Ventricular Tachycardia

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Continuing Education Activity

Ventricular tachycardia is characterized as a wide complex tachyarrhythmia. It is classified by duration as non-sustained or sustained. Non-sustained ventricular tachycardia lasts less than 30 seconds and presents with tachyarrhythmia with more than 3 beats of ventricular origin. When the rhythm lasts longer than 30 seconds or hemodynamic instability occurs in less than 30 seconds, it is considered sustained ventricular tachycardia. This activity reviews the evaluation and management of ventricular tachycardia and highlights the role of interprofessional team members in collaborating to provide well-coordinated care and enhance outcomes for affected patients.


  • Explain the pathophysiologic basis of ventricular tachycardia.
  • Characterize the differential diagnosis of ventricular tachycardia.
  • Explain how to properly manage a patient affected by ventricular tachycardia.
  • Explain the importance of improving care coordination, with particular emphasis on communication between interprofessional medical teams, to enhance prompt and thorough delivery of care to patients with ventricular tachycardia.


Ventricular tachycardia is characterized as a wide complex (QRS duration greater than 120 milliseconds) tachyarrhythmia at a heart rate greater than 100 beats per minute. It is classified by duration as non-sustained or sustained. Non-sustained ventricular tachycardia is defined as more than 3 beats of ventricular origin at a rate greater than 100 beats per minute that lasts less than 30 seconds in duration.[1] When the rhythm lasts longer than 30 seconds or hemodynamic instability occurs in less than 30 seconds, it is considered sustained ventricular tachycardia.[1]

Further classification is made into monomorphic and polymorphic on the basis of QRS morphology. Monomorphic ventricular tachycardia demonstrates a stable QRS morphology from beat to beat while polymorphic ventricular tachycardia has changing or multiform QRS variance from beat to beat.[1] Torsades de pointes is a polymorphic ventricular tachycardia that occurs in the setting of a long QT interval and appears as waxing and waxing QRS amplitude on ECG.[1]

The final form of ventricular tachycardia is bidirectional ventricular tachycardia which has a beat-to-beat alternation in the QRS frontal plane axis.[1] It is associated with digitalis toxicity or catecholaminergic polymorphic VT.

The most common cause of VT is ischemic heart disease.


Ventricular tachycardia accounts for approximately 8% of cases of wide complex tachycardia.[2] The most common cause of ventricular tachycardia is underlying ischemic heart disease. Other causes include adult and congenital structural heart disease, acquired and inherited channelopathies, infiltrative cardiomyopathy, electrolyte imbalances (hypokalemia, hypocalcemia, hypomagnesemia), illicit drugs such as cocaine or methamphetamine, and digitalis toxicity.[3] Infiltrative cardiomyopathy can result from: systemic lupus erythematosus, sarcoidosis, amyloidosis, rheumatoid arthritis, and hemochromatosis.[4]

A common trigger is hypokalemia followed by hypomagnesemia. Some cases may also be triggered by hyperkalemia, especially in patients with structural heart disease. sleep apnea and atrial fibrillation can also trigger V.

QT prolongation either acquired or inherited, is fast becoming recognized as a trigger for VT. In both cases, the repolarization phase is prolonged leading to torsade de pointes.

In young people, the cause of VT includes:

  • Myocarditis
  • Hypertrophic cardiomyopathy
  • Long QT syndrome
  • Right ventricular cardiomyopathy
  • Congenital coronary artery anomalies

Catecholaminergic polymorphic VT is known to be triggered by exercise, stress and intense emotional states.

The Brugada syndrome is characterized by RBBB and ST-segment elevation in the early precordial leads (V1-V3) can also cause VT and is often associated with sudden death.


Ventricular tachycardia and ventricular fibrillation cause most cases of sudden cardiac death with an estimated rate of 300,000 deaths each year in the United States.[5][6] This accounts for approximately half of the deaths related to cardiac causes.[6] Risk factors for ventricular tachycardia are hypertension, previous myocardial infarction, chronic obstructive pulmonary disease (COPD), and ST-segment changes at presentation.[7] Patients presenting with acute myocardial infarction have ventricular fibrillation or ventricular tachycardia at a rate of 5% to 10%.[1][8] Ventricular tachycardia 48 hours after hospital presentation is associated with an increased risk of death compared to ventricular tachycardia occurring within the first 48 hours of hospital presentation.[9]

VT is rare in children but can occur in the presence of structural heart disease. Overall, VT is more common in men than in women.


