Ventricular premature contractions are very common arrhythmias, with an incidence of 1% to 4% in the general population and a detection rate of up to 75% in those who undergo ambulatory electrocardiography. Among healthy people aged 45-65 years, 6% of them have detectable ventricular prematureities, and among those who undergo 24-hour Holter examinations, 39% have at least one ventricular premature, 4% have more than 100 ventricular premature, and 1% have frequent ventricular premature (more than 20% of total beats). Although for the vast majority of healthy individuals, ventricular premature beats are benign and neither symptomatic nor clinically significant. However, in a small percentage of patients with severe structural heart disease, ventricular premature beats may have adverse consequences. Previously, it was thought that in people with structurally normal hearts, even frequent ventricular premature beats were a benign manifestation with no effect on cardiac function, but newer studies have found that frequent ventricular premature beats can lead to cardiac enlargement and a decrease in cardiac function, even if the original heart structure and function are normal and can be partially or fully restored after effective treatment of ventricular premature beats, which we call ventricular premature cardiomyopathy. In 1998, foreign scholars found that cardiac function improved in patients with idiopathic dilated cardiomyopathy after antiarrhythmic treatment. As a result, the concept of “ventricular premature beat induced cardiomyopathy” was introduced. In recent years, this concept has received a lot of attention in the field and is called “premature ventricular cardiomyopathy”. The journal JACC reviewed arrhythmogenic cardiomyopathy, noting that tachycardia, atrial fibrillation, and premature ventricular beats can all induce cardiomyopathy. I. Mechanism of ventricular premature cardiomyopathy The exact mechanism of ventricular premature cardiomyopathy is unknown, but there are several possible mechanisms as follows: 1. Tachycardia: Frequent ventricular premature leads to an increase in total heart beats, thus resembling tachycardia cardiomyopathy, resulting in cardiac dysfunction and heart enlargement. 2. Right and left ventricular asynchrony: Asynchrony of right and left ventricular contraction during ventricular premature, as well as loss of atrial function during ventricular premature, leads to ventricular premature cardiomyopathy. 3.Decreased effective beat volume: In ventricular premature, insufficient ventricular filling and loss of atrial systolic function both lead to insufficient effective beat volume. Although the electrocardiogram shows premature beats and an increase in the number of heart beats, many of them are actually ineffective beats, similar to bradycardia, and the effective beat volume is decreased, which leads to the occurrence of ventricular premature cardiomyopathy. 4, cellular calcium regulation disorder: ventricular premature cardiomyopathy can also be found at the cellular level abnormalities, many studies have confirmed that frequent ventricular premature causes calcium overload and calcium accumulation in cardiomyocytes, which leads to increased oxygen consumption in cardiomyocytes, leading to ventricular premature cardiomyopathy in the long run. Second, how is ventricular premature cardiomyopathy diagnosed? There is no clear diagnosis of ventricular premature cardiomyopathy, and it is difficult to identify it in the early stages. At present, it is considered that the diagnosis of ventricular premature cardiomyopathy is made when there is no underlying heart disease, frequent ventricular premature beats are treated with radiofrequency ablation or medication, and the LVEF returns to normal or increases by 15% from the baseline value and the left ventricular end-diastolic diameter decreases, i.e., the heart function and structure are reversed after the effective elimination of ventricular premature beats. The following clinical features are often indicative of ventricular premature cardiomyopathy: 1) absence of organic heart disease and cardiovascular complications; 2) premature ventricular contractions precede impaired cardiac function; 3) total ventricular premature contractions of ≥10,000/24h, with a prevalence of ≥20,000/24h, as monitored by ambulatory electrocardiography; 4) premature ventricular contractions are often monomorphic and of right ventricular outflow tract and Purkinje fibrous network origin 5. After control of ventricular premature beats, cardiac function can be completely reversed and the ejection fraction can be normalized or rebounded by >15% from the baseline value. Echocardiography shows decreased left ventricular ejection fraction, increased left ventricular end-systolic and end-diastolic internal diameters, diffuse ventricular wall motion abnormalities, and mitral regurgitation; valvular disease, segmental wall motion abnormalities, and myocardial abnormalities can also be excluded. Cardiac MRI is useful to rule out arrhythmogenic right ventricular cardiomyopathy; it can also detect myocardial scarring and clarify whether premature ventricular contractions are caused by myocardial scarring or fibrosis. In patients with hypoplastic left heart with risk factors for ischemic heart disease, coronary angiography should be performed to exclude severe coronary artery disease. III. How is ventricular premature cardiomyopathy treated? The treatment of ventricular premature cardiomyopathy is mainly to suppress or eliminate ventricular premature beats, and patients with cardiac insufficiency need to improve cardiac function treatment. For patients with symptomatic ventricular premature cardiomyopathy with compensated cardiac function, beta-blockers, angiotensin-converting enzyme inhibitors (ACEI) and angiotensin receptor antagonists (ARB) can be the drugs of choice. when beta-blockers are ineffective, the use of flecainide or propafenone can be considered. Amiodarone is effective in controlling premature ventricular contractions and is safer for those with severe cardiac insufficiency, but extracardiac adverse effects are more frequent, so it is difficult to use long-term, especially for children. Drug therapy is not an eradication therapy, and the efficiency is low. Patient compliance and tolerance are important factors to be considered. 2. Catheter ablation Ventricular premature cardiomyopathy can be reversed successfully by catheter ablation. The success rate of catheter ablation depends on the site of origin of the target – 93% in patients with ventricular premature beats originating from the right ventricular outflow tract, but only 67% in patients with ventricular premature beats originating from the epicardium. In synthesis of the treatment strategies for ventricular premature cardiomyopathy in the literature, early identification of people with high ventricular premature load and aggressive treatment of ventricular premature beats with catheter ablation are important to avoid deterioration of cardiac function and even to reverse heart failure, and can effectively improve the prognosis. Patients with frequent ventricular premature beats detected by ECG should not be easily let go. Even in young patients without underlying cardiac disease and without symptoms of cardiac insufficiency, ambulatory ECG is mandatory and specialist cardiology evaluation is necessary.