Cardioprotective Role of Remote Ischemic Periconditioning in Primary Percutaneous Coronary Intervention

Rentoukas, Ilias; Γιαννόπουλος, Γεώργιος; Kaoukis, Andreas; Kossyvakis, Charalampos; Raisakis, Konstantinos; Driva, Metaxia; Panagopoulou, Vasiliki; Tsarouchas, Konstantinos; Vavetsi, Sofia; Pyrgakis, Vlasios; Deftereos, Spyridon

doi:10.1016/j.jcin.2009.10.015

Cited by 211 publications

(163 citation statements)

References 26 publications

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“…A metaanalysis including 244 patients treated by PPCI suggested that preconditioning resulted in lower mean peak creatine kinase release, and improved left ventricular ejection fraction and myocardial reperfusion, compared with controls. 44 Interestingly, Rentoukas et al 45 showed that the beneficial effect of remote IPC on ST-segment resolution in patients treated by PPCI was increased by the concomitant administration of morphine. Remote preconditioning is unique in that it can be applied during myocardial ischaemia, prior to reperfusion.…”

Section: Prevention and Treatment Of Ischaemia-reperfusion Injurymentioning

confidence: 99%

Pharmacological and physical prevention and treatment of no-reflow after primary percutaneous coronary intervention in ST-segment elevation myocardial infarction

Guo

Sheng²,

Xu³

et al. 2013

J Int Med Res

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After successful primary percutaneous coronary intervention in ST-segment elevation myocardial infarction, adequate myocardial reperfusion is not achieved in up to 50% of patients. This phenomenon of no-reflow is associated with a poor in-hospital and long-term prognosis. Four main factors are thought to contribute to the occurrence of no-reflow: ischaemic injury; reperfusion injury; distal embolization; susceptibility of the microcirculation to injury. This review evaluates the literature, and in particular the clinical trials, concerned with pharmacological and physical methods for prevention and treatment of no-reflow. A number of drugs may improve no-reflow experimentally and clinically, but some have not yet been associated with conclusive improvements in clinical outcome. The complex interacting factors in no-reflow make it unlikely that any single agent will be effective for all patients. Confirmed methods known to be beneficial in the prevention of no-reflow (such as aspirin therapy, chronic statin therapy, blood glucose control, thrombus aspiration in patients with a high thrombus burden and ischaemic preconditioning) should be offered to patients as often as possible, to prevent and treat no-reflow.

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Section: Prevention and Treatment Of Ischaemia-reperfusion Injurymentioning

confidence: 99%

Pharmacological and physical prevention and treatment of no-reflow after primary percutaneous coronary intervention in ST-segment elevation myocardial infarction

Guo

Sheng²,

Xu³

et al. 2013

J Int Med Res

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show abstract

“…Primary PCI is the gold standard, and the first study to examine RIC in this setting included 33 patients in each group, but was negative 95. Interestingly, in this study, while RIC did not provide additional benefit over the control group, a third group that received morphine in addition to RIC had less myocardial injury, suggesting a synergistic role for RIC with an opioid.…”

Section: Ric In Stemi Patients Treated By Primary Pcimentioning

confidence: 76%

Remote ischaemic conditioning: cardiac protection from afar

2015

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For patients with ischaemic heart disease, remote ischaemic conditioning may offer an innovative, non‐invasive and virtually cost‐free therapy for protecting the myocardium against the detrimental effects of acute ischaemia‐reperfusion injury, preserving cardiac function and improving clinical outcomes. The intriguing phenomenon of remote ischaemic conditioning was first discovered over 20 years ago, when it was shown that the heart could be rendered resistant to acute ischaemia‐reperfusion injury by applying one or more cycles of brief ischaemia and reperfusion to an organ or tissue away from the heart – initially termed ‘cardioprotection at a distance’. Subsequent pre‐clinical and then clinical studies made the important discovery that remote ischaemic conditioning could be elicited non‐invasively, by inducing brief ischaemia and reperfusion to the upper or lower limb using a cuff. The actual mechanism underlying remote ischaemic conditioning cardioprotection remains unclear, although a neuro‐hormonal pathway has been implicated. Since its initial discovery in 1993, the first proof‐of‐concept clinical studies of remote ischaemic conditioning followed in 2006, and now multicentre clinical outcome studies are underway. In this review article, we explore the potential mechanisms underlying this academic curiosity, and assess the success of its application in the clinical setting.

