eMedicine Specialties > Cardiology > Arrhythmias
Ventricular Tachycardia: Treatment & Medication
Updated: Oct 24, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Medical Care
Acute ventricular tachycardia
The acute emphasis is to achieve an accurate diagnosis and arrhythmia conversion. Ventricular tachycardia (VT) associated with loss of consciousness or hypotension is a medical emergency requiring immediate cardioversion. In a normal-sized adult, this is typically accomplished with a 100-to 200-J biphasic cardioversion shock using standard advanced cardiac life support (ACLS) protocols.
If the hemodynamic status is stable, and no evidence for coronary ischemia or infarction is present, then rhythm conversion may be achieved with either cardioversion or intravenous medication. An intravenous line is placed, and 12-lead ECG obtained prior to conversion. If left ventricular function is impaired, amiodarone, then lidocaine, are favored over procainamide because of the latter drug's potential for exacerbating congestive heart failure. If medical therapy is unsuccessful, synchronized cardioversion (50-200 J monophasic) following sedation is appropriate.
If runs of polymorphic VT are observed punctuated by sinus rhythm with QT prolongation, then attempts should be made to correct torsades with magnesium, isoproterenol, and/or pacing. Phenytoin and lidocaine may also help by shortening the QT interval in this setting, but procainamide is contraindicated because of its QT prolonging effects. Efforts should be made to correct hypokalemia and withdraw any chronic medications associated with QT-interval prolongation.
Occasionally, patients present with wide QRS complex tachycardia of unknown mechanism. In the absence of pacing, the differential diagnosis includes VT and aberrantly conducted supraventricular tachycardia (SVT). If hemodynamic compromise is present or if any doubt exists about the rhythm diagnosis, the safest strategy is to treat the undiagnosed rhythm as VT. If the clinical situation permits, a 12-lead ECG should be obtained prior to conversion of the rhythm. The ECG criteria of Brugada et al15 may be useful in differentiating the arrhythmia mechanism as outlined above.
Rarely, patients present with repetitive runs of nonsustained VT, as in the following ECG. Prolonged exposure to this (or any other) tachycardia may cause a tachycardia-induced cardiomyopathy, which typically improves with medical or ablative therapy of the VT.12
Repetitive monomorphic ventricular tachycardia (VT) from an asymptomatic 45-year-old female wind surfer with a structurally normal heart. This ECG pattern is typical for idiopathic VT arising from the right ventricular outflow tract. This rhythm is often exertional and, unlike ischemic VT, suppressed by beta blockade or verapamil. The prognosis is good, with the following exceptions: (1) sudden death may be seen if right ventricular dysplasia or exceptionally rapid VT is encountered, and (2) occasionally, patients with incessant VT develop congestive heart failure due to tachycardia-induced cardiomyopathy or frequent ectopy. The cardiomyopathy resolves when the tachycardia is treated.
Ventricular tachycardia postconversion
Following conversion of VT, the clinical emphasis shifts to determining the severity of heart disease, prognosis, and best long-term management plan. Options, depending on the severity of symptoms and degree of structural heart disease, include medications, ICD implantation, and catheter ablation. Combinations of these therapies are often used when structural heart disease is present. Because monomorphic VT patients with structurally normal hearts have a low risk of sudden death, ICDs are rarely necessary in this setting. These patients are almost always managed with medications or ablation.
Antiarrhythmic drug trials have been disappointing, particularly in patients with left ventricular dysfunction. Some antiarrhythmic drugs may actually increase sudden death mortality in this group. This is of particular concern with Vaughn Williams Class I antiarrhythmics, which slow propagation and reduce tissue excitability through sodium channel blockade. Current clinical practice favors class III antiarrhythmics, which prolong myocardial repolarization through potassium channel blockade.
