Abstract
The aim of the present paper is to review the evolution of concepts regarding the use of Class I and III antiarrhythmic drugs (AADs) in myocardial infarction over the past four decades. Results of animal experiments carried out by the authors and papers published between 1970 and 2012 in journals and the PubMed search system were used. Animal experiments carried out as early as the 1970s showed that Class IB and IC AADs lose their antiarrhythmic effect and electrically destabilize ventricles in the very early phase of myocardial ischemic focus formation. The cause of this is interaction between Class IB and IC AADs as well as Class III AADs with sympathetic neural activation (SNA) of the heart in the early phase of myocardial ischemia. Given the extremely high and uneven distribution of noradrenaline in tissue, SNA results in dispersion of the depolarization and repolarization processes in the ventricles. The clinical sequels of the interaction between the effects of AADs and SNA are as follows: the antiarrhythmic effect of AADs is restored in AMI once SNA has resolved; membrane-destabilization of the ventricles can be restored any time in the presence of randomly occurring SNA not only due to increasing myocardial ischemia but, also, as a result of psychological stress (emotions), and any pre-existing structural heart disease will enhance the pro-fibrillatory effect of a randomly occurring SNA. Despite the above risks, AADs continue to play an irreplaceable role in suppressing post-myocardial arrhythmias and in preventing sudden cardiac death following ICD placement. The risk of AADs' proarrhythmic effect in SNA can be reduced by combining them with beta-blockers. The last recourse when attempting to suppress malignant ventricular tachyarrhythmias is left sympathetic denervation of the heart.
Highlights
A review of randomized controlled trials was published in 1993 to summarize the effect of prophylactic therapy with antiarrhythmic drugs (AADs) on mortality in patients with acute myocardial infarction (AMI)
Results of the analysis suggest that the risk of arrhythmic cardiac death is increased by amiodarone in the presence of higher sympathetic neural activation of the heart while being decreased with the amiodarone/beta-blocker combination
Class IB antiarrhythmics do not prevent the decrease in electrical stability of ischemic tissue on interaction with sympathetic neural activation (SNA)
Summary
A review of randomized controlled trials was published in 1993 to summarize the effect of prophylactic therapy with antiarrhythmic drugs (AADs) on mortality in patients with acute myocardial infarction (AMI) (ref.[1]). Animal experiments carried out as early as the 1970s showed that Class IB and IC AADs lose their antiarrhythmic effect and electrically destabilize ventricles in the very early phase of myocardial ischemic focus formation. The cause of this is interaction between Class IB and IC AADs as well as Class III AADs with sympathetic neural activation (SNA) of the heart in the early phase of myocardial ischemia. The last recourse when attempting to suppress malignant ventricular tachyarrhythmias is left sympathetic denervation of the heart
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