Ischaemic postconditioning revisited: lack of effects on infarct size following primary percutaneous coronary intervention

Freixa, Xavier; Bellera, Neus; Ortiz-Pérez, Josè T.; Jiménez, Marcelo; Paré, Carles; Bosch, Xavier; Caralt, Teresa M. de; Betriu, Amadeo; Masotti, Mónica

doi:10.1093/eurheartj/ehr297

Cited by 208 publications

(210 citation statements)

References 31 publications

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“…In 2013 a single‐center study by Freixa et al showed rather a significant deterioration in the myocardial salvage and the myocardial salvage index along with reduced pump function 6 months after myocardial ischemia 9. These results correspond to data published by Hahn et al from a multicenter study of 700 patients (POST [Effects of Postconditioning On Myocardial Reperfusion] trial, https://clinicaltrials.gov/show/NCT00942500) that was conducted between 2009 and 2012, also showing no cardiprotective effect 10.…”

Section: Introductionmentioning

confidence: 99%

Adverse Effects on β‐Adrenergic Receptor Coupling: Ischemic Postconditioning Failed to Preserve Long‐Term Cardiac Function

Schreckenberg

Bencsik

Weber

et al. 2017

JAHA

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BackgroundIschemic preconditioning (IPC) and ischemic postconditioning (IPoC) are currently among the most efficient strategies protecting the heart against ischemia/reperfusion injury. However, the effect of IPC and IPoC on functional recovery following ischemia/reperfusion is less clear, particularly with regard to the specific receptor‐mediated signaling of the postischemic heart. The current article examines the effect of IPC or IPoC on the regulation and coupling of β‐adrenergic receptors and their effects on postischemic left ventricular function.Methods and ResultsThe β‐adrenergic signal transduction was analyzed in 3‐month‐old Wistar rats for each of the intervention strategies (Sham, ischemia/reperfusion, IPC, IPoC) immediately and 7 days after myocardial infarction. Directly after the infarction a cardioprotective potential was demonstrated for both IPC and IPoC: the infarct size was reduced, apoptosis and production of reactive oxygen species were lowered, and the myocardial tissue was preserved. Seven days after myocardial ischemia, only IPC hearts showed significant functional improvement. Along with a deterioration in fractional shortening, IPoC hearts no longer responded adequately to β‐adrenergic stimulation. The stabilization of β‐adrenergic receptor kinase‐2 via increased phosphorylation of Mdm2 (an E3‐ubiquitin ligase) was responsible for desensitization of β‐adrenergic receptors and identified as a characteristic specific to IPoC hearts.ConclusionsImmediately after myocardial infarction, rapid and transient activation of β‐adrenergic receptor kinase‐2 may be an appropriate means to protect the injured heart from excessive stress. In the long term, however, induction and stabilization of β‐adrenergic receptor kinase‐2, with the resultant loss of positive inotropic function, leads to the functional picture of heart failure.

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Section: Introductionmentioning

confidence: 99%

Adverse Effects on β‐Adrenergic Receptor Coupling: Ischemic Postconditioning Failed to Preserve Long‐Term Cardiac Function

Schreckenberg

Bencsik

Weber

et al. 2017

JAHA

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“…Further, patients with larger infarcts or those with an anterior MI are more likely to benefit from such an intervention. 5,6,27,32 Indeed, in our initial study, there was a trend toward a stronger effect of sevoflurane in patients with an anterior MI on assessing myocardial injury by release of cardiac enzymes. 20 In the current study, we did not observe an overall clinically meaningful effect of sevoflurane on the long-term assessment of LV function, myocardial scarring, or hibernating myocardium.…”

Section: Discussionmentioning

confidence: 79%

“…4,5 However, other recent studies, including a study published by our group, did not show clinical benefit from ischemic conditioning, suggesting that the precise mode of applying ischemic conditioning should be explored further. 6,7 In particular, it seems that it is important to apply the ischemic conditioning intervention as early as possible. Administration of a pharmacological agent that mimics ischemic conditioning can be initiated early and may be suitable for all patients with STEMI receiving reperfusion therapy, including fibrinolysis and pPCI.…”