- Amiodarone is a complex antiarrhythmic drug that deserves special mention. It is generally listed as a class III drug but has measurable class I, II, and IV effects. Unlike class I antiarrhythmics, amiodarone appears to be safe in patients with left ventricular dysfunction. Class III antiarrhythmics are preferred in most patients with left ventricular dysfunction.
- In the setting of congestive heart failure, the best proven but nonspecific antiarrhythmic drug strategies include beta-receptor blocking drugs carvedilol, metoprolol, and bisoprolol; angiotensin-converting enzyme (ACE) inhibitors; and aldosterone antagonists. Statin therapy may also have nonspecific but salutory effects on both atrial and ventricular arrhythmias.
Surgical Care
In the 1980s, ventricular arrhythmia surgery was explored at several centers, using excision and cryoablation of infarct zones to prevent recurrent ventricular tachycardia (VT). This strategy has been essentially abandoned due to high mortality rates and the advent of both ICD and ablative therapies.
Implantable cardioverter-defibrillator
The implantable cardioverter-defibrillator (ICD) has changed the face of ventricular arrhythmia management. Like pacemakers, these devices can be implanted transvenously in a brief, low-risk procedure. Once installed, the ICD can detect ventricular tachyarrhythmias and terminate them with defibrillation shocks or antitachycardia pacing algorithms. These devices can also function as backup pacemakers in patients with bradyarrhythmias. The advent of transvenous ICD technology triggered several trials comparing the ICD to conventional antiarrhythmic therapies.
In patients with prior ventricular tachycardia/ventricular fibrillation, ICD therapy was compared with the best available antiarrhythmic drugs, amiodarone and sotalol. The Antiarrhythmics Versus Implantable Defibrillators (AVID) study; the Canadian Implantable Defibrillator Study (CIDS); and the Cardiac Arrest Study, Hamburg (CASH) demonstrated better survival in patients randomized to ICD therapy. The survival difference was significant in AVID, of borderline statistical significance in CIDS (P <0.06), and of no statistical difference in CASH. A meta-analysis of the 3 trials suggested a 28% reduction in the relative risk of death related to ICD implantation in this clinical setting.17
Endocardial catheter ablationEndocardial catheter ablation is used early in idiopathic monomorphic VT (ie, structurally normal heart) but can also be used to reduce arrhythmia burden in the presence of cardiomyopathy. Ablation is used to treat symptomatic VT rather than to reduce sudden death risk. In patients with cardiomyopathy, the usual goal is to minimize the number of ICD shocks.
In some patients, percutaneous epicardial ablation can be used successfully when endocardial lesions fail. Current techniques include 3-dimensional scar, isopotential, or activation mapping, followed by high-energy radiofrequency ablation with irrigated-tip catheters capable of creating deeper lesions in the thicker LV wall.
- Reentrant VT requires a slow conduction zone, and this is usually located along the border of a scarred zone of myocardium.
- The small physical size of the slow conduction zone makes it an ideal target for focal ablation procedures.
- Cell disruption can be achieved using radiofrequency energy or cryoablation via transvenous catheters during closed-chest procedures.
- Because patients with ischemic VT often have multiple reentrant circuits, ablation is typically used as an adjunct to ICD therapy.
- If VT arises from an automatic focus, the focus can be targeted for ablation.
- In patients with structurally normal hearts, the most common form of VT arises from the right ventricular outflow tract (RVOT). The typical outflow tract ectopic beat shows a positive QRS axis in the inferior leads. Abnormal or triggered automaticity is the most likely mechanism, and focal ablation is curative in these patients. Ablation cure rates are typically greater than 95% if the arrhythmia can be induced in the electrophysiology laboratory.
- Reentrant tachycardia may arise from the RVOT in patients with right ventricular dysplasia or repaired tetralogy of Fallot. These circuits are usually amenable to catheter ablation.