The mechanism for ventricular tachyarrhythmias includes enhancement of normal automaticity or abnormal automaticity, activity triggered by early or late afterdepolarizations, and reentry.[10] In acute myocardial infarction, the transient ischemia results in an increased concentration of extracellular potassium, which causes partial depolarization of the resting membrane potential.[10] This creates injury currents between the infarcted tissue and healthy myocardium that may trigger spontaneous activity.

History and Physical

A good history and physical can help you differentiate ventricular tachycardia from supraventricular tachycardia. Patients presenting with ventricular tachycardia are more likely to be older with a history of heart disease. A past medical history of heart failure, recent angina, and prior myocardial infarction all have a greater than 9% positive predictive value for ventricular tachycardia.[11] 

The physical examination findings of cannon A waves and variable intensity of the S1 heart sound suggest AV dissociation, a criterion favoring the diagnosis of ventricular tachycardia.[11]

Patients may present with hypotension, altered mental status, diaphoresis, and pallor.


The first step in the evaluation of presumed ventricular tachycardia is a 12-lead electrocardiogram (ECG).[12][13] Patients with ventricular tachycardia symptoms associated with exertion, ischemic heart disease, or catecholaminergic polymorphic ventricular tachycardia should undergo further testing with a treadmill stress test.[14] Patients having syncope, presyncope or palpitations with no arrhythmia detected on a single 12-lead ECG should undergo further evaluation with ambulatory ECG monitoring.[15] In patients with ventricular tachycardia and possible structural heart disease, .an echocardiogram is recommended.[16][17] Patients who undergo an episode of unexplained sudden cardiac arrest secondary to a ventricular tachyarrhythmia, CT, or coronary angiography can be used to confirm the presence or absence of ischemic heart disease.[18][19]

 If there is a family history of prolonged QT interval, hypertrophic cardiomyopathy or right ventricular dysplasia, then siblings should be offered genetic testing.

Appropriate laboratory workup is necessary. Levels of potassium, magnesium, calcium, and phosphate should be measured serially. Levels of digoxin and a toxicology screen should be obtained. Cardiac enzymes should be obtained to rule of an MI.

Echocardiography is useful in patients at risk for sudden death. The technique can assess ejection fraction, myocardial infiltrative disease, and presence of any wall motion abnormality.

A myocardial biopsy is only done in patients with infiltrative cardiomyopathies.  If no cause is found, electrophysiologic studies may be required to determine the presence of reentry circuits.

Treatment / Management

Asymptomatic patients with non-sustained ventricular tachycardia (VT) and no underlying cardiac comorbidities require no additional therapy.  Patients that are symptomatic and without cardiac comorbidities should be started on a beta-blocker due to favorable efficacy and safety profile.[20][21] If these patients continue to have episodes of non-sustained VT despite beta-blocker therapy, or cannot tolerate beta-blocker therapy, a calcium channel with atrioventricular nodal action such as verapamil or diltiazem can be used. The previously mentioned nondihydropyridine calcium channel blockers are contraindicated in the setting of structural heart disease or heart failure with reduced ejection fraction.[22]

Patients with sustained monomorphic ventricular tachycardia (SMVT) that are unstable should be managed following advanced cardiac life support (ACLS) guidelines. Hemodynamically stable patients should be pharmacologically cardioverted using an anti-arrhythmic medication. Intravenous amiodarone or procainamide can be used for this purpose. Procainamide will terminate between 50% and 80% of ventricular tachycardias, and it will slow the conduction of those that it does not terminate.[23][24] Amiodarone will convert about 30% of patients to sinus rhythm but is very effective in reducing the reversion rate of refractory SMVT.[25][26][27]

The first-line therapy for chronic treatment of patients with ischemic heart disease and VT is a beta-blocker therapy which is associated with a reduced risk of sudden cardiac death.[20][18][21] In patients with ischemic heart disease who have recurrent VT despite beta-blocker therapy, amiodarone or sotalol can be initiated however neither therapy has been associated with a decrease in mortality.[28][29][30] Amiodarone plus a beta-blocker has been associated with a greater decrease in the number of ICD shocks compared to sotalol monotherapy.[31][30][29]

Patients with ischemic heart disease that survive sudden cardiac arrest due to ventricular tachycardia, or experience hemodynamically unstable or stable sustained ventricular tachycardia, should have an implantable cardiac defibrillator (ICD) placed if their estimated meaningful survival is greater than 1 year.[32][33][34] Patients with syncope who have ischemic cardiomyopathy, non-ischemic cardiomyopathy, or adult congenital heart disease who do not meet criteria for an ICD can undergo an electrophysiological study to assess the risk of sustained ventricular tachycardia; however, performing the study solely for risk stratification is not indicated.[35][36][19]

Catheter ablation has a class 1 recommendation for patients with a history of myocardial infarction who continue to suffer from symptomatic sustained VT, or have failed or are intolerant of amiodarone or other antiarrhythmic medications.[37][38][39]


If a patient with VT is hemodynamically unstable, immediate cardioversion is necessary. This is accomplished by a 100-200J biphasic shock. All reversible factors must be corrected. VT in patients with an MI should be treated with lidocaine. If the patient has torsade de pointes then magnesium sulfate is preferred.

