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Background —Amiodarone is the most promising drug for the treatment of life-threatening tachyarrhythmias in patients with structural heart disease. The pharmacological effects of amiodarone on cardiac ion channels are complex and may differ for short-term and long-term administration.Methods and Results —The delayed rectifier K+ current (IK ) of ventricular myocytes isolated from rabbit hearts was recorded with the whole-cell voltage-clamp technique. IK was separated into 2 components by use of specific blockers for either IKs (chromanol 293B, 30 μmol/L) or IKr (E-4031, 10 μmol/L). Short-term application of amiodarone caused a concentration-dependent decrease in IKr with an IC50 of 2.8 μmol/L (n=8) but only a minimal reduction in IKs . The short-term effects of amiodarone were also determined inXenopus oocytes expressing the cloned human channels that conduct IKr and IKs (HERG and KvLQT1/minK). HERG current in oocytes was reduced by amiodarone (IC50 =38 μmol/L), whereas KvLQT1/minK current was unaffected by 300 μmol/L amiodarone. To study the effects of long-term drug administration, rabbits were treated for 4 weeks with oral amiodarone (100 mg · kg−1 · d−1 ) before cell isolation. Long-term administration of amiodarone decreased IK to 55% (n=10) in control rabbits and altered the relative density of IKr and IKs . The majority (92%) of current was IKr . mRNA levels of rabbitERG ,KVLQT1 , andminK in left ventricular myocardium did not differ between control and long-term amiodarone.Conclusions —Amiodarone has differential effects on the 2 components of IK , depending on the application period; short-term treatment inhibits primarily IKr , whereas long-term treatment reduces IKs .

Short- and Long-Term Effects of Amiodarone on the Two Components of Cardiac Delayed Rectifier K + Current

Short- and Long-Term Effects of Amiodarone on the Two Components of Cardiac Delayed Rectifier K ⁺ Current