Abstract
Despite a decline in mortality from cardiovascular disease in the last decade, the number of sudden cardiac deaths (SCD) has remained constant and is estimated to be at least 300,000 deaths annually. The most common mechanism of SCD is ventricular fibrillation. Antiarrhythmic drugs (AARx) that modulate cardiac ion channels have been shown to be effective in a variety of experimental models in possibly decreasing the risk of arrhythmic death and held the promise of possibly reducing the incidence of SCD. However, translation of these animal experiments to human studies has been disappointing, largely because AARx have been shown to be proarrhythmic in clinical settings in which there was great promise to reduce the incidence of SCD in susceptible populations. Unfortunately, drugs that block sodium or potassium channels overall have been ineffective in preventing SCD and in many cases have, paradoxically, increased the risk of life-threatening ventricular arrhythmias. In contrast, in a number of studies of patients after myocardial infarction and those with heart failure, other classes of drugs, such as angiotensin-converting enzyme (ACE) inhibitors and beta blockers, that are not considered traditional antiarrhythmic drugs, have been shown to be effective in reducing overall mortality and potentially sudden death mortality in patients with underlying structural heart disease. This chapter will review those drugs and also describe potential pathophysiological mechanisms by which these agents may reduce sudden death.
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Ilkhanoff, L., Kadish, A.H., Jacobson, J.T. (2013). Non-antiarrhythmic Drugs in Sudden Death Prevention. In: Gussak, I., Antzelevitch, C. (eds) Electrical Diseases of the Heart. Springer, London. https://doi.org/10.1007/978-1-4471-4978-1_34
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