation, discharge (48 h) and 6-8 weeks, to assess platelet reactivity, coagulation, and endogenous fibrinolysis using the Global Thrombosis Test and thromboelastography. Baseline thrombotic status was similar in the two groups. At discharge, there was some evidence that the time to in vitro thrombotic occlusion under high shear stress was longer with RIC compared to sham (454 ± 105 s vs. 403 ± 105 s; mean difference 50.1 s; 95% confidence interval 93.7-6.4, P = 0.025), but this was no longer apparent at 6-8 weeks. There was no difference in clot formation or endogenous fibrinolysis between the study arms at any time point. CONCLUSION: RIC may reduce platelet reactivity in the first 48 h post-STEMI. Further research is needed to delineate mechanisms through which RIC may reduce platelet reactivity, and whether it may improve outcomes in patients with persistent high on-treatment platelet reactivity. Published on behalf of the European Society of Cardiology. All rights reserved.
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