proarrhythmic

Proarrhythmic refers to substances, conditions, or scenarios that increase the likelihood of cardiac arrhythmias or worsen an existing arrhythmia. It is an important consideration in the development and clinical use of drugs, as many agents can have proarrhythmic potential in certain patients.

Mechanisms of proarrhythmia often involve disturbance of the cardiac electrical cycle. A common pathway is prolongation of the QT interval on the electrocardiogram, which can enable dangerous forms of ventricular tachycardia such as torsades de pointes. Other mechanisms include triggered activity from early or delayed afterdepolarizations and the promotion of reentrant circuits in diseased or damaged tissue. The risk is influenced by factors such as electrolyte abnormalities, bradycardia, structural heart disease, and interactions with other QT-prolonging drugs.

Examples and risk factors. Proarrhythmic risk is not limited to antiarrhythmic drugs; many non-cardiac medications can contribute to QT prolongation and arrhythmia. Among antiarrhythmics, class I and III agents carry notable proarrhythmic potential, including certain drugs in these classes. Amiodarone has a relatively lower risk but can still be proarrhythmic in rare situations. Other drugs associated with proarrhythmia include some macrolide antibiotics, fluoroquinolones, and certain antipsychotics. Individual risk increases with higher doses, electrolyte disturbances, preexisting conduction disease, and congenital long QT syndromes.

Management and monitoring focus on minimizing risk. This includes baseline and follow-up ECGs, correcting electrolytes, avoiding concurrent QT-prolonging medications, and careful dose selection. If proarrhythmia occurs, discontinuation of the offending agent, magnesium administration, electrolyte optimization, and, in some cases, temporary pacing or pacing support may be employed.