This is a posteroanterior view of a right ventricular endocardial activation map during ventricular tachycardia in a patient with a prior septal myocardial infarction. Earliest activation is recorded in red; late activation shows as blue to magenta. Fragmented low amplitude diastolic local electrograms were recorded adjacent to the earliest (red) breakout area, and local ablation in this scarred zone (red dots) resulted in termination and noninducibility of this previously incessant arrhythmia.
Consultations
Cardiac electrophysiology is a subspecialty devoted to the diagnosis and management of cardiac arrhythmias. Patients with ventricular tachycardia should be referred to general cardiologists or electrophysiologists for specialized care.
Diet
Patients with ischemic ventricular tachycardia (VT) may benefit from low-cholesterol and/or low-salt diets. Patients with idiopathic VT may notice a reduction in symptoms when stimulants, such as caffeine, are avoided.
Activity
Ventricular tachycardia (VT) may be precipitated by increased sympathetic tone during strenuous physical exertion. One goal of successful VT management is to allow the patient to return to an active lifestyle through medications, ICD implantation, and/or ablation therapy.
Medication
Intravenous medications are used to suppress acute monomorphic ventricular tachycardia (VT). In the United States, these are limited to procainamide, lidocaine, amiodarone, and a handful of intravenous beta-adrenergic blocking agents (metoprolol, esmolol, propranolol). Bretylium is no longer available. In patients with cardiac arrest, intravenous amiodarone is the drug of choice. Although intravenous lidocaine is effective at suppressing peri-infarction VT, it may increase the overall mortality risk. Amiodarone has been shown to be superior to lidocaine or placebo in resuscitated cardiac arrest, but has not been as well studied in stable, monomorphic VT.
In patients with idiopathic VT (associated with structurally normal hearts), medications are often avoided entirely through the use of curative catheter-based ablation.
Oral medications are used to chronically suppress recurrent VT. As noted earlier in this article, current evidence favors class III antiarrhythmic drugs over class I drugs. No large studies compare the currently available class III drugs, amiodarone, and sotalol. Both drugs require careful monitoring during initiation and long term follow-up. Sotalol is loaded on an inpatient basis, with telemetry and ECG monitoring for bradycardia, ventricular proarrhythmia, and excessive QT prolongation. Many centers then follow sotalol patients on a quarterly basis to reassess renal function, QT intervals, and to watch for new drug interactions. Amiodarone initiation requires baseline and serial liver, thyroid, and pulmonary function testing.
When VT is observed in a patient receiving an antiarrhythmic drug, discrimination must be made between VT recurrence and drug-induced ventricular proarrhythmia. The most common form of proarrhythmia is torsades de pointes (see Torsade de Pointes) associated with QT-interval prolongation, usually due to excessive potassium channel blockade.
In patients with hemodynamically significant ventricular tachycardia/ventricular fibrillation, implantable cardioverter-defibrillator (ICD) implantation has superseded medication as primary therapy. Because ICDs treat, rather than prevent, ventricular arrhythmias, as many as 50% of ICD patients require therapy with antiarrhythmic drugs to reduce the potential for ICD shocks. Once an ICD has been implanted, adjunctive drug and catheter ablation therapies can be used to reduce the number of ICD discharges.
Antiarrhythmics
Intravenous administration is used for suppression of acute VT. Agents alter the electrophysiologic mechanisms responsible for arrhythmia. Medications are generally used to prevent recurrence of VT in susceptible patients.
Careful attention must be paid to drug pharmacokinetics due to relatively narrow therapeutic windows involved.
Most antiarrhythmic drugs may actually cause ventricular arrhythmias, and risks generally increase with serum drug levels.
To monitor for drug proarrhythmia, patients are usually admitted to the hospital during initiation of oral antiarrhythmic medication. The patient is then monitored by telemetry and serial ECGs during 5-6 drug half-lives to be sure that the drug is well tolerated.
