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On the basis of our knowledge of human biology, thyroid hormone deficiency and excess could increase risks for atherosclerosis, heart failure, and cardiac dysrhythmias (6). The thyroid hormones alter cholesterol and homocysteine metabolism, endovascular functions, and coagulability; they influence systolic and diastolic myocardial performance; and they affect the cardiac conducting system, particularly the sinoatrial node and potentially aberrant atrial region pacemaker cells. Sensitive serologic markers, imaging techniques, and electrophysiologic measurements demonstrate these effects. Clinical investigators have used various research designs: case–control studies, small controlled trials, cross-sectional epidemiologic analyses, prospective observational studies, and in recent years, meta-analyses of these studies to determine whether these effects cause clinical disease. In this issue, Ochs and colleagues (7) report a meta-analysis of selected population-based cohort studies, in which researchers have tested the hypothesis that disorders of thyroid function increase coronary heart disease (CHD) events and mortality. Ten studies reported risks associated with subclinical hypothyroidism, and 5 examined risks associated with subclinical thyrotoxicosis.
For subclinical hypothyroidism, the relative risks for CHD events and cardiovascular and overall mortality were 1.2, 1.2, and 1.1, respectively, with 95% CIs that, in each case, extended slightly below 1.0. Limiting analyses to studies with the most rigorous methodologies slightly decreased these risk estimates, whereas including studies that used convenience samples of patients increased them. On the basis of these studies, the independent CHD risk that subclinical hypothyroidism poses seems to be very modest, if it exists at all.
medicine endocrinology subclinical hypothyroidism cardiology preventive medicine
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