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. However, mild thyroid gland failure, evidenced solely by elevation of the serum thyrotropin (TSH) concentration, may be associated with increased morbidity, particularly for cardiovascular disease, and subtly decreased myocardial contractility. In SH, both cardiac structures and function remain normal 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 vasodilatation, a marker of endothelial function, is significantly impaired in SH, and decreased heart rate variability, a marker of autonomic activity, suggests hypofunctional abnormalities in the parasympathetic nervous system. SH does result in a small increase in low-density lipoprotein (LDL) cholesterol (C) and a decrease in high-density lipoprotein (HDL)-C, changes that enhance the risk for development of atherosclerosis and coronary artery disease (CAD). After coronary revascularization, a trend toward higher rates of chest pain, dissection, and reocclusion has been noted in SH subjects. Smoking may contribute to the high incidence of SH and may aggravate its metabolic 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 than 10 mU/L and smoking habits have the highest risk for cardiovascular complications. The magnitude of the lipid changes and the subtle impairment of left ventricular function and cardiopulmonary exercise capacity in SH may justify use of hormone replacement. Early levothyroxine (LT4) treatment in SH may reduce the C level by an average of 8% and normalize all metabolic effects in smokers, nevertheless, in some patients, LT4 therapy may exacerbate angina pectoris or an underlying cardiac arrhythmia. Longitudinal follow-up to define the actual cardiovascular disease risk associated with SH is warranted.
Kahaly
G J
GJ
Department of Medicine and Endocrinology/Metabolism, Gutenberg University Hospital, Mainz, Germany. kahaly@endokrinologie.klinik.uni-mainz.de
D000818:Animals; D001161:Arteriosclerosis / Q000209:etiology*; D002318:Cardiovascular Diseases / Q000209:etiology*; D008078:Cholesterol, LDL / Q000097:blood; D003327:Coronary Disease / Q000209:etiology; D005080:Exercise Test; D006339:Heart Rate; D006801:Humans; D007037:Hypothyroidism / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology; D012907:Smoking / Q000009:adverse effects; D013963:Thyroid Hormones / Q000502:physiology
D008078:Cholesterol, LDL; D013963:Thyroid Hormones