Cardioinhibitory syncope: from pathophysiology to treatment—should we think on cardioneuroablation?

Vasovagal syncope (VVS) is the most common type of syncope; the lone cardioinhibitory syncope represents only a small group of patients; however, the “cardioinhibitory component” is highly prevalent in reflex syncope and can be severe enough to produce asystole, lasting for a few seconds followed by a recovery to sinus beats. The environment in which syncope occurs can compromise life, and in-depth knowledge of the disease can prevent deaths and guide the appropriate management. The therapeutic cornerstone is general measures (increase water and salt) followed by pharmacologic therapy; for cardioinhibitory syncope, both treatments fail most of the time, and the next therapeutic option is pacemaker implantation. However, although the pacemaker causes a reduction in syncope, recurrence is high, and a one-time, effective, and safe intervention would be ideal. Cardioneuroablation (CNA) therapy has been proposed as a pacemaker alternative with these characteristics. CNA has shown a high reduction or even complete syncope elimination during 3 years of follow-up in some studies. Patients also reported prolonged prodromal periods, which allowed them enough time to abort the syncope. Invasive therapies like CNA require further extensive cohort studies, randomized clinical trials, and more substantial follow-up to evaluate adverse side effects. This review highlights syncope pathophysiology, dividing it into a central theory and a peripheral theory, the diagnosis explaining the head-up tilt test protocols, and treatments like CAN, representing it with figures for a simplified understanding.