The effects of antiarrhythmic therapy on the immature heart
from Section 2 - Fetal disease
Published online by Cambridge University Press: 05 February 2013
Introduction
Supraventricular tachyarrhythmias (SVT) belong to the common cardiac causes of fetal hydrops and perinatal death [1, 2]. With cross-sectional echocardiography providing the non-invasive means to detect and monitor tachyarrhythmias in utero, the fetus has increasingly become the target of pharmacological treatment to prevent or treat heart failure. Survival in excess of 95% is now possible for fetal SVT when existing recommendations are implemented. These include the principles that the best treatment is one targeted specifically to the disease mechanism, and that the potential benefits of drug administration should outweigh the risks to the fetus and the co-treated mother. Hence, successful antiarrhythmic therapy necessitates a thorough knowledge of fetal-maternal physiology, arrhythmia mechanisms, treatment indications and limitations, pharmacokinetics, and effects of the elected drug. Antiarrhythmic agents affect the generation and/or propagation of the cardiac rhythm by their actions on one or several ion channel currents (channel blocker) and/or the autonomous nervous system (beta-blocker; digoxin; adenosine). The Singh Vaughan Williams (SVW) classification is often used to describe the specific drug actions. Class I agents (e.g. flecainide) block cardiac Na+ channels; class II agents are anti-sympathetic agents (beta-blocker); class III agents (sotalol; amiodarone) affect K+ efflux; and class IV agents (verapamil) inhibit calcium channels. Digoxin and adenosine have actions that were not included in the original SVW classification. The main focus of this chapter will be on five antiarrhythmic agents (digoxin; flecainide; sotalol; amiodarone; adenosine) which, due to their relative safety and efficacy, are considered the foundation of transplacental and/or direct pharmacological therapy of fetal SVT.
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