Lidocaine (Xylocaine, Nervocaine, LidoPen, Duo-Trach)
Class IB antiarrhythmic that increases electrical stimulation threshold of the ventricle, suppressing automaticity of conduction through the tissue. Although lidocaine may terminate VT successfully, it may increase the overall mortality in peri-infarction VT. Evidence for effectiveness is considered "Indeterminate" in the 2000 American Heart Association Emergency Cardiovascular Care guidelines.
Adult
1-1.5 mg/kg IV push, followed by 0.5-0.75 mg/kg IV push to a maximum of 3 mg/kg
Continuous 1–4 mg/min infusion should be started after arrhythmia is suppressed
Pediatric
Endotracheal, intraosseous, and IV loading dose: 1 mg/kg, may repeat twice at 10- to 15-min intervals if necessary; follow with continuous IV infusion of 20-50 mcg/kg/min
Coadministration with cimetidine or beta-blockers, increases toxicity of lidocaine; coadministration with procainamide and tocainide may result in additive cardiodepressant action; may increase effects of succinylcholine
Documented hypersensitivity to amide-type local anesthetics; avoid in Adams-Stokes syndrome and Wolf-Parkinson-White syndrome; avoid in severe sinoatrial, atrioventricular (AV), or intraventricular block if artificial pacemaker not in place
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Do not use a drug solution that contains preservatives; caution in heart failure, hepatic disease, hypoxia, hypovolemia or shock, respiratory-depression, and bradycardia; elderly patients may be at increased risk for CNS and cardiac adverse effects due to increased half-life or decreased clearance of the drug; high plasma concentrations can cause seizures, heart block, and AV conduction abnormalities; has been associated with malignant hyperthermia
Procainamide (Procanbid, Pronestyl)
A Class IIB level therapy used for VT refractory to defibrillation and epinephrine. Increases refractory period of atria and ventricles.
Myocardial excitability is reduced by increase in threshold for excitation and inhibition of ectopic pacemaker activity.
Adult
20-30 mg/min continuous IV infusion until arrhythmia suppressed, patient becomes hypotensive, QRS widens 50% above baseline, or maximum dose of 17 mg/kg is administered; once arrhythmia is suppressed, may be infused at rate of 1-4 mg/min continuously
Long-acting formulation: 1000 mg PO bid; adjust dose based on levels of procainamide and NAPA
Pediatric
Not established; suggested dosage is 15-50 mg/kg/d PO divided q3-6h to maximum 4 g/d
Alternatively, 20-30 mg/kg/d IM divided q4-6h to maximum 4 g/d or 3-6 mg/kg per dose IV infused over 5 min
Maintenance: 20-80 mcg/kg/min IV by continuous infusion; not to exceed 100 mcg per dose or 2 g/d
Can expect increased levels of procainamide metabolite NAPA in patients taking cimetidine, ranitidine, beta-blockers, amiodarone, trimethoprim, and quinidine; procainamide may increase effect of skeletal muscle relaxants, quinidine, lidocaine, and neuromuscular blockers; ofloxacin inhibits tubular secretion of procainamide and may increase bioavailability; when taken concurrently with sparfloxacin, may increase risk of cardiotoxicity
Complete heart block or second- or third-degree heart block, if pacemaker not in place; torsade de pointes; documented hypersensitivity; systemic lupus erythematosus
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Monitor for hypotension; plasma concentrations of procainamide and active metabolite, NAPA, may increase in renal failure; high or toxic concentrations may induce AV block or abnormal automaticity; caution in complete AV block, digitalis intoxication, organic heart disease, renal disease, and hepatic insufficiency
Amiodarone (Cordarone, Pacerone)
Now the drug of choice in treatment of unstable ventricular arrhythmias. Currently considered a Class IIb intervention by the American Heart Association 2000 Emergency Cardiovascular Care Guidelines. Prehospital studies currently suggest that amiodarone is safe and efficacious for use in out-of-hospital cardiac arrest. Often used for life-threatening ventricular arrhythmias in patients who have relative contraindications to its use.
