Remote Ischemic Conditioning Reduces Myocardial Infarct Size and Edema in Patients With ST-Segment Elevation Myocardial Infarction

White, Steven K; Fröhlich, Georg; Sado, Daniel; Maestrini, Viviana; Fontana, Marianna; Treibel, Thomas A.; Tehrani, Shana; Flett, Andrew; Meier, Pascal; Ariti, Cono; Davies, John R.; Moon, James; Yellon, Derek M.; Hausenloy, Derek J.

doi:10.1016/j.jcin.2014.05.015

Cited by 211 publications

(225 citation statements)

References 40 publications

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“…180 In patients with acute STsegment elevation myocardial infarction undergoing PCI, remote ischemic perconditioning with 4 cycles of 5-minute arm ischemia/5-minute reperfusion at hospital admission reduced both infarct size and edema on MRI. 181 Also in patients with acute myocardial infarction undergoing PCI, remote ischemic postconditioning by 3 cycles of lower limb ischemia/reperfusion reduced edema (MRI) and infarct size (MRI, biomarker), improved ST-segment resolution during reperfusion, but did not improve TIMI frame count or myocardial blush grading. 182 In the recent LIPSIA (from Leipzig) conditioning trial in patients undergoing primary PCI for acute ST-segment elevation myocardial infarction, postconditioning alone with 4 cycles of 30-second reocclusion/reperfusion failed to improve myocardial salvage and microvascular obstruction by MRI, but combined postconditioning with remote ischemic perconditioning by 3 cycles of 5-minute upper arm ischemia/5-minute reperfusion improved myocardial salvage, albeit reduced microvascular obstruction only nonsignificantly.…”

Section: Coronary Vascular Protection By Remote Ischemic Conditioningmentioning

confidence: 96%

The Coronary Circulation as a Target of Cardioprotection

Heusch

2016

Circulation Research

206

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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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Section: Coronary Vascular Protection By Remote Ischemic Conditioningmentioning

confidence: 96%

The Coronary Circulation as a Target of Cardioprotection

Heusch

2016

Circulation Research

206

160

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“…All studies that used an ischemic perconditioning protocol of repeated arm or leg ischemia/reperfusion in patients with acute STEMI found reduced infarct size, which was significant in most of them, no matter whether reperfusion was by primary PCI 96,[106][107][108][109][110][111] or thrombolysis 112 and no matter whether biomarker release or imaging was used to assess infarct size ( Figure 3). A retrospective analysis of the CONDI trial (Effect of Remote Ischemic Conditioning on Clinical Outcome in (Table 3).…”

Section: Remote Ischemic Conditioningmentioning

confidence: 99%

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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“…Remote ischemic conditioning by repetitive limb ischemia/reperfusion also reduces myocardial damage in patients undergoing elective interventional2 or surgical coronary revascularization3, 4, 5, 6 and in those with reperfused acute myocardial infarction 7, 8, 9, 10, 11, 12, 13. Cardioprotection was confirmed by reduced release of cardiac biomarkers2, 3, 4, 5, 6, 10 or by increased salvage in cardiac imaging7, 8, 9, 11 but also resulted in improved short‐5, 8 and more long‐term2, 4, 13, 14, 15 clinical outcome in retrospective analyses. Recently, the first prospective, randomized trial on patients with reperfused acute myocardial infarction confirmed improved clinical outcome as a primary end point of remote ischemic conditioning during follow‐up for 3.6 years 13.…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial and Contractile Function of Human Right Atrial Tissue in Response to Remote Ischemic Conditioning

Kleinbongard

Gedik

Kirca

et al. 2018

JAHA

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BackgroundRemote ischemic preconditioning (RIPC) by repeated brief cycles of limb ischemia/reperfusion attenuates myocardial ischemia/reperfusion injury. We aimed to identify a functional parameter reflecting the RIPC‐induced protection in human. Therefore, we measured mitochondrial function in right atrial tissue and contractile function of isolated right atrial trabeculae before and during hypoxia/reoxygenation from patients undergoing coronary artery bypass grafting with RIPC or placebo, respectively.Methods and ResultsOne hundred thirty‐seven patients under isoflurane anesthesia underwent RIPC (3×5 minutes blood pressure cuff inflation on the left upper arm/5 minutes deflation, n=67) or placebo (cuff uninflated, n=70), and right atrial appendages were harvested before ischemic cardioplegic arrest. Myocardial protection by RIPC was assessed from serum troponin I/T concentrations over 72 hours after surgery. Atrial tissue was obtained for isolation of mitochondria (RIPC/placebo: n=10/10). Trabeculae were dissected for contractile function measurements at baseline and after hypoxia/reoxygenation (60 min/30 min) and for western blot analysis after hypoxia/reoxygenation (RIPC/placebo, n=57/60). Associated with cardioprotection by RIPC (26% decrease in the area under the curve of troponin I/T), mitochondrial adenosine diphosphate–stimulated complex I respiration (+10%), adenosine triphosphate production (+46%), and calcium retention capacity (+37%) were greater, whereas reactive oxygen species production (−24%) was less with RIPC than placebo. Contractile function was improved by RIPC (baseline, +7%; reoxygenation, +24%). Expression and phosphorylation of proteins, which have previously been associated with cardioprotection, were not different between RIPC and placebo.ConclusionsCardioprotection by RIPC goes along with improved mitochondrial and contractile function of human right atrial tissue.Clinical Trial RegistrationURL: https://www.clinicaltrials.gov. Unique identifier: NCT01406678.

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Remote Ischemic Conditioning Reduces Myocardial Infarct Size and Edema in Patients With ST-Segment Elevation Myocardial Infarction

Abstract: This randomized study demonstrated that in ST-segment elevation myocardial infarction patients treated by PPCI, RIC, initiated prior to PPCI, reduced MI size, increased myocardial salvage, and reduced myocardial edema.

Cited by 211 publications

References 40 publications

The Coronary Circulation as a Target of Cardioprotection

The Coronary Circulation as a Target of Cardioprotection

Time to Give Up on Cardioprotection?

Mitochondrial and Contractile Function of Human Right Atrial Tissue in Response to Remote Ischemic Conditioning

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