A 67-year-old man with history of Hashimoto thyroiditis was attending a routine clinic appointment and was found to have a resting heart rate of 40 beats per min and was referred to the emergency department. The patient had not been evaluated by a physician for two years and previous heart rates were unknown. He was not taking any medications and denied any illicit drug use. The patient denied any dizziness, syncopal episodes, chest pain, dyspnea at rest or with exertion, or palpitations. He did report dry skin and hair loss but denied intolerance to heat or cold, diarrhea, constipation, and significant weight changes.
Physical examination revealed a heart rate of 39; all other vitals normal. The patient was resting comfortably, alert and oriented. Examination also revealed mild thinning of his hair and dry skin. He had no jugular venous distention. Cardiac auscultation revealed normal heart sounds and no murmur. Lungs were clear to auscultation. He had no pretibial edema bilaterally. The electrocardiogram showed a complete atrioventricular (AV) block with junctional escape rhythm of 38 beats/minute. Laboratory findings revealed serum thyroid stimulate hormone (TSH) 250 micro-units/mL, free T4 of <0.25 micrograms/dL. Other laboratory findings were unremarkable. Chest radiograph showed a mildly enlarged heart. Transthoracic echocardiography showed normal left ventricular wall motion and ejection fraction. The patient was subsequently admitted and monitored on telemetry, remained asymptomatic with no arrythmias, and did not require temporary pacing. He was started on levothyroxine 25 mcg/day and discharged from the hospital with a Holter monitor and subspecialty referrals to cardiology and endocrinology to re-evaluate indication for permanent pacemaker should the patient have no improvement in heart rate.
Discussion:
We present an unusual case of atrioventricular block in the setting of severe untreated hypothyroidism. Hypothyroidism can cause prolonged PR/QTc intervals, bradycardia, second- and third-degree AV block. The mechanism mediating the effect of thyroid hormone on cardiac conduction system is not well understood but speculated to involve an increase in the number of adrenergic receptors in the heart. In patients with severe hypothyroidism with AV block, reversal to normal sinus rhythm may occur within days to weeks after initiation of therapy, and in these patients unnecessary pacemakers maybe avoided.
Conclusions:
Atrial ventricular (AV) block may be secondary to ischemic event, medications, neuromuscular disease, or electrolyte abnormalities. Hypothyroidism should always be considered as a cause of AV block even in relatively asymptomatic patients. Recognition and treatment may mitigate the need for urgent pacemaker placement.