The spectrum of thyroid disease and risk of new onset atrial fibrillation: a large population cohort study

Abstract

Objectives To examine the risk of atrial fibrillation in relation to the whole spectrum of thyroid function in a large cohort of patients.Design Population based cohort study of general practice patients identified by linkage of nationwide registries at the individual level.Setting Primary care patients in the city of Copenhagen.Subjects Registry data for 586 460 adults who had their thyroid function evaluated for the first time by their general practitioner during 2000-10 and who were without previously recorded thyroid disease or atrial fibrillation.Main outcome measure Poisson regression models used to estimate risk of atrial fibrillation by thyroid function. Results Of the 586 460 individuals in the study population (mean (SD) age 50.2 (16.9) years, 39% men), 562 461 (96.0%) were euthyroid, 1670 (0.3%) had overt hypothyroidism, 12 087 (2.0%) had subclinical hypothyroidism, 3966 (0.7%) had overt hyperthyroidism, and 6276 (1.0%) had subclinical hyperthyroidism. Compared with the euthyroid individuals, the risk of atrial fibrillation increased with decreasing levels of thyroid stimulating hormone (TSH) from high normal euthyroidism (incidence rate ratio 1.12 (95% CI 1.03 to 1.21)) to subclinical hyperthyroidism with reduced TSH (1.16 (0.99 to 1.36)) and subclinical hyperthyroidism with supressed TSH (1.41 (1.25 to 1.59)). Both overt and subclinical hypothyroidism were associated with a lower risk of atrial fibrillation.Conclusion The risk of atrial fibrillation was closely associated with thyroid activity, with a low risk in overt hypothyroidism, high risk in hyperthyroidism, and a TSH level dependent association with risk of atrial fibrillation across the spectrum of subclinical thyroid disease.

Prevalence of normal TSH value among patients with autonomously functioning thyroid nodule

“…Even if long-term functional outcome was not evaluated in the papers selected for the present analysis, it has also been described in the literature that nontoxic autonomous thyroid nodules show a conversion rate to a toxic state of about 4% per year, so that there is a considerable likelihood that a patient who is now nontoxic will be in fact converted to thyrotoxicosis with associated risks within 10 years of time [34]. In addition, even if the risk for atrial fibrillation, risk of thromboembolism, stroke and other embolic events and a reduction in axial bone mineral density are higher in patients with suppressed TSH, low values within the normal references have been recently proved to be related to increased risk of atrial fibrillation [35]. Patients with euthyroid AFTN are at potential high risk of overt hyperthyroidism when exposed to iodine overload (i.e.…”

The Clinical Profile and Pathophysiology of Atrial Fibrillation

“…Although overt hyperthyroidism has long been associated with an increased risk of AF (3-to 6-fold increased incidence versus those with normal thyroid function), an apparent linear relationship between thyroid function and AF risk has been noted with the risk of AF increasing with decreasing levels of thyroid-stimulating hormone (relative risk 1.1 with high normal euthyroidism to 1.2 with subclinical hyperthyroidism, to 1.4 with subclinical hyperthyroidism and suppressed thyroid-stimulating hormone compared with those with normal thyroid function). [73][74][75][76] This is postulated to reflect increases in β-adrenergic tone, as well as the direct effects of thyroid hormone on pulmonary vein cardiomyocytes (increased automaticity and enhanced triggered activity).…”

Radioiodine therapy increases the risk of cerebrovascular events in hyperthyroid and euthyroid patients

“…This leads to some of the mild subclinical hyperthyroid (defined as TSH below normal range but above 0.1 and normal T 4 and free T 3 ) being included in the euthyroid group. This could lead to an overestimation of the risk of cerebrovascular events in this group, as these individuals have an increased risk of AF (22). However, whether subclinical hyperthyroidism leads to an increased risk of stroke is a subject of debate.…”