Complement factors in Acute Myocardial Infarction and Unstable Angina

Coronary artery disease (CAD) is one of the most important and lethal diseases in the world. CAD represents a board spectrum of disease from silent ischemia at one end to sudden cardiac death at the other end. The middle of this spectrum consists of acute myocardial infarction (AMI) and unstable angina pectoris (UA). Recent data show that the inflammatory process plays a major role in the pathogenesis of acute coronary syndrome. In this study we evaluated the difference in complement factors C3 and C4 between AMI and UA, and the relation between early completions of AMI and UA and the amount of C3 and C4. In this cross – sectional analytic study, 30 patients with AMI and 30 patients with UA were compared with healthy subjects. Clinical and laboratory data were collected. Blood samples were obtained on arrival and at 12.24 and 48 hours. electrocardiography and echocardiography were performed. All patients were monitored for 14 days after discharging from hospital. For all patients ECG was take on arrival and then daily bat. Complement activation occurred in patients with AMI and UA. In AMI activation of complement factors was significantly higher than in UA (p<0.01). In Qwave MI and congestive heart failure, this elevation of activity was prominent (p<0.01). In AMI a positive relation was found between complement factors and Cratin phospho kinas level (r=0.71). There was a positive relation between complement and mortality, and an inverse relation with ejection fraction (r=0.71). There was significant difference among complement factors in the UA, AMI, and control group (p<0.01). Elevated levels of complement factors in AMI were related to the degree of left ventricular ejection fraction (LVEF). Q-wave MI, and mortality. However, in UA, elevated levels of complement factors were unrelated, with the exception of the serum C3 level, which was related to LVEF.