Abstract

Faintness and syncopal attacks for five months compelled this 57 year-old woman to enter our hospital for treatment. Some attacks were severe and were followed by complete unconsciousness and urinary incontinence. Bradycardia was evident in the first episode. At this time a 2: 1 auriculoventricular block was recorded. She had no history of hypertension, coronary insufficiency or myocardial infarction. She did not smoke. On admission, the blood pressure was 120/65 mm. Hg, the radial pulse rate, 42/min., and the jugular pulse rate, 84/min. The heart was not enlarged on physical or x-ray examination. She had no congestive heart failure. The laboratory tests showed stigma of thalassemia, hemoglobin 11.9 gm.%, red blood cells 5,350,OOO per cu. mm., hematocrit 39 per cent, marked increase of AZ hemoglobin and blood serum iron 179.3 pg. per cent. The electrolytes, liver function tests, serum oxalacetic transaminase, serologic tests, urinalysis, x-ray studies of cervical ribs and gallbladder were normal. Although the esophagram revealed a saccular expansion of the esophagus below the aortic arch, the patient never experienced any syncopal episode during swallowing. The electrocardiogram (Fig. 1) revealed a 2: 1 A-V block and ST-T changes suggesting ischemia. The low R waves in VI, Vp and Va and the inverted T waves in V? and VB suggested damage in the anterior myocardial wall. Therefore, scarring in the A-V node was considered the cause of the impaired conduction. The effects of sympathomimetic agents (isoproterenol and ephedrine) and atropinization were only temporary; they were slowly discontinued within three days, and digitalis was given to produce complete A-V block. The patient received oral digoxin 0.25 mg. twice a day. Six days later, normal A-V conduction proved by esophageal leads was reestablished and maintained thereafter by digoxin. The second electrocardiogram (Fig. 2) showed improvement of the anterior wall ischemia and ST-T changes suggesting digitalis effect. Although the electrocardiogram suggested left ventricular hypertrophy, there was no history of hypertension or any clinical or radiologic evidence to substantiate this diagnosis.

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