INTRAMYOCARDIAL ELECTROGRAM RECORDINGS (I MEG) IN HUMORAL REJECTION AFTER HEART-TRANSPLANTATION

Measuring intramyocardial ECG amplitude is a clinical non-invasive pro cedure used for diagnosing rejection after heart transplantation. In r ecent years, as the importance of humoral mediated rejection has incre asingly been recognized, the fact that endomyocardial biopsies often p roduce false negative results due to the absence of lymphocytic infilt rates has become a matter of concern. In order to test the reliability of IMEG diagnosis of this form of rejection, heterotopic neck-heart t ransplantation was performed on eight beagles which were previously se nsitized through several skin transplantations. Over the course of the study IMEG registrations were performed daily as well as echocardiogr aphic examinations to determine left ventricular wall thickness and ma ximal diastolic relaxation velocity. Donor-specific antibodies in seru m (IgG, IgM) were also determined daily. Myocardial biopsies, performe d once every 2 days, were examined for the presence of edema and lymph ocytic infiltrate (according to the guidelines of the international So ciety of Heart and Lung Transplantation, ISHLT) and examined under imm unofluorescent microscopy for IgG and IgM. Under triple drug immunosup pression with cyclosporine A, azathioprine, and cortisone accelerated rejection occurred on the fifth postoperative day (range: 4th-5th). Al l eight episodes were detected through IMEG diagnosis (sensitivity 100 %), while the myocardial biopsies graded according to ISHLT guideline s indicated only one case of relevant lymphocytic infiltrate (Grade 3A ) (sensitivity 12.5 %). In each case rejection was recognized so early that it was possible to perform therapy with restitutio ad integrum. This proved that, as opposed to endomyocardial biopsy, IMEG diagnosis detected humoral mediated rejection early and with high reliability. F urthermore, the immediate recovery in IMEG during therapy indicates th at the voltage decrease caused by rejection cannot be explained by an irreversible loss of myocardium (myocytolysis), but rather may be due to a quickly reversible functional impairment.