Arrhythmogenic effect of propafenone administered for a "wrong" clinical diagnosis.

Dear Editor, we have read with great interest the work by pintarić et al. 1 about the administration of propafenone in terminating atrioventricular nodal reentrant tachy-cardia and atrioventricular reentrant tachycardia, where propafenone is presented as a safe and efficient antiarrhythmic drug. That inspired us to present an interesting case which demonstrates how propafenone, if administered in a " wrong " clinical indication, is a potentially extremely harmful medication. propafenone is an iC class antiarrhythmic agent which acts by blocking na + channels and partially blocking ß-adrenergic receptors and Ca 2+ channels. propafenone thus acts as a stabilizer of ion permeability of cardiac muscle cell membrane in cardiac pathologic conditions such as arrhythmias. propafenone prolongs both pr interval and Qrs complex on electrocardio-grams, while it has no effect on Qt interval 2,3. it is metabolized in the liver through cytochrome p-450 2d6. patients are distinguished as " slow " and " fast " metabolizers. in " slow " metabolizers, better prophy-lactic effect of propafenone was observed in preventing atrial fibrillation, but not in conversion to sinus rhythm. " fast " metabolizers have less ß-adrenergic blocking effect. maximum blood level of propafenone is achieved in 2-3 hours after its application. The main clinical indications for administration of propafenone are supraventricular tachycardias, including the ones occurring in wpw syndrome and atrial fibrillation in patients without structural heart disease. in general , propafenone is not administered in cases of ven-tricular rhythm disturbances, particularly in patients with preexisting structural heart disease. if given to patients with these cardiac pathologies, propafenone can induce proarrhythmic rather than antiarrhythmic effects with potentially detrimental consequences 4,5. An 80-year-old patient was admitted to the intensive care unit due to electrocardiographically recorded atrial fibrillation with slow ventricular rate of up to 20 beats per minute with rr pauses of up to 3.2 seconds (fig. 1), accompanied by dizziness and acute heart failure. The patient had a history of heart disease; he had survived two myocardial infarctions (fifteen and four years before) that consequentially led to the development of ischemic cardiomyopathy with reduced systol-ic function of the left ventricle (Ef 40% 2d simpson's biplane analysis) and moderate mitral regurgitation. Thirteen years before, the patient underwent CABg x 3 (LAd, rCA, om1-Vsm). recoronarography performed in 2002 showed occluded bypasses on rCA and om1. Consequently, pCi of LAd-Vsm bypass was performed and one stent was implanted. The results of recoronarography performed two years before …