ISSN: 2474-9214
Authors: Centurion OA*, García LB, Torales JM, and Scavenius KE
In the last three decades with the increasing evidence regarding molecular basis of channellopathies, there was an impressive interest and revival of quinidine therapy due to the unique pharmacological multichannel properties of the drug. Currently available data from observational studies and small reports suggest that quinidine may represent a potential treatment option for ventricular fibrillation either idiopathic or associated to other channellopaties. Quinidine shows a very complex profile of electrophysiological effects that is still not completely understood. The principal therapeutic action of quinidine in patients with either ventricular or atrial arrhythmias is to cause frequency-dependent increases in relative tissue refractoriness, leading to interruption of reentry. Prolongation of the ventricular effective refractory period in relation to the duration of the action potential is strongly dependent on frequency and is correlated with the suppression of ventricular tachycardia. Slowing of conduction may also contribute to the antiarrhythmic action of quinidine. This pharmacological agent remains one of the oldest cardiac drugs still available in the modern era of antiarrhythmic therapy, although not in every country. Currently, quinidine has been proved to be a live-saving antiarrhythmic drug able to control ventricular tachycardias and ventricular fibrillations in patients with channellopathies, specially the Brugada’s syndrome. The therapy of VF with electrophysiologically-guided quinidine may be implemented after demonstrating that VF is no longer inducible after quinidine therapy. Drug therapy with quinidine in ICD patients is usually beneficial by reducing the frequency of appropriate shocks, which can improve the patient's quality of life. Nowadays, quinidine is not only useful in VF-related channellopathies, but it is also a lifesaving pharmacological agents in these patients. Therefore, Quinidine should be available in every hospital, in every drug store, anywhere in the world.
Keywords: Quinidine; Ventricular fibrillation; Channellopathies; Brugada syndrome
