Cardiovascular Consequences of Subclinical Thyroid Dysfunction: More Smoke but No Fire

Physicians delight in diagnosing and treating patients with overt thyroid dysfunction—those with a serum thyroxine level above or below the normal range—expecting that most or all of their symptoms will resolve and that serious, even life-threatening, complications will be avoided. At the same time, physicians recommend that individuals who have symptoms or such conditions as hypercholesterolemia, heart failure, atrial fibrillation and osteoporosis, but also normal free thyroxine and thyroid-stimulating hormone (TSH) levels, seek nonthyroidal causes and solutions for their clinical problems. Physicians remain uncertain, however, whether to treat patients who have pituitary thyrotropic cells that show that their thyroid hormone action is insufficient or excessive, even though their serum thyroid hormone concentrations remain within the population reference range.

The controversy over whether to treat subclinical hypothyroidism and subclinical thyrotoxicosis—both unfortunately named because they are biochemically and not clinically defined—hinges on 2 questions: What is the precise threshold at which thyroid hormone deficiency or excess is severe enough to make a clinical difference? Is the pituitary thyrotroph a perfect reporter of optimal thyroid hormone responses in other target tissues, such as the brain, liver, heart, and skeleton, particularly in elderly persons?

Both forms of subclinical thyroid dysfunction satisfy many of the criteria for a disorder worth screening to diagnose and treat. They are common enough: Approximately 15% of older persons have subclinical hypothyroidism, and 1% to 5% have subclinical thyrotoxicosis (1). The TSH test used to diagnose these disorders is accurate, safe, and inexpensive. Treatments are highly effective, are economical, and infrequently cause side effects. The sole uncertainty is whether their consequences are clinically important …