Modification of N-(2,6-dimethylphenyl)- N, N-diethylglycinamide and 4-amino- N[2-(diethylamino)ethyl]benzamide in order to increase their antiarrhythmic effect.

A structure-antiarrhythmic activity relationship has been investigated using a chloroform model of arrhythmia in rats. A mathematical model capable of predicting and recognizing antiarrhythmic activity with 84% reliability is formulated. Optimization of the molecular design of lidocaine and procainamide, which have weak antiarrhythmic activity, has resulted in modeling and predicting 51 much more effective antiarrhythmic compounds that can be synthesized for further testing. [ABSTRACT FROM AUTHOR]