EVALUATION OF MYOCARDIAL-CELL DAMAGE BY IN-111-MONOCLONAL ANTIMYOSIN ANTIBODIES IN PATIENTS UNDER CHRONIC TRICYCLIC ANTIDEPRESSANT DRUG-TREATMENT

Background The capability of chronic tricyclic antidepressant drug (TAD) treatment to elicit myocardial damage has been a subject of debate. Lack of an adequate noninvasive method to detect such damage has prevented an in-depth study. Methods and Results A prospective study with In-111-monoclonal antimyosin antibodies was undertaken in a series of 21 young patients with major depression on TADs and a control group of 19 healthy subjects. A heart-to-lung ratio (HLR) of antimyosin uptake was used to discriminate normal from abnormal scans. HLR in healthy subjects was 1.39+/-0.08. Patients on imipramine (HLR, 1.41+/-0.09) or clomipramine (HLR, 1.44+/-0.06) showed normal studies. Those under amitriptyline had a higher HLR (1.58+/-0.12) compared with nonamitriptyline or normal groups (P<.05). None of the 15 patients on imipramine or clomipramine showed abnormal HLR, while 3 of 6 on amitriptyline did (P<.01). In these 3 patients, uptake decreased or disappeared after drug withdrawal. Ejection fraction was normal in every patient. Conclusions Monoclonal antimyosin antibody studies are normal in imipramine- and clomipramine-treated patients. Antibody uptake in those under amitriptyline treatment, which disappears after drug withdrawal, would suggest early evidence of myocardial toxicity.