A previously well 85-year-old Thai woman consulted for a two-month history of dyspnea. The dyspnea was constant and not apparently aggravated by exertion. She also noted associated leg edema, constipation, cold intolerance and dry skin. She did not experience orthopnea, paroxysmal nocturnal dyspnea, chest pain, syncope, urinary symptoms or unusual weight loss. She had hypertension and dyslipidemia for approximately 2 years, but had no maintenance medication. She did not have any history of thyroid problems; heart disease; and irradiation to, or surgery to the neck area.

On physical examination, she was conscious and cooperative but appeared tired. Her vital signs were as follows: temperature 36.7 °C, blood pressure 120/90, pulse rate 40 beats/minute, and respiratory rate 18 breaths/minute. She had coarse hair, facial puffiness and thinning of the lateral third of the eyebrows. She had no macroglossia. The right lobe of the thyroid gland was not palpable, while the left lobe was firm and mildly enlarged. No superficial lymphadenopathy was detected. Careful examination of the cardiovascular system revealed bradycardia; normal S1 and S2; and no cardiac murmur. Examination of the extremities showed dry, cracked skin with no apparent yellowing of the palms. She had full and slow pulses, and grade 1 bipedal pitting edema. Neuromuscular examination revealed slow relaxation of reflexes.

Laboratory results were as follows: fasting plasma glucose 88 mg/dL, blood urea nitrogen 17 mg/dL, and serum creatinine 1.4 mg/dL. Her lipid profile revealed a total cholesterol level of 180 mg/dL, low-density lipoprotein cholesterol (LDL-C) of 114 mg/dL, high-density lipoprotein (HDL-C) of 31 mg/dL and triglyceride level of 154 mg/dL. Troponin-T level was within normal limits. Her thyroid function tests revealed elevated thyroid stimulating hormone (TSH) (> 75 mIU/L, normal value 0.4 to 4.0 mIU/L), low free T3 (1.0 pg/mL, normal value 2.0 to 4.0 pg/mL), and low free T4 (< 0.30 ng/dL, normal value 1.0 to 2.0 ng/dL). Antithyroglobulin antibody (anti-TG Ab) was > 3,000 IU (normal value 0 to 40 IU), and antithyroperoxidase antibody (anti-TPO Ab) was > 100 IU (normal value 0 to 35 IU).

Her chest x-ray demonstrated normal lung parenchyma and thoracic cage, and mild cardiomegaly. A 12-lead electrocardiogram (ECG) showed complete heart block (Figure 1).

Figure 1. Complete heart block pattern on 12-lead ECG showing unconducted P waves (bold arrows) and idioventricular rhythm ( dashed arrows).

She underwent temporary pacemaker insertion with an output of 40 mA and a set rate 60 beats/minute. The ECG done after the procedure is shown in Figure 2.

Figure 2. Twelve-lead ECG after temporary pacemaker insertion.

On admission, the patient was started on levothyroxine at a dose of 25 mcg/day. This dose was adjusted by increments of 25 mcg every three days until a dose of 100 mcg/day was reached by the tenth hospital day. Her heart rate increased, and some electrical activity was found to be conducted through the atrioventricular node as shown in Figure 3.

Figure 3. Twelve-lead ECG after 10 days of levothyroxine treatment.

On the second week of levothyroxine replacement, her free T4 level became normal (1.04 pg/mL). Her ECG was compatible with a Mobitz type I atrioventricular block (Figure 4). The temporary pacemaker was subsequently removed. No new conduction blocks were observed on close monitoring during the following week. She was discharged on the third week of her hospital stay.

Figure 4. Twelve-lead ECG after 21 days of levothyroxine treatment.

The patient returned for follow-up 2 weeks after discharge. She did not experience dizziness, dyspnea or syncope. Subsequent ECGs done (Figures 4 and 5) shows persistence of the same Mobitz type I AV block pattern. Free T4 level was within normal (1.54 pg/mL).

Figure 5. Twelve-lead ECG on the fifth week of levothyroxine treatment.