Ventricular arrhythmias
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor: Cafer Zorkun, M.D., Ph.D. [2] Vishnu Vardhan Serla M.B.B.S. [3] Nehal Eid, M.D.[4]
Overview
Ventricular arrhythmias (VAs) are abnormal cardiac rhythms originating from the ventricles, encompassing a spectrum from benign premature ventricular complexes (PVCs) to life-threatening ventricular tachycardia (VT) and ventricular fibrillation (VF). VAs are the most common cause of sudden cardiac death (SCD), which accounts for approximately 50% of all cardiovascular deaths in the United States.Al-Khatib SM, Stevenson WG, Ackerman MJ, Bryant WJ, Callans DJ, Curtis AB, Deal BJ, Dickfeld T, Field ME, Fonarow GC, Gillis AM, Granger CB, Hammill SC, Hlatky MA, Joglar JA, Kay GN, Matlock DD, Myerburg RJ, Page RL (2018). "2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death". J Am Coll Cardiol. 72 (14): e91–e220. doi:10.1016/j.jacc.2017.10.054. PMID 29097320. The 2017 AHA/ACC/HRS guideline and the 2022 ESC guideline provide the primary frameworks for the evaluation, risk stratification, and management of patients with VAs and for the prevention of SCD.Könemann H, Ellermann C, Zeppenfeld K, Eckardt L (2023). "Management of Ventricular Arrhythmias Worldwide: Comparison of the Latest ESC, AHA/ACC/HRS, and CCS/CHRS Guidelines". JACC Clin Electrophysiol. 9 (5): 715–728. doi:10.1016/j.jacep.2022.12.008. PMID 37225314 Check |pmid= value (help).
Historical Perspective
The recognition of ventricular arrhythmias dates to the early days of electrocardiography. The development of the implantable cardioverter-defibrillator (ICD) by Michel Mirowski in the 1980s revolutionized the management of life-threatening VAs. Landmark trials including MADIT, MADIT-II, SCD-HeFT, and AVID established the role of ICDs in both primary and secondary prevention of SCD. The CAST trial in 1989 demonstrated that suppression of PVCs with class IC antiarrhythmic drugs (flecainide, encainide) paradoxically increased mortality in post-myocardial infarction patients, fundamentally changing the approach to pharmacologic management of VAs.
Classification
Ventricular arrhythmias are classified by morphology, duration, and clinical context:
| Type | Definition |
|---|---|
| Premature ventricular complex (PVC) | A premature depolarization originating from the ventricles |
| Nonsustained VT (NSVT) | ≥3 consecutive ventricular beats at a rate >100 bpm lasting 30 seconds and not requiring termination due to hemodynamic compromise |
| Sustained VT | VT lasting ≥30 seconds or requiring termination due to hemodynamic compromise in 30 seconds |
| Monomorphic VT | Sustained VT with a stable single QRS morphology |
| Polymorphic VT | Sustained VT with a changing or multiform QRS morphology at cycle length between 600 and 180 ms |
| Torsades de pointes | Polymorphic VT associated with a prolonged QT or QTc, characterized by twisting of the QRS peaks around the isoelectric line |
| Bundle-branch re-entrant tachycardia | VT due to re-entry involving the His-Purkinje system, usually with LBBB morphology; typically occurs in the setting of cardiomyopathy |
| Bidirectional VT | VT with beat-to-beat alternation in the QRS frontal plane axis; often associated with digitalis toxicity or catecholaminergic polymorphic ventricular tachycardia ↗ |
| Ventricular flutter | Regular ventricular arrhythmia at approximately 300 bpm with monomorphic appearance and no isoelectric interval between successive QRS complexes |
| Ventricular fibrillation | Rapid (usually >300 bpm), grossly irregular ventricular rhythm with marked variability in QRS cycle length, morphology, and amplitude |
| Electrical storm | ≥3 episodes of sustained VT, VF, or appropriate ICD shocks within 24 hours |
Zipes DP, Camm AJ, Borggrefe M, Buxton AE, Chaitman B, Fromer M, Gregoratos G, Klein G, Moss AJ, Myerburg RJ, Priori SG, Quinones MA, Roden DM, Silka MJ, Tracy C (2006). "ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death". J Am Coll Cardiol. 48 (5): e247–346. doi:10.1016/j.jacc.2006.07.010. PMID 16949478.