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“…In recent decades, IR injury has become a topic of particular interest in the context of liver surgery and research. Studies have predominantly focused on RIPC, which is a strategy for harnessing the body's endogenous protective capabilities against the injury that is incurred during IR (5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17). NO is an essential mediator of the protection that is afforded by hind-limb RIPC against liver IR injury (25).…”

Section: Discussionmentioning

confidence: 99%

“…Increasing evidence indicates that remote ischemic preconditioning (RIPC) represents a strategy for harnessing the body's endogenous protective capabilities to counter the injury that is incurred by IR in various organs (5)(6)(7)(8)(9)(10)(11)(12)(13), including the normal liver (14)(15)(16)(17). The protective mechanism of RIPC is highly complex (18)(19)(20)(21)(22) and involves the improvement of hepatic oxygenation (23), reduction of serum cytokine-induced neutrophil chemoattractant-1 levels (24), modulation of hepatic microcirculation (15) and activation of the soluble guanylate cyclase-cyclic guanosine monophosphate pathway (20), resulting in protective effects against IR injury.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-29a/b/c targets iNOS and is involved in protective remote ischemic preconditioning in an ischemia-reperfusion rat model of non-alcoholic fatty liver disease

et al. 2017

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Abstract. Remote ischemic preconditioning (RIPC) protects against the injury that is incurred by ischemia and reperfusion (IR); however, the role of RIPC in liver IR injury in non-alcoholic fatty liver disease (NAFLD) remains unclear. In this study, a NAFLD rat model was utilized in a series of different surgical procedures and molecular experiments. Rats of the IR group and the RIPC+IR group exhibited more severe injury than NAFLD control rats (in which the liver was prodded following a median-incision laparotomy). The liver condition, measured by serum alanine transaminase and aspartate transaminase levels, of the RIPC+IR group was better than that of the IR group. In addition, alanine transaminase and aspartate transaminase levels were lower in the RIPC+IR group compared with the IR group (P<0.001). Flow cytometry revealed that the cell apoptosis ratio was significantly lower in the RIPC+IR group than in the IR group (P<0.001). Reverse transcription-polymerase chain reaction (RT-qPCR) was used to assess miR-29a/b/c levels, revealing that they were significantly reduced in the RIPC and RIPC+IR groups, but did not vary in the IR group compared with the control group. RT-qPCR also revealed that iNOS mRNA levels were not significantly different among any of the NAFLD groups; however, western blot analysis indicated that iNOS protein levels were increased in the RIPC group and the RIPC+IR group compared with the control and IR groups. A luciferase reporter assay demonstrated that transfection with miR-29a/b/c mimics significantly decreased the luciferase activities of plasmids containing the wild-type iNOS 3'-untranslated region (UTR) (relative fluorescence intensity: 0.47±0.06 for miR-29a, 0.36±0.07 for miR-29b, 0.41±0.04 for miR-29c; P<0.001), whereas the activities of plasmids containing the mutant iNOS 3'-UTR sequence were not markedly affected [relative fluorescence intensity: 0.99±0.08 for miR-29a (P=0.1349), 0.99±0.09 for miR-29b (P= 0.1607), 0.97±0.07 for miR-29c (P= 0.1824)]. This suggested that miR-29a/b/c downregulates iNOS by directly targeting its 3'-UTR. In summary, the results suggest that RIPC has a protective effect in NAFLD liver IR injury, which may be due to reduced miR-29a/b/c levels in the skeletal muscle, leading to increased iNOS and, therefore, nitric oxide.

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Cardioprotective Role of Remote Ischemic Periconditioning in Primary Percutaneous Coronary Intervention

Cited by 211 publications

References 26 publications

Pharmacological and physical prevention and treatment of no-reflow after primary percutaneous coronary intervention in ST-segment elevation myocardial infarction

Pharmacological and physical prevention and treatment of no-reflow after primary percutaneous coronary intervention in ST-segment elevation myocardial infarction

Remote ischaemic conditioning: cardiac protection from afar

MicroRNA-29a/b/c targets iNOS and is involved in protective remote ischemic preconditioning in an ischemia-reperfusion rat model of non-alcoholic fatty liver disease

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