When we do an electrocardiogram, there is occasionally “ventricular premature” in the conclusion; or when we do a 24-hour ambulatory electrocardiogram, there is often “ventricular premature” in the description of the conclusion. What exactly does “ventricular premature” mean? Ventricular premature is an abbreviation for “premature ventricular contraction”, or more commonly referred to as “ventricular preterm contraction”. Premature ventricular contractions are ventricular electrical events that occur earlier than the underlying normal rhythm (mostly sinus rhythm) and are produced by the ectopic pacing points below the branch of the bundle of Hirschsprung, either alone or in pairs. If more than three ventricular tachycardias occur in a row, they become ventricular tachycardia (ventricular tachycardia), which in some patients may be characterized by short bouts of ventricular tachycardia or sustained ventricular tachycardia. Ventricular tachycardia is the most common ventricular arrhythmia and can trigger ventricular tachycardia and ventricular flutter or fibrillation. The arrhythmia can occur in patients of any age with organic heart disease or in normal subjects. Ventricular premature and short-onset ventricular tachycardia are like twin brothers and are present together in many patients. Some episodic ventricular premature events have no significant discomfort or only symptoms of the primary disease. In the case of frequent ventricular premature, there are palpitations, cardiac arrest, and throat pulling discomfort, which are often described as “heart beating in the throat,” “missed pulse,” or “pulse that is a little faster all at once. The symptoms are often described as “heart beating in the throat”, “missed pulse”, “pulse going fast”, etc. However, it is also common to see patients who have tolerated frequent ventricular premature events without significant symptoms. Ventricular tachycardia, on the other hand, is very different, mainly manifesting as tachycardia, which can be relatively regular or irregular, in addition, the time of appearance can be long or short, and there is great variability. In general, ventricular premature and short-onset ventricular tachycardia are mostly benign and have minimal impact on the patient. However, frequent ventricular prematureities need to be watched carefully and need to be observed on follow-up. Prolonged, frequent ventricular premature events can cause clinical manifestations of cardiac enlargement and heart failure (so-called “tachycardia cardiomyopathy”). Studies have found that frequent symptomatic ventricular premature beats (premature load >5%) have a significant effect on cardiac function in patients without organic heart disease, causing a decrease in left heart function and an increase in left ventricular end-diastolic internal diameter. The risk of premature ventricular load-mediated cardiomyopathy is greatest at 24% (sensitivity 79%, specificity 78%). In addition, ventricular prematureness can induce malignant ventricular arrhythmias, such as ventricular fibrillation and polymorphic ventricular tachycardia. Therefore, the presence of ventricular prematureness is still a cause for concern. Ventricular premature and ventricular tachycardia can arise in different patients with the following: 1. various organic heart diseases, such as acute myocardial ischemia or old myocardial infarction from coronary heart disease, heart valve disease leading to ventricular dilatation or hypertrophy, myocarditis and cardiomyopathy, hypertensive ventricular hypertrophy, post-surgical repair of congenital heart disease, and heart failure from various causes. 2. people with normal heart structure and function. Ventricular premature occurs frequently in patients with normal cardiac structure and function. Common pacing sites include the right ventricular outflow tract, the left ventricular outflow tract or ectopic excitation foci caused by the aortic sinus and the left ventricular septum. In addition to the etiology, other common causes should be considered, such as stress, anxiety, fatigue, and excitatory drinks such as alcohol, coffee, and strong tea; drugs, such as the arrhythmogenic effects of antiarrhythmic drugs, especially digitalis; toxic side effects of tricyclic antidepressants, certain antibiotics (e.g., erythromycin) can cause ventricular premature contractions; and electrolyte disorders, such as severe hypokalemia or hypomagnesemia.