Ventricular arrhythmias include premature ventricular beats, ventricular tachycardia (ventricular tachycardia), monomorphic ventricular tachycardia: sustained and nonsustained, polymorphic ventricular tachycardia: sustained and nonsustained, and ventricular flutter and fibrillation.
Incidence of sudden cardiac death
The annual number of sudden cardiac death worldwide is 9,000,000, with an average survival rate of less than 1%, including 300,000/year in Western Europe, with an average survival rate of 2%-3%, 250,000-350,000/year in the United States, and about 540,000/year in China. Sudden cardiac death has become one of the biggest threats to human health.
Sudden cardiac death classification and risk factors
The incidence of sudden cardiac death is 62% for ventricular tachycardia, 8% for primary ventricular fibrillation, 13% for tip-twist ventricular tachycardia, and 17% for chronic arrhythmias. Risk factors for sudden cardiac death include the occurrence of sudden cardiac death events, ventricular tachycardia, post-myocardial infarction patients, coronary artery disease, heart failure with hypertrophic cardiomyopathy, long QT syndrome, and Brugada syndrome. In contrast, among survivors of sudden cardiac death, having had a sudden cardiac death event is the most risk factor, and within one year, 30% to 50% of survivors of sudden cardiac death will still have a sudden cardiac death event, and patients with sudden cardiac death are closely associated with heart attack and cardiac arrest. In patients who have already had a ventricular tachycardia event, ventricular tachycardia with syncope or low ejection fraction (LVEF < 40%) increases the risk of sudden cardiac death, and the risk of sudden cardiac death in this group of patients is 20% to 50%. The 5-year risk was 32% for post-infarction, nonsustained, inducible, nonsuppressible ventricular tachycardia with LV ejection fraction < 40%. Autopsies in patients with coronary artery disease showed the presence of coronary artery disease in 90% of sudden cardiac deaths, and >50% of sudden cardiac deaths had no significant coronary artery disease prior to the sudden death event. Approximately half of patients with heart failure die from sudden arrhythmias, and low left ventricular ejection fraction increases the risk of sudden cardiac death, and unexplained syncope in NYHA class II C IV patients is predictive of sudden cardiac death. Sudden cardiac death is the most common cause of death in patients with hypertrophic cardiomyopathy. The population prevalence of hypertrophic cardiomyopathy is approximately 0.2%, approximately 10% of patients with hypertrophic cardiomyopathy are considered to be at risk for sudden cardiac death, and recent studies suggest that >50% of high-risk patients will experience sudden cardiac death within 10 years, with hypertrophic cardiomyopathy being the leading cause of sudden cardiac death in athletes under 35 years of age.
Risk stratification of ventricular arrhythmias
Risk stratification for ventricular arrhythmias is determined by the type of ventricular arrhythmia, the presence of organic heart disease, and the presence of a family history of syncope and sudden death. The different classifications of ventricular tachycardia, according to the presence or absence of heart disease, are idiopathic ventricular tachycardia, organic heart disease ventricular tachycardia, coronary ventricular tachycardia, precoronary ventricular tachycardia, arrhythmogenic right ventricular cardiomyopathy ventricular tachycardia; according to the duration of ventricular tachycardia, persistent ventricular tachycardia, nonpersistent ventricular tachycardia, restless ventricular tachycardia; according to the mechanism of ventricular tachycardia, bundle branch folding ventricular tachycardia, coronary ventricular tachycardia, idiopathic left ventricular tachycardia Increased autoregulation includes arrhythmogenic right ventricular cardiomyopathy ventricular tachycardia, idiopathic right ventricular tachycardia, and triggered activity. Fast ventricular rate ventricular tachycardia and slow ventricular rate ventricular tachycardia are classified according to the frequency of ventricular tachycardia.
The earliest risk stratification for ventricular arrhythmias, the LOWN classification of ventricular arrhythmias.
