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Am Fam Physician. 2003;67(7):1590-1593

Clinical thyroid dysfunction has well-recognized effects on the heart. Subclinical thyroid dysfunction, with abnormal thyroid-stimulating hormone (TSH) and normal free thyroxine and triiodothyronine levels, also is associated with cardiac changes. Biondi and associates reviewed clinical studies of the effect of subclinical thyroid dysfunction on the heart.

The prevalence of subclinical thyroid dysfunction ranges from 1.3 to 17.5 percent and can be caused by exogenous and endogenous factors. Subclinical hypothyroidism is more common in thyroid antibody–positive patients than in those who are antibody–negative. Impaired left ventricular diastolic function at rest and systolic dysfunction with effort have been observed in persons with subclinical hypothyroidism. Normalization of TSH levels with thyroid hormone supplementation can improve systolic function, possibly as a result of improved myocardial contractility. Persons with subclinical hypothyroidism may have a higher risk for coronary artery disease, which could be caused by lipid abnormalities or other problems with vascular reactivity.

Subclinical hyperthyroidism can be caused exogenously by the overzealous use of L-thyroxine to suppress TSH levels in patients with thyroid nodular disease or prevent thyroid cancer progression after surgery, or endogenously by Graves' disease, multinodular goiter, or a hyperfunctioning thyroid nodule. Exogenous subclinical hyperthyroidism lowers the pre-ejection period and the ventricular contraction time. Often, left ventricular mass also is enhanced, and an increase in atrial premature beats and atrial fibrillation is noted, with no increase in ventricular arrhythmias. Beta blockade seems to eliminate these changes.

Endogenous subclinical hyperthyroidism appears to cause an increase in heart rate and a rise in left ventricular mass. Treatment with thyroid suppression reverses these changes. The effect of these changes on left ventricular function is less clear, making the significance of the increased left ventricular mass difficult to determine. There appears to be an increased risk of death from cardiac causes among persons with subclinical hyperthyroidism, but the exact cause is unknown.

The authors conclude that minimal changes in thyroid hormone levels can cause changes in the heart. Among elderly persons, subclinical hypothyroidism is associated with increased risk for atherosclerosis and coronary artery disease, while subclinical hyperthyroidism is associated with increased mortality from all causes, but especially from cardiac disease. The cut-off point for the diagnosis of subclinical hypothyroidism requiring treatment should probably be a TSH level above 4 μU per mL (4 mU per L) rather than 10 μU per mL (10 mU per L), especially if thyroid antibodies are present. Treatment can improve lipid profiles, possibly reduce the risk for atherosclerotic and coronary artery disease, prevent cardiac functional and morphologic changes, and decrease the possibility of progression to overt thyroid disease (see accompanying table). Beta blockade can be used in patients who are hyper responsive to necessary L-thyroxine supplementation. Because morbidity risk is increased in patients with subclinical hyperthyroidism who are older than 60 years, treatment of this condition is a higher imperative in this group. Suppressive therapy should maintain the TSH level at the low end of normal and be monitored regularly, including periodic cardiovascular assessment.

Assess cardiac conditions before initiating treatment to decrease risk of ischemic heart disease exacerbation.
Use doses lower than those used for overt hypothyroidism. Start with 12.5 to 25 mcg of l-thyroxine and use lower doses in older patients.
Monitor TSH levels regularly to reach goal of 1 to 2 µU per mL (1 to 2 mU per L).
When the appropriate replacement dose is achieved, obtain follow-up TSH determinations every six to 12 months.

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