Thyroid hormones have a significant impact on heart function, mediated by genomic and non-genomic effects. Consequently, thyroid hormone deficiencies, as well as excesses, are expected to result in profound changes in cardiac function regulation and cardiovascular hemodynamics.
Thyroid hormones upregulate the expression of the sarcoplasmic reticulum calcium-activated ATPase and downregulate the expression of phospholamban.
Overall, hyperthyroidism is characterized by an increase in resting heart rate, blood volume, stroke volume, myocardial contractility, and ejection fraction.
The development of high-output heart failure in hyperthyroidism may be due to tachycardia-mediated cardiomyopathy.
On the other hand, in a hypothyroid state, thyroid hormone deficiency results in lower heart rate and weakening of myocardial contraction and relaxation, with prolonged systolic and early diastolic times.
Cardiac preload is decreased due to impaired diastolic function. Cardiac afterload is increased, and chronotropic and inotropic functions are reduced.
Subclinical thyroid dysfunction is relatively common in patients over 65 years of age. In general, subclinical hypothyroidism increases the risk of coronary heart disease ( CHD ) mortality and CHD events, but not of total mortality.
The risk of CHD mortality and atrial fibrillation ( but not other outcomes ) in subclinical hyperthyroidism is higher among patients with very low levels of thyrotropin.
Medications such as Amiodarone ( Cordarone ) may induce hypothyroidism ( mediated by the Wolff-Chaikoff ), as well as hyperthyroidism ( mediated by the Jod-Basedow effect ). In both instances, the underlying cause is the high concentration of iodine in this medication. ( Xagena )
Vargas-Uricoechea H et al, Clin Investig Arterioscler 2014;26:296-309