Class 0 – no premature ventricular contractions
Grade 1 – occasional solitary ventricular premature beats (1/myocardial infarction n or <30/h)
Grade 2 – frequent ventricular premature (>1/myocardial infarction n or >30/h)
Grade 3 – Multi-source ventricular premature
Grade 4 – A: paired ventricular premature; B: 3 or more consecutive ventricular premature
Class 5 – R-ON-T ventricular premature
The LOWN stratification of ventricular arrhythmia risk places too much emphasis on the ventricular premature itself, ignoring the underlying pathology and cardiac condition, leading to overtreatment of ventricular premature by clinicians. The administration of the strong antiarrhythmic drug cortolone to a patient with ventricular premature beats without organic heart disease, good cardiac function, and no family history of sudden death violates the principles of standardized treatment. In this group of patients, even with frequent ventricular premature beats or even non-sustained ventricular tachycardia, the prognosis is good, the risk of sudden death is extremely low, and no antiarrhythmic drug treatment can be used if there are no significant symptoms. In the risk stratification of ventricular premature beats, normal healthy population: good prognosis, non-ischemic cardiomyopathy: premature beats and non-sustained ventricular tachycardia can increase mortality, left ventricular hypertrophy is a high risk factor for sudden death, and the Framingham study showed that mortality in those with left ventricular hypertrophy was 8 times higher than in those with normal left ventricles, but high mortality was only partially associated with ventricular prematureness. The prognostic impact of premature and nonsustained ventricular tachycardia on patients with coronary artery disease depends on the timing of the arrhythmia during the disease course. Frequent premature and nonsustained ventricular tachycardia are independent risk factors for total cardiac mortality and sudden cardiac death, with a 3-year cumulative mortality rate of 33% and 15%, respectively. Left ventricular ejection fraction, late potentials, T-wave electrical alternans, heart rate variability, QT dispersion, pressure reflex sensitivity, family history of sudden death, survivors of sudden death, and those with long QT syndrome with syncope. Typical Brugada waves with syncope are also an independent risk factor for determining ventricular arrhythmias. Based on the prognosis of ventricular arrhythmias, the presence or absence of significant associated symptoms and hemodynamic disturbances are classified as benign ventricular arrhythmias including premature or nonsustained ventricular tachycardia without organic heart disease; ventricular arrhythmias with prognostic significance including premature or nonsustained ventricular tachycardia with organic heart disease; and malignant ventricular arrhythmias including sustained ventricular tachycardia with hemodynamic disturbances and ventricular fibrillation. The risk stratum for ventricular tachycardia is based on the presence or absence of combined organic heart disease, myocardial ischemia, cardiac insufficiency, syncope, and family history of sudden death. In clinical practice, unless ventricular tachycardia with hemodynamic instability requires immediate termination of the tachycardia, the search for evidence of organic heart disease should be given priority, and the functional status of the heart should be evaluated to determine the principles of treatment. The risk of sudden death is related to the degree of left ventricular insufficiency, and a poor long-term prognosis is predicted if the LVEF is <40%. (80% of patients have ventricular premature within 24 h after infarction), and nonsustained ventricular tachycardia is also an independent risk factor for sudden cardiac death, especially in patients with left ventricular insufficiency, and its prognosis is worse. The risk stratification of late potentials for predicting ventricular arrhythmias is 90% negative for sudden cardiac death and ventricular arrhythmias and only 16%-31% positive if the patient has cardiac insufficiency, which increases the sensitivity, specificity and positive rate. The incidence of sudden cardiac death is high if the LVEF is <40%, the late potentials are positive, and the Holter shows premature and nonsustained ventricular tachycardia. Role of signal level ECG in risk stratification of ventricular arrhythmias: In the MUSTT study, it was an independent risk factor for death and sudden cardiac death, and other studies have concluded that the exact role of late potentials with other noninvasive risk stratification methods needs to be further clarified, with only 20% predictive value of positive late potentials in post-infarction patients. Children and young patients with hypertrophic cardiomyopathy with a family history of sudden cardiac death are poor prognosticators if they have recurrent exercise syncope, and young patients with severe symptoms are at high risk; some studies have shown a high incidence of sudden cardiac death in patients with hypertrophic cardiomyopathy with nonsustained ventricular tachycardia, and other studies do not support this conclusion; patients with hypertrophic cardiomyopathy <40 years of age who have an abnormal blood pressure response are prone to Most studies have shown that patients with hypertrophic cardiomyopathy are susceptible to sudden cardiac death if they have electrophysiologically induced ventricular arrhythmias.
Treatment of ventricular arrhythmias
These include antiarrhythmic drug therapy, radiofrequency catheter ablation, cardioverter-defibrillators (ICDs), surgical treatment and gene therapy.
The goals of ventricular arrhythmia drug therapy are: to stop acute attacks; to prevent recurrences; and to improve hemodynamics by slowing the ventricular rate.
Pharmacologic treatment of ventricular arrhythmias: Drug selection is based on underlying cardiac lesions, functional status, drug side effects, and overall mortality. In the case of combined cardiac insufficiency, amiodarone is the ideal drug; sotalol is not suitable for heart failure combined with ventricular tachycardia; β-blockers can reduce the sudden death rate of heart failure and ventricular tachycardia after infarction; Class I drugs should be avoided because of their strong negative inotropic and arrhythmogenic effects.
