Premature ventricular contraction (ventricular premature) or ventricular prophase contraction is the most common clinical arrhythmia. Ventricular premature contractions are common in patients with organic heart disease, but can also be seen in people with normal heart structure, known as idiopathic ventricular premature.
Premature ventricular contractions are abnormal ventricular electrical activity that occurs earlier than sinus rhythm and is produced by ectopic pacing points in and below the branches of the bundle of Hirschsprung, either alone or in pairs. If more than 3 ventricular premature events occur in a row, they become ventricular tachycardia, and in some patients, they may manifest as short bursts of ventricular tachycardia or persistent ventricular tachycardia. Premature ventricular tachycardia 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.
Symptoms of ventricular prematureness: There is great variability in symptoms, ranging from completely asymptomatic, with mild palpitations and breath-holding discomfort, to premature beats triggering malignant ventricular arrhythmias resulting in syncope or even sudden death. The most common symptom of ventricular premature beats is palpitations. Patients with episodic ventricular premature beats are usually asymptomatic or have occasional palpitations, chest tightness, and other discomfort. Some patients describe the symptoms as “heart beating in the throat”, “pulse missing or stopping”, “heart beating faster all of a sudden”, and even angina pectoris. Patients may even experience angina pectoris, a feeling of tightness and crushing pain in the precordial region during ventricular premature attacks.
The palpitations are mainly caused by the enhanced heartbeat and compensatory intervals after premature beats (i.e., long intervals after ventricular premature beats), and when ventricular premature beats occur frequently or in duplex rhythm, they can lead to a significant decrease in cardiac output and dizziness. When ventricular premature beats occur frequently for a long period of time, it can cause a decline in heart function and, in severe cases, heart failure. Therefore, chest tightness and chest pain are not symptoms specific to angina pectoris in coronary heart disease.
A. Clinical examination of ventricular premature and short-onset ventricular tachycardia
1, 12-lead electrocardiogram: routine examination, clear diagnosis, at the same time can be used to determine the origin of ventricular premature, ventricular tachycardia.
2, 24-hour dynamic electrocardiogram (holter): to clarify how many ventricular premature or ventricular tachycardia in a day (24 hours), which has a great impact on the choice of treatment.
3, cardiac imaging: mainly for echocardiography (heart ultrasound), chest X-ray and even cardiac magnetic resonance imaging. Generally, routine cardiac ultrasound can clarify whether there are any abnormal changes in the anatomical structure 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 tests: mainly to exclude other reversible factors leading to ventricular premature, ventricular tachycardia.
5, other concomitant disease examination: according to the age and symptoms to exclude such as coronary heart disease, hypertension and other disease examination.
Second, the treatment of ventricular premature and short-onset ventricular tachycardia
The treatment of ventricular premature and short-onset ventricular tachycardia requires consideration of various factors: age, underlying heart disease, general condition of the patient, medication, family history of sudden death or syncope, electrolyte disorders, metabolic imbalance, arrhythmogenic effects of drugs; ischemic heart disease should be excluded in patients aged 40 years and above with ventricular premature, and non-ischemic causes should be considered in those aged below 40 years, including hypertension, valvular disease, cardiomyopathy and ion channel diseases such as long QT syndrome. The overall treatment goal of radiofrequent ventricular premature beats is to completely eradicate the ventricular trigger lesion and avoid deterioration of cardiac function
A few premature ventricular contractions may occur in normal people during emotional stress, tension, or overexertion, and usually do not exceed 100 contractions/24 hours. For episodic premature ventricular contractions without organic heart disease, we do not need to apply anti-arrhythmic drugs for treatment. Ventricular premature contractions can disappear with proper rest, elimination of mental tension and change of bad habits.
Generally speaking, if ventricular premature contractions are not frequent and there is no organic heart disease, in principle, drugs are not needed. However, you can first adjust your living habits, such as paying attention to rest, avoiding stimulating foods or drugs, such as strong tea and coffee, and avoiding bad habits such as drinking alcohol and staying up late.
If the symptoms are very pronounced or frequent, or if the frequency of ventricular prematureness exceeds 5%-10% of the total heart rate, interventional treatment should be considered.
The current treatment is pharmacological and interventional catheter ablation. Generally, pharmacological treatment is considered first, mainly including mexiletine, cardioplegia, beta-blockers and amiodarone, i.e., dactylone.
However, the choice of drugs is significantly different between organic heart disease and those without organic heart disease. Ventricular premature beats in organic heart disease cannot be easily selected from cardiac rhythm. beta-blockers have a good prognostic effect, and amiodarone can be selected if the treatment is not effective, but amiodarone has a large side effect, which can damage thyroid function, lung function and even pulmonary fibrosis, especially in patients taking the drug for a long time, and these indicators need to be reviewed regularly. The choice of specific medication depends on the patient’s situation, and it is not recommended that patients self-medicate, but rather require physician consultation before medication can be administered.
The focus of attention is on ventricular premature without organic heart disease, which is also known as idiopathic ventricular tachycardia, and requires the attention and understanding of our clinicians and patients. The traditional view is that ventricular prematureness with no cause can be treated without symptoms, but clinical studies have proven this view to be wrong and even harmful.
Many studies have shown that frequent ventricular premature beats and short bursts of ventricular tachycardia can cause tachycardia and cardiomyopathy even if there are no symptoms, manifesting as enlarged hearts and clinical manifestations of cardiac insufficiency. 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. As tachycardia cardiomyopathy and early heart failure due to premature ventricular tachycardia are reversible, complete treatment of premature ventricular beats can restore the size and function of the heart, and the patient’s quality of life is restored. Therefore, it is important to control the frequency of ventricular premature episodes or even eradicate them completely to avoid cardiomyopathy.
If premature beats are still more frequent after drug therapy or if drug therapy is ineffective, radiofrequency ablation therapy is recommended to be considered if necessary. The efficiency of radiofrequency ablation treatment is more than 90%. Catheter ablation may be an option if frequent episodes of premature ventricular contractions are present, and 24-hour ambulatory monitoring of patients without organic heart disease who find more than 10,000 premature ventricular contractions is also an indication for catheter ablation. In some patients with significant symptoms, catheter ablation may also be considered when the premature beats are above 4000-5000, if necessary. There are also patients with special occupations, such as pilots and drivers, who should be treated more aggressively and early.
Ventricular premature contractions with organic heart disease can also be treated with catheter ablation. However, the success rate of catheter ablation in patients with ventricular tachycardia with organic heart disease is not high, and some of them may 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.
In conclusion, for frequent ventricular premature beats, we should not be paralyzed and should pay attention to its harmful effects. We should actively search for the causes of ventricular premature beats and correct them in time, including the adjustment of living habits (pay attention to rest, avoid stimulating foods and drugs, such as strong tea and coffee, etc.) For those who are not well controlled by drugs, we should actively choose radiofrequency ablation treatment at an early stage, and should not miss the good opportunity of treatment.