Adult
150 mg IV infused over 10 min, follow with 1 mg/min constant infusion for 6 h, then maintenance infusion at 0.5 mg/min
Oral dosing generally 400 mg/d following load
Pediatric
Not established; weight-based dosing suggested; consider for refractory ventricular arrhythmias in children
Increases effect and blood levels of theophylline, quinidine, procainamide, phenytoin, methotrexate, flecainide, digoxin, cyclosporine, beta-blockers, and anticoagulants; cardiotoxicity of amiodarone is increased by ritonavir, sparfloxacin, and disopyramide; coadministration with calcium channel blockers may cause an additive effect and decrease myocardial contractility further; cimetidine may increase amiodarone levels
Documented hypersensitivity; sinus node dysfunction; atrioventricular conduction disorders; underlying hepatic, pulmonary, or thyroid disease
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Hypotension, bradycardia, and AV block may occur; hypotension is most common adverse effect during intravenous administration; acute life-threatening pulmonary or hepatic toxicity may complicate acute or chronic use of this drug; elevation of serum hepatic enzymes and/or TSH requires that patients be monitored carefully during amiodarone therapy; rarely, irreversible blindness from optic neuritis is observed with chronic use
Sotalol (Betapace)
Primarily a potassium channel (IKr)–blocking drug, with weak beta-blocker effect. In ESVEM study, sotalol was compared with 6 other drugs (not including amiodarone) in VT patients.
Survival was best in the sotalol group.
Adult
80-120 mg PO q12h initially; occasionally, doses as high as 240 mg q12h are used with careful monitoring for toxicity
Pediatric
Not established; weight-based dosing recommended; can be considered for refractory ventricular arrhythmias in pediatric population
Increases effect and blood levels of theophylline, quinidine, procainamide, phenytoin, methotrexate, flecainide, digoxin, cyclosporine, beta-blockers, and anticoagulants; cardiotoxicity of amiodarone is increased by ritonavir, sparfloxacin, and disopyramide; coadministration with calcium channel blockers may cause an additive effect and decrease myocardial contractility further; cimetidine may increase amiodarone levels
Documented hypersensitivity; complete AV block; intraventricular conduction defects; patients taking ritonavir or sparfloxacin
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Risk of proarrhythmia increases with dose; monitor for QT prolongation, dyspnea, fatigue, depression, bradycardia, and syncope due to torsade de pointes
Mexiletine (Mexitil)
A class Ib sodium channel blocker, and the closest oral analog to lidocaine. Generally well tolerated and occasionally used in patients with VT responding to intravenous lidocaine. Class Ib sodium channel–blocking drugs generally felt to be safer than Ic drugs, but no large comparative trials exist.
Adult
150 mg PO q8h initially; may increase to 300-450 PO q8h
Pediatric
Not established; weight-based dosing recommended; consider for refractory ventricular arrhythmias
Medications that decrease mexiletine levels include aluminum-magnesium hydroxide compounds, atropine, narcotics, hydantoins, rifampin, and urinary acidifiers; metoclopramide and urinary alkalinizers may increase mexiletine levels; cimetidine can either increase or decrease mexiletine levels; medications whose levels are increased by mexiletine include caffeine and theophylline
Documented hypersensitivity; mexiletine may exacerbate congestive heart failure or hypotension; clearance is reduced in hepatic failure
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Second- or third-degree AV block (without a pacemaker) is a contraindication; can be used cautiously in patients who have pacemakers and second- or third- degree block; in those with first-degree AV blocks, sinus node dysfunction, intraventricular conduction abnormalities, hypotension, or congestive heart failure, consultation with a cardiologist is recommended before using this medication; liver injury reported, particularly in conjunction with congestive heart failure or cardiac ischemia; monitor liver enzymes; rarely, leukopenia or agranulocytosis has been observed; CBC should be monitored; convulsions have occurred in about 0.2% of patients on this medication, caution is indicated if history of seizures is present; avoid other drugs that significantly modify the pH of urine
Flecainide (Tambocor)
Treats life-threatening ventricular arrhythmias. Causes a prolongation of refractory periods and decreases action potential without affecting duration. Blocks sodium channels, producing a dose-related decrease in intracardiac conduction in all parts of the heart, with greatest effect on the His-Purkinje system (HV conduction). Effects on AV nodal conduction time and intra-atrial conduction times, although present, are less pronounced than on ventricular conduction velocity.
