Postoperative immunological response against contractile proteins after coronary bypass surgery.

Abstract

The pathogenesis of post-cardiac injury syndronme 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.Post-cardiac injury syndrome is a frequent complication of cardiac surgery' -7; it is seen less often after acute myocardial infarction,7 8 despite the generally more severe myocardial damage produced by infarction. Furthermore, post-cardiac injury syndrome was found to be significantly more frequent after valve replacement surgery than after coronary bypass operation.69 According to Engle et al more severe myocardial damage after valve replacement explains this observation.9 Aortic valve replacement gives rise to a greater cumulative enzyme release of creatine kinase, creatine kinase MB, and a hydroxybutyrate dehydrogenase than coronary artery bypass grafting which in turn gives rise to greater cumulative enzyme release than mitral valve replacement.10o 1 Thus the reason for the significantly Requests for reprints to Dr Ivan De Scheerder, higher frequency of post-cardiac injury syndrome after valve replacement surgery than after coronary artery bypass grafting remains controversial. De Scheerder etal demonstrated that the difference in occurrence of post-cardiac injury syndrome after cardiac surgery and acute myocardial infarction correlated well with the difference of post-cardiac injury humoral immune response against myocardial tissue and the major contractile proteins, actin and myosin,7 suggesting that this immune response is important in the pathogenesis or postcardiac injury syndrome.We have studied the correlation between the tissue damage during coronary artery bypas...

Acute Pleuropericarditis After Coronary Stenting A Case Report

“…They found a significant correlation between the frequency and intensity of the syndrome and the ratio of post-operative to pre-operative titers of antiactin and anti-myosin antibodies. 13 Contrary to these reports suggesting a pathogenetic importance of AHA, Hoffman et al reported that the development of AHA was epiphenomenon rather than cause of PCIS. They examined the time course of the appearance and disappearance of AHA in the circulation in 20 patients undergoing elective coronary artery bypass grafting.…”

Dressler’s syndrome as a complication of apical ballooning cardiomyopathy

“…[28] The development of Dressler's syndrome is considered to be immune-mediated with involvement of pericardium, pleura and lungs. [29][30][31] In the case of our patient, Takotsubo cardiomyopathy developed into Dressler's syndrome 2 weeks later. To note, a complete immune panel was unfortunately not established.…”

Immunogenetic basis of myocarditis: Role of fibrillary antigens

“…A low correlation may be particularly associated with viral myocarditis and idiopathic cardiomyopathy, where there is a protracted interval between the initial damage to the myocardium and the development of disease. Another factor may be that these antibodies are produced only in a subset of patients, since not all individuals undergoing cardiac surgery or who incur myocardial infarcts develop PCIS [16][17][18][19]. It is likely that those individuals who develop myosin autoantibodies are genetically predisposed to inflammatory heart disease.…”

“…Only a few investigators have attempted to demonstrate a myosin-specific response [16][17][18][19]. Myosin antibodies have been detected using an enzyme-linked immunosorbant assay (ELISA) with rabbit cardiac heavy meromyosin as the target.…”