Pathophysiology
The mechanisms underlying ventricular arrhythmias include:
Re-entry: The most common mechanism in structural heart disease. Scar tissue from prior myocardial infarction or fibrosis creates zones of slow conduction bordered by areas of functional or anatomic block, forming a re-entrant circuit. The border zone between viable and fibrotic tissue is the typical substrate for monomorphic VT in ischemic cardiomyopathy.Natale A, Raviele A, Al-Ahmad A, Alfieri O, Aliot E, Almendral J, Breithardt G, Brugada J, Calkins H, Callans D, Cappato R, Chiang CE, Coumel P, Della Bella P, Delacretaz E, Di Biase L, Haissaguerre M, Hindricks G, Ho SY, Jackman W, Jalife J, Jais P, Kalman J, Keane D, Kim YH, Kirchhof P, Klein G, Kottkamp H, Kumagai K, Lindsay BD, Mansour M, Marchlinski FE, McCarthy PM, Mont JL, Morady F, Nademanee K, Nam GB, Packer DL, Pappone C, Prystowsky E, Reddy V, Ruskin JN, Scanavacca M, Shivkumar K, Soejima K, Stevenson W, Swarup V, Tanner H, Thibault B, Tung R, Verma A, Wilber DJ, Yamane T (2010). "Venice Chart International Consensus Document on Ventricular Tachycardia/Ventricular Fibrillation Ablation". J Cardiovasc Electrophysiol. 21 (3): 339–79. doi:10.1111/j.1540-8167.2009.01686.x. PMID 20487903. Triggered activity: Caused by afterdepolarizations. Delayed afterdepolarizations (DADs) are the mechanism of outflow tract VT and digitalis-induced arrhythmias. Early afterdepolarizations (EADs) underlie torsades de pointes in the setting of QT prolongation. Abnormal automaticity: Enhanced automaticity in ventricular tissue, particularly in ischemic or injured myocardium, or in Purkinje fibers. Channelopathies: Genetic mutations affecting cardiac ion channels (e.g., long QT syndrome, Brugada syndrome ↗, catecholaminergic polymorphic ventricular tachycardia, short QT syndrome) create spatial electrical heterogeneity that predisposes to VF.
Causes
Structural Heart Disease
Coronary artery disease: The most common cause of VT and VF, accounting for 76–82% of clinically documented cases Dilated cardiomyopathy Hypertrophic cardiomyopathy Arrhythmogenic right ventricular cardiomyopathy (ARVC) Cardiac sarcoidosis ↗ Myocarditis Congenital heart disease (e.g., tetralogy of Fallot ↗) Valvular heart disease (e.g., aortic stenosis, mitral valve prolapse) Left ventricular noncompaction
Inherited Channelopathies (Structurally Normal Heart)
Long QT syndrome (LQTS) Brugada syndrome Catecholaminergic polymorphic ventricular tachycardia (CPVT) Short QT syndrome (SQTS) Early repolarization syndrome Idiopathic VF
Idiopathic VT (Structurally Normal Heart)
Outflow tract VT: Right ventricular outflow tract (RVOT) or left ventricular outflow tract (LVOT), including aortic sinus of Valsalva origin Idiopathic left ventricular tachycardia: Left posterior fascicular (verapamil-sensitive), left anterior fascicular, or high septal fascicular VT Papillary muscle VT Mitral or tricuspid annular VT
Prystowsky EN, Padanilam BJ, Joshi S, Fogel RI (2012). "Ventricular Arrhythmias in the Absence of Structural Heart Disease". J Am Coll Cardiol. 59 (20): 1733–44. doi:10.1016/j.jacc.2012.01.036. PMID 22575310.