Adult
100 mg PO bid q12h; increase q4d to a maximum of 400 mg/d
Pediatric
3-6 mg/kg/d or 100-150 mg/m2/d divided PO tid to 11 mg/kg/d or 200 mg/m2/d
Amiodarone, cimetidine, and digoxin may increase plasma concentrations of flecainide; beta-adrenergic blockers, verapamil, and disopyramide may have additive inotropic effects when administered with flecainide; ritonavir may increase cardiotoxicity of flecainide
Documented hypersensitivity; third-degree AV block; myocardial depression
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in renal or hepatic impairment
Propafenone (Rythmol)
Treats life-threatening arrhythmias. Possibly works by reducing spontaneous automaticity and prolonging the refractory period.
Adult
150 mg PO q8h and increase at 3- to 4-d intervals up to 300 mg q8h
Pediatric
Not established
Decreases serum levels of rifampin; cimetidine, quinidine, warfarin, and beta-blockers may increase serum levels of propafenone
Documented hypersensitivity; bronchospastic disorders; conduction disorders; bradycardia; uncontrolled heart failure
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Should only be used for life-threatening arrhythmias; caution in patients with congestive heart failure, myocardial infarction, or hepatic or renal dysfunction
Quinidine (Quinidex, Quinora, Quinalan, Cardioquin)
Depresses myocardial excitability and conduction velocity.
Adult
200 mg IV q2-3h for 5-8 doses with subsequent daily increases until sinus rhythm is restored or adverse effects occur; not to exceed 3-4 g/d in any regimen
Quinidine gluconate: 324 mg PO tid; adjust based on quinidine levels
Pediatric
30 mg/kg/d PO in 5 divided doses
Phenytoin, rifampin, and phenobarbital may decrease quinidine concentrations; toxicity of quinidine is increased when taken with ritonavir, sparfloxacin, beta-blockers, amiodarone, verapamil, cimetidine, alkalinizing agents, or nondepolarizing and depolarizing muscle relaxants; may enhance effect of anticoagulants
Documented hypersensitivity; complete AV block or intraventricular conduction defects; presently taking ritonavir or sparfloxacin
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in G-6-PD deficiency and those with a tendency to develop granulocytopenia; avoid use in myocardial depression, hepatic or renal insufficiency, and myasthenia gravis
More on Ventricular Tachycardia |
| Overview: Ventricular Tachycardia |
| Differential Diagnoses & Workup: Ventricular Tachycardia |
 Treatment & Medication: Ventricular Tachycardia |
| Follow-up: Ventricular Tachycardia |
| Multimedia: Ventricular Tachycardia |
| References |
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References
Segal OR, Chow AW, Wong T, et al. A novel algorithm for determining endocardial VT exit site from 12-lead surface ECG characteristics in human, infarct-related ventricular tachycardia. J Cardiovasc Electrophysiol. Feb 2007;18(2):161-8. [Medline]. [Full Text].
Arya A, Piorkowski C, Sommer P, et al. Idiopathic outflow tract tachycardias: current perspectives. Herz. May 2007;32(3):218-25. [Medline]. [Full Text].
Noda T, Shimizu W, Taguchi A, et al. Malignant entity of idiopathic ventricular fibrillation and polymorphic ventricular tachycardia initiated by premature extrasystoles originating from the right ventricular outflow tract. J Am Coll Cardiol. Oct 4 2005;46(7):1288-94. [Medline]. [Full Text].
