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The Vaughan Williams classification [1] was introduced in 1970 by Miles Vaughan Williams. [2] Vaughan Williams was a pharmacology tutor at Hertford College, Oxford. One of his students, Bramah N. Singh, [3] contributed to the development of the classification system. The system is therefore sometimes known as the Singh-Vaughan Williams ...
Miles Vaughan Williams. (Edward) Miles Vaughan Williams (8 August 1918 – 31 August 2016) was a British cardiac pharmacologist and academic. He is best known for the Vaughan Williams classification of antidysrhythmic drugs. [1] From 1955 to 1985, he was a Fellow of Hertford College, Oxford, and its Tutor in medicine. [2]
Procainamide. Procainamide (PCA) is a medication of the antiarrhythmic class used for the treatment of cardiac arrhythmias. It is a sodium channel blocker of cardiomyocytes; thus it is classified by the Vaughan Williams classification system as class Ia.
Sodium channel blockers are used in the treatment of cardiac arrhythmia. They are classified as "Type I" in the Vaughan Williams classification. Class I antiarrhythmic agents interfere with the (Na +) channel. Class I agents are grouped by their effect on the Na + channel, and by their effect on cardiac action potentials.
These agents are commonly classified by the type of ion they manipulate and named the Vaughan Williams classification: Class I — Sodium channel blockers. Class Ia — Fast sodium channels (quinidine, ajmaline, procainamide, disopyramide) Class Ib — Sodium channels (lidocaine, phenytoin, mexiletine, tocainide)
In 1969, Singh was awarded a Nuffield travelling fellowship and moved to Oxford to work with Miles Vaughan Williams. There, he worked on the anti-arrhythmic properties of drugs including amiodarone. [4] [5] Such work helped to refine the characteristics of Class III compounds in the developing Vaughan Williams classification. [6]
Considering the fact that aconitine acts as an agonist of the sodium channel receptor, antiarrhythmic agents which block the sodium channel (Vaughan-Williams' classification I) might be the first choice for the therapy of aconitine induced arrhythmias. [26] Animal experiments have shown that the mortality of aconitine is lowered by tetrodotoxin.
Proarrhythmia. Proarrhythmia is a new or more frequent occurrence of pre-existing arrhythmias, paradoxically precipitated by antiarrhythmic therapy, which means it is a side effect associated with the administration of some existing antiarrhythmic drugs, as well as drugs for other indications. In other words, it is a tendency of antiarrhythmic ...