Cardiovascular effects of overt and subclinical hyperthyroidism: focus on differentiated thyroid cancer

Thera P Links; Trynke van der Boom; Wouter T Zandee; Joop D Lefrandt

doi:10.1530/EC-20-0539

Cardiovascular effects of overt and subclinical hyperthyroidism: focus on differentiated thyroid cancer

Thera P Links^*, Trynke van der Boom, Wouter T Zandee, Joop D Lefrandt

^*Corresponding author for this work

Research output: Contribution to journal › Review article › peer-review

6 Citations (Scopus)

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Abstract

Thyroid hormone stimulates cardiac inotropy and chronotropy via direct genomic and non-genomic mechanisms. Hyperthyroidism magnifies these effects, resulting in an increase in heart rate, ejection fraction and blood volume. Hyperthyroidism also affects thrombogenesis and this may be linked to a probable tendency towards thrombosis in patients with hyperthyroidism. Patients with hyperthyroidism are therefore at higher risk for atrial fibrillation, heart failure and cardiovascular mortality. Similarly, TSH suppressive therapy for differentiated thyroid cancer is associated with increased cardiovascular risk. In this review, we present the latest insights on the cardiac effects of thyroid suppression therapy for the treatment of thyroid cancer. Finally, we will show new clinical data on how to implement this knowledge into the clinical practice of preventive medicine.

Original language	English
Article number	EC-20-0539
Pages (from-to)	R43-R51
Number of pages	9
Journal	Endocrine Connections
Volume	10
Issue number	1
Early online date	1-Dec-2020
DOIs	https://doi.org/10.1530/EC-20-0539
Publication status	Published - Jan-2021

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title = "Cardiovascular effects of overt and subclinical hyperthyroidism: focus on differentiated thyroid cancer",

abstract = "Thyroid hormone stimulates cardiac inotropy and chronotropy via direct genomic and non-genomic mechanisms. Hyperthyroidism magnifies these effects, resulting in an increase in heart rate, ejection fraction and blood volume. Hyperthyroidism also affects thrombogenesis and this may be linked to a probable tendency towards thrombosis in patients with hyperthyroidism. Patients with hyperthyroidism are therefore at higher risk for atrial fibrillation, heart failure and cardiovascular mortality. Similarly, TSH suppressive therapy for differentiated thyroid cancer is associated with increased cardiovascular risk. In this review, we present the latest insights on the cardiac effects of thyroid suppression therapy for the treatment of thyroid cancer. Finally, we will show new clinical data on how to implement this knowledge into the clinical practice of preventive medicine.",

author = "Links, {Thera P} and {van der Boom}, Trynke and Zandee, {Wouter T} and Lefrandt, {Joop D}",

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AU - Links, Thera P

AU - van der Boom, Trynke

AU - Zandee, Wouter T

AU - Lefrandt, Joop D

PY - 2021/1

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N2 - Thyroid hormone stimulates cardiac inotropy and chronotropy via direct genomic and non-genomic mechanisms. Hyperthyroidism magnifies these effects, resulting in an increase in heart rate, ejection fraction and blood volume. Hyperthyroidism also affects thrombogenesis and this may be linked to a probable tendency towards thrombosis in patients with hyperthyroidism. Patients with hyperthyroidism are therefore at higher risk for atrial fibrillation, heart failure and cardiovascular mortality. Similarly, TSH suppressive therapy for differentiated thyroid cancer is associated with increased cardiovascular risk. In this review, we present the latest insights on the cardiac effects of thyroid suppression therapy for the treatment of thyroid cancer. Finally, we will show new clinical data on how to implement this knowledge into the clinical practice of preventive medicine.

AB - Thyroid hormone stimulates cardiac inotropy and chronotropy via direct genomic and non-genomic mechanisms. Hyperthyroidism magnifies these effects, resulting in an increase in heart rate, ejection fraction and blood volume. Hyperthyroidism also affects thrombogenesis and this may be linked to a probable tendency towards thrombosis in patients with hyperthyroidism. Patients with hyperthyroidism are therefore at higher risk for atrial fibrillation, heart failure and cardiovascular mortality. Similarly, TSH suppressive therapy for differentiated thyroid cancer is associated with increased cardiovascular risk. In this review, we present the latest insights on the cardiac effects of thyroid suppression therapy for the treatment of thyroid cancer. Finally, we will show new clinical data on how to implement this knowledge into the clinical practice of preventive medicine.

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