Current Recommendations

  1. Patients with CHF and reduced ejection fraction should be managed with a beta-blocker, ACE inhibitor, angiotensin receptor blocker or a mineralocorticoid receptor blocker to lower the risk of sudden death.
  2. In patients with ischemic heart disease and sustained monomorphic VT, medical therapy is needed besides revascularization.
  3. In patients with nonischemic cardiomyopathy, heart failure and an ejection fraction of 35% or less, place an ICD.
  4. Catheter ablation is recommended in patients with previous MI, VT storm or refractoriness to amiodarone or not tolerating antiarrhythmic drug therapy.

Differential Diagnosis

If possible, ventricular tachycardia should be differentiated from supraventricular tachycardia with aberrant conduction as the treatment strategies are different. Factors favoring the diagnosis of ventricular tachycardia include: QRS width greater than 0.14 seconds with right bundle branch block pattern or greater than 0.16 seconds with left bundle branch block pattern, AV dissociation, RS interval longer than 100 milliseconds in a precordial lead (Brugada's sign), QRS with negative concordance in the precordial leads, and ventricular fusion beats.[37]


The prognosis of VT depends on the cause and cardiac status. Patients who develop VT can suffer from hemodynamic failure and the mortality can exceed 30% if no treatment is provided. In the setting of percutaneous coronary intervention, VT occurring prior to revascularization is associated with very high mortality. The prognosis does not correlate with ejection fraction. Patients with hypertrophic cardiomyopathy, long QT syndrome and right ventricular dysplasia often have normal heart function but yet are a high risk for sudden death.

Postoperative and Rehabilitation Care

Patients who have monomorphic VT with normal heart anatomy are at low risk for sudden death and can be managed by medications or ablation

In the presence of LV dysfunction, the antiarrhythmic drugs have been disappointing. The drug of choice is amiodarone and can be combined with beta-blockers.

Enhancing Healthcare Team Outcomes

Early recognition, bystander CPR, and public access defibrillation have all helped to increase the rate of survival for patients who have an out-of-hospital cardiac arrest however survival remains low at under 10%.[40][41][42] (Level I) After arrival at the hospital, post-arrest care order sets that pay significant attention to temperature control and cardio-cerebral resuscitation, have further improved survival.[43] (Level 2)

In-hospital cardiac arrest shares the similarity with out-of-hospital cardiac arrest in that early cardiopulmonary resuscitation (CPR), and defibrillation are important factors in survival. (Level I) Every minute that treatment is delayed reduces survival by approximately 10%.[44] This makes the resuscitation team an important part in improving outcomes of in-hospital cardiac arrest. However, there is significant variation amongst different hospitals in efficacy. Resuscitation teams universally consist of physicians, nurses, anesthesia, and respiratory therapists coordinating their efforts. Hospitals that were high performing included more support staff (pharmacy, clerical, security, spiritual staff).[45] 

Patients with ischemic heart disease should be seen by a dietitian because they may benefit from low cholesterol and low sodium diet. Strenuous exercise should be avoided as it may precipitate VT in some patients. All patients should be encouraged to discontinue smoking. The pharmacist should educate the patient on medication compliance and the need to follow up with the cardiologist. They should also assist the clinical team in managing drug-drug interactions and making appropriate drug treatment selection.

