Cardioprotective role of ischemic postconditioning in acute myocardial infarction: A systematic review and meta-analysis

Khan, Abdur Rahman; Binabdulhak, Aref A.; Alastal, Yaseen; Khan, Sobia; Faricy-Beredo, Bridget M.; Luni, Faraz Khan; Lee, Wade M.; Khuder, Sadik A.; Tinkel, Jodi

doi:10.1016/j.ahj.2014.06.021

Cited by 37 publications

(22 citation statements)

References 42 publications

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“…A consistent reduction of infarct size by biomarker release and by imaging was confirmed in recent meta-analyses. 104,105 Several the above studies also reported clinical outcome over relatively short periods of time as secondary end point (Table 2). In only one study in patients with acute STEMI was there a significantly better outcome with ischemic postconditioning, that is, a reduced development of heart failure at 3 months.…”

Section: Ischemic Postconditioningmentioning

confidence: 99%

Time to Give Up on Cardioprotection?

Heusch

Rassaf

2016

Circulation Research

176

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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: Ischemic Postconditioningmentioning

confidence: 99%

Time to Give Up on Cardioprotection?

Heusch

Rassaf

2016

Circulation Research

176

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“…Previous observations showed beneficial effects on both animal and human studies, like limition of infarct size, preservation of left ventricular function [17, 18], reduction of myocardial edema [19] and prevention of coronary microembolization [20]. These cardioprotective phenotypes from IPoC are attributed to secondary to its effect on various cellular mechanisms: the kinase pathway, survival activating factor enhancement pathway, Janus signal transducer and activator system, reduction in formation of reactive oxygen or nitrogen species, and attenuation of calcium overload [21, 22]. …”

Section: Introductionmentioning

confidence: 99%

Hydrogen Gas Attenuates Myocardial Ischemia Reperfusion Injury Independent of Postconditioning in Rats by Attenuating Endoplasmic Reticulum Stress-Induced Autophagy

Gao

Yang

Chi

et al. 2017

Cell Physiol Biochem

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Background/Aims: To study the effect of inhaling hydrogen gas on myocardial ischemic/reperfusion(I/R) injury in rats. Methods: Seventy male Wistar albino rats were divided into five groups at random as the sham group (Sham). The I/R group (I/R), The ischemic postconditioning group (IPo), The I/R plus hydrogen group (IH₂) and the ischemic postconditioning plus hydrogen group (IPoH₂). The Sham group was without coronary occlusion. In I/R group, Ischemic/reperfusion injury was induced by coronary occlusion for 1 hour. Followed by 2 hours of reperfusion. In the IPo and IPoH2 group, four cycles of 1 min reperfusion/1 min ischemia was given at the end of 1 hour coronary occlusion. While 2% hydrogen was administered by inhalation 5 min before reperfusion till 2 hours after reperfusion in both the IPoH2 and IH2 group. The heart and blood samples were harvested at the end of the surgical protocol. Then the myocardium cell endoplasmic reticulum(ER) stress and autophagy was observed by electron microscope. In addition, the cardiac ER stress and autophagy related proteins expression were detected by Western blotting analysis. Results: Both inhaling 2% hydrogen and ischemic postconditioning treatment reduced the ischemic size and serum troponin I level in rats with I/R injury, and inhaling hydrogen showed a more curative effect compared with ischemic postconditioning treatment. Meanwhile inhaling hydrogen showed a better protective effect in attenuating tissue reactive oxygen species. Malondialdehyde levels and immunoreactivities against 8-hydroxy-2’-deoxyguanosine and inhibiting cardiac endoplasmic reticulum stress and down-regulating autophagy as compared with ischemic postconditioning treatment. Conclusion: These results revealed a better protective effect of hydrogen on myocardial ischemic/reperfusion injury in rats by attenuating endoplasmic reticulum stress and down-regulating autophagy compared with ischemic postconditioning treatment.

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“…2 Growing evidence from experimental studies and small-size proof-of-concept clinical trials shows that reperfusion injury contributes greatly to the final infarct size. [3][4][5] Preclinical studies indicate that the opening of the mitochondrial permeability transition pore (PTP) in the inner mitochondrial membrane plays a major role in reperfusion injury. 6,7 Either genetic or pharmacologic inhibition of cyclophilin D, a major component of the PTP, reduces the severity of myocardial reperfusion injury.…”

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confidence: 99%

Cyclosporine before PCI in Patients with Acute Myocardial Infarction

et al. 2015

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BACKGROUNDExperimental and clinical evidence suggests that cyclosporine may attenuate reperfusion injury and reduce myocardial infarct size. We aimed to test whether cyclosporine would improve clinical outcomes and prevent adverse left ventricular remodeling. METHODSIn a multicenter, double-blind, randomized trial, we assigned 970 patients with an acute anterior ST-segment elevation myocardial infarction (STEMI) who were undergoing percutaneous coronary intervention (PCI) within 12 hours after symptom onset and who had complete occlusion of the culprit coronary artery to receive a bolus injection of cyclosporine (administered intravenously at a dose of 2.5 mg per kilogram of body weight) or matching placebo before coronary recanalization. The primary outcome was a composite of death from any cause, worsening of heart failure during the initial hospitalization, rehospitalization for heart failure, or adverse left ventricular remodeling at 1 year. Adverse left ventricular remodeling was defined as an increase of 15% or more in the left ventricular end-diastolic volume. RESULTSA total of 395 patients in the cyclosporine group and 396 in the placebo group received the assigned study drug and had data that could be evaluated for the primary outcome at 1 year. The rate of the primary outcome was 59.0% in the cyclosporine group and 58.1% in the control group (odds ratio, 1.04; 95% confidence interval, 0.78 to 1.39; P = 0.77). Cyclosporine did not reduce the incidence of the separate clinical components of the primary outcome or other events, including recurrent infarction, unstable angina, and stroke. No significant difference in the safety profile was observed between the two treatment groups. CONCLUSIONSIn patients with anterior STEMI who had been referred for primary PCI, intravenous cyclosporine did not result in better clinical outcomes than those with placebo and did not prevent adverse left ventricular remodeling at 1 year. ( n engl j med 373;11 nejm.org September 10, 2015 1022T h e ne w e ngl a nd jou r na l o f m e dicine O ver the past three decades, major progress has been made in the treatment of patients with ST-segment elevation myocardial infarction (STEMI).1 Nevertheless, the rates of death, heart failure, and recurrent ischemic events occurring in the first year after infarction remain unacceptably elevated in this highrisk population. Although many advances have been made in the development of methods to reopen the culprit coronary artery and prevent reocclusion, there is currently no specific treatment that targets myocardial reperfusion injury, which is a paradoxical form of myocardial damage that occurs as a result of the restoration of vessel patency.2 Growing evidence from experimental studies and small-size proof-of-concept clinical trials shows that reperfusion injury contributes greatly to the final infarct size.3-5 Preclinical studies indicate that the opening of the mitochondrial permeability transition pore (PTP) in the inner mitochondrial membrane plays a major role in reperfusion injury. ...

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Cardioprotective role of ischemic postconditioning in acute myocardial infarction: A systematic review and meta-analysis

Cited by 37 publications

References 42 publications

Time to Give Up on Cardioprotection?

Time to Give Up on Cardioprotection?

Hydrogen Gas Attenuates Myocardial Ischemia Reperfusion Injury Independent of Postconditioning in Rats by Attenuating Endoplasmic Reticulum Stress-Induced Autophagy

Cyclosporine before PCI in Patients with Acute Myocardial Infarction

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