• 대한임상독성학회지
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• 제9권2호
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• pp.105-108
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• 2011

Aconitine is an anti-inflammatory agent with therapeutic uses in oriental medicine as an analgesic and for treatment of stroke. Because of its sodium channel effect, aconitine can promote undesirable, wide complex tachyarrhythmia. If tachycardia develops during use of aconitine, class Ia and class III anti arrhythmic drugs can be utilized for treatment. However there are no single anti-arrhythmia agents which are uniformly effective. We report a case, characterized by wide complex tachyarrhythmia and severe hypotension, which was successfully treated by simultaneous injections of amiodarone and lidocaine. A 59-year-old woman exhibiting clinical signs of drowsiness as a result of ingesting 6 g of aconitine, was admitted to the emergency department. Initially, wide complex tachyarrhythmia (ventricular tachycardia and pulse rate of 180 beats/min) and severe hypotension (blood pressure of 53/26 mmHg) was observed. After simultaneous injection of amiodarone and lidocaine, the patient's rhythm pattern changed to an accelerated junctional rhythm with ventricular premature complex. Two hours later, the patient's heart pattern became a sinus rhythm. As demonstrated by this case, simultaneous injections of amiodarone and lidocaine can be useful in treating ventricular arrhythmia induced by aconitine.

• Korean Circulation Journal
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• 제53권4호
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• pp.239-250
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• 2023

Background and Objectives: Brugada syndrome (BrS) is an inherited arrhythmia syndrome that presents as sudden cardiac death (SCD) without structural heart disease. One of the mechanisms of SCD has been suggested to be related to the uneven dispersion of transient outward potassium current (I_to) channels between the epicardium and endocardium, thus inducing ventricular tachyarrhythmia. Artemisinin is widely used as an antimalarial drug. Its antiarrhythmic effect, which includes suppression of I_to channels, has been previously reported. We investigated the effect of artemisinin on the suppression of electrocardiographic manifestations in a canine experimental model of BrS. Methods: Transmural pseudo-electrocardiograms and epicardial/endocardial transmembrane action potentials (APs) were recorded from coronary-perfused canine right ventricular wedge preparations (n=8). To mimic the BrS phenotypes, acetylcholine (3 μM), calcium channel blocker verapamil (1 μM), and I_to agonist NS5806 (6-10 μM) were used. Artemisinin (100-150 μM) was then perfused to ameliorate the ventricular tachyarrhythmia in the BrS models. Results: The provocation agents induced prominent J waves in all the models on the pseudo-electrocardiograms. The epicardial AP dome was attenuated. Ventricular tachyarrhythmia was induced in six out of 8 preparations. Artemisinin suppressed ventricular tachyarrhythmia in all 6 of these preparations and recovered the AP dome of the right ventricular epicardium in all preparations (n=8). J wave areas and epicardial notch indexes were also significantly decreased after artemisinin perfusion. Conclusions: Our findings suggest that artemisinin has an antiarrhythmic effect on wedge preparation models of BrS. It might work by inhibition of potassium channels including I_to channels, subsequently suppressing ventricular tachycardia/ventricular fibrillation.

• The Korean Journal of Physiology and Pharmacology
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• 제27권4호
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• pp.399-406
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• 2023

Voltage-dependent K⁺ (Kv) channels are widely expressed on vascular smooth muscle cells and regulate vascular tone. Here, we explored the inhibitory effect of encainide, a class Ic anti-arrhythmic agent, on Kv channels of vascular smooth muscle from rabbit coronary arteries. Encainide inhibited Kv channels in a concentration-dependent manner with an IC₅₀ value of 8.91 ± 1.75 μM and Hill coefficient of 0.72 ± 0.06. The application of encainide shifted the activation curve toward a more positive potential without modifying the inactivation curve, suggesting that encainide inhibited Kv channels by altering the gating property of channel activation. The inhibition by encainide was not significantly affected by train pulses (1 and 2 Hz), indicating that the inhibition is not use (state)-dependent. The inhibitory effect of encainide was reduced by pretreatment with the Kv1.5 subtype inhibitor. However, pretreatment with the Kv2.1 subtype inhibitor did not alter the inhibitory effects of encainide on Kv currents. Based on these results, encainide inhibits vascular Kv channels in a concentration-dependent and use (state)-independent manner by altering the voltage sensor of the channels. Furthermore, Kv1.5 is the main Kv subtype involved in the effect of encainide.

• Journal of Chest Surgery
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• 제46권2호
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• pp.98-103
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• 2013

Background: Atrial fibrillation (AF) is a common complication in elderly patients with atrial septal defect (ASD). The purpose of this study was to examine the efficacy of the maze procedure in these patients. Materials and Methods: Between February 2000 and May 2011, 46 patients underwent the maze procedure as a concomitant operation with ASD closure. Three patients who underwent a right-sided maze were excluded, and one patient was lost to follow-up. The mean follow-up duration was $3.2{\pm}2.5$ years. Electrocardiography was performed 1 month, 3 months, 6 months, and 1 year after surgery, and checked annually after that. Results: AF persisted in 4 patients after surgery. One year after surgery, among 38 patients, 55.3% remained in sinus rhythm without antiarrhythmic drugs. However, when including the patients who took antiarrhythmic drugs, 92.1% were in sinus rhythm. Freedom from AF recurrence at 3 months, 6 months, 1 year, 2 years, 3 years, and 5 years after surgery were $97.4{\pm}2.6$, $94.4{\pm}3.8$, $91.2{\pm}4.9$, $87.8{\pm}5.8$, $79.5{\pm}7.6$, and $68.2{\pm}12.4$, respectively. There was no early mortality after operation. Conclusion: Concomitant treatment with the maze procedure and ASD closure is safe and effective for restoring the sinus rhythm.