Chest
Complement Activation after Myocardial Infarction
Section snippets
PATIENTS
Fifty-six patients admitted with myocardial infarction, diagnosed on the clinical presentation and associated ECG and serum enzyme changes, were studied. They were divided into four groups as follows:
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Postmyocardial infarction syndrome: 13 patients (mean age 56 years) had pericardial friction occurring after the first postinfarction week (mean duration eight days), pyrexia of more than seven days' duration, and a maximum ESR of greater than 60 mm in the first hour. The chest x-ray films
Specimens
For C3 and C4 estimations, 5 ml venous blood was taken into plain tubes, separated, and frozen within one hour of collection at — 70°C. All patients had blood taken at least twice weekly. In 15 patients, additional samples were taken at daily intervals to ascertain dynamic changes in C3d concentrations.
Serum C3, C4, and C3d Estimations
The C3d antiserum was prepared by coating rabbit erythrocytes with human C3d and then injecting them back into the same rabbit, as described by Merry et al.8 The specificities of the resulting
C3d Plasma Concentrations
The mean C3d values (expressed as a percentage of native C3) showed significant differences between the control subjects and the other three groups (p<0.001). By far, the most striking difference was between the control subjects and the PMIS patients (Table 1). Figure 1 is a scattergram of all the C3d results recorded at twice weekly intervals. The results in the control subjects showed an apparent cut-off at the 7 to 8 percent level. Of the eight patients whose C3d exceeded 8 percent, seven
DISCUSSION
It has been established that following myocardial infarction, complement levels rise roughly in parallel with the ESR (complement being acute phase proteins),12 and this probably explains why the maximum serum C3 and C4 concentrations were higher in the prolonged pyrexia and pulmonary embolism groups when compared to the control subjects. However, the PMIS patients, despite all having ESR levels in excess of 60 mm in the first hour, had slightly lower C3 levels than the control subjects. The
ACKNOWLEDGMENTS
We thank Dr. Milford Ward for his help with the complement investigations, Drs. Merry and Rawlinson for their help in preparing the C3d antiserum, and Professor Mollison for allowing us to have some of his C3d antiserum. We also thank all the physicians and the staff of the Heart Care Unit at Hope Hospital, Salford.
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