Ventricular premature contractions (ventricular premature) are the most common type of arrhythmia in China. One ventricular premature contraction may trigger ventricular fibrillation and even cause sudden death, while tens of thousands of ventricular premature contractions per day may accompany a person for the rest of his or her life without any loss of health. As you can see, ventricular prematureness is like a kaleidoscope of variability and mystery that deserves and needs to be explored in depth.
Premature ventricle: the “prime mover” of cardiac arrhythmia
Ventricular premature is originated from abnormal electrical excitation of ventricular muscle, which can be issued singly or in pairs (paired ventricular premature), or even in bunches of 3~5 times (bunches of ventricular premature), and can occur occasionally or frequently (frequent ventricular premature, >30 times/hour). The QRS wave pattern of ventricular premature can be monomorphic or polymorphic and can originate from a single site in the ventricle (monogenic) or from multiple sites (polymorphic). Many ventricular premature events occur in healthy individuals, but they are also common in patients with organic heart disease.
Ventricular premature is the leading cause of arrhythmias in China and worldwide. The detection rate of ventricular premature is as high as 70% to 90% in the general population. It is important to note that there is a pattern to the various types of ventricular premature.
In general, the incidence and complexity of ventricular premature increases with age. In people aged 75-85 years, a 24-hour ambulatory electrocardiogram can record ventricular premature in more than 90% of the subjects, and gender also has an effect on ventricular premature. The number of ventricular premature is also in circadian rhythm, with two peaks of 24-hour ventricular premature in the early morning and 3:00~5:00 pm, and the sympathetic excitability is higher in these phases.
In addition, most functional ventricular prematures decrease after exercise, while pathological ventricular prematures are new or increase in number after exercise.
Holiday syndrome: a consequence of sympathetic ventricular prematureness
Holiday syndrome is a disorder that occurs during the holiday season and has a high incidence in Western countries. The initial cases occur during the holidays when friends and family are excitedly gathering and someone may have a sudden onset of severe heartburn with pallor, profuse sweating, or even complaints of a breathless, near-death feeling. After the patient is brought to the emergency room and undergoes various related tests, the family is often told that “only frequent ventricular prematureness is recorded on the ECG, blood pressure and cardiopulmonary function are normal, and the patient needs quiet rest and observation”.
Over time and with the accumulation of similar cases, a separate and specific condition eventually developed – holiday syndrome, which stems from excessive alcohol, tea or coffee consumption, smoking and excessive excitement during the holidays leading to a sharp increase in sympathetic excitability and causing sudden ventricular premature and even short bursts of ventricular tachycardia. These symptoms disappear quickly after appropriate rest, because the patient has never experienced similar conditions and feels nervous and uncomfortable.
The holiday syndrome suggests that a variety of pathological and physiological factors in daily life can cause arrhythmias, with the highest incidence of ventricular prematureness. 70% to 90% of the general population can have ventricular prematureness recorded after 7 consecutive days of ambulatory electrocardiography, and the detection rate increases with the duration of the examination. Ventricular prematureness can occur in every individual throughout life, but the age of onset, number and accompanying symptoms vary.
Functional ventricular prematureness: common but not treated
Functional ventricular prematureness is a condition that occurs in patients without organic heart disease who have normal physical examination and echocardiographic findings. Patients may have abnormal autonomic function, especially increased sympathetic excitability.
The characteristics of functional ventricular prematureness are as follows.
(1) Most of them are young people, while ventricular prematureness in the elderly or children often has a cause;
②The attacks are often accompanied by increased sympathetic excitation or excitation triggers;
(3) The complaints of ventricular premature episodes are many and dramatic, on the contrary, ventricular premature episodes without any complaints and found in physical examination are mostly pathological;
④The efficacy of antiarrhythmic drugs is poor;
⑤ The ECG is not accompanied by atrioventricular or intraventricular block, and there is no left ventricular hypertrophy or other abnormalities;
(6) The QRS wave amplitude of ventricular premature is high and the time limit is short, on the contrary, the morphology of pathological ventricular premature is often stumpy, i.e., the QRS wave is wide and low. Functional ventricular premature is not accompanied by hemodynamic changes and is a benign ventricular arrhythmia, so no treatment is needed.
Natural variability of ventricular prematureness: objective evaluation of the total number of ventricular prematureness
Some physicians and patients place too much emphasis on the number of ventricular premature events, especially those reported on an ambulatory ECG. When the total number of premature ventricles decreases from 6,000 to 4,000 ventricles per day, it is optimistic that the condition is improving or that drug therapy is working, while the opposite is true: the condition is considered to be worsening. However, judgments based solely on the increase or decrease in the total number of ventricular premature events are often one-sided and blind.
