抄録
The free thyroxine (FT4) values has been known to increase in the patients with various cardiac disorders such as supraventicular tachycardias, atrial fibrillation and myocardial infarction. However, the mechanisms and details of the chages in FT4 concentration in these patients are not clear. Therefore, the changes and physiological significance of FT4 in the paltients with various cardiac disorders were investigated in this study, and in order to obtain supporting data for clinical results the changes in FT4 were also followed in the dogs with experimentally induced myocardial infarction and experimental cardioversion.
Serum samples were obtained from patients with chronic and atrial fibrillation, sinus tachycardias, paroxysmal ventricular and supraventricular tachycardias, acute myocardial infarction and cardioversion, and from the dogs with experimentally induced myocardial infarction and experimental cardioversion. Thyroxine, FT4 values, thyroxine-binding globuline, thyroxine-binding pre-albumine (TBPA) capacity and CPK values of these samples were measured.
Increased FT4 and decraesed TBPA capacity were observed in 12 out of 22 cases with chronic atrial fibrillation and in 2 out of 3 cases in supraventricular tachycardias.
In myocardial infarction, decreased TBPA capacity was observed 24 hours after and increased FT4 24-48 hours after attack of myocardial infarction.
In the dogs with experimentally induced myocardial infarction, FT4 and CPK were observed to increase 48 hours after infarction.
TBPA capacity was observed to decrease immediately after cardioversion and FT4 increase 24 hours after and CPK increase 48 hours after cardioversion.
In the dogs with experimentally induced cardioversion under pentbarbital anesthesia, FT4 began to increase immediately after cardioversion and FT4 and CPK increased their maximum values 24 hours after cardioversion. Of the dogs anesthetised with pentobarbital and gallamine, FT4 began to increase immediately after cardioversion, but, FT4and CPK increased to their maximum values 3 hours after cardioversion.
From these data, it is concluded that the FT4 increases in chronic atrial fibrrillation, supraventricular tachycardias, acute myocardial infarction and cardioversion. It is probable that the increase in FT4 is due to 1) a decreased hepatic synthesis of TBPA in chronic atrial fibrillation and supraventricular tachycardias, 2) a decreased TBPA capacity and escaped FT4 from myocardial muscle in acute myocardial infarction, and 3) escaped FT4 from skeletal muscle rather than the decreased TBPA capacity in the case of cardioversion.
