Cardiovascular and atherogenic aspects of subclinical hypothyroidism

Subclinical hypothyroidism (SH) is common, especially among elderly women. There is no clear evidence to date that SH causes clinical heart disease. H owever, mild thyroid gland failure, evidenced solely by elevation of the se rum thyrotropin (TSH) concentration, may be associated with increased morbi dity, particularly for cardiovascular disease, and subtly decreased myocard ial contractility. In SH, both cardiac structures and function remain norma l at rest, but impaired ventricular function as well as cardiovascular and respiratory adaptation to effort may become unmasked during exercise. These changes are reversible when euthyroidism is restored. Flow-mediated vasodi latation, a marker of endothelial function, is significantly impaired in SH , and decreased heart rate variability, a marker of autonomic activity, sug gests hypofunctional abnormalities in the parasympathetic nervous system. S H does result in a small increase in low-density lipoprotein (LDL) choleste rol (C) and a decrease in high-density lipoprotein (HDL)-C, changes that en hance the risk for development of atherosclerosis and coronary artery disea se (CAD). After coronary revascularization, a trend toward higher rates of chest pain, dissection, and reocclusion has been noted in SH subjects. Smok ing may contribute to the high incidence of SH and may aggravate its metabo lic effects. Subjects with SH with marked TSH elevation and high titers of thyroid autoantibodies are at higher risk of unnoticed progression to overt hypothyroidism. Especially women over 50 years with TSH levels greater tha n 10 mU/L and smoking habits have the highest risk for cardiovascular compl ications. The magnitude of the Lipid changes and the subtle impairment of l eft ventricular function and cardiopulmonary exercise capacity in SH may ju stify use of hormone replacement. Early levothyroxine (LT4) treatment in SH may reduce the C level by an average of 8% and normalize all metabolic eff ects in smokers, nevertheless, in some patients, LT4 therapy may exacerbate angina pectoris or an underlying cardiac arrhythmia. Longitudinal follow-u p to define the actual cardiovascular disease risk associated with SH is wa rranted.