The principles of combination of antiarrhythmic drugs: combination of non-similar drugs, combination of different mechanisms of action, combination of low doses, attention to the side effects of the combination, and attention to the combination of different underlying pathologies. Problems noted in antiarrhythmic drug therapy: negative inotropic effects of certain drugs such as beta-blockers, calcium antagonists, etc.; arrhythmogenic effects, i.e., aggravation of existing arrhythmias, emergence of new arrhythmias (torsional ventricular tachycardia), severe bradycardia (sinus node and atrioventricular node function inhibition), etc. Other side effects are the effects of amiodarone on thyroid function, liver function, lung and cornea. Treatment of arrhythmogenic effects of antiarrhythmic drugs: If toxic effects of an antiarrhythmic drug are identified immediately discontinue the drug and treat aggressively with lidocaine to prevent new arrhythmias. Patients with hemodynamic instability are treated with resuscitation and defibrillation, patients with bradycardia are treated with temporary pacing, those with quinidine toxicity can be treated with magnesium preparations, β-blockers are used to counteract arrhythmias caused by flecainide and enkephalin, and digoxin toxicity is treated with phenytoin sodium.
New classification of antiarrhythmic drugs
Classification
Channel of action
Repolarization time
Representative drugs
Ia
Sodium channel blocker++
Prolongation
quinidine, procainamide
Ⅰb
Sodium channel blocker +
Shortening
Mexilate
Ic
Sodium channel blocker ++++
Unchanged
Propafenone
Ⅰb/Ⅰc
Sodium channel blocker ++++
Shortening
Maurethizide
II
Inhibition of 4-phase depolarization current attenuates L-ICa
unchanged
Beta blockers
Principles of pharmacological treatment of ventricular prematureness
Ventricular premature without organic heart disease or symptoms generally does not require treatment, but if the symptoms are obvious, pharmacological treatment can be considered: β-blockers
The treatment of ventricular prematureness without organic heart disease or symptoms generally requires treatment. Ventricular premature in organic heart disease does not necessarily require drug treatment, but if the symptoms are obvious, myocardial infarction, poor left heart function, drug treatment
Principles of pharmacological treatment of ventricular tachycardia
Termination of acute attacks
Idiopathic ventricular tachycardia: verapamil, propafenone. Ventricular tachycardia of organic heart disease: cortolone, lidocaine
Prevention of recurrence
Idiopathic ventricular tachycardia: verapamil, propafenone. Ventricular tachycardia of organic heart disease: beta-blockers, cortolone Ventricular flutter and ventricular fibrillation: pharmacological treatment as above, but electrical cardioversion or electrical defibrillation preferred
Catheter ablation of idiopathic ventricular tachycardia/premature ventricle
Catheter ablation of ventricular premature is in principle a non-strong indication, and trial ablation can be considered only in the following cases: 1) obvious symptoms, ineffective pharmacological treatment, ventricular premature burden ≥ 20%; 2) catheter ablation of ventricular premature for triggered ventricular fibrillation: triggered primary ventricular fibrillation, long QT syndrome, Brugada syndrome, coronary ventricular fibrillation and other ventricular premature. Radiofrequency ablation of idiopathic left ventricular tachycardia: the success rate is generally about 85%, or even up to 90% or more. Some of the ventricular tachycardia QRS patterns are similar to right ventricular outflow tract ventricular tachycardia, but actually originate from the left ventricular outflow tract, and attention should be paid to the small r waves in V1 leads and other thoracic lead migration. Ablation of ventricular tachycardia originating in the left ventricular outflow tract should only be performed by experienced physicians. Radiofrequency ablation of idiopathic right ventricular outflow tract ventricular tachycardia: success rate of more than 95% and low complications. It is worth mentioning that some ventricular tachycardias originating in the right ventricular outflow tract may be associated with organic heart disease, such as dilated cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy.
Treatment of ventricular tachycardia in organic heart disease
Ventricular tachycardia in coronary artery disease: drug and ICD therapy are preferred; catheter ablation is considered for monomorphic, hemodynamically stable, restless ventricular tachycardia that fails to respond to drug therapy and for slow ventricular rate ventricular tachycardia after ICD implantation. Ventricular tachycardia after correction of congenital heart disease: ventricular tachycardia originating in the right ventricular outflow tract may be considered for catheter ablation. Ventricular tachycardia in dilated cardiomyopathy: the success rate of catheter ablation of bundle branch folding ventricular tachycardia is up to 100%; the success rate of catheter ablation of non-bundle branch folding ventricular tachycardia is low, and ICD or drug therapy is preferred. Hypertrophic ventricular tachycardia: drug or ICD therapy is preferred, and catheter ablation has a low success rate. Arrhythmogenic right ventricular cardiomyopathy: drug or ICD therapy is preferred. Catheter ablation may be considered for ventricular tachycardia originating in the right ventricular outflow tract, but recurrence of ventricular tachycardia is desirable.