PubMed · 9341068
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J R Biddle. 1997-10-15. Amiodarone and thyroid function.. https://doi.org/10.7326/0003-4819-127-8_part_1-199710150-00020
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Although implantable cardioverter-defibrillators (ICDs) can successfully terminate ventricular arrhythmias, antiarrhythmic drugs are often required to prevent recurrent events. Class III antiarrhythmic agents have emerged as the safest, most effective, and widely used agents in the 40-70% of ICD patients who require concomitant antiarrhythmic medication. Antiarrhythmic agents can influence the effectiveness of ICDs to terminate arrhythmias through their effect on defibrillation threshold. All class III agents share the ability to prolong ventricular refractoriness and those with "pure" class III activity consistently decrease defibrillation threshold in the normal canine heart model. Sotalol, amiodarone, and bretylium all have other Vaughan Williams class actions that influence their respective effects on defibrillation threshold. Sotalol has been associated with a decrease in defibrillation threshold in both animal and in clinical studies, whereas amiodarone has been associated with variable effects in animal models and an increase in defibrillation threshold in clinical studies. Additionally, antiarrhythmic agents may prolong ventricular tachycardia (VT) cycle length, which may affect the ability to pace terminate or cardiovert VT. Amiodarone has a moderate slowing effect on the VT cycle length. Finally, class III drugs also have proarrhythmic potential that may affect the defibrillator's function. Sotalol can be associated with dose-related torsade de pointes, whereas amiodarone may slow the VT cycle length below the tachycardia detection rate cutoff. In conclusion, class III pharmacotherapy can be safely administered in conjunction with ICD therapy as long as the interaction between these therapeutic modalities is appreciated.
Treatment of patients with amiodarone, a potent anti arrhythmic drug, increases plasma LDL cholesterol levels, similar to that seen during hypothyroidism. This increase is the result of a decreased expression of the hepatic LDL receptor gene. We investigated the effects of thyroid hormone, amiodarone and desethylamiodarone on the first 687 bp upstream of the first ATG of the human LDL receptor gene by co-transfection with TRbeta1 into HepG2 cells. Promoter activity showed a dose-dependent increase upon addition of thyroid hormone up to a maximum of 600% at 10(-6) M T3. Using 5'-deletions it was found that a functional TRE(s) is present between -687 bp and -160 bp upstream of the ATG of the LDL receptor gene. Amiodarone and desethylamiodarone at 10(-6) M reduced basal LDL receptor promoter activity further then with the TRbeta1 alone (to 30% vs. 50% respectively, p<0.01) but interestingly in combination with T3 these compunds show a synergistic effect on promoter activity (to 225% T3 alone vs. 380% respectively, p<0.01).
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