Reversible / Secondary Causes
Electrolyte abnormalities (hypokalemia, hypomagnesemia, hypocalcemia) Myocardial ischemia or acute myocardial infarction Drug-induced (QT-prolonging medications, digitalis toxicity, sympathomimetics, class IC antiarrhythmics in structural heart disease) Hypoxia Acidosis Thyroid disorders Cocaine or other stimulant use
Differentiating Ventricular Arrhythmias from Other Diseases
The differential diagnosis of a wide QRS complex tachycardia includes:
| Diagnosis | Key Distinguishing Features |
|---|---|
| Ventricular tachycardia | AV dissociation, capture/fusion beats, concordance in precordial leads, QRS >140 ms (RBBB) or >160 ms (LBBB), northwest axis |
| Supraventricular tachycardia with aberrant conduction | Typical RBBB or LBBB morphology, preceding P waves, prior ECG showing bundle branch block |
| Supraventricular tachycardia with pre-excitation (Wolff-Parkinson-White syndrome) | History of pre-excitation on baseline ECG, irregular rate (pre-excited atrial fibrillation) |
| Pacemaker-mediated tachycardia | Pacing spikes visible, device interrogation confirms diagnosis |
| Artifact | Baseline rhythm visible between artifact deflections, patient clinically stable |
The Brugada algorithm is a widely used stepwise approach for differentiating VT from SVT with aberrancy, with reported sensitivity and specificity exceeding 95%.
Epidemiology and Demographics
SCD accounts for approximately 230,000 to 350,000 deaths per year in the United States. The estimated total annual burden of out-of-hospital cardiac arrest is approximately 356,500, with an additional 209,000 in-hospital cardiac arrests occurring annually.
Age: Risk of SCD in the general population beginning at age 35 is estimated at approximately 1 per 1,000 per year. In children, adolescents, and young adults, the annual risk is approximately 1 per 100,000. Sex: SCD is more common in men than in women across all age groups. Underlying substrate: Ischemic heart disease remains the most common substrate associated with SCD, although its relative contribution appears to be decreasing, with various forms of cardiomyopathy increasing. PVCs: Found on longer-term monitoring in approximately 50% of all people with or without heart disease. Frequent PVCs (≥1 PVC on a 12-lead ECG or >30 PVCs per hour) are associated with increased cardiovascular risk and mortality.
Risk Factors
Reduced left ventricular ejection fraction (LVEF) Prior myocardial infarction Heart failure Coronary artery disease Family history of SCD Inherited cardiomyopathy or channelopathy Electrolyte abnormalities QT-prolonging medications Stimulant drug use
Natural History, Complications, and Prognosis
The prognosis of ventricular arrhythmias depends on the underlying substrate:
PVCs in structurally normal hearts: Generally benign prognosis. Very frequent PVCs (>10,000–20,000 per day) may cause PVC-induced cardiomyopathy, which is potentially reversible with PVC suppression. NSVT: In the absence of structural heart disease, prognosis is generally favorable. In patients with ischemic or nonischemic cardiomyopathy, NSVT is associated with increased risk of SCD.Katritsis DG, Zareba W, Camm AJ (2012). "Nonsustained Ventricular Tachycardia". J Am Coll Cardiol. 60 (20): 1993–2004. doi:10.1016/j.jacc.2011.12.063. PMID 23083773. Sustained VT/VF: Associated with high mortality without treatment. Electrical storm is associated with increased mortality. Out-of-hospital cardiac arrest: Overall survival rate is estimated at approximately 10%. Survival is better when the initial rhythm is shockable (VF or pulseless VT) compared with pulseless electrical activity or asystole. Idiopathic VT: Outflow tract VT and fascicular VT in structurally normal hearts carry an excellent prognosis.
