"Sub-laboratory" hypothyroidism and the empirical use of Armour® Thyroid

Alternative Medicine Review, June, 2004 by Alan R. Gaby

Cardiovascular Disease

Longstanding hypothyroidism is associated with an increased risk of cardiovascular disease, presumably due in part to the hypercholesterolemia that often accompanies hypothyroidism. An elevated plasma concentration of homocysteine, which is an independent risk factor for cardiovascular disease, also occurs frequently in people with hypothyroidism. In one study, treatment of hypothyroid patients with levothyroxine reduced the mean plasma homocysteine concentration by 38 percent; (38) in another study, thyroid-replacement therapy reduced the median plasma homocysteine level by 44 percent. (36) As mentioned previously. hypothyroidism is associated with hypertension (another cardiac risk factor), and the correction of hypothyroidism often reduces elevated blood pressure.

While the relationship between subclinical or subtle hypothyroidism and cardiovascular disease has been debated extensively, recent evidence supports the concept that mild hypothyroidism increases the risk of heart disease. In a population-based, cross-sectional study of 1,149 women (mean age 69) participating in the Rotterdam Study, subclinical hypothyroidism (defined as a TSH level greater than 4.0 mUlL. with a normal serum free-T4 concentration) was associated with an increased age-adjusted risk of aortic atherosclerosis (odds ratio, 1.7 [95% CI. 1.12.6]) and myocardial infarction (odds ratio, 2.3 [959] CI, 1.3-4.0]). (37) Further adjustment for body mass index, cholesterol level, blood pressure, and smoking status did not affect the results.

Anecdotal evidence suggests that the cardiovascular benefits of thyroid hormone also extend to those with sub-laboratory hypothyroidism. In a study of 1,569 patients treated empirically with desiccated thyroid and followed fl)r a total of 8,824 patient-years. Barnes observed only four new cases of coronary heart disease, although 72 new cases would have been expected in a similar group of patients, according to data from the Framingham Study. (38)

Angina pectoris can result from hypothyroidism and sometimes responds to thyroid hormone, (39) as in Case 6. However, treatment with thyroid hormone may also exacerbate pre-existing angina, or trigger its appearance in patients with established coronary heart disease (CHD). (40) Furthermore, the use of excessive doses of thyroid hormone can trigger atrial fibrillation in susceptible individuals, particularly in the elderly. For these reasons, administration of thyroid hormone to people with CHD should be undertaken with extreme caution, starting with low doses. In some cases, full correction of hypothyroidism is not possible, as the diseased cardiovascular system is not able to tolerate the increased metabolic demand created by the administration of thyroid hormone.

Case 6.

A 57-year-old woman complained
of fatigue, nonexertional chest pat n, and palpitations,
beginning nine years previously.
At that time another physician treated her
with 0.1 mg levothyroxine daily (it was not
clear whether thyroid-function tests were
performed), which resulted in an improvement
in her symptoms. Seven years later (two
years prior to her first visit with this author),
she was taken off levothyroxine, which resulted
in a return of her previous symptoms.
She underwent a stress thallium test, which
revealed coronary artery disease with 80-90
percent probability, and her chest pain was
diagnosed its angina pectoris. Treatment with
a calcium-channel blocker (diltiazem) reduced
the frequency of anginal episodes. The
addition of coenzyme [Q.sub.10] and L-carnitine
three months prior to her first visit resulted
in some additional improvement, but her
symptoms persisted. Past medical history
was significant for a partial thyroidectomy
at age 14. Recent thyroid-function tests were
normal.

Based on her history, a therapeutic
trial was begun with 15 mg Armour thyroid
daily, increasing to 30 mg daily after two
weeks. The patient wits advised to reduce
the dose or to discontinue treatment if the
angina became worse. Instead, there wits a
rapid improvement in symptoms and at her
follow-up visit two months later she reported
her angina, fatigue, and palpitations had disappeared.
Although it was not possible to rule
out a delayed response to coenzyme [Q.sub.10] and
L-carnitine as the reason for her improvement,
the patient was convinced the benefit
was attributable primarily to the desiccated
thyroid. She did experience a recurrence of
angina when she tried to discontinue
diltiazem; therefore, she was maintained on
diltiazem plus 30 mg Armour thyroid daily
and continued to do well the next two years,
after which she was lost to follow-up.