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Pexelizumab Does Not "Complement" Percutaneous Coronary Intervention in Patients With ST-Elevation Myocardial Infarction
John W. Eikelboom, MBBS;
Martin O’Donnell, MB
JAMA. 2007;297:91-92.
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Timely restoration of coronary artery blood flow using thrombolytic therapy, percutaneous coronary intervention (PCI), or coronary artery bypass graft (CABG) surgery salvages threatened myocardium and decreases cardiac morbidity and mortality. Reperfusion of ischemic tissues can, however, be associated with life-threatening reperfusion injury that can cause arrhythmias, myocardial stunning, microvascular dysfunction, and cell death.1 Accordingly, therapies that modulate reperfusion injury would be expected to enhance the effectiveness of thrombolysis and primary percutaneous coronary intervention for preserving myocardium and reducing mortality in patients with ST-elevation myocardial infarction (STEMI).
Complement activation plays a key role in the acute inflammatory response associated with ischemia and reperfusion injury.2-3 The anaphylotoxins, C3a and C5a, and the C5b-9 membrane attack complex that are formed during complement activation promote tissue injury by increasing vascular permeability, activating endothelial and inflammatory cells, activating hemostasis, inducing apoptosis, and causing cell lysis. Targeting the complement . . . [Full Text of this Article]
Author Affiliations: Department of Medicine, McMaster University, Hamilton, Ontario.
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