Kannankeril PJ, Roden DM. Drug-induced long QT and torsade de pointes: recent advances. Curr Opin Cardiol. Jan 2007;22(1):39-43. [Medline]. [Full Text].
Brugada J, Brugada R, Brugada P. Channelopathies: a new category of diseases causing sudden death. Herz. May 2007;32(3):185-91. [Medline]. [Full Text].
Wolpert C, Schimpf R, Veltmann C, et al. Clinical characteristics and treatment of short QT syndrome. Expert Rev Cardiovasc Ther. Jul 2005;3(4):611-7. [Medline]. [Full Text].
Sumitomo N, Harada K, Nagashima M, Yasuda T, Nakamura Y, Aragaki Y. Catecholaminergic polymorphic ventricular tachycardia: electrocardiographic characteristics and optimal therapeutic strategies to prevent sudden death. Heart. Jan 2003;89(1):66-70. [Medline]. [Full Text].
Chugh SS, Jui J, Gunson K, Stecker EC, John BT, Thompson B. Current burden of sudden cardiac death: multiple source surveillance versus retrospective death certificate-based review in a large U.S. community. J Am Coll Cardiol. Sep 15 2004;44(6):1268-75. [Medline]. [Full Text].
Tsatsopoulou AA, Protonotarios NI, McKenna WJ. Arrhythmogenic right ventricular dysplasia, a cell adhesion cardiomyopathy: insights into disease pathogenesis from preliminary genotype--phenotype assessment. Heart. Dec 2006;92(12):1720-3. [Medline]. [Full Text].
Rassi A Jr, Rassi A, Rassi SG. Predictors of mortality in chronic Chagas disease: a systematic review of observational studies. Circulation. Mar 6 2007;115(9):1101-8. [Medline]. [Full Text].
Nademanee K, Veerakul G, Mower M, et al. Defibrillator Versus beta-Blockers for Unexplained Death in Thailand (DEBUT): a randomized clinical trial. Circulation. May 6 2003;107(17):2221-6. [Medline].
Yarlagadda RK, Iwai S, Stein KM, et al. Reversal of cardiomyopathy in patients with repetitive monomorphic ventricular ectopy originating from the right ventricular outflow tract. Circulation. Aug 23 2005;112(8):1092-7. [Medline]. [Full Text].
Bogun F, Crawford T, Reich S, et al. Radiofrequency ablation of frequent, idiopathic premature ventricular complexes: comparison with a control group without intervention. Heart Rhythm. Jul 2007;4(7):863-7. [Medline]. [Full Text].
Gordon T, Kannel WB. Premature mortality from coronary heart disease. The Framingham study. JAMA. Mar 8 1971;215(10):1617-25. [Medline].
Brugada P, Brugada J, Mont L, et al. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation. May 1991;83(5):1649-59. [Medline]. [Full Text].
Vereckei A, Duray G, Szenasi G, et al. New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachycardia. Heart Rhythm. Jan 2008;5(1):89-98. [Medline]. [Full Text].
Connolly SJ, Hallstrom AP, Cappato R, et al. Meta-analysis of the implantable cardioverter defibrillator secondary prevention trials. AVID, CASH and CIDS studies. Antiarrhythmics vs Implantable Defibrillator study. Cardiac Arrest Study Hamburg . Canadian Implantable Defibrillator Study. Eur Heart J. Dec 2000;21(24):2071-8. [Medline].
Goldschlager N, Epstein AE, Naccarelli GV, et al. A practical guide for clinicians who treat patients with amiodarone: 2007. Heart Rhythm. Sep 2007;4(9):1250-9. [Medline].
Akhtar M, Shenasa M, Denker S, et al. Role of cardiac electrophysiologic studies in patients with unexplained recurrent syncope. Pacing Clin Electrophysiol. Mar 1983;6(2 Pt 1):192-201. [Medline].