Management
Patients Without Heart Disease
In the absence of heart disease, PVCs are associated with little or no increased risk of developing a dangerous arrhythmia. In this situation, the risk-to-benefit ratio of antiarrhythmic drug therapy does not support routine treatment.[1] It is important to review medications, determine if stimulants are being used, and correct electrolyte abnormalities. If no underlying cause is found, the optimal approach is patient reassurance. Patients should be made aware of the potential dangers of antiarrhythmic drug therapy as determined in the Cardiac Arrhythmia Suppression Trials (CAST and CAST II).[2] [3]
CAST showed that the risk of dying increased, rather than decreased, with successful long-term suppression of premature ventricular complexes after myocardial infarction in older patients. At best, CAST II showed no impact on long-term survival from drug treatment that successfully suppressed premature ventricular complexes. If patients with multiple premature ventricular complexes have severe, disabling symptoms, beta blockers are the safest initial choice.Referral to a cardiologist is indicated if beta-blocker therapy is not effective. In this situation, the next agents to be tried would be class I antiarrhythmic drugs, such as flecainide (Tambocor) and amiodarone (Cordarone), although radiofrequency ablation of an ectopic focus may also be an appropriate treatment.
Patients with Structural Heart Disease
The occurrence of premature ventricular complexes in patients with structural heart disease has been shown to significantly increase the risk of subsequent morbidity and mortality. Coronary heart disease, cardiomyopathy, and congestive heart failure are the major cardiac diseases associated with unfavorable outcomes in patients with premature ventricular complexes.
Ventricular Tachycardia
Ventricular tachycardia refers to a rhythm originating from a ventricular ectopic focus at a rate >100 bpm. The electrocardiogram shows a wide complex tachycardia with no associated P waves.
In patients with bundle branch block,Wolff-Parkinson-White syndrome, or aberrant conduction, supraventricular tachycardia can resemble ventricular tachycardia. Because of the morbidity and mortality associated with untreated ventricular tachycardia, any wide-complex tachycardia should be assumed to be ventricular tachycardia until proved otherwise. Physicians should keep in mind that patients with ventricular tachycardia can have minimal symptoms.
Management of Ventricular Tachycardia
The mortality rate within two years is reported to be higher than 30% in patients with non sustained ventricular tachycardia on Holter monitoring and impaired left ventricular function.[4] Two large multicenter trials [5] [6] showed a clear advantage for automatic cardioverter defibrillator implantation over drug therapy in patients who had a malignant ventricular arrhythmia or who had been resuscitated from sudden cardiac death. The selection of high-risk patients for defibrillator implantation should be based on left ventricular function and the findings of electrophysiologic studies.
Implantable defibrillators appear to be most beneficial in patients with a low ejection fraction who are noted to have frequent premature ventricular complexes, non sustained ventricular tachycardia on Holter monitoring, and a history of syncope or nearsyncope. It is critical to rule out coronary heart disease and to optimize the treatment of congestive heart failure in these patients. When ventricular tachycardia is diagnosed in relatively asymptomatic patients, medical treatment should be attempted. New recommendations from the American Heart Association [7] emphasize the initial use of 300 mg of iv. administered amiodarone, followed by repeated 150 mg iv. doses every 8-10 minutes, in patients with pulseless VT.
Patients with stable ventricular tachycardia should be given 150 mg of amiodarone intravenously over 10 minutes, followed by an infusion at 1 mg/minute for 6 hours and then at 0.5 mg/minute until the VT converts to sinus rhythm or another less dangerous rhythm. The alternative treatment is intravenously administered lidocaine (Xylocaine), given first in a 100 mg bolus (or 1 mg/kg) and then in an infusion at 1-4 mg/minute.
In hemodynamically unstable patients, electrical cardioversion should be attempted in accordance with the recently revised advanced cardiac life support (ACLS) protocols.
Automatic implantable cardioverter defibrillators (ICD) are considered the most effective treatment for patients with life-threatening VT or VF. According to expert recommendations, implantation of an automatic cardioverter defibrillator should be considered in these situations[8]:
1. Cardiac arrest resulting from ventricular fibrillation or tachycardia not caused by a transient or reversible cause
2. Spontaneous, sustained ventricular tachycardia
3. Syncope of undetermined origin and sustained VT or ventricular fibrillation (VF) induced during electrophysiologic studies
4. Non sustained VT with coronary artery disease and LV dysfunction if VT or VF is induced during electrophysiologic studies.
