Active myocardial damage in hyperthyroidism. A concurrent mechanism of heart failure reversed by treatment.
A patient with hyperthyroidism, heart failure, and depressed ejection fraction, in whom myocardial damage was evidenced by In111-labelled monoclonal antimyosin antibodies, is presented. Both myocardial damage and left ventricular dysfunction disappeared after antithyroid therapy. This suggests that, in addition to volume overload, heart failure in hyperthyroidism could be also due to the presence of potentially reversible concurrent myocardial damage.
D000328:Adult; D000911:Antibodies, Monoclonal; D013956:Antithyroid Agents / Q000627:therapeutic use*; D002231:Carbimazole / Q000627:therapeutic use*; D009202:Cardiomyopathies / Q000000981:diagnostic imaging* / Q000188:drug therapy; D005500:Follow-Up Studies; D006333:Heart Failure / Q000000981:diagnostic imaging* / Q000188:drug therapy; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D006801:Humans; D006980:Hyperthyroidism / Q000000981:diagnostic imaging* / Q000188:drug therapy; D007205:Indium Radioisotopes / Q000627:therapeutic use; D008297:Male; D009218:Myosins / Q000276:immunology*; D011877:Radionuclide Imaging; D016277:Ventricular Function, Left / Q000187:drug effects / Q000502:physiology
D000911:Antibodies, Monoclonal; D013956:Antithyroid Agents; D007205:Indium Radioisotopes; D002231:Carbimazole; D009218:Myosins