It should be understood that the natural variability of ventricular prematureness is 70%, i.e., it can increase or decrease by 70% at different times, a phenomenon known as the natural variability of ventricular prematureness. Understanding this characteristic of ventricular premature can help to reduce the blindness of excessive pessimism or optimism, and the natural variability of ventricular premature should be taken into account when judging the efficacy of antiarrhythmic drugs, only drugs that reduce the total number of ventricular premature by 70% or more are considered effective, while natural reduction cannot be excluded for changes within 70%.
There is no unanimous opinion on the evaluation of normal or abnormal number of ventricular premature in ECG reports. Most of the literature suggests that a normal total number of ventricular premature events is ≤100/24 hours and >100/24 hours is considered as frequent ventricular premature events, while others suggest that intervention should be started when the total number of ventricular premature events is ≥10% of the total daily heart rate. In fact, the total number of ventricular premature reported by ECG is only a reference indicator, and has no independent significance in judging the prognosis, which must be considered in conjunction with the clinical situation.
Hazards of ventricular prematureness: Lown grading should not be abused.
The Lown classification was proposed in 1971 to stratify the risk of different ventricular premature events in patients with myocardial infarction, with grade III or below being mild ventricular premature, while grade ≥III ventricular premature events have a high risk of sudden death and should be treated with appropriate intervention.
It is worth noting that the word “myocardial infarction” is often omitted in the application of the Lown classification method in China, which makes the classification method mistakenly considered to be applicable to all people. In fact, most ventricular premature and short-onset ventricular tachycardias are benign ventricular arrhythmias with no adverse prognostic significance. It is important that clinicians apply the Lown classification with a clear distinction.
The possibility of ventricular tachycardia and ventricular fibrillation is the essence of the fear of ventricular prematureness. In the risk stratification of ventricular premature, R on T ventricular premature is the most potentially dangerous and is classified as the most severe class V of the Lown classification. It should be understood that the peak of the T wave of the ECG is the dividing line between the two types of ventricular nonstimulation, which are preceded and followed by the effective nonstimulation and the relative nonstimulation, respectively.
The excitability of the ventricular muscle will gradually recover from zero to 100% during the relative non-response period, while the 20-30 ms before the peak of the T wave is called the ventricular fibrillation period, i.e., this time period is in the electrical asynchronous state of the ventricle, and the starting time of the recovery of the excitability of the ventricular muscle in different parts is different, and the recovery speed is also different, and the dispersion of the non-response period is the greatest at this moment.
Theoretically and practically, it has been proven that ventricular fibrillation can often be induced by ventricular premature R on T. R on T ventricular premature is classified into type I and type II according to the patient’s previous absence or presence of QT interval prolongation. Because of the risk of ventricular fibrillation in R on T ventricular prematurely, clinicians who encounter it are like the enemy, and they are rather afraid to talk about it.
The correct evaluation of R on T ventricular premature is crucial, first of all, it should be clear that the incidence of this ventricular premature is very low, accounting for only 2% of the total number of ventricular premature in the 24 hours before acute myocardial infarction. In addition, not all R on T ventricular prematureities can trigger ventricular tachycardia and ventricular fibrillation; the incidence of R on T ventricular prematureities is 8% within 10 min after the onset of acute coronary syndrome, but only 4% of ventricular tachycardia or ventricular fibrillation is triggered by R on T ventricular prematureities during this period.
The ability of R on T ventricular premature to trigger ventricular tachycardia and ventricular fibrillation is related to a number of factors, particularly the underlying cardiac status, sympathetic activity, and the patient’s threshold for ventricular fibrillation. In buried cardioverter-defibrillator placement, the application of R on T ventricular premature induces ventricular fibrillation almost 100% of the time due to the high energy of the delivered artificial ventricular premature, often with a voltage of 700 volts or more. Therefore, R on T ventricular premature should be highly valued and objectively evaluated, and should not be overly feared and subsequently overtreated.
Insights from the CAST trial: treatment must be cautious
The ventricular premature suppression trial (CAST) in patients with myocardial infarction (infarction) is the most important evidence-based development in the field of ventricular premature research in recent years. The incidence of ventricular prematureness in patients with acute infarction is as high as 60% to 100%, and ventricular prematureness can increase mortality in patients. Physicians hope to reduce mortality in infarction patients by suppressing ventricular premature or short-onset ventricular tachycardia with antiarrhythmic drugs, but the validity of this good intention still needs to be verified.
The CAST trial is a 10-year prospective, multicenter, randomized, double-blind, controlled study conducted by the Heart, Lung, and Blood Institute in the United States, in which the antiarrhythmic drugs used (inconamide, flecainide, and emethazine) were effective in long-term control of ventricular premature (over 70%) and short-onset ventricular tachycardia (over 90%) in infarction patients. However, follow-up results showed a 2.8- to 7.7-fold increase in mortality in the treated group compared with the untreated control group, forcing early termination of the CAST trial.
This result warns us that the decision to treat or not to treat ventricular premature should be made carefully, not only considering the immediate efficacy but also the long-term prognostic impact of the treatment. Treatment of ventricular prematureness should be limited to patients with significant symptoms or significant hemodynamic changes.
