Ventricular premature contractions (ventricular premature) are like a kaleidoscope of variability and mystery. The principle of ventricular premature treatment is not to provide targeted treatment, let alone long-term antiarrhythmic drug therapy for asymptomatic ventricular premature. It is necessary to treat ventricular premature with clear etiology, and for frequent, complex ventricular premature with obvious symptoms, both Chinese and Western drug therapy can be chosen.
1. Insight from CAST trial: treatment must be cautious
Ventricular premature suppression test (CAST) in patients with myocardial infarction (infarction) is the most important evidence-based progress 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 was 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, considering not only the immediate efficacy but also the impact of treatment on the long-term prognosis. Treatment of ventricular prematureness should be limited to patients with significant symptoms or significant hemodynamic changes.
2.Most ventricular premature: no treatment required
Most ventricular premature, including episodic ventricular premature and frequent ventricular premature (even formed triplet rhythm or diphasic rhythm), do not need treatment. This is also true for functional ventricular premature and pathological ventricular premature. 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 may 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).
3, ventricular premature after myocarditis: overtreatment prevails
Clinically, viral myocarditis is common, with viral myocarditis occurring in about 4% of patients per influenza. Although the outbreak of viral myocarditis is serious and dangerous course, but only seen in a very small number of patients, the vast majority of patients with mild disease, or even no symptoms have been self-healing. 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 does fatal arrhythmia occur.
At present, the phenomenon of 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 or suspended from school, which is not only unhelpful to treatment, but also increases the mental burden of children, and even causes psychological disorders.
4.Radiofrequency ablation: a helpless choice
Many patients believe that too much ventricular premature will affect the heart function and general health, and are eager to be cured by radiofrequency ablation. Radiofrequency ablation can indeed cure ventricular premature (especially those located in the right ventricular outflow tract), but it is worth emphasizing that radiofrequency ablation treatment for ventricular premature is still a class IIb indication, i.e., this treatment should not be used as much as 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, most of the ventricular premature is not easy or not suitable for radiofrequency ablation treatment, coupled with the high cost of the procedure and certain failure rate and recurrence rate, so we must be extra cautious when choosing.
5.Partial ventricular premature: full attention must be paid
While emphasizing that most ventricular premature is a benign arrhythmia, it does not mean that all ventricular premature can be ignored. Evidence has confirmed 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, the following conditions should be taken into account when patients with ventricular prematureness are present.
(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 conclusion, 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.
6. Myerburg classification of risk of ventricular prematureness
The Myerburg classification of risk based on the frequency and morphology of ventricular premature is called the Myerburg classification (Table 1) and has been shown to be effective in patients with chronic heart disease. The data show that the risk of fatal arrhythmias is significantly higher for ventricular prematureities with frequency class 3 or higher in the Myerburg classification. Paired ventricular prematureities have a higher risk than monomorphic or episodic polymorphic ventricular prematureities, and those with morphology grade D or higher have a higher risk of cardiac events.
In healthy individuals without organic heart disease, ventricular prematureities below grade 2 are benign, whereas in patients with acute infarction or cardiac insufficiency they may be malignant and can even cause sudden death. Therefore, combining Myerburg grading method with the severity of underlying heart disease and left ventricular ejection fraction is the only way to correctly assess the risk of ventricular premature in patients with chronic heart disease and use it to guide clinical practice.
7.Heart rate shock after ventricular premature: a new technique for warning sudden death
Heart rate turbulence refers to the short-term fluctuation of sinus heart rate after a ventricular premature, that is, under normal circumstances, the sinus heart rate after ventricular premature should appear fast and then slow, and the disappearance of this phenomenon is abnormal. The main detection indexes are oscillation onset (TO) and oscillation slope (TS). a normal TO means that the RR interval after ventricular premature is temporarily fast first. a normal TO < 0 means that the sinus rate after ventricular premature is accelerated. a normal TS is the maximum slope of any 5 RR intervals out of 20 sinus rhythms after ventricular premature. a normal TS > 2.5 ms/RR indicates that the sinus rate after ventricular premature is posterior slowing.
Evidence-based medical evidence suggests that in patients with ischemic heart disease, TO and TS are two independent predictors of high risk of death, with TO ≥ 0 and TS ≤ 2.5 ms/RR being abnormal. One study (MPIP) showed a 2-year mortality rate of 11% for TO<0 and 20% for TO≥0, compared with 11% and 27%, respectively, in another study (EMITA).
In the MPIP study, the 2-year mortality rate was 9% in those with normal TS (negative) and 27% in those with positive, compared with 9% and 26%, respectively, in the EMITA study. This shows that the risk of sudden death is increased in those with positive TO or TS, and both are abnormal with greater predictive power. In conclusion, the absence of characteristic sinus heart rate oscillations after ventricular premature is a predictor of increased sudden death in patients with acute heart attack and heart failure.