2006 ACC/AHA/ESC Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death (DO NOT EDIT) [9]
Diagnostic Evaluation
Electrocardiographic Techniques and Measurements (DO NOT EDIT)[9]
| Class IIa |
| "1. It is reasonable to use TWA to improve the diagnosis and risk stratification of patients with ventricular arrhythmias or who are at risk for developing lifethreatening ventricular arrhythmias. (Level of Evidence: A) " |
| Class IIb |
| "1. ECG techniques such as signal-averaged ECG (SAECG), heart rate variability (HRV), baroflex sensitivity, and heart rate turbulence may be useful to improve the diagnosis and risk stratification of patients with ventricular arrhythmias or who are at risk of developing life-threatening ventricular arrhythmias. (Level of Evidence: B) " |
Resting Electrocardiogram (DO NOT EDIT)[9]
| Class I |
| "1. Resting 12-lead ECG is indicated in all patients who are evaluated for ventricular arrhythmias. (Level of Evidence: A). " |
Ambulatory Electrocardiography Recommendations (DO NOT EDIT)[9]
| Class I |
| "1. Ambulatory ECG is indicated when there is a need to clarify the diagnosis by detecting arrhythmias, QT interval changes, T-wave alternans (TWA), or ST changes, to evaluate risk, or to judge therapy. (Level of Evidence: A) " |
| "2. Event monitors are indicated when symptoms are sporadic to establish whether or not they are caused by transient arrhythmias. (Level of Evidence: B) " |
| "3. Implantable recorders are useful in patients with sporadic symptoms suspected to be related to arrhythmias such as syncope when a symptom-rhythm correlation cannot be established by conventional diagnostic techniques. (Level of Evidence: B) " |
Exercise Testing Recommendations (DO NOT EDIT)[9]
| Class I |
| "1. Exercise testing is recommended in adult patients with ventricular arrhythmias who have an intermediate or greater probability of having CHD by age, gender, and symptoms* to provoke ischemic changes or ventricular arrhythmias. (Level of Evidence: B) *See Table 4 in the ACC/AHA 2002 Guideline Update for Exercise Testing (141) for further explanation of CHD probability." |
| "2. Exercise testing, regardless of age, is useful in patients with known or suspected exercise-induced ventricular arrhythmias, including catecholaminergic VT, to provoke the arrhythmia, achieve a diagnosis, and determine the patient’s response to tachycardia. (Level of Evidence: B)" |
| Class III |
| "1. See Table 1 in the ACC/AHA 2002 Guideline Update for Exercise Testing (141) for contraindications. (Level of Evidence: C)" |
| Class IIa |
| "1. Exercise testing can be useful in evaluating response to medical or ablation therapy in patients with known exercise-induced ventricular arrhythmias. (Level of Evidence: B)" |
| Class IIb |
| "1. Exercise testing may be useful in patients with ventricular arrhythmias and a low probability of CHD by age, gender, and symptoms.* (Level of Evidence: C) *See Table 4 in the ACC/AHA 2002 Guideline Update for Exercise Testing (141) for further explanation of CHD probability." |
| "2. Exercise testing may be useful in the investigation of isolated premature ventricular complexes (PVCs) in middle-aged or older patients without other evidence of CHD. (Level of Evidence: C)" |
Left Ventricular Function and Imaging (DO NOT EDIT)[9]
| Class I |
| "1. Echocardiography is recommended in patients with ventricular arrhythmias who are suspected of having structural heart disease. (Level of Evidence: B)" |
| "2. Echocardiography is recommended for the subset of patients at high risk for the development of serious ventricular arrhythmias or SCD, such as those with dilated, hypertrophic, or RV cardiomyopathies, AMI survivors, or relatives of patients with inherited disorders associated with SCD. (Level of Evidence: B)" |
| "3. Exercise testing with an imaging modality (echocardiography or nuclear perfusion [single-photon emission computed tomography (SPECT)]) is recommended to detect silent ischemia in patients with ventricular arrhythmias who have an intermediate probability of having CHD by age, symptoms, and gender and in whom ECG assessment is less reliable because of digoxin use, LVH, greater than 1-mm ST-segment depression at rest, WPW syndrome, or LBBB. (Level of Evidence: B)" |
| "4. Pharmacological stress testing with an imaging modality (echocardiography or myocardial perfusion SPECT) is recommended to detect silent ischemia in patients with ventricular arrhythmias who have an intermediate probability of having CHD by age, symptoms, and gender and are physically unable to perform a symptom-limited exercise test. (Level of Evidence: B)" |
| Class IIa |
| "1. MRI, cardiac computed tomography (CT), or radionuclide angiography can be useful in patients with ventricular arrhythmias when echocardiography does not provide accurate assessment of LV and RV function and/or evaluation of structural changes. (Level of Evidence: B)" |