Section: Résumémentioning

confidence: 99%

One-year outcome of the sevoflurane in acute myocardial infarction randomized trial

Lavi

Alemayehu

McCarty

et al. 2015

Can J Anesth/J Can Anesth

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Background Sevoflurane is an inhalation anesthetic that has cardioprotective effects. There is limited information regarding its use outside of the operating room and its potential protective effect for patients presenting with myocardial infarction. Methods In the Sevoflurane In Acute Myocardial Infarction trial, patients with a first acute ST-elevation myocardial infarction (STEMI) who were treated by primary percutaneous coronary intervention were randomized to inhalation of sevoflurane or oxygen (control). From the time of the patient's arrival for cardiac catheterization, the anesthesia team administered sevoflurane or oxygen for 30 min using a tight-fitting mask.In this substudy, we report the one-year outcomes. Patients were followed clinically for one year; they underwent a thallium cardiac viability study at six months and an echocardiogram at one year. Results Forty-six patients completed follow-up. One patient in the sevoflurane group died. The mean [standard deviation (SD)] ejection fraction by singlephoton emission computed tomography at six months was 51.7 (7.7)% in the sevoflurane group and 51 (9.1)% in the control group (mean difference, 0.7%; 95% confidence interval [CI], -5.9 to 7.3; P = 0.831). The median [interquartile range] amount of scarring at six months was 0% [0 -8] in the sevoflurane group and 2.5% [0 -7.1] in control group (mean difference, -0.1%; 95% CI, -4.6 to 4.4; P = 0.700). The mean (SD) percentage of hibernating myocardium was similar in both groups 0% [0, 5] (mean difference, -1.3%; 95% CI, -3.4 to 0.9; P = 0.259). The mean (SD) ejection fraction at one year increased compared with baseline by 8.0 (9.1)% (P \ 0.001).Conclusions In this study, we did not find an effect of sevoflurane on left ventricular function or myocardial injury at one year post STEMI. This trial was registered at www.clinicaltrials.gov; identifier: NCT00971607. RésuméContexte Le sévoflurane est un anesthésique inhalé qui a des effets cardioprotecteurs. On ne dispose que de peu Meeting presentation: Presented in part at the Canadian Cardiovascular Congress in Vancouver, 2014 and published as an abstract (Can J Cardiol 2014, 30 (10): s62.).

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“…Clinical trials reported conflicting results of POC application during the percutaneous coronary intervention of the infarct related artery. POC triggered cardioprotection [8] or did not protect myocardium against I/R injury at all [18]. Such observed discrepancies may be related to diverse scenarios of coronary artery occlusion.…”

Section: Discussionmentioning

confidence: 96%

The co-application of hypoxic preconditioning and postconditioning abolishes their own protective effect on systolic function in human myocardium

Roleder

Gołba²,

Kunecki³

et al. 2013

Cardiol J

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NE application, as compared to Control (30.35 ± 2.25 vs. 41.89 ± 2.25, 56.26 ± 7.73 vs. 65.98 ± 5.39, respectively). This was in contrary to the effects observed when IPC and POC were applied separately. Conclusions:The co-application of IPC and POC abolishes the cardioprotection of either intervention alone against simulated I/R injury in fragments of the human right heart atria. (Cardiol J 2013; 20, 5: 472-477)

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Ischaemic postconditioning revisited: lack of effects on infarct size following primary percutaneous coronary intervention

Abstract: This randomized study suggests that p-cond during primary PCI does not reduce infarct size or improve myocardial function recovery at both short- and long-term follow-up and might have a potential harmful effect.

Cited by 208 publications

References 31 publications

Adverse Effects on β‐Adrenergic Receptor Coupling: Ischemic Postconditioning Failed to Preserve Long‐Term Cardiac Function

Adverse Effects on β‐Adrenergic Receptor Coupling: Ischemic Postconditioning Failed to Preserve Long‐Term Cardiac Function

One-year outcome of the sevoflurane in acute myocardial infarction randomized trial

The co-application of hypoxic preconditioning and postconditioning abolishes their own protective effect on systolic function in human myocardium

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