Evaluation of myocardial cell damage by In-111-monoclonal antimyosin antibodies in patients under chronic tricyclic antidepressant drug treatment.

Abstract

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.