Why the study?
Platelet thrombus formation is a critical determinant of STEMI outcomes, but whether the beneficial effects of remote ischaemic conditioning relate to thrombotic parameters remains unclear.
Does remote ischaemic conditioning reduce platelet reactivity and improve endogenous fibrinolysis in patients with STEMI undergoing primary PCI?
Does remote ischaemic conditioning reduce platelet reactivity and improve endogenous fibrinolysis in patients with STEMI undergoing primary PCI?
Remote ischaemic conditioning may transiently reduce platelet reactivity in the first 48 hours post-STEMI, providing a potential mechanistic insight into its effects.
RIC shows no consistent effect on thrombotic parameters in STEMI; leaves open alternative mechanisms for any infarct size reduction.
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.
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Gorog et al. (2020) studied this question.
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