Arrhythmogenic

Arrhythmogenic refers to something that can cause or promote arrhythmias, or irregular heart rhythms. The term is used broadly in medicine to describe substrates, tissues, diseases, or substances with the potential to disrupt the heart’s electrical activity and lead to abnormal heartbeats.

In cardiology, arrhythmogenic substrates are conditions that predispose to arrhythmias. Arrhythmogenic cardiomyopathy (ACM) is a hereditary heart-muscle disorder in which myocardium is progressively replaced by fibrofatty tissue, most notably in the right ventricle. This remodeling disrupts electrical conduction and creates a substrate for ventricular tachyarrhythmias, which can cause syncope or sudden cardiac death, particularly in young people and athletes. Genetic mutations in desmosomal proteins (such as PKP2, DSP, DSG2, DSC2) and other genes contribute to disease risk. Diagnosis involves a combination of clinical history, imaging (often cardiac MRI), ECG findings, arrhythmia documentation, family history, and sometimes genetic testing. Management aims to reduce arrhythmic risk and may include activity modification, antiarrhythmic medications, catheter ablation, and implantable cardioverter-defibrillators in high-risk individuals.

In pharmacology, arrhythmogenic describes drugs with proarrhythmic potential, meaning they can provoke or worsen arrhythmias. This property is assessed by their effects on cardiac repolarization and the QT interval, as well as their interactions with electrolytes and other medications. Examples include certain antiarrhythmic drugs and non-cardiac medications known to prolong QT and increase the risk of torsades de pointes. Clinicians weigh benefits and risks, monitor for electrolyte disturbances, and consider drug interactions to minimize proarrhythmic risk.

Understanding arrhythmogenic mechanisms supports prevention, diagnosis, and treatment of abnormal heart rhythms across clinical contexts.