concanavalin-a and Cardiomyopathies

Expression of interleukin 2 (IL-2) receptor on peripheral blood lymphocytes after stimulation with concanavalin A (Con A) or anti-T3 monoclonal antibody was analyzed in patients with dilated cardiomyopathy (DCM) in order to clarify the abnormalities of lymphocyte activation mechanism in DCM. The expression of IL-2 receptor after the stimulation with either Con A or anti-T3 monoclonal antibody was found to be reduced in the patients with DCM when the results were compared with those of controls. A significant correlation was noticed between the expression of IL-2 receptor after Con A stimulation and T4+/T8+ cell ratio, and between the expression of IL-2 receptor after anti-T3 monoclonal antibody stimulation and the left ventricular end-diastolic pressure (LVEDP). The results suggest that there are abnormalities of lymphocyte activation in DCM and that the alteration may be associated with the cause or clinical conditions of DCM.

Topics: Adult; Antibodies, Monoclonal; Antigens, Surface; Cardiomyopathies; Concanavalin A; Female; Humans; Interleukin-2; Lymphocyte Activation; Male; Middle Aged; Receptors, Immunologic; Receptors, Interleukin-2; T-Lymphocytes

Leucocyte migration inhibition in patients with ischaemic heart disease was evaluated as an assay for progressive myocardial damage. Abnormal results were observed in 50% of patients with ischaemic cardiac disease. The prevalence of abnormal leucocyte migration inhibition was unrelated to clinical presentation, extent of coronary artery disease, or degree of impairment of left ventricular function. Six of the eight patients with unstable angina pectoris and abnormal leucocyte migration inhibition developed life threatening cardiac complications in the follow-up period compared with five patients with unstable angina and normal tests who developed no complications. A similar association between abnormal leucocyte migration inhibition and complications was not observed in patients with angina pectoris or previous myocardial infarction. Thus, leucocyte migration inhibition may be useful as a prognostic marker in unstable angina and may be an important additional variable to identify a high risk subset.

Topics: Adult; Angina Pectoris; Cardiomyopathies; Cell Migration Inhibition; Concanavalin A; Coronary Disease; Female; Follow-Up Studies; Humans; Leukocytes; Male; Middle Aged; Myocardial Infarction; Myocardium; Prognosis; Tissue Extracts

Several diseases with autoimmune features have recently been shown to be characterised by defects in suppressor cell immune regulation. Aberrant immune mechanisms of primary importance have been sought but not yet demonstrated for idiopathic congestive cardiomyopathy and rheumatic heart disease. We tested whether defective immunoregulatory function might explain certain features of these diseases. Peripheral blood mononuclear cells from patients with both diseases showed normal proliferative responses in the mixed leucocyte reaction. Concanavalin A induced similar suppressor activity, quantified in mixed leucocyte reaction as a suppression index, among control subjects, patients with rheumatic heart disease, and patients with idiopathic congestive cardiomyopathy. Similarly, patient serum supported induction of suppressor activity in normal leucocytes equal to that of control serum. A chronic immunoregulatory defect thus does not appear necessary for the development of idiopathic congestive cardiomyopathy or rheumatic heart disease.

Topics: Adolescent; Adult; Aged; Cardiomyopathies; Concanavalin A; Female; Humans; Leukocytes; Lymphocyte Culture Test, Mixed; Male; Middle Aged; Rheumatic Heart Disease; T-Lymphocytes, Regulatory

Topics: Adolescent; Adult; Binding Sites; Cardiomyopathies; Cell Adhesion; Concanavalin A; Female; Heart Failure; Humans; Lymphocyte Culture Test, Mixed; Male; Middle Aged; T-Lymphocytes; Time Factors