Can elevated thyroid‑stimulating hormone (TSH) cause electrocardiogram (EKG) changes?

Can High TSH Cause EKG Changes?

Yes, elevated TSH can directly cause EKG changes, particularly through cardiac electrical remodeling that affects repolarization and increases arrhythmia risk, even when thyroid hormone levels remain normal.

Mechanisms of TSH-Induced Cardiac Electrical Changes

The relationship between elevated TSH and EKG abnormalities operates through two distinct pathways:

Direct TSH Effects on Cardiac Tissue

High TSH levels directly suppress cardiac potassium channels through TSH-receptor/protein kinase A pathway activation in the heart, independent of thyroid hormone deficiency 1. This mechanism explains why:

• TSH reduces expression of KCND3 and KCNQ1 (genes encoding repolarizing potassium currents) in human cardiac myocytes through protein kinase A-dependent pathways 1
• Primary hypothyroidism (high TSH) causes more severe cardiac electrical remodeling and arrhythmia vulnerability than central hypothyroidism (low TSH), despite similar thyroid hormone deficiency 1
• In vitro TSH treatment for 24 hours enhances isoproterenol-induced spontaneous activity in ventricular cells and diminishes transient outward potassium current density 1

Thyroid Hormone Deficiency Effects

When TSH elevation accompanies overt hypothyroidism (low T3/T4), additional EKG changes occur 2:

• Subtle decreases in myocardial contractility detected by echocardiography 2
• Cardiac dysfunction including delayed relaxation and abnormal cardiac output 2
• Systemic vascular resistance increases 2

Specific EKG Abnormalities Associated with Elevated TSH

Common Findings in Hypothyroidism

The most frequently observed EKG changes include 3:

• Low voltage QRS complexes (25% of patients) - caused by combination of severe thyroid hormone deficiency and pericardial effusion when present 4
• T-wave inversions (23.5% of patients) 3
• Sinus bradycardia (10.3% of patients) 3
• QRS prolongation - TSH level positively associated with QRS interval duration in men 5
• PR interval changes - U-shaped association between TSH and PR interval in both men and women 5

Repolarization Abnormalities

Primary hypothyroidism with high TSH shows electrocardiographic repolarization abnormalities and increased ventricular arrhythmia incidence, particularly during adrenergic stimulation 1. These changes result from:

• Decreased transient outward potassium current (Ito) density in cardiomyocytes 1
• Enhanced occurrence of early afterdepolarizations under β-adrenergic stimulation 1
• Prolonged QTc intervals in some patients 3

TSH Level Thresholds and Clinical Significance

Subclinical Hypothyroidism (Normal T3/T4, Elevated TSH)

Even with normal thyroid hormone levels, elevated TSH alone can produce cardiac electrical remodeling 6. This is particularly relevant because:

• Subclinical hypothyroidism affects approximately 10% of the population 6
• Different combinations of TSH and thyroid hormones generate different forms of cardiac electrical remodeling 6
• The question of whether serum TSH reference ranges should be redefined is being raised based on cardiac effects 6

Overt Hypothyroidism (Low T3/T4, High TSH)

More severe EKG changes occur when both thyroid hormone deficiency and TSH elevation coexist 2, 1:

• Cardiac dysfunction with delayed relaxation 2
• Increased susceptibility to cardiac arrhythmias 1
• Pericardial effusion (44.4% of hypothyroid patients), which contributes to low voltage when present 4

Population-Level Evidence

In the general population, variation in thyroid hormone levels, even within the normal range, associates with various EKG changes 5:

• Positive linear association between serum T4 and heart rate in men 5
• U-shaped association between T4 and PR interval in both sexes 5
• TSH positively associated with QRS interval in men 5
• U-shaped association between TSH and QRS in women 5

Clinical Implications and Monitoring

When to Suspect TSH-Related EKG Changes

Patients with abnormal EKG and echocardiography without other cardiovascular risk factors should be evaluated for hypothyroidism 3. Key clinical presentations include:

• Fatigue/weakness (67.6% of hypothyroid patients) 3
• Dyspnea (42.6% of patients) 3
• Bradycardia with mean pulse rate 81.50 ± 16.16 3
• Pallor (22.1% of patients) 3

Reversibility with Treatment

Low voltage QRS complexes can improve after thyroid replacement therapy, even when large pericardial effusion persists 4. This demonstrates that:

• Thyroid hormone deficiency contributes independently to low voltage beyond mechanical effects of pericardial fluid 4
• Multi-variate analysis shows low voltage relates to large pericardial effusion, patient age, and low T4 levels 4
• Elderly patients over 60 years have low voltage more frequently than younger patients 4

Critical Pitfalls to Avoid

• Do not attribute all EKG changes in hypothyroidism solely to pericardial effusion - severe thyroid hormone deficiency and high TSH contribute independently 4
• Do not overlook subclinical hypothyroidism as a cause of cardiac electrical abnormalities - high TSH alone can cause changes even with normal thyroid hormones 1, 6
• Do not assume central hypothyroidism (low TSH) produces the same cardiac electrical remodeling as primary hypothyroidism (high TSH) - TSH elevation is critical for arrhythmia vulnerability 1
• Consider age as a risk factor - elderly patients demonstrate more frequent low voltage complexes 4