Complement activation after myocardial infarction.

Complement activation as reflected by C3, C4, and C3d levels was studied in 56 patients following myocardial infarction, 13 with the postmyocardial infarction syndrome (PMIS); 12 with prolonged postinfarction pyrexia; six with clinical evidence of pulmonary embolism; and 25 control patients without apparent complications. In most patients, C3d levels were elevated during the first ten postinfarction days and at the time of any pulmonary embolism; this probably represented local nonimmunologic complement utilization. The PMIS patients had much higher C3d levels associated with significantly lower concentrations of C3 at the time of disease activity. It is suggested that heart reactive antibodies combine with circulating cardiac antigens to form soluble immune complexes, and in the PMIS, these may become deposited in various sites resulting in complement-mediated tissue damage. The high C3d levels associated with the PMIS may also be of value in differentiating this condition from pulmonary embolism, as both problems may have similar clinical and roentgenographic features.