What is it about?
A systematic review by researchers from Bochum and Recklinghausen in Germany and Singapore analysed the results of 32 studies with a record total of 1.3 million participants. A pooled statistical evaluation with consecutive meta-analysis found both subclinical hypothyroidism and subclinical hyperthyroidism to predict the risk for cardiovascular mortality. In particular, serum concentrations of the free thyroid hormone T4 (FT4) correlated directly with the probability of cardiac death and other adverse cardiovascular events. Their results suggest that cardiovascular risk increases continuously with the FT4 concentration, whereas a complex U-shaped risk relationship exists with the concentration of the controlling hormone thyrotropin (TSH). Two different patterns of thyroid-mediated arrhythmia may explain this dualism. In one form ("dyshomeostatic type"), primary thyroid disease directly elevates the concentration of thyroid hormones and thereby increases cardiovascular risk. The other form ("allostatic type") results from an elevated set point of the feedback loop linking the pituitary and the thyroid gland so that indirect elevations of thyroid hormone promote arrhythmia.
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Why is it important?
It is known for more than 200 years that severe thyrotoxicosis may lead to cardiac arrhythmia (irregular heartbeat), one of the major reasons for sudden cardiac death. Today, overt thyroid dysfunction is recognised as an established risk factor for major adverse cardiovascular events (MACE). However, the situation remained equivocal in mild thyroid dysfunction. Whereas in some studies, minimal elevations of thyroid hormones and even high-normal concentrations within the reference range for healthy people predicted an increased risk for sudden cardiac death, other studies had not shown such a relationship. Until very recently, the jury is still out on whether to treat those with subclinical forms of hyperthyroidism and hypothyroidism.
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This page is a summary of: Minor perturbations of thyroid homeostasis and major cardiovascular endpoints—Physiological mechanisms and clinical evidence, Frontiers in Cardiovascular Medicine, August 2022, Frontiers,
DOI: 10.3389/fcvm.2022.942971.
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