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Letter by Dietrich et al Regarding Article, "Thyroid Dysfunction in Heart Failure and Cardiovascular Outcomes".

April 2019 1 To the Editor: The article by Lakshmi Kannan et al1 is an important contribution because it provides both new insights and a unified view on earlier observations describing positive correlations between cardiovascular risk and TSH (thyrotropin) or free T4 concentrations,2 as well as a negative relation to T3 levels.3 However, difficulties arise when one tries to interpret the results on a pathophysiological basis. Particularly, possible low-T3 syndrome under severe heart failure urges us to exercise caution. It should also be applied to risk stratification of sudden cardiac death in heart failure patients. Thyroid function may be used as an additional hazard indicator though current guidelines for primary prevention emphasize left ventricular ejection fraction as sole risk factor. Reported increased TSH concentrations may indicate primary hypothyroidism, secondary hyperthyroidism, resistance to thyroid hormone, and an elevated set point of thyroid homeostasis. Although secondary hyperthyroidism and congenital resistance to thyroid hormone are rare and the authors controlled for acquired resistance to thyroid hormone because of amiodarone therapy, both primary hypothyroidism and a high set point are common causes. Conditions associated with an elevated set point include certain genetic polymorphisms in thyroid signaling and type 2 thyroid allostasis, for example, psychiatric diseases and obesity.4 Increased free T4 concentrations may represent thyrotoxicosis, and, again, resistance to thyroid hormone or a raised set point.4 Low T3-concentrations usually result from reduced step-up deiodination in illness (including heart failure) and severe hypothyroidism. To distinguish these pathophysiologies, future studies should report parameters like thyroid’s secretory capacity (SPINA-GT), step-up deiodinase activity (SPINA-GD) and, as a marker for the set point, Jostel’s TSH index.4 The authors’ conclusion that T3 administration might be beneficial in heart failure should be treated with caution. The majority of studies investigating substitution with L-T3 in nonthyroidal illness syndrome did not find a favorable outcome of this intervention, yet some reported considerable adverse effects.5 Potential interventional studies should, therefore, include extensive safety measures.