Ventricular premature beats are one of the most common clinical arrhythmias. Their clinical symptoms are highly variable and can be asymptomatic, or they can present with palpitations, chest pain, shortness of breath, and dizziness. Some patients with frequent ventricular premature beats can cause symptoms such as cardiac enlargement and cardiac insufficiency, the exact mechanism of which is not clear. Studies have speculated that prolonged ventricular premature beats causing tachycardia may lead to myocardial high-energy phosphate depletion, increased renin-angiotensin-aldosterone activity, abnormal subendocardial to subepicardial blood flow ratio, reduced coronary blood flow to myocardial ischemia, and other causes of cardiac insufficiency. The aim of treatment of premature ventricular contractions is to improve the clinical symptoms and long-term prognosis of patients. Currently, antiarrhythmic drugs commonly used to treat ventricular premature beats include sodium channel blockers (e.g., cardioplegia, mexilate, etc.), betalactone, and potassium channel blockers (e.g., sotalol, amiodarone, etc.). However, research has found that: anti-arrhythmic drugs can have arrhythmogenic effects, and some of them can worsen the arrhythmia; in addition, some anti-arrhythmic drugs have negative variability and worsen cardiac function; some anti-arrhythmic drugs have organ toxicity effects when applied for a long time. With the increasing development of cardiac electrophysiology, the use of radiofrequency ablation for the treatment of premature ventricular beats has gained more and more attention. The 2006 ACC/AHA/ESC guidelines for the treatment of ventricular arrhythmias and prevention of sudden cardiac death provide the following indications for radiofrequency ablation of ventricular premature beats: (1) Patients with low risk of sudden cardiac death (SCD), but with frequent monomorphic ventricular premature beats with symptoms, drug resistance (ineffective use of drugs), intolerance to drugs (discomfort or side effects of drugs), or unwillingness to take long-term drug therapy Patients with ventricular premature ablation (IIa) are eligible. (2) Some recent studies have found that some ventricular tachycardia and ventricular fibrillation are induced by premature ventricular beats, and radiofrequency ablation of these ventricular tachycardia and ventricular fibrillation can reduce the onset of ventricular tachycardia and fibrillation. Radiofrequency ablation of potential points of origin of ventricular premature beats (IIb) can be performed in patients with multiple induced ventricular arrhythmic storms due to similar monomorphic paroxysmal ventricular premature beats. (3) Arrhythmogenic cardiomyopathy caused by ventricular premature beats may be a potentially reversible factor causing cardiac insufficiency, and radiofrequency ablation (IIb) may be performed in asymptomatic patients with frequent ventricular premature beats to avoid or treat arrhythmogenic cardiomyopathy. Through clinical practice in recent years, it has been confirmed that frequent ventricular premature beats can be eradicated and clinical symptoms improved by radiofrequency ablation in some patients, and in some patients with already enlarged hearts and symptoms of cardiac insufficiency, ventricular premature beats are eradicated by radiofrequency ablation, and the patients’ heart size is restored to normal and cardiac function is improved.