6i6 The Heart in Myxedema 



myxedema the amplitude was constantly low, while in coronary sclerosis the 

 Q-R-S complexes though frequently low may be high. In the one condition 

 the electrocardiogram returns to normal with thyroid therapy, in the other it 

 remains unaffected. In only one of the thirty-five cases of myxedema was there 

 a suspicion of pericardial effusion on fluoroscopic and roentgenographic ex- 

 amination. The fact that in general the cardiac pulsations returned to normal 

 under thyroid therapy with very little change in the size of the heart makes the 

 presence of pericardial effusion in those cases at least unlikely. 



Pardee"" also says the S-T segment may show an upward convexity suggest- 

 ing the coronary T wave but in contrast to the usual appearance of the coro- 

 nary T the voltage of T in myxedema is small. The A-V time is frequently 

 prolonged. These changes, he thinks, are due to physiological variations in 

 the muscle metabolism and not to pathological changes, because the adminis- 

 tration of thyroid brings about their reversal. 



Katz" thinks the electrocardiographic changes in myxedema are due to 

 changes in the water and protein content of the heart and surrounding tissues 

 brought about by removal of the normal action of thyroid secretion. The 

 changes comprise (i) sinus bradycardia, (2) low Q-R-S complexes in the limb 

 leads, (3) small or inverted T waves, and (4) S-T depressions. Gross changes 

 in the heart include dilatation, sluggish pulsations, pericardial effusions. Coro- 

 nary insufficiency may develop in either hyperthyroidism or hypothyroidism. 

 In the latter case it is probably due to the combined effect of the frequently 

 present anemia and interference with oxgen by the myxedematous cardiac 

 muscle. 



As for large pericardial effusions in myxedema. Freeman,"* and Gordon" 

 have reported such cases. In each instance the patient made satisfactory recov- 

 ery with thyroid therapy. Suspicion naturally arises that the slight and the 

 moderate "cardiac" enlargements seen so frequently in myxedema might be 

 due to small pericardial effusions and not, as at first thought, to dilatation of 

 the heart. Pericardial effusions are frequent in thyroidectomized animals, but 

 in human myxedema their presence or absence can be settled only through 

 many post-mortem examinations or through the hazardous aspiration of the 

 "moderately enlarged hearts." Pathologists rarely have the opportunity to 

 examine a person dead of untreated myxedema. Furthermore, myxedema is 

 by no means a very common malady. In the following report of a case of 

 enormous pericardial effusion in myxedema, the later changes in the size of 

 the heart shadow were quite probably due to recurrences of the effusion. 



Case Report 



D. C, male, farmer; age 5^ years; myxedema; hies; enormous pericardial effu- 

 sion; ascites; pleural effusion; atony bladder; co^nplete disappearance of peri- 

 cardial effusion after ^ cc. Salyrgan intraveyiously; typical electrocardiographic 

 changes; recovery xuith thyroid therapy. 



This man entered the Colorado General Hospital on January 27, 1935, with 



