How should a new or unexplained cardiac arrhythmia be evaluated and managed in relation to thyroid hormone abnormalities?

Evaluation and Management of Arrhythmias in Thyroid Hormone Abnormalities

Immediate Assessment: Check Thyroid Function in All New Arrhythmias

Thyroid function testing (TSH and free T4) should be performed in every patient presenting with a new or unexplained cardiac arrhythmia, as both hyperthyroidism and hypothyroidism can precipitate life-threatening rhythm disturbances. 1

Hyperthyroidism and Arrhythmias

Atrial fibrillation is the most common arrhythmia in hyperthyroidism, occurring in 5-15% of patients, with higher frequency in those over 60 years of age. 1

Treatment Algorithm for Hyperthyroid-Related AF:

• Primary treatment is restoration of euthyroid state—antiarrhythmic drugs and cardioversion typically fail while thyrotoxicosis persists. 1

• Beta blockers are the first-line rate control agents because the elevated catecholamine state drives the arrhythmia. 1

• If beta blockers cannot be used, nondihydropyridine calcium channel antagonists (diltiazem or verapamil) are recommended for rate control. 1

• Defer cardioversion attempts until the patient is euthyroid, as spontaneous reversion to sinus rhythm usually occurs once thyroid hormone levels normalize. 1

• Anticoagulation decisions should be guided by CHA2DS2-VASc score, not thyroid status alone—embolic risk is not necessarily increased independent of other stroke risk factors. 1

Ventricular Arrhythmias in Thyrotoxicosis:

Ventricular tachycardia and sudden cardiac death are extremely uncommon in thyrotoxicosis but may occur with concomitant electrolyte disturbances (particularly hypokalemia and hypomagnesemia). 1

• Correct electrolyte imbalances (potassium, magnesium, calcium) immediately as first-line management. 1

• Persistent life-threatening ventricular arrhythmias should be treated conventionally (including ICD implantation if indicated) in patients receiving chronic optimal medical therapy with reasonable expectation of survival. 1

Hypothyroidism and Arrhythmias

Hypothyroidism more commonly causes bradyarrhythmias, but can paradoxically precipitate supraventricular and ventricular tachyarrhythmias through QT prolongation and altered myocardial electrophysiology. 1, 2, 3

Mechanism and Clinical Presentation:

• QT interval prolongation is the basic underlying mechanism for arrhythmias in hypothyroidism, creating substrate for torsades de pointes and polymorphic VT. 1

• Severe hypothyroidism can present with supraventricular tachycardia or polymorphic ventricular tachycardia, though this is rare. 2, 3

• Bradycardia is the hallmark cardiac finding, with low cardiac output caused by three mechanisms: bradycardia, decreased ventricular filling, and decreased cardiac contractility. 4

Treatment Approach:

• Thyroxine replacement therapy usually corrects the arrhythmia and prevents recurrence once euthyroid state is restored. 1, 2, 3

• In emergency situations with life-threatening arrhythmias, procainamide has been used successfully while awaiting thyroid hormone normalization. 1

• Arrhythmias typically resolve completely after restoration of euthyroidism, suggesting hypothyroidism was the direct cause. 2, 3

Amiodarone-Induced Thyroid Dysfunction

Amiodarone causes thyroid dysfunction in 10-20% of patients, creating a bidirectional problem: the drug treats arrhythmias but can cause thyroid disease that precipitates arrhythmias. 1, 5, 6

Management Strategy:

• Obtain baseline thyroid function tests (TSH, free T4) before initiating amiodarone, then monitor at 6-month intervals. 5, 6

• If iatrogenic hyperthyroidism develops during amiodarone treatment, discontinue the drug after carefully weighing risks and benefits. 1

• Amiodarone inhibits T4 to T3 conversion, resulting in decreased T3 and slightly increased T4 in euthyroid patients—this is expected and does not require intervention. 7, 5

• TSH is the first hormone to change significantly (within 24 hours), followed by reverse T3, T4, and T3 during amiodarone loading. 7

Critical Pitfalls to Avoid

Never assume sinus bradycardia in hypothyroidism excludes the possibility of tachyarrhythmias—severe hypothyroidism can paradoxically cause supraventricular or ventricular tachycardia through QT prolongation. 2, 3

Do not attempt cardioversion in hyperthyroid patients with AF until euthyroid state is achieved—success rates are extremely low and arrhythmia will likely recur immediately. 1

Always correct electrolyte abnormalities (K+, Mg2+, Ca2+) before attributing arrhythmias solely to thyroid dysfunction—these disturbances frequently coexist and are directly arrhythmogenic. 1

Monitor thyroid function every 6 months in all patients on amiodarone—both hyper- and hypothyroidism can develop insidiously and worsen the underlying arrhythmia being treated. 5, 6

Prognosis and Follow-up

Cardiac abnormalities caused by thyroid dysfunction are typically reversible—return to normal thyroid levels corrects the arrhythmias in most cases. 6

Left ventricular dysfunction associated with severe hypothyroidism and arrhythmias normalizes completely after thyroid hormone replacement, often without need for long-term antiarrhythmic therapy. 3

Complications of AF in hyperthyroidism include heart failure and thromboembolism, making prompt recognition and treatment essential to prevent morbidity and mortality. 1