Top-performing hospitals were also more likely to have a dedicated resuscitation team that had no clinical responsibilities that interfered with their participation in the team. Effective communication among team members was also identified as a positive factor in improving outcomes.[45]

(Click Image to Enlarge)
Ventricular Tachycardia rhythm example
Ventricular Tachycardia rhythm example
Contributed by Tammy J. Toney-Butler, AS, RN, CEN, TCRN, CPEN

(Click Image to Enlarge)
Ventricular Tachycardia, [SATA]
Ventricular Tachycardia, [SATA]
Contributed by Steve Bhmji, MS, MD, PhD
Article Details

Article Author

Christopher Foth

Article Author

Manesh Kumar Gangwani

Article Editor:

Heidi Alvey


8/8/2022 8:39:21 PM



American College of Cardiology/American Heart Association Task Force on Clinical Data Standards (ACC/AHA/HRS Writing Committee to Develop Data Standards on Electrophysiology).,Buxton AE,Calkins H,Callans DJ,DiMarco JP,Fisher JD,Greene HL,Haines DE,Hayes DL,Heidenreich PA,Miller JM,Poppas A,Prystowsky EN,Schoenfeld MH,Zimetbaum PJ,Goff DC,Grover FL,Malenka DJ,Peterson ED,Radford MJ,Redberg RF, ACC/AHA/HRS 2006 key data elements and definitions for electrophysiological studies and procedures: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Data Standards (ACC/AHA/HRS Writing Committee to Develop Data Standards on Electrophysiology). Circulation. 2006 Dec 5     [PubMed PMID: 17130345]


Alzand BS,Crijns HJ, Diagnostic criteria of broad QRS complex tachycardia: decades of evolution. Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology. 2011 Apr     [PubMed PMID: 21131372]


Koplan BA,Stevenson WG, Ventricular tachycardia and sudden cardiac death. Mayo Clinic proceedings. 2009 Mar     [PubMed PMID: 19252119]


Bejar D,Colombo PC,Latif F,Yuzefpolskaya M, Infiltrative Cardiomyopathies. Clinical Medicine Insights. Cardiology. 2015     [PubMed PMID: 26244036]


Tang PT,Shenasa M,Boyle NG, Ventricular Arrhythmias and Sudden Cardiac Death. Cardiac electrophysiology clinics. 2017 Dec     [PubMed PMID: 29173411]


McNally B,Robb R,Mehta M,Vellano K,Valderrama AL,Yoon PW,Sasson C,Crouch A,Perez AB,Merritt R,Kellermann A,Centers for Disease Control and Prevention., Out-of-hospital cardiac arrest surveillance --- Cardiac Arrest Registry to Enhance Survival (CARES), United States, October 1, 2005--December 31, 2010. Morbidity and mortality weekly report. Surveillance summaries (Washington, D.C. : 2002). 2011 Jul 29     [PubMed PMID: 21796098]


Al-Khatib SM,Granger CB,Huang Y,Lee KL,Califf RM,Simoons ML,Armstrong PW,Van de Werf F,White HD,Simes RJ,Moliterno DJ,Topol EJ,Harrington RA, Sustained ventricular arrhythmias among patients with acute coronary syndromes with no ST-segment elevation: incidence, predictors, and outcomes. Circulation. 2002 Jul 16     [PubMed PMID: 12119245]


Dumas F,Cariou A,Manzo-Silberman S,Grimaldi D,Vivien B,Rosencher J,Empana JP,Carli P,Mira JP,Jouven X,Spaulding C, Immediate percutaneous coronary intervention is associated with better survival after out-of-hospital cardiac arrest: insights from the PROCAT (Parisian Region Out of hospital Cardiac ArresT) registry. Circulation. Cardiovascular interventions. 2010 Jun 1     [PubMed PMID: 20484098]


Volpi A,Cavalli A,Franzosi MG,Maggioni A,Mauri F,Santoro E,Tognoni G, One-year prognosis of primary ventricular fibrillation complicating acute myocardial infarction. The GISSI (Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto miocardico) investigators. The American journal of cardiology. 1989 May 15     [PubMed PMID: 2565684]


Cherry EM,Fenton FH,Gilmour RF Jr, Mechanisms of ventricular arrhythmias: a dynamical systems-based perspective. American journal of physiology. Heart and circulatory physiology. 2012 Jun 15     [PubMed PMID: 22467299]


Pellegrini CN,Scheinman MM, Clinical management of ventricular tachycardia. Current problems in cardiology. 2010 Sep     [PubMed PMID: 20887902]


Wellens HJ,Bär FW,Lie KI, The value of the electrocardiogram in the differential diagnosis of a tachycardia with a widened QRS complex. The American journal of medicine. 1978 Jan     [PubMed PMID: 623134]


Pérez-Rodon J,Martínez-Alday J,Barón-Esquivias G,Martín A,García-Civera R,Del Arco C,Cano-Gonzalez A,Moya-Mitjans A, Prognostic value of the electrocardiogram in patients with syncope: data from the group for syncope study in the emergency room (GESINUR). Heart rhythm. 2014 Nov     [PubMed PMID: 24993462]


