Subclinical Hypothyroidism Does Not Cause Heart Block
Subclinical hypothyroidism is not associated with heart block or ventricular conduction abnormalities. The cardiac manifestations of subclinical hypothyroidism are limited to diastolic dysfunction, reduced exercise capacity, and modest effects on heart rate—but not conduction system disease or heart block 1.
Cardiac Effects of Subclinical Hypothyroidism
What Actually Occurs
Diastolic dysfunction with delayed relaxation is the primary cardiac manifestation, consistently demonstrated across multiple studies 2.
Impaired systolic function on exertion leading to reduced exercise capacity occurs, though resting systolic function typically remains normal 2, 3.
Bradycardia may develop, but this represents sinus node slowing rather than conduction block 4.
Elevated pulmonary arterial pressures and reduced peak oxygen consumption have been documented in heart failure patients with subclinical hypothyroidism 3.
What Does NOT Occur
No association with ventricular arrhythmias or conduction abnormalities has been established in subclinical hypothyroidism 1.
The guideline evidence specifically addresses arrhythmias in thyroid disease but focuses entirely on atrial fibrillation in subclinical hyperthyroidism (low TSH), not heart block in subclinical hypothyroidism (high TSH) 1.
Important Clinical Distinction
The provided evidence discusses subclinical hyperthyroidism (low TSH) causing atrial arrhythmias, which is the opposite thyroid state from subclinical hypothyroidism (elevated TSH). This is a critical distinction:
Subclinical hyperthyroidism increases risk of atrial fibrillation 3-5 fold when TSH <0.1 mIU/L 1.
Subclinical hypothyroidism causes bradycardia and diastolic dysfunction but not conduction block 4, 2.
Cardiovascular Risks That Do Exist
While heart block is not a concern, subclinical hypothyroidism does carry other cardiovascular risks:
Increased coronary heart disease events and mortality when TSH ≥10 mIU/L, with hazard ratios of 1.89 for CHD events and 1.58 for CHD mortality 5.
Elevated LDL cholesterol and total cholesterol, contributing to atherosclerotic risk 6, 7.
Adverse prognosis in existing heart failure, with higher cardiac event rates and all-cause mortality 3.
Impaired endothelial function and decreased heart rate variability, suggesting autonomic dysfunction rather than conduction block 7.
Clinical Pitfall to Avoid
If a patient with subclinical hypothyroidism presents with heart block, search for alternative etiologies. Heart block in this setting is coincidental, not causal. Consider:
- Ischemic heart disease (which subclinical hypothyroidism may worsen through lipid effects) 5.
- Infiltrative diseases, medications, or primary conduction system disease 4.
- The possibility that severe, unrecognized overt hypothyroidism (not subclinical) is present, though even overt hypothyroidism more commonly causes sinus bradycardia than heart block 4.
Treatment Considerations
Levothyroxine replacement reverses the diastolic dysfunction and improves exercise capacity in subclinical hypothyroidism 2.
Treatment is particularly indicated when TSH >10 mIU/L due to cardiovascular and mortality risks 5.
Caution is warranted when initiating treatment in patients with underlying coronary disease, as levothyroxine may exacerbate angina, but this relates to increased metabolic demand, not conduction abnormalities 7.