Administration of C1-esterase inhibitor during emergency coronary artery bypass surgery in acute ST-elevation myocardial infarction☆

Thielmann, Matthias; Marggraf, G.; Neuhäuser, Markus; Forkel, Jörg; Herold, Ulf; Kamler, Markus; Massoudy, Parwis; Jakob, Heinz

doi:10.1016/j.ejcts.2006.04.022

Cited by 49 publications

(23 citation statements)

References 22 publications

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“…Prior studies conducted on patients with acute myocardial infarction have shown that treatment with intravenous C1-INH may reduce myocardial injury. 30,31 Based on our findings it can be assumed that supplementation with C1-INH during the postoperative period might be beneficial in the prevention of restenosis in patients with CEA.…”

Section: Discussionmentioning

confidence: 99%

Low C1-Inhibitor Levels Predict Early Restenosis After Eversion Carotid Endarterectomy

Varga

Laki

Dósa

et al. 2007

ATVB

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Objective-Homozygotes for the normal (A) allele of mannose-binding lectin (MBL2) gene have higher risks to develop an early restenosis after eversion carotid endarterectomy (CEA). Activation of the lectin pathway is regulated by C1-inhibitor (C1-INH). The objective of the present study was to determine the predictive value of C1-INH in restenosis after CEA. Methods and Results-C1-INH and MBL-associated serine protease-2 (MASP-2) were determined in samples serially taken from 64 patients with CEA, who were followed-up with carotid duplex scan (CDS) examinations for 14 months. MBL2 genotypes were also determined.

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Section: Discussionmentioning

confidence: 99%

Low C1-Inhibitor Levels Predict Early Restenosis After Eversion Carotid Endarterectomy

Varga

Laki

Dósa

et al. 2007

ATVB

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“…In humans, C1-inhibitor half-life was calculated to be Ϸ35 hours, and administration of C1-inhibitor (40 IU/kg) to patients during bypass surgery after myocardial infarction has been shown to be beneficial, without adverse effects or complications. 47 In a porcine model, C1-inhibitor at 40 IU/kg was effective and had no associated adverse effects, but used at a higher dose (100 and 200 IU/kg), it provoked severe side effects and coagulation disorders. 48 In mice, however, treatment with the C1-inhibitor (at 15 IU per mouse, which corresponds to Ϸ400 IU/kg) was well-tolerated, and no adverse effects, infections, or bleeding disorders were observed.…”

Section: Shagdarsuren Et Al C1-esterase Inhibitor Reduces Neointima Fmentioning

confidence: 99%

C1-Esterase Inhibitor Protects Against Neointima Formation After Arterial Injury in Atherosclerosis-Prone Mice

