Cardiovasc Prev Pharmacother.  2023 Jan;5(1):1-14. 10.36011/cpp.2023.5.e1.

Adverse reactions to antiarrhythmic drugs

• Do U

• KMID: 2540035
• DOI: http://doi.org/10.36011/cpp.2023.5.e1

Abstract

There are various types of adverse reactions to antiarrhythmic drugs (AADs). Proarrhythmia, which refers to an exacerbation of the preexisting arrhythmia or occurrence of a new arrhythmia, may occur under the therapeutic concentration of an AAD. Bradyarrhythmia is the most common type of proarrhythmia due to AADs, and prior myocardial infarction and old age are known risk factors. Atrial flutter with 1:1 atrioventricular conduction usually occurs during rhythm control of atrial fibrillation with class IC AADs. QT prolongation due to AADs, mainly class III AADs, elevates the risk of torsade de pointes by triggered activity due to early afterdepolarization. The addition of clinical factors that promote QT prolongation, such as hypokalemia, hypomagnesemia, female sex, and bradycardia, increases the risk of developing torsade de pointes. Proarrhythmic monomorphic ventricular tachycardia usually occurs as a result of slow conduction and disparity of refractoriness due to class IC AADs. In patients with preexisting left ventricular systolic dysfunction or structural heart disease, the risk of hypotension or cardiogenic shock caused by negative inotropic effects due to AADs should be considered. To prevent these major adverse reactions to AADs, we need to understand the electrophysiologic properties of AADs in detail. Furthermore, the risk of proarrhythmia could be heightened by interplay with clinical factors, such as electrolyte unbalances, heart rate, and hepatic/renal or myocardial dysfunction. Sufficient awareness about drug-drug interactions, which may affect the metabolism of AADs, will improve patient safety during the management of arrhythmia.

Keyword

Anti-arrhythmia agents; Proarrhythmia; Drug interactions

Figure

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  Fig. 1. Atrial flutter with 1:1 atrioventricular conduction. (A) This 51-year-old male patient was transferred due to wide QRS complex tachycardia. He had been treated with flecainide and verapamil due to paroxysmal atrial fibrillation. (B) The tachycardia was not terminated by adenosine, and the rhythm postadenosine infusion was compatible with typical atrial flutter. Subsequently during catheter ablation for his atrial fibrillation, atypical atrial flutter was induced by burst pacing under intravenous flecainide infusion. (C) The QRS complex morphology of the induced atrial flutter was the same as that of the initial electrocardiography of wide QRS tachycardia. This could be accepted as a finding providing further support that (A) the QRS widening of electrocardiography occurred by aberrant conduction, affected by flecainide.

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  Fig. 2. Monomorphic ventricular tachycardia. This 44-year-old female patient underwent cavotricuspid isthmus ablation and implantation of a permanent pacemaker (DDDR mode) due to typical atrial flutter and sick sinus syndrome. She had taken flecainide (50 mg twice daily), and diltiazem (30 mg twice daily) due to paroxysmal atrial fibrillation. She visited the emergency room due to palpitation. Her blood pressure was 90/60 mmHg. (A) Initial electrocardiography showed wide QRS tachycardia of 180 beats/min. The tachycardia was not responsive to intravenous adenosine, and electrical cardioversion was performed for sinus conversion. (B) Interrogation of the pacemaker showed that the clinical tachycardia was compatible with ventricular tachycardia. The morphology of the QRS complex during tachycardia resembles a sine wave.

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  Fig. 3. Amiodarone-induced pulmonary toxicity. (A) Chest radiography and (B) a high-resolution computed tomography of a 58-year-old male patient with amiodarone-induced pulmonary toxicity. This patient with persistent atrial fibrillation had been treated with oral amiodarone. (A) Chest radiography was performed due to mild dyspnea during exertion, and increased opacity in the right middle and lower lung fields was observed. (B) Diffuse peribronchial consolidations with ground-glass opacity and nodular density at both lung fields were detected on computed tomography.

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