Beneficial Impact of Preconditioning During PTCA on Creatine Kinase Release

Laskey, Warren K.

doi:10.1161/01.cir.99.16.2085

Cited by 58 publications

(37 citation statements)

References 39 publications

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“…3,13,22,23) Appropriate balloon ischemia has been shown to suppress lactate production during coronary angioplasty in patients with stable angina pectoris 3) and creatine kinase elevation after coronary angioplasty in patients with unstable ischemic syndromes. 22) Yasuda, et al 13) reported that pre-administration of nicorandil suppresses lactate production during angioplasty, suggesting that pharmacological preconditioning is induced by nicorandil. Jenkins, et al 23) reported that short periods of ischemia at the beginning of the revascularization operation reduce TnT release in patients undergoing coronary artery bypass surgery.…”

Section: Discussionmentioning

confidence: 99%

Nicorandil-Induced Preconditioning as Evidenced by Troponin T Measurements after Coronary Angioplasty in Patients with Stable Angina Pectoris.

et al. 2002

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SUMMARYNicorandil has been reported to have a preconditioning effect which suppresses the ST-segment shift or lactate production during coronary angioplasty in patients with stable angina pectoris. The present study investigated whether the preconditioning effect of nicorandil affects troponin T (TnT) levels after coronary angioplasty. Twenty-four patients with stable angina pectoris were randomized to receive a 1-minute intravenous infusion of nicorandil (100 µg/kg) or normal saline. Five minutes later they underwent three 2-minute balloon inflations 5 minutes apart. The sum of ST-segment elevation in all leads (∑ST) was determined at the end of each balloon inflation. Serum levels of TnT were measured 6 and 18 hours after the procedure, and the higher value of the two measurements was compared between the groups. ∑ST decreased progressively during the three sequential balloon inflations in both groups and was less in the nicorandil group than in the control group. The TnT level after the procedure was significantly lower in the nicorandil group than in the control group (0.05±0.05 vs 0.11±0.10 ng/mL). In conclusion, pretreatment with intravenous nicorandil suppresses TnT release after coronary angioplasty as well as ST-segment elevation during coronary angioplasty, suggesting pharmacological preconditioning by nicorandil. (Jpn Heart J 2002; 43: 443-453)

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Section: Discussionmentioning

confidence: 99%

Nicorandil-Induced Preconditioning as Evidenced by Troponin T Measurements after Coronary Angioplasty in Patients with Stable Angina Pectoris.

et al. 2002

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“…[41][42][43] Less pain was the reported clinical end point. 41,42 There were then several smaller proof-of-concept studies on ischemic preconditioning in patients undergoing surgical revascularization by CABG or valve surgery.…”

Section: Ischemic Preconditioningmentioning

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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“…It is known that exercise can mimic the protective effect of IP (9,12,21,51). Evidence for preconditioning in humans derives also from in vitro studies (42) and observations made during coronary angioplasty and cardiac surgery (12,21,51).…”

Section: Physiological Significance Of the Findings In Cardioprotectionmentioning

confidence: 99%

“…Evidence for preconditioning in humans derives also from in vitro studies (42) and observations made during coronary angioplasty and cardiac surgery (12,21,51). Also, the warm-up phenomenon (i.e., enhanced resistance to further ischemia in patients suffering from angina a few minutes after a previous effort) has been attributed to a preconditioning-like effect (9,46).…”

Section: Physiological Significance Of the Findings In Cardioprotectionmentioning

confidence: 99%

Platelet-activating factor induces cardioprotection in isolated rat heart akin to ischemic preconditioning: role of phosphoinositide 3-kinase and protein kinase C activation

Penna

Alloatti

Cappello³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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. Platelet-activating factor induces cardioprotection in isolated rat heart akin to ischemic preconditioning: role of phosphoinositide 3-kinase and protein kinase C activation. Am J Physiol Heart Circ Physiol 288: H2512-H2520, 2005. First published January 6, 2005; doi:10.1152/ajpheart.00599.2004.-Ischemic preconditioning (IP) is a cardioprotective mechanism against myocellular death and cardiac dysfunction resulting from reperfusion of the ischemic heart. At present, the precise list of mediators involved in IP and the pathways of their mechanisms of action are not completely known. The aim of the present study was to investigate the role of platelet-activating factor (PAF), a phospholipid mediator that is known to be released by the ischemic-reperfused heart, as a possible endogenous agent involved in IP. Experiments were performed on Langendorff-perfused rat hearts undergoing 30 min of ischemia followed by 2 h of reperfusion. Treatment with a low concentration of PAF (2 ϫ 10 Ϫ11 M) before ischemia reduced the extension of infarct size and improved the recovery of left ventricular developed pressure during reperfusion. The cardioprotective effect of PAF was comparable to that observed in hearts in which IP was induced by three brief (3 min) periods of ischemia separated by 5-min reperfusion intervals. The PAF receptor antagonist WEB-2170 (1 ϫ 10 Ϫ9 M) abrogated the cardioprotective effect induced by both PAF and IP. The protein kinase C (PKC) inhibitor chelerythrine (5 ϫ 10 Ϫ6 M) or the phosphoinositide 3-kinase (PI3K) inhibitor LY-294002 (5 ϫ 10 Ϫ5 M) also reduced the cardioprotective effect of PAF. Western blot analysis revealed that following IP treatment or PAF infusion, the phosphorylation of PKC-⑀ and Akt (the downstream target of PI3K) was higher than that in control hearts. The present data indicate that exogenous applications of low quantities of PAF induce a cardioprotective effect through PI3K and PKC activation, similar to that afforded by IP. Moreover, the study suggests that endogenous release of PAF, induced by brief periods of ischemia and reperfusion, may participate to the triggering of the IP of the heart. ischemia-reperfusion; WEB-2170; LY-294002 ISCHEMIC PRECONDITIONING (IP) is the phenomenon whereby brief periods of ischemia and reperfusion increase the resistance to myocardial infarction and contractile dysfunction induced by a subsequent sustained episode of ischemia (9, 34 -36). In all species tested, the beneficial effects of IP include protection against necrotic and apoptotic cell death. In some species, it has been shown that IP also induces the prevention of ischemia-reperfusion-induced arrhythmias, a faster recovery from reperfusion-induced myocardial stunning, and a protection of microvasculature function (for reviews, see Refs. 33 and 35

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Beneficial Impact of Preconditioning During PTCA on Creatine Kinase Release

Abstract: A standardized protocol to elicit preconditioning during PTCA results in a significant reduction in the rate of CK elevation in a high-risk population. These observations support the clinical relevance of ischemic preconditioning in humans.

Cited by 58 publications

References 39 publications

Nicorandil-Induced Preconditioning as Evidenced by Troponin T Measurements after Coronary Angioplasty in Patients with Stable Angina Pectoris.

Nicorandil-Induced Preconditioning as Evidenced by Troponin T Measurements after Coronary Angioplasty in Patients with Stable Angina Pectoris.

Time to Give Up on Cardioprotection?

Platelet-activating factor induces cardioprotection in isolated rat heart akin to ischemic preconditioning: role of phosphoinositide 3-kinase and protein kinase C activation

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