Akhtar M, Shenasa M, Jazayeri M, et al. Wide QRS complex tachycardia. Reappraisal of a common clinical problem. Ann Intern Med. Dec 1 1988;109(11):905-12. [Medline].
Altemose GT, Buxton AE. Idiopathic ventricular tachycardia. Annu Rev Med. 1999;50:159-77. [Medline].
American Heart Association, International Liaison Committee on Resuscitation. Guidelines 2000 Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 6: advanced cardiovascular life support: 7C: a guide to the International ACLS algorithms. AHA in collaboration with International Liaison Committee on Resuscitation. Circulation. Aug 22 2000;102(8 Suppl):I142-57. [Medline].
AVID Investigators. 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. Nov 27 1997;(22):1576-83. [Medline].
Bardy GH, Lee KL, Mark DB, et al. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. N Engl J Med. Jan 20 2005;352(3):225-37. [Medline]. [Full Text].
Buxton AE, Lee KL, Fisher JD, et al. A randomized study of the prevention of sudden death in patients with coronary artery disease. Multicenter Unsustained Tachycardia Trial Investigators. N Engl J Med. Dec 16 1999;341(25):1882-90. [Medline].
Connolly SJ, Hallstrom AP, Cappato R, et al. Meta-analysis of the implantable cardioverter defibrillator secondary prevention trials. AVID, CASH and CIDS studies. Antiarrhythmics vs Implantable Defibrillator study. Cardiac Arrest Study Hamburg. Canadian Implantable Defibrillator Study. Eur Heart J. Dec 2000;21(24):2071-8. [Medline].
Fontaine G, Fontaliran F, Frank R. Arrhythmogenic right ventricular cardiomyopathies: clinical forms and main differential diagnoses. Circulation. Apr 28 1998;97(16):1532-5. [Medline].
Klein LS, Shih HT, Hackett FK, et al. Radiofrequency catheter ablation of ventricular tachycardia in patients without structural heart disease. Circulation. May 1992;85(5):1666-74. [Medline].
Mason JW. A comparison of electrophysiologic testing with Holter monitoring to predict antiarrhythmic-drug efficacy for ventricular tachyarrhythmias. Electrophysiologic Study versus Electrocardiographic Monitoring Investigators. N Engl J Med. Aug 12 1993;329(7):445-51. [Medline].
Mason JW. A comparison of seven antiarrhythmic drugs in patients with ventricular tachyarrhythmias. Electrophysiologic Study versus Electrocardiographic Monitoring Investigators. N Engl J Med. Aug 12 1993;329(7):452-8. [Medline].
Moss AJ, Hall WJ, Cannom DS, 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. Dec 26 1996;335(26):1933-40. [Medline].
Moss AJ, Zareba W, Hall WJ, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med. Mar 21 2002;346(12):877-83. [Medline]. [Full Text].
Stevenson WG, Friedman PL, Kocovic D, et al. Radiofrequency catheter ablation of ventricular tachycardia after myocardial infarction. Circulation. Jul 28 1998;98(4):308-14. [Medline].
The CASCADE Investigators. Randomized antiarrhythmic drug therapy in survivors of cardiac arrest (the CASCADE Study). Am J Cardiol. Aug 1 1993;72(3):280-7. [Medline].
Viskin S. Long QT syndromes and torsade de pointes. Lancet. Nov 6 1999;9190:1625-33. [Medline].
Further Reading
Keywords
ventricular tachycardia, VT, ischemic heart disease, ventricular fibrillation, VF, monomorphic VT, polymorphic VT, long QT syndrome, short QT syndrome, idiopathic VF, Brugada syndrome, familial adrenergic polymorphic VT, bradycardia, ischemic cardiomyopathy, dilated cardiomyopathy, hypertrophic cardiomyopathy, Chagas disease, right ventricular dysplasia, torsade de pointes, hypertrophic cardiomyopathy, right ventricular cardiomyopathy, myocarditis, coronary artery disease, hypokalemia, hyperkalemia
