Measurement of autoimmune response against collagen types I, III, and IV by enzyme-linked immunosorbent assay, and its application in infective endocarditis.

In these enzyme-linked immunosorbent assays for determination of autoantibodies (IgG, IgM) against collagen type I (ACA I), III (ACA III), and IV (ACA IV), we use commercially available antigen preparations. Inhibition curves showed limited cross-reactivity between these different collagen preparations, the major interference being observed after addition of collagen type III in the ACA I procedures. Imprecision (CVs) for high- and low-titer samples ranged between 1.5% and 7.9% (within-run) and 5.5% and 12.7% (between-run) for ACA I, between 2.2-8.7% and 4.5-10.7% for ACA III, and between 1.3-5.9% and 7.4-11.6% for ACA IV. Significantly increased humoral immune response against collagen types I and III (P less than 0.001) could be demonstrated during the first month of infective endocarditis. In contrast, only borderline increases, however constant, of autoimmune response against basement-membrane collagen (ACA IV) were noticed during 90 days of follow-up.

Postoperative immunological response against contractile proteins after coronary bypass surgery.

The pathogenesis of post-cardiac injury syndrome was studied prospectively in 62 patients who underwent coronary bypass grafting. Preoperative and serial postoperative titres of actin and myosin antibodies were measured by an enzyme linked immunosorbent assay. Perioperative cumulative release of serum aspartate and alanine aminotransferases, lactate dehydrogenase, and creatine kinase was calculated by approximation formulas that are used to estimate infarct size. Complete post-cardiac injury syndrome developed in eight (13%) patients and an incomplete syndrome developed in 16 (26%). There was a significant correlation between frequency and intensity of the syndrome and the ratio of postoperative to preoperative titres of actin and myosin antibodies. Furthermore, there was a significant correlation between the cumulative release of lactate dehydrogenase, serum aspartate aminotransferase, and creatine kinase and the number of coronary vessels that were grafted, but no correlation was found between the incidence of post-cardiac injury syndrome and the number of coronary bypasses grafted or between the cumulative enzyme release and the postoperative immunological response against the major contractile proteins, actin and myosin. The amount of enzymes released during coronary bypass surgery seems to be a good indicator of the extent of myocardial damage during operation but it does not determine either the incidence of post-cardiac injury syndrome or the postoperative immunological response against the main contractile proteins actin and myosin.

Macro CK type 1 as a marker for autoimmunity in coronary heart disease.

In a group of 3000 hospital patients the prevalence of immunoglobulin bound creatine kinase (macro CK type 1) was 4.3%. The relative frequency was greater in the older age categories. The highest prevalence was found in patients with rheumatic and cardiac diseases. In a group of 556 cardiac patients selected for coronary angiography a prevalence of 13.8% was observed. No significant correlation was obtained between the findings of the coronary angiography and the activity of macro CK type 1. CK MB results determined by ion-exchange or immuno-inhibition techniques in macro CK type 1 positive patients are falsely positive. Macro CK type 1 may be seen as an antigen-antibody complex against CK BB, which originates at least partly from the vascular wall.

Post-cardiac injury syndrome and an increased humoral immune response against the major contractile proteins (actin and myosin).

To better understand the pathogenesis of the post-cardiac injury syndrome (PCIS) 2 models of cardiac injury were studied. One hundred twenty-nine patients who underwent cardiac surgery and 80 patients with acute myocardial infarction (AMI) were prospectively followed and the levels of anti-heart antibodies (AHA), anti-actin antibodies (AAA) and anti-myosin antibodies (AMA) were determined. In the surgical group, PCIS developed in 27 patients (21%) and incomplete PCIS in 36 (28%). In the AMI group, PCIS did not develop in any patient, but incomplete PCIS developed in 11 patients (14%) (p less than 0.001). The surgical group showed a significantly higher humoral immune response than the AMI group when analyzed for AHA and anti-contractile protein antibodies. After cardiac surgery, AHA developed in 59 patients (46%), AAA developed in 33 (26%) and AMA developed in 49 (38%); in the AMI group, significant levels of AHA, AAA and AMA developed in 16 (20%), 7 (9%) and 13 patients (16%), respectively. These studies show a significant correlation between the PCIS clinical classification and auto-antibodies raised against heart contractile proteins.