Most ventricular premature: no treatment required
Most ventricular premature events, including episodic ventricular premature events and frequent ventricular premature events (even those that have developed a triplet or duplex rhythm), do not require treatment. This is also true for functional and pathologic ventricular prematureness. Pathologic ventricular prematureness in young people is more common in patients with viral or rheumatic myocarditis, and in older adults is more common in those with combined coronary artery disease, hypertension, or heart failure. Even when the number of pathological ventricular premature is high, even with symptoms, antiarrhythmic drug treatment for ventricular premature is not necessary, but should take appropriate measures for the cause (such as improving cardiac function, lowering blood pressure, crown expansion, improving myocardial blood supply, etc.).
When the patient’s symptoms have affected quality of life or hemodynamics, pharmacological treatment can be given, but the potential hazards of antiarrhythmic drugs must be taken into account. β-blockers are the drug of choice, which can treat both the symptoms and the cause of the arrhythmia (the arrhythmia itself and the cause), and are moderately effective in controlling ventricular prematureness, but have very little arrhythmogenic effect and are safer to use.
Ventricular prematureness after myocarditis: overtreatment is common
Viral myocarditis is clinically common, occurring in approximately 4% of patients per influenza. Although fulminant viral myocarditis is severe and has a dangerous course, it is seen in only a very small number of patients, and the vast majority of patients have mild or even no symptoms and have recovered spontaneously. About 90% of patients may develop various arrhythmias, with ventricular prematureness being the most common.
Clinically, viral myocarditis is divided into four phases.
(1) Acute phase: viral infection with cardiac symptoms, within 6 months.
②Recovery phase: gradual improvement of cardiac symptoms, duration of disease within 1 year.
(3) Chronic phase: the disease is repeatedly prolonged and the duration of the disease is more than 1 year.
④After-effects phase: no cardiac symptoms, only stable arrhythmias.
Treatment of ventricular premature in patients with viral myocarditis must also follow the above principles. A few patients with severe symptoms can be treated with targeted medications, and treatment should be continued for 2-3 months after symptoms disappear, followed by ambulatory electrocardiography to determine the next step of treatment. When the patient still has complex ventricular prematureness, treatment must be continued for 2 to 3 months. In general, antiarrhythmic drugs are no longer administered after 6 months of the acute phase, because overtreatment is harmful, and ventricular prematureness in patients at this time is related to local inflammatory scar formation and not to the long-term prognosis, which neither affects normal life and work nor causes fatal arrhythmias.
At present, over-treatment of ventricular premature after viral myocarditis is more common, as shown by the excessive duration of antiarrhythmic drug treatment (>6 months), and children are even required to be exempted from physical education classes or suspended from school, which is not only unhelpful to treatment, but also increases the mental burden of children and even causes psychological disorders.
Radiofrequency ablation: a helpless choice
Many patients believe that excessive ventricular prematureness will affect cardiac function and general health, and are eager to be cured by radiofrequency ablation. Radiofrequency ablation can indeed cure ventricular prematureness (especially those located in the right ventricular outflow tract), but it is worth emphasizing that radiofrequency ablation treatment for ventricular prematureness is still a Class IIb indication, which means that this treatment should not be used if possible. In addition, when patients are considered for radiofrequency ablation treatment, they should also choose a well-equipped hospital and an experienced physician to receive the treatment selectively.
Indications for radiofrequency ablation of ventricular premature include excessive total number of ventricular premature (>10,000/day), high level of concomitant symptoms, pre-existing or potential cardiac insufficiency, and low natural variability of ventricular premature. Therefore, the majority of ventricular premature is not easy or suitable for radiofrequency ablation treatment, coupled with the high cost of the procedure and certain failure rate and recurrence rate, so extra caution must be taken when selecting.
Partial ventricular premature: full attention must be paid
While emphasizing that the majority of ventricular premature events are benign arrhythmias, it does not mean that all ventricular premature events can be ignored. Evidence has shown that the prognosis of cardiac patients is related to the number and complexity of ventricular premature events. Clinicians should pay attention to “complex ventricular premature”, i.e., patients with organic heart disease who present with ECG abnormalities in addition to ventricular premature.
In addition, patients with ventricular prematureness should also be taken seriously when they have the following conditions.
(1) Clinical manifestations such as vertigo, black haze or aura syncope.
(2) Organic heart disease (such as coronary artery disease, acute heart attack, cardiomyopathy, heart valve disease, hypertension, etc.).
(③) There have been structural and functional changes of the heart (such as enlarged heart, left ventricular ejection fraction <0.40 or heart failure, etc.).
④History of hereditary arrhythmias or family history.
⑤ Presence of multiple sources, paired and cascading ventricular premature on ECG, as well as R on T ventricular premature on the basis of acute infarction or QT prolongation.
In summary, isolated ventricular prematureness is not clinically significant, and physicians should never take patients with combined organic heart disease or a history of malignant ventricular arrhythmias lightly.