Effect of Remote Ischemic Preconditioning on Platelet Activation Induced by Coronary Procedures

Lanza, Gaetano Antonio; Stazi, Alessandra; Villano, Angelo; Torrini, Flavia; Milo, Maria; Laurito, Marianna; Flego, Davide; Aurigemma, Cristina; Liuzzo, Giovanna; Crea, Filippo

doi:10.1016/j.amjcard.2015.10.056

Cited by 29 publications

(30 citation statements)

References 26 publications

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“…A retrospective analysis of the CONDI trial (Effect of Remote Ischemic Conditioning on Clinical Outcome in (Table 3). A similar pattern with infarct size reduction in the majority but not all studies (with 2 small extreme outlier studies reporting even increased infarct size by remote ischemic preconditioning 114,115 ) emerged for elective PCI when either remote ischemic pre- [116][117][118][119][120][121][122][123] or postconditioning 124,125 was used for cardioprotection. In some of these studies, clinical outcome was reported as a secondary outcome, and it was either not different 106,119,124 or improved.…”

Section: Remote Ischemic Conditioningmentioning

confidence: 77%

Time to Give Up on Cardioprotection?

Heusch

Rassaf

2016

Circulation Research

174

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Abstract:The mortality from acute myocardial infarction (AMI) remains significant, and the prevalence of postmyocardial infarction heart failure is increasing. Therefore, cardioprotection beyond timely reperfusion is needed. Conditioning procedures are the most powerful cardioprotective interventions in animal experiments. However, ischemic preconditioning cannot be used to reduce infarct size in patients with AMI because its occurrence is not predictable; several studies in patients undergoing surgical coronary revascularization report reduced release of creatine kinase and troponin. Ischemic postconditioning reduces infarct size in most, but not all, studies in patients undergoing interventional reperfusion of AMI, but may require direct stenting and exclusion of patients with >6 hours of symptom onset to protect. Remote ischemic conditioning reduces infarct size in patients undergoing interventional reperfusion of AMI, elective percutaneous or surgical coronary revascularization, and other cardiovascular surgery in many, but not in all, studies. Adequate dose-finding phase II studies do not exist. There are only 2 phase III trials, both on remote ischemic conditioning in patients undergoing cardiovascular surgery, both with neutral results in terms of infarct size and clinical outcome, but also both with major problems in trial design. We discuss the difficulties in translation of cardioprotection from animal experiments and proof-ofconcept trials to clinical practice. Given that most studies on ischemic postconditioning and all studies on remote ischemic preconditioning in patients with AMI reported reduced infarct size, it would be premature to give up on cardioprotection. (Circ Res. 2016;119:676-695.

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Section: Remote Ischemic Conditioningmentioning

confidence: 77%

Time to Give Up on Cardioprotection?

Heusch

Rassaf

2016

Circulation Research

174

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“…Pedersen and colleagues demonstrated that RIPC decreased platelet‐monocyte aggregate formation after ischemia‐reperfusion injury . In another study, patients undergoing coronary angiography were resistant to the effects of ADP‐induced platelet‐monocyte aggregate formation and CD41 and CD62 expression after RIPC; in another, RIPC inhibited ADP‐induced platelet activation after exercise …”

Section: Discussionmentioning

confidence: 99%

Remote ischemic preconditioning inhibits platelet αIIbβ3 activation in coronary artery disease patients receiving dual antiplatelet therapy: A randomized trial

Lau

Pennings

Reddel

et al. 2020

Journal of Thrombosis and Haemostasis

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Objectives:We investigated whether remote ischemic preconditioning (RIPC) inhibits agonist-induced conformational activation of platelet α IIb β 3 in patients with coronary artery disease already receiving conventional antiplatelet therapy. Patients/Methods:Consecutive patients with angiographically confirmed coronary artery disease were randomized to RIPC or sham treatment. Venous blood was collected before and immediately after RIPC/sham. Platelet aggregometry (ADP, arachidonic acid) and whole blood platelet flow cytometry was performed for CD62P, CD63, active α IIb β 3 (PAC-1 binding) before and after stimulation with ADP, thrombin ± collagen, or PAR-1 thrombin receptor agonist.Results: Patients (25 RIPC, 23 sham) were well matched, 83% male, age (mean ± standard deviation) 63.3 ± 13.2 years, 95% aspirin, 81% P2Y 12 inhibitor. RIPC did not affect platelet aggregation, nor agonist-induced expression of CD62P, but selectively and significantly decreased α IIb β 3 activation after stimulation with either PAR-1 agonist peptide or the combination of thrombin + collagen, but not after ADP nor thrombin alone. The effect of RIPC on platelet α IIb β 3 activation was evident in patients receiving both aspirin and P2Y 12 inhibitor, and was not associated with an increase in vasodilator-stimulated phosphoprotein phosphorylation. Conclusions:Remote ischemic preconditioning inhibits conformational activation of platelet α IIb β 3 in response to exposure to thrombin and collagen in patients with coronary artery disease receiving dual antiplatelet therapy. These findings indicate agonist-specific inhibition of platelet activation by RIPC in coronary artery disease that is not obviated by the prior use of P2Y 12 inhibitors.

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“…183 Remote ischemic preconditioning reduces leukocyte adhesion and phagocytosis in healthy volunteers, 184 and it attenuates the increased platelet reactivity and formation of monocyte-platelet aggregates in patients undergoing ablation for atrial fibrillation 185 and in patients undergoing coronary procedures. 186 Remote ischemic preconditioning activates erythrocyte nitric oxide synthase 187 and improves erythrocyte deformability, 188 thus potentially antagonizing stasis.…”

Section: Coronary Vascular Protection By Remote Ischemic Conditioningmentioning

confidence: 99%

The Coronary Circulation as a Target of Cardioprotection

Heusch

2016

Circulation Research

204

160

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Abstract:The atherosclerotic coronary vasculature is not only the culprit but also a victim of myocardial ischemia/ reperfusion injury. Manifestations of such injury are increased vascular permeability and edema, endothelial dysfunction and impaired vasomotion, microembolization of atherothrombotic debris, stasis with intravascular cell aggregates, and finally, in its most severe form, capillary destruction with hemorrhage. In animal experiments, local and remote ischemic pre-and postconditioning not only reduce infarct size but also these manifestations of coronary vascular injury, as do drugs which recruit signal transduction steps of conditioning. Clinically, no-reflow is frequently seen after interventional reperfusion, and it carries an adverse prognosis. The translation of cardioprotective interventions to clinical practice has been difficult to date. Only 4 drugs (brain natriuretic peptide, exenatide, metoprolol, and esmolol) stand unchallenged to date in reducing infarct size in patients with reperfused acute myocardial infarction; unfortunately, for these drugs, no information on their impact on the ischemic/reperfused coronary circulation is available. (Circ Res.

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Effect of Remote Ischemic Preconditioning on Platelet Activation Induced by Coronary Procedures

Cited by 29 publications

References 26 publications

Time to Give Up on Cardioprotection?

Time to Give Up on Cardioprotection?

Remote ischemic preconditioning inhibits platelet αIIbβ3 activation in coronary artery disease patients receiving dual antiplatelet therapy: A randomized trial

The Coronary Circulation as a Target of Cardioprotection

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