Add time:09/27/2019         Source:sciencedirect.com

1.1. Six hypertensive patients receiving protoveratrine developed various forms of cardiac arrhythmias on nine occasions. These arrhythmias consisted of sinus bradycardia, sinus arrest, wandering pacemaker, first-degree atrioventricular block, and partial and complete atrioventricular dissociation. All of these mechanisms reverted to normal sinus rhythm with time or with the administration of atropine.2.2. These arrhythmias are believed to result from excessive vagal stimulation by the drug, producing depression of the sinoauricular and atrioventricular nodes of the heart. A direct toxic effect of protoveratrine on the myocardium cannot definitely be excluded.3.3. It is emphasized that protoveratrine may produce either atrioventricular block or atrioventricular dissociation, or both. Atrioventricular dissociation may occur by virtue of excessive sinus slowing and ventricular escape (default) or increased ventricular automaticity (usurpation). In the present series of cases, the effect in depressing the sinoauricular node was paramount.4.4. At times these toxic effects appeared to be related to a certain critical threshold dosage of the drug; at other times, they occurred on maintenance dosage previously tolerated without toxic symptoms.5.5. Digitalis preparations were being used concomitantly in four of the six patients. No definite conclusion as to the possible synergistic action of these two drugs in the production of these arrhythmias can be made from this small series of cases.

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