Antiarrhythmic Drugs are a group of pharmaceuticals that are used to suppress abnormal rhythms of the hear.
The choice to start an antiarrhythmic treatment depends on the nature, severity of the arrhythmia, and the possible effect on any other cardiological problems. Generally, any underlying diseases, such as high blood pressure, heart failure, or thyroid disease, are treated first.
These drugs can be administered in acute situations, for example to stop an arrhythmia, such as paroxysmal supraventricular tachycardias, atrial fibrillation, or ventricular tachycardias (so-called “pharmacological cardioversion”). These drugs can also be used for chronic therapies, to control and reduce the incidence of arrhythmias (such as supraventricular or ventricular extrasystoles or atrial fibrillation).
Patients taking antiarrhythmic drugs must be followed meticulously to promptly identify the appearance of any side effects, and in particular the recurrence of any arrhythmias similar to those for which the antiarrhythmic drug has been prescribed, or the onset of new rhythm disorders that in some rare cases can be caused by antiarrhythmic drugs (so-called pro-arrhythmic effect).
Antiarrhythmic drugs are classified according to a special classification, called the Vaughan Williams Classification:
|Class I: inhibition of rapid sodium channels.|
|Ia subgroup (quinidine, disopyramide, procainamide)|
|Ib subgroup (lidocaine, mexiletine, diphenylhydantoin)|
|Ic subgroup (flecainide, propafenone, cibenzoline)|
|Class II: Blockers of beta adrenergic receptors|
|Class III: Blockers of the potassium channels iK (amiodarone, bretilio, sotalol)|
|Class IV: slow calcium channel inhibitors (verapamil)|
In addition to the Vaugham-Williams classification, there is also a classification called “Sicilian Gambit”, proposed by P.J. Schwartz in 2005, which proposes a synoptic view of the electrophysiological properties of antiarrhythmic drugs.
Class II antiarrhythmic drugs are beta-blockers and mainly act on tissues with slow channels (sinus-atrial and atrioventricular node), where they reduce automation, conduction speed and increase the refractory period. Therefore, the heart rate drops, the PR interval lengthens, and the atrioventricular node conducts rapid atrial depolarizations at a lower rate. Class II drugs are used mainly to treat supraventricular tachycardias, including sinus tachycardia, re-entry tachycardias of the atrioventricular node, atrial fibrillation and atrial flutter. These drugs are also used to treat ventricular tachycardia, increase the ventricular fibrillation threshold in ischemic cells and reduce the ventricular pro-arrhythmic effects of beta-adrenergic receptor stimulation. Beta blocker drugs are also used for the treatment of heart failure, ischemic heart disease and high blood pressure. Beta blockers can also be used in the treatment of glaucoma, thyrotoxicosis, somatic manifestations of anxiety, essential tremor and in the prophylactic treatment of migraine. Beta blockers are generally well tolerated; adverse effects include apathy, sleep disturbances and gastrointestinal disturbances. Beta-blockers are divided into cardioselective beta 1 receptors (mainly located at the cardiac, renal and ocular levels), are non-cardioselective, and are endowed with intrinsic sympathomimetic activity. Non-cardioselective beta-blockers are contraindicated in patients with pneumopathies with bronchial hyperreactivity.
|Beta 1-selective beta blockers||Beta blockers not selective for beta 1||Beta-blockers with sympathetic mimetic activity (ISA)|
|Atenolol (water soluble)||Nadolol||Pindolol|
It should be noted that digoxin and adenosine are not included in the Vaughan Williams classification.
WHAT IS THE PROARITHMIC EFFECT?
Class Ia drugs, in predisposed patients, may cause prolongation of the QT interval and cause torsade de pointes type ventricular tachycardia. Class Ia drugs can organize and slow down atrial tachyarrhythmias in such a way as to allow 1:1 atrioventricular conduction with a marked increase in the ventricular response.
Class Ic drugs, in predisposed subjects, can induce the Brugada ECG pattern and favor the onset of ventricular tachyarrhythmias. Thus, it may happen that the diagnosis of Brugada syndrome occurs during therapy with Class Ic drugs, which may be administered, for example, for the prevention or cardioversion of atrial fibrillation. In predisposed patients, Class Ic drugs can cause prolongation of the QT interval and cause torsade de pointes type ventricular tachycardia. Finally, Class Ic drugs can organize and slow down atrial tachyarrhythmias in such a way as to allow 1:1 atrioventricular conduction with a marked increase in the ventricular response.
Class III drugs, which prolong the QT interval, have a risk of ventricular proarrhythmia, especially torsade de pointes type ventricular tachycardia, and are not used in patients with this type of tachycardia.
Patients taking antiarrhythmic drugs should be carefully monitored to identify any recurrence or worsening of the arrhythmic picture. For example, patients taking antiarrhythmic drugs should be educated to check their pulse to promptly identify any pathological rhythms.
Patients must undergo electrocardiographic checks using the various ECG recording methods available, to be evaluated according to the clinical picture: basal ECG, dynamic ECG according to Holter, prolonged multi-week Holter ECG, Cardiotelephone.
In case of patients with implantable cardiac devices (implantable loop recorder, pacemaker, cardiac defibrillator, resynchronizers) the patient can be followed by remote monitoring of cardiac devices.