Unlocking the Potential of Left Cardiac Sympathetic Denervation: A Scoping Review of a Promising Approach for Long QT Syndrome

Left cardiac sympathetic denervation (LCSD) has emerged as an alternative therapy for individuals diagnosed with long QT syndrome (LQTS), a genetic disorder characterized by abnormal electrical activity in the heart and sudden cardiac death (SCD). This review examines the history and rationale behind LCSD in LQTS treatment, as well as the procedure, its efficacy, and indications along with the adverse effects that may be associated with it. LQTS presents with prolonged QT intervals on an electrocardiogram and can manifest as seizures, fainting, and SCD. Beta-blockers are the primary treatment for LQTS but some patients do not respond well to these medications or experience side effects. Additionally, implantable cardioverter-defibrillators (ICDs) are not always effective in preventing arrhythmias and can lead to complications. LCSD might offer an alternative approach by disrupting sympathetic activity in the heart. In humans, LCSD reduces the release of norepinephrine, normalizes the QT interval, and decreases the likelihood of life-threatening heart rhythms. The procedure does not impair heart rate or cardiac function due to the compensatory effects of the right cardiac sympathetic nerves. The surgical procedure for LCSD involves the removal of the lower half of the stellate ganglion and thoracic ganglia. Complete denervation is essential for optimal outcomes, while incomplete procedures are considered unacceptable. Traditional and minimally invasive approaches, such as video-assisted thoracic surgery (VATS), are available, with VATS offering shorter hospital stays and fewer complications. In conclusion, LCSD provides a viable treatment option for individuals with LQTS who do not respond well to beta-blockers or require additional protection beyond medication or ICDs. Further research and clinical experience are needed to enhance its acceptance and implementation in routine practice.