| "2. Coronary angiography can be useful in establishing or excluding the presence of significant obstructive CHD in patients with life-threatening ventricular arrhythmias or in survivors of SCD, who have an intermediate or greater probability of having CHD by age, symptoms, and gender. (Level of Evidence: C)" |
| "3. LF imaging can be useful in patients undergoing biventricular pacing. (Level of Evidence: C)" |
Electrophysiological Testing (DO NOT EDIT)[9]
| Class I |
| "1. EP testing is recommended for diagnostic evaluation of patients with remote MI with symptoms suggestive of ventricular tachyarrhythmias, including palpitations, presyncope, and syncope. (Level of Evidence: B)" |
| "2. EP testing is recommended in patients with CHD to guide and assess the efficacy of VT ablation. (Level of Evidence: B)" |
| "3. EP testing is useful in patients with CHD for the diagnostic evaluation of wide QRS complex tachycardias of unclear mechanism. (Level of Evidence: B)" |
| Class IIa |
| "1. EP testing is reasonable for risk stratification in patients with remote MI, NSVT, and LVEF equal to or less than 40%. (Level of Evidence: B)" |
Management of Special Patient Populations
Management of Ventricular Arrhythmias in Pregnancy (DO NOT EDIT)[9]
| Class I |
| "1. Pregnant women developing hemodynamically unstable VT or VF should be electrically cardioverted or defibrillated. (Level of Evidence: B) (See Section 7.)" |
| "2. In pregnant women with the LQTS who have had symptoms, it is beneficial to continue beta-blocker medications throughout pregnancy and afterward, unless there are definite contraindications. (Level of Evidence: C)" |
Management of Ventricular Arrhythmias in Elderly Patients (DO NOT EDIT)[9]
| Class I |
| "1. Elderly patients with ventricular arrhythmias should generally be treated in the same manner as younger individuals. (Level of Evidence: A)" |
| "2. The dosing and titration schedule of antiarrhythmic drugs prescribed to elderly patients should be adjusted to the altered pharmacokinetics of such patients. (Level of Evidence: C)" |
| Class III |
| "1. Elderly patients with projected life expectancy less than 1 y due to major comorbidities should not receive ICD therapy. (Level of Evidence: C)" |
Management of Ventricular Arrhythmias in Pediatric Patients (DO NOT EDIT)[9]
| Class I |
| "1. An ICD should be implanted in pediatric survivors of a cardiac arrest when a thorough search for a correctable cause is negative and the patients are receiving optimal medical therapy and have reasonable expectation of survival with a good functional status for more than 1 y. (Level of Evidence: C)" |
| "2. Hemodynamic and EP evaluation should be performed in the young patient with symptomatic, sustained VT. (Level of Evidence: C)" |
| "3. ICD therapy in conjunction with pharmacological therapy is indicated for high-risk pediatric patients with a genetic basis (ion channel defects or cardiomyopathy) for either SCD or sustained ventricular arrhythmias. The decision to implant an ICD in a child must consider the risk of SCD associated with the disease, the potential equivalent benefit of medical therapy, as well as risk of device malfunction, infection, or lead failure and that there is reasonable expectation of survival with a good functional status for more than 1 y. (Level of Evidence: C)" |
| Class III |
| "1. Pharmacological treatment of isolated PVCs in pediatric patients is not recommended. (Level of Evidence: C)" |
| "2. Digoxin or verapamil should not be used for treatment of sustained tachycardia in infants when VT has not been excluded as a potential diagnosis. (Level of Evidence: C)" |
| "3. Ablation is not indicated in young patients with asymptomatic NSVT and normal ventricular function.(Level of Evidence: C)" |
| Class IIa |
| "1. ICD therapy is reasonable for pediatric patients with spontaneous sustained ventricular arrhythmias associated with impaired (LVEF of 35% or less) ventricular function who are receiving chronic optimal medical therapy and who have reasonable expectation of survival with a good functional status for more than 1 y. (Level of Evidence: B)" |
| "2. Ablation can be useful in pediatric patients with symptomatic outflow tract or septal VT that is drug resistant, when the patient is drug intolerant or wishes not to take drugs. (Level of Evidence: C)" |
Resources
1. Zipes DP, Camm AJ, Borggrefe M, et al., ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death A Report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death)Circulation 2006;114;e385-e484
2. Kesh Hebbar A, Hueston WJ, Management of Common Arrhythmias: Part II.Ventricular Arrhythmias and Arrhythmias in Special Populations Am Fam Physician 2002;65:2491-6.
