Atrial Fibrillation and Hyperthyroidism: Summary

Atrial Fibrillation and Hyperthyroidism

Pathophysiology

Atrial fibrillation is caused by chaotic electrical activity, leading to micro-reentrant tachycardia. In hyperthyroidism, elevated thyroid hormone alters cardiac receptors, increasing sympathetic function and decreasing atrial refractory period.

Thyroid hormone effects:

  1. Decreased L-type Calcium channel mRNA expression

  2. Increased expression of Kv 1.5 mRNA

  3. Increased outward current and decreased inward current

  4. Shorter action potential duration

Subclinical Hyperthyroidism

Subclinical hyperthyroidism is also associated with an increased risk of atrial fibrillation, particularly in individuals over 60. Lower TSH levels increase risk.

Cardioversion and Catheter Ablation

  • Cardioversion may be considered after achieving a euthyroid state with anticoagulation.

  • Catheter ablation may be considered for refractory atrial fibrillation after restoring euthyroid state, but multiple ablations are often required.

Thrombotic Risk

Contradictory evidence exists regarding the independent thrombotic risk of hyperthyroidism in atrial fibrillation. The decision to initiate anticoagulation should be done on an individual basis.

Management of Atrial Fibrillation

Initial management includes B-blockers and anti-thyroid agents (PTU or methimazole).

  • Digoxin may be considered in hemodynamically unstable patients, but caution is needed due to altered pharmacokinetics.

  • Amiodarone may be used acutely but requires caution due to the risk of atrial stunning.

During thyroid storm, elevated thyroxine levels theoretically increase thrombotic risk, but the decision to anticoagulate is per clinician discretion.

Pharmacological Rhythm Control

Rhythm control is generally not recommended initially, as many patients revert to normal sinus rhythm after achieving a euthyroid state. Amiodarone should be used cautiously due to the risk of amiodarone-induced thyrotoxicosis (AIT).

  • AIT Type I: Increased hormone production due to iodine load.

  • AIT Type 2: Autoimmune destructive thyroiditis.

Preventing Atrial Fibrillation

Treatment of overt hyperthyroidism is warranted to reduce the risk of atrial fibrillation. Treatment of subclinical hyperthyroidism should be done in individuals older than 65 and with a TSH level of <0.1 mU/L.

Clinical Implications

Routine TSH screening after an atrial fibrillation diagnosis may aid in early hyperthyroidism detection.Introduction

Atrial fibrillation is a common arrhythmia, and hyperthyroidism is a recognized cause. This review addresses the relationship between atrial fibrillation and hyperthyroidism, pathophysiology, management, and clinical implications.

  • Overt hyperthyroidism: Suppressed TSH, elevated T3 and/or free T4.

  • Subclinical hyperthyroidism: Low TSH, normal T3 and free T4.

Hyperthyroidism and Atrial Fibrillation

New-onset hyperthyroidism is associated with an increased risk of atrial fibrillation. Patients with atrial fibrillation have a higher incidence of hyperthyroidism, especially males aged 51-60. Routine screening for hyperthyroidism may be considered in patients with new-onset atrial fibrillation.