Ventricular premature contractions are ventricular electrical activity that occurs earlier than the basal rhythm (mostly sinus rhythm) and is produced by ectopic pacing points in the Hirschsprung’s bundle and below, either alone or in pairs. If more than three ventricular premature contractions occur in a row, they become ventricular tachycardia (ventricular tachycardia), which in some patients may be characterized by short bursts of ventricular tachycardia or sustained ventricular tachycardia. Ventricular asystole 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 twins and are present together in many patients. Some episodic ventricular premature contractions have no significant discomfort or only symptoms of the primary disease. Frequent ventricular precontractions are associated with palpitations, cardiac arrest, and throat pulling discomfort, often described as “heart beating in the throat,” “missed pulse,” or “pulse that is a little faster all at once “etc. However, it is also common to see a proportion of patients clinically 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 a large variability. In general, ventricular premature and short-onset ventricular tachycardia are mostly benign and have minimal impact on the patient. However, frequent ventricular premature contractions need to be beware and need to be followed up and observed. Prolonged, frequent ventricular premature contractions can cause clinical manifestations of cardiac enlargement and cardiac insufficiency (so-called “tachycardia cardiomyopathy”). Studies have found that frequent symptomatic ventricular premature contractions (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 a cause for caution. The mechanisms of ventricular premature and ventricular tachycardia include the following three: folded excitation, triggered activity, and increased excitability of ectopic pacing points. Ventricular premature and ventricular tachycardia can be produced in different patients as follows: 1, various organic heart diseases, such as acute myocardial ischemia or old myocardial infarction in 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 caused by various reasons, can lead to the occurrence of ventricular premature beats. 2. In patients with normal heart structure and function, ventricular premature beats also often occur in patients with normal heart structure and function. Common pacing sites include the right ventricular outflow tract, left ventricular outflow tract or ectopic excitation foci caused by the aortic sinus and left ventricular septum. In addition to the etiology, other common causes need to be considered, such as stress, anxiety, fatigue, and the consumption of excitatory beverages such as alcohol, coffee, and strong tea; drugs, such as the arrhythmogenic effects of antiarrhythmic drugs, especially digitalis is the most common; the toxic side effects of tricyclic antidepressants, certain antibiotics (such as erythromycin) can cause ventricular premature contractions; electrolyte disorders, such as severe hypokalemia or hypomagnesemia. How should I be examined if I have ventricular premature and short-onset ventricular tachycardia? 1, 12-lead ECG: this is necessary, mainly to clarify the diagnosis, and can be used to determine the origin of ventricular premature and ventricular tachycardia. 2, dynamic electrocardiogram or telemetry electrocardiogram: also known as holter and other tests, mainly to clarify how many ventricular premature or ventricular tachycardia in 24 hours a day, which has a great impact on the choice of treatment. 3, cardiac imaging: mainly including echocardiography (cardiac ultrasound), cardiac magnetic resonance, etc.. The echocardiogram can clarify whether there are any abnormal changes in the anatomy of the heart and whether there are any organic changes in the heart. In some patients, further MRI, nuclear imaging, etc. may be required. 4, thyroid function, electrolytes and other hematological examinations: mainly to exclude other reversible factors leading to ventricular premature and ventricular tachycardia. 5, the examination of other concomitant diseases: such as coronary heart disease, hypertension and other diseases of the examination. Of course, the need for all of these tests needs to be further considered after the clinician’s evaluation, and sometimes it is difficult to fully evaluate them during online consultation. Therefore, it is recommended that all patients should visit an outpatient clinic if necessary. What is the treatment for ventricular premature and short-onset ventricular tachycardia? The current concern for ventricular premature and ventricular tachycardia is to distinguish between the presence of organic heart disease and the presence of reversible etiology or predisposing factors. Treatment of ventricular premature and short-onset ventricular tachycardia requires consideration of a variety of factors: age, underlying heart disease, overall patient condition, medication use, family history of sudden death or syncope, electrolyte disturbances, metabolic imbalances, and arrhythmogenic effects of medications; ischemic heart disease should be excluded in patients aged 40 years and older with ventricular premature, and non-ischemic causes should be considered in those younger than 40 years, including hypertension, valvular disease, cardiomyopathy, and ion channel diseases such as long QT syndrome. In general, premature ventricular contractions do not require drugs in principle if they are infrequent and there is no organic heart disease. However, it is possible to start with lifestyle modification, such as taking rest, avoiding stimulating foods or drugs, such as strong tea and coffee, and avoiding bad habits such as drinking alcohol and staying up late. However, if the symptoms are very obvious or frequent, further intervention should be considered, generally when the frequency of ventricular premature exceeds 5%-10% of the total heart rate. Of course, the main methods of intervention are drugs and interventions, with drugs being considered first. However, the choice of drugs for ventricular premature beats with organic heart disease and without organic heart disease is obviously different. Amiodarone is generally rarely used because of its large side effects. The choice of specific medication depends on the patient’s condition, and it is not recommended to use medication on your own, but only after medical consultation. If the number of premature beats is still high after drug therapy or if drug therapy is not effective, radiofrequency ablation therapy is recommended if necessary. Catheter ablation may be indicated in patients with frequent ventricular premature contractions and in patients without organic heart disease who have more than 10,000 premature ventricular contractions detected by 24-hour ambulatory monitoring. In some patients with significant symptoms, catheter ablation may also be considered when the premature beats are above 4000-5000, if necessary. Ventricular premature contractions with organic heart disease can also be treated with catheter ablation. However, patients with ventricular tachycardia with organic heart disease do not have a high success rate of catheter ablation, and some deteriorate into ventricular flutter or ventricular fibrillation. Fast ventricular tachycardia or ventricular flutter or ventricular fibrillation are causes of sudden death. In addition to the treatment of underlying heart disease, implantation of an ICD (buried cardioverter-defibrillator) can prevent sudden cardiac death. Therefore, the treatment of ventricular premature and ventricular tachycardia can be broadly summarized as follows: In general, the treatment of premature beats requires consideration of various factors. However, it is possible to start with lifestyle modifications (rest, avoiding stimulating foods and medications, such as strong tea and coffee, etc.), followed by medication if necessary (the decision will depend on the relevant data). If the number of premature contractions is still high after medication or if medication is ineffective, radiofrequency ablation may be considered if necessary.