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World J Cardiol. Feb 26, 2026; 18(2): 111032
Published online Feb 26, 2026. doi: 10.4330/wjc.v18.i2.111032
Ryanodine receptor 2 mutations in catecholaminergic polymorphic ventricular tachycardia: From molecular mechanisms to precision medicine
Vaibhav Sharma
Vaibhav Sharma, Internal Medicine, Medstar Washington Hospital Center, Washington, DC 20010, United States
Author contributions: Sharma V conceived and designed the study, conducted the comprehensive literature search, performed data synthesis and analysis, drafted the manuscript, created all figures and tables, and critically revised the manuscript for important intellectual content. The author takes full responsibility for the integrity of the work and the accuracy of the data analysis.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Vaibhav Sharma, MD, Resident Physician, Internal Medicine, Medstar Washington Hospital Center, Washington, DC 20010, United States. vsharma3090@gmail.com
Received: June 23, 2025
Revised: August 1, 2025
Accepted: December 17, 2025
Published online: February 26, 2026
Processing time: 233 Days and 7.1 Hours
Core Tip

Core Tip: Catecholaminergic polymorphic ventricular tachycardia serves as a paradigm of precision cardiology in which a mechanistic unravelling of the ryanodine receptor 2-mediated calcium ion channel abnormality helps in formulating a genotype-oriented treatment approach. Recent studies regarding the pathopharmacology of store overload-induced calcium ion release, together with mitochondrial interactions, posit the possibility of a more complex pathophysiology than the classic electrical disorders. Recent milestones in the application of the clustered regularly interspaced short palindromic repeats gene editing tool together with artificial intelligence-assisted diagnostic techniques in association with a personalized form of pharmacotherapy have resulted in the successful treatment of 80%-90% of the affected subjects.