The relationship between hypothyroi...

The relationship between hypothyroidism and atherosclerosis has been confirmed from case-control studies and autopsy; the relationship is often clearer in patients with apparent hypothyroidism than in patients with subclinical disease. apparent hypothyroidism increases low-density lipoprotein (LDL) cholesterol evens induces diastolic hypertension, alters coagulability, and negatively affects vascular plain muscle function. Treatment of patent hypothyroidism can moderate these negative drifts but the effect of treatment is les clear in patients with subclinical hypothyroidism. Reductions in total cholesterol flushs are highest in patients who had the highest pretreatment thyroid-stimulating hormone (TSH) and lipid plains Hypothyroidism treatment also can lessen hypertension and improve vascular even muscle function. Treatment of subclinical hypothyroidism may lower cholesterol evens in patients with hypercholesterolemia. Cappola and Ladenson reviewed the most numerous recent information about hypothyroidism and cardiovascular risk factors.

Patients with hypothyroidism appear to have elevated homocysteine and C-reactive protein (CRP) flats and altered flow-mediated, endothelium-dependent vasodilatation; coagulation capacity also may be affected. Thyroxine ([Tsub4]) therapy can cut short homocysteine and CRP levels significantly in somebodys with overt hypothyroidism, but it may not be as useful in patients with subclinical disease.

Hypothyroidism may benefit patients with atherosclerotic disease because decreased peripheral oxygen utilization and bradycardia end in decreased cardiac work. Thyroid hormone replacement may turn topsy-turvy this benefit and increase myocardial ischemia. However, closer examination reveals that hormone therapy may be beneficial in these patients because of decreased peripheral vascular resistance, improved myocardial contractility, reduc preload, and decreased risk of left ventricular dilation. These consequences result in improved myocardial efficiency. Hormone replacement should be started at a reasonable dosage (12.5 to 25 mcg by day) and slowly titrated (in 125- to 25-mcg increments at four- to six-week intervals) until serum TSH reaches normal flushs Angina symptoms can be treated according to revascularization, pharmacotherapy, or a temporary reduction in thyroid hormone dosage.

The authors end that overt hypothyroidism can cause atherosclerosis and other cardiac risk factors. Careful management of hypothyroidism can improve morbidity resulting from cardiac events

Cappola AR, Ladenson PW Hypothyroidism and atherosclerosis. J Clin Endocrinol Metab June 2003;88:2438-44

EDITOR'S NOTE: The benefit of treating patients with open hypothyroidism is clear. Although there are many advocates for treating subclinical hypothyroidism, cardiovascular benefits are unclear. Physicians have a variety of preparations available to use for thyroid hormone supplementation. A consideration by Dong and associates (1) showed that sum of two units brand-name preparations, Levoxyl and Synthroid, and brace generic preparations distributed by Geneva Generics and Rugby Laboratories were bioequivalent. Each fruit when taken over a six-week period in a four-way crossover design consideration demonstrated similar bioavailability parameters of total [Tsub4] triiodothyronine, and resin thyroxine uptake. Although not all brands were standarded it appears that thyroid hormone supplementation can be exhibited reliably with generic preparations.--R.S.

REFERENCES

(1) Dong BJ Hauck WW Gambertoglio JG Gee L White JR Bubp JL et al. Bioequivalence of generic and brand-name levothyroxine results in the treatment of hypothyroidism. JAMA 1997;277:1205-13

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