Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2013, 157(2):114-124 | DOI: 10.5507/bp.2013.030
Class I and III antiarrhythmic drugs for prevention of sudden cardiac death and management of postmyocardial infarction arrhythmias. A review
- a Experimental Department and Department for Medical Electronics, Institute for Clinical and Experimental Medicine, Prague, Czech Republic
- b Department of Epidemiology, Third Faculty of Medicine, Charles University in Prague, Prague
- c Department of Cardiac Surgery, University Hospital Olomouc, Olomouc
- d Department of Cardiology, Institute for Clinical and Experimental Medicine, Prague
Background: 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.
Methods: 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.
Results: 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.
Conclusions: 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.
Keywords: antiarrythmics, sympathetic neural activation, sudden cardiac death, postmyocardial arrhythmias
Received: December 19, 2012; Accepted: April 17, 2013; Prepublished online: May 7, 2013; Published: June 21, 2013Show citation
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