References
- ↑ Kennedy HL, Whitlock JA, Sprague MK, Kennedy LJ, Buckingham TA, Goldberg RJ. Long-term follow-up of asymptomatic healthy subjects with frequent and complex ventricular ectopy. N Engl J Med 1985;312:193-7.
- ↑ Echt DS, Liebson PR, Mitchell LB, Peters RW, Obias-Manno D, Barker AH, et al. Mortality and morbidity in patients receiving encainide, flecainide, or placebo. The Cardiac Arrhythmia Suppression Trial. N Engl J Med 1991;324:781-8
- ↑ Effect of the antiarrhythmic agent moricizine on survival after myocardial infarction. The Cardiac Arrhythmia Suppression Trial II Investigators. N Engl J Med 1992;327:227-33.
- ↑ Wilber DJ, Garan H, Finkelstein D, Kelly E, Newell J, McGovern B, et al. Out-of-hospital cardiac arrest. Use of electrophysiologic testing in the prediction of long-term outcome. N Engl J Med 1988;318:19-24.
- ↑ Moss AJ, Hall WJ, Cannom DS, Daubert JP, Higgins SL, Klein H, et al. Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. Multicenter Automatic Defibrillator Implantation Trial Investigators. N Engl J Med 1996;335:1933-40.
- ↑ A comparison of antiarrhythmic drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias. The Antiarrhythmics versus Implantable Defibrillators (AVID) Investigators. N Engl J Med 1997;337:1576-83.
- ↑ Gazmuri RJ, Nadkarni VM, Nolan JP et al., Scientific Knowledge Gaps and Clinical Research Priorities for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Identified During the 2005 International Consensus Conference on E and CPR Science With Treatment Recommendations A Consensus Statement From the International Liaison Committee on Resuscitation (American Heart Association, Australian Resuscitation Council, European Resuscitation Council, Heart and Stroke Foundation of Canada, Inter American Heart Foundation, Resuscitation Council of Southern Africa, and the New Zealand Resuscitation Council); the American Heart Association Emergency Cardiovascular Care Committee; the Stroke Council; and the Cardiovascular Nursing Council. Circulation 2007 http://circ.ahajournals.org/cgi/content/full/116/21/2501
- ↑ Gregoratos G, Cheitlin MD, Conill A, Epstein AE, Fellows C, Ferguson TB Jr, et al. ACC/AHA guidelines for implantation of cardiac pacemakers and antiarrhythmia devices: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Pacemaker Implantation). Circulation 1998;97:1325-35.
- ↑ 9.00 9.01 9.02 9.03 9.04 9.05 9.06 9.07 9.08 9.09 Zipes DP, Camm AJ, Borggrefe M, Buxton AE, Chaitman B, Fromer M; et al. (2006). "ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (writing committee to develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society". Circulation. 114 (10): e385–484. doi:10.1161/CIRCULATIONAHA.106.178233. PMID 16935995.