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Jan 13, 2001 - Abstract Intron 9 contains the complete endogenous retrovirus HERV-K(C4) as a 6.4-kb insertion in 60% of human C4 genes. The retroviral ...
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507004 research-article2013
ACC3110.1177/2048872613507004European Heart Journal: Acute Cardiovascular CareHolt et al.
EUROPEAN SOCIETY OF CARDIOLOGY ®
Original scientific paper
Association between endogenous complement inhibitor and myocardial salvage in patients with myocardial infarction
Charlotte B Holt1,2, Steffen Thiel2, Kim Munk1, Jakob A Østergaard1, Hans E Bøtker1 and Troels K Hansen1
Abstract Background: Many pathogenic processes and diseases are the result of an erroneous activation of the complement cascade and a number of inhibitors of complement have thus been examined for anti-inflammatory actions. It was recently demonstrated that supraphysiological concentrations of the endogenous complement inhibitor MAp44 (also denoted MAP1) protect against myocardial reperfusion injury. In the present study, we examined the association between outcome after acute myocardial infarction (MI) and the plasma levels of MAp44 and its related proteins MASP1 and MASP-3 in patients with first-time MI. In addition, we compared plasma levels of MAp44, MASP-1, and MASP-3 in MI patients to levels in a healthy control group. Methods: A total of 192 MI patients and 140 control persons were included. Plasma samples were obtained and analysed with time-resolved immunofluorometric assays determining the plasma levels of MAp44, MASP-1, and MASP3. The myocardial outcomes (salvage index and final infarct size) were measured by gated single-photon emission CT. Results: MI patients had 18 % higher plasma levels of MAp44 (IQR 11–25%) as compared to the healthy control group (p
