Acute effects of intravenous amiodarone on sulphate metabolites of thyroid hormones in arrhythmic patients

Abstract

Our data indicate that a loading dose of intravenous amiodarone in patients with cardiac dysrhythmias is followed by a very rapid and progressive increase in circulating T3-S levels, possibly due to an inhibition of type 1-iodothyronine de-iodinase. Since T2-S and T1-S, common final metabolites of the thyroid hormone sulphation pathways remained unchanged, our data suggest that the total amount of thyroid hormone degraded by sulphation pathways remains unaltered during amiodarone treatment. Finally our findings are compatible with the view that sulphation represents an important pathway for T3 metabolism in vivo in man.

Understanding the impact of left atrial epicardial adipose tissue thickness on atrial fibrillation: A literature review

“…Moreover, individuals with thicker epicardial adipose tissue (EAT) have exhibited an inferior response to antiarrhythmic therapy (Ahmet et al, 2015). The research revealed that EAT thickness and left atrial volume index (LAVI) were independent predictors of prolonged atrial electromechanical delay (AEMD), and both were closely associated (Iervasi et al, 1998). This may account for the poorer response to antiarrhythmic therapy seen in patients with thicker EAT.…”

Understanding the Impact of Left Atrial Epicardial Adipose Tissue Thickness on Atrial Fibrillation: A Literature Review

“…Moreover, individuals with thicker epicardial adipose tissue (EAT) have exhibited an inferior response to antiarrhythmic therapy (57). The research revealed that EAT thickness and left atrial volume index (LAVI) were independent predictors of prolonged atrial electromechanical delay (AEMD), and both were closely associated (58). This may account for the poorer response to antiarrhythmic therapy seen in patients with thicker EAT.…”