et al. 2008

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Background-Although activation of the complement system has been implicated in the progression of human atherosclerosis, its function during arterial remodeling after injury has not been investigated. Here, we examined the contribution of the complement cascade to neointima formation in apolipoprotein E-deficient mice using a C1-esterase inhibitor (C1-inhibitor). Methods and Results-Apolipoprotein E-deficient mice fed an atherogenic diet were subjected to wire-induced endothelial denudation of the carotid artery and treated with C1-inhibitor (Berinert; 15 IU IV) or vehicle perioperatively and subsequently every 2 days. The effectiveness of C1-inhibitor treatment was confirmed by measurement of plasma C1-inhibitor activity. A significant reduction in serum triglyceride levels was observed in C1-inhibitor-treated mice, whereas cholesterol levels did not differ. After 3 weeks, neointimal area was significantly reduced in C1-inhibitor-treated mice versus controls, whereas medial area was unaltered. This was associated with a significant decrease in neointimal and medial macrophage and CD3 ϩ T-cell content. Expression of C3 mRNA was significantly reduced in plaques of C1-inhibitor-treated mice 10 days after injury, as assessed by reverse-transcription polymerase chain reaction. The peak in serum C3 levels after injury was markedly downregulated by C1-inhibitor, as evidenced by ELISA. Immunohistochemistry revealed strong expression of C3 and C3c, which colocalized to plaque macrophages and was reduced in C1-inhibitor-treated mice. C1-inhibitor impaired monocyte arrest on activated endothelium and platelets under flow conditions in vitro and leukocyte recruitment to carotid arteries 1 day after injury in vivo. Conclusions-C1-inhibitor limits neointimal plaque formation and inflammation. This may involve blockade of complement activation, inhibition of leukocyte recruitment, and reduced triglyceride levels, thus providing a multimodal approach to treat arterial disease. (Circulation. 2008;117:70-78.)Key Words: atherosclerosis Ⅲ inflammation Ⅲ cell adhesion molecules Ⅲ complement A therosclerosis is an inflammatory disease that is strongly affected by the action of monocytes/macrophages and T cells. 1 Emerging evidence further suggests that the complement system plays a role in atherosclerosis, although its exact functions and mechanisms of action remain unclear. 2,3 In atherosclerotic plaques, activation of the classic complement pathway has been observed. In addition, mRNA of complement components, including C3 activation products and membrane attack complex, are also detectable in diseased arteries. Membrane attack complex depositions colocalize with lipoproteins, which are known to be potent activators of the complement system in the aortic intima in rabbits at early stages of atherogenesis and in human atherosclerotic lesions, 4 and they correlate with the severity of arterial damage. 5,6 Clinical Perspective p 78However, complement regulatory proteins have not been found to be upregulated in human plaque tissue. 7 ...

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“…However, despite these profound experimental data, the only available clinical trial addressing the role of sCR1 in ischemia-reperfusion injury yielded disappointing therapeutic results [128]. In contrast, the efficacy of C1-Esterase inhibitor (C1-INH) in preventing reperfusion injury has been shown experimentally in rats [129] and pigs [83,130] as well as clinically [131], where application of C1-INH in patients with coronary bypass surgery in acute ST-elevation myocardial infarction resulted in reduced myocardial reperfusion injury [132,133] and improved cardiac function [134].…”

Section: Contemporary Treatment Strategiesmentioning

confidence: 99%

Ischemia-Reperfusion Injury

Dorweiler

Pruefer²,

Andrási³

et al. 2007

Eur J Trauma Emerg Surg

116

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The term ischemia-reperfusion injury describes the experimentally and clinically prevalent finding that tissue ischemia with inadequate oxygen supply followed by successful reperfusion initiates a wide and complex array of inflammatory responses that may both aggravate local injury as well as induce impairment of remote organ function. Conditions under which ischemia-reperfusion injury is encountered include the different forms of acute vascular occlusions (stroke, myocardial infarction, limb ischemia) with the respective reperfusion strategies (thrombolytic therapy, angioplasty, operative revascularization) but also routine surgical procedures (organ transplantation, free-tissue-transfer, cardiopulmonary bypass, vascular surgery) and major trauma/shock. Since the first recognition of ischemia-reperfusion injury during the 1970s, significant knowledge has accumulated and the purpose of this review is to present an overview over the current literature on the molecular and cellular basis of ischemia-reperfusion injury, to outline the clinical manifestations and to compile contemporary treatment and prevention strategies. Although the concept of reperfusion injury is still a matter of debate, it is corroborated by recent and ongoing clinical trials that demonstrated ischemic preconditioning, inhibition of sodium-hydrogen-exchange and administration of adenosine to be effective in attenuating ischemia-reperfusion injury.

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Administration of C1-esterase inhibitor during emergency coronary artery bypass surgery in acute ST-elevation myocardial infarction☆

Abstract: C1-INH administration in emergency CABG with acute STEMI is safe and effective to inhibit complement activation and may reduce myocardial ischemia-reperfusion injury as measured by cTnI.

Cited by 49 publications

References 22 publications

Low C1-Inhibitor Levels Predict Early Restenosis After Eversion Carotid Endarterectomy

Low C1-Inhibitor Levels Predict Early Restenosis After Eversion Carotid Endarterectomy

C1-Esterase Inhibitor Protects Against Neointima Formation After Arterial Injury in Atherosclerosis-Prone Mice

Ischemia-Reperfusion Injury

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