Elhendy A,Chandrasekaran K,Gersh BJ,Mahoney D,Burger KN,Pellikka PA, Functional and prognostic significance of exercise-induced ventricular arrhythmias in patients with suspected coronary artery disease. The American journal of cardiology. 2002 Jul 15     [PubMed PMID: 12106835]


Barrett PM,Komatireddy R,Haaser S,Topol S,Sheard J,Encinas J,Fought AJ,Topol EJ, Comparison of 24-hour Holter monitoring with 14-day novel adhesive patch electrocardiographic monitoring. The American journal of medicine. 2014 Jan     [PubMed PMID: 24384108]


Solomon SD,Zelenkofske S,McMurray JJ,Finn PV,Velazquez E,Ertl G,Harsanyi A,Rouleau JL,Maggioni A,Kober L,White H,Van de Werf F,Pieper K,Califf RM,Pfeffer MA,Valsartan in Acute Myocardial Infarction Trial (VALIANT) Investigators., Sudden death in patients with myocardial infarction and left ventricular dysfunction, heart failure, or both. The New England journal of medicine. 2005 Jun 23     [PubMed PMID: 15972864]


Gula LJ,Klein GJ,Hellkamp AS,Massel D,Krahn AD,Skanes AC,Yee R,Anderson J,Johnson GW,Poole JE,Mark DB,Lee KL,Bardy GH, Ejection fraction assessment and survival: an analysis of the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT). American heart journal. 2008 Dec     [PubMed PMID: 19033019]


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, 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: Executive summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Heart rhythm. 2018 Oct     [PubMed PMID: 29097320]


Al-Khatib SM,Stevenson WG,Ackerman MJ,Bryant WJ,Callans DJ,Curtis AB,Deal BJ,Dickfeld T,Field ME,Fonarow GC,Gillis AM,Hlatky MA,Granger CB,Hammill SC,Joglar JA,Kay GN,Matlock DD,Myerburg RJ,Page RL, 2017 AHA/ACC/HRS Guideline 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 on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation. 2017 Oct 30     [PubMed PMID: 29084731]


Pedersen CT,Kay GN,Kalman J,Borggrefe M,Della-Bella P,Dickfeld T,Dorian P,Huikuri H,Kim YH,Knight B,Marchlinski F,Ross D,Sacher F,Sapp J,Shivkumar K,Soejima K,Tada H,Alexander ME,Triedman JK,Yamada T,Kirchhof P,Lip GY,Kuck KH,Mont L,Haines D,Indik J,Dimarco J,Exner D,Iesaka Y,Savelieva I, EHRA/HRS/APHRS expert consensus on ventricular arrhythmias. Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology. 2014 Sep     [PubMed PMID: 25172618]


Reiter MJ,Reiffel JA, Importance of beta blockade in the therapy of serious ventricular arrhythmias. The American journal of cardiology. 1998 Aug 20     [PubMed PMID: 9737650]


Gill JS,Blaszyk K,Ward DE,Camm AJ, Verapamil for the suppression of idiopathic ventricular tachycardia of left bundle branch block-like morphology. American heart journal. 1993 Nov     [PubMed PMID: 8237755]


Gorgels AP,van den Dool A,Hofs A,Mulleneers R,Smeets JL,Vos MA,Wellens HJ, Comparison of procainamide and lidocaine in terminating sustained monomorphic ventricular tachycardia. The American journal of cardiology. 1996 Jul 1     [PubMed PMID: 8712116]


Komura S,Chinushi M,Furushima H,Hosaka Y,Izumi D,Iijima K,Watanabe H,Yagihara N,Aizawa Y, Efficacy of procainamide and lidocaine in terminating sustained monomorphic ventricular tachycardia. Circulation journal : official journal of the Japanese Circulation Society. 2010 May     [PubMed PMID: 20339190]


Marill KA,deSouza IS,Nishijima DK,Stair TO,Setnik GS,Ruskin JN, Amiodarone is poorly effective for the acute termination of ventricular tachycardia. Annals of emergency medicine. 2006 Mar     [PubMed PMID: 16492484]


deSouza IS,Martindale JL,Sinert R, Antidysrhythmic drug therapy for the termination of stable, monomorphic ventricular tachycardia: a systematic review. Emergency medicine journal : EMJ. 2015 Feb     [PubMed PMID: 24042252]


Schützenberger W,Leisch F,Kerschner K,Harringer W,Herbinger W, Clinical efficacy of intravenous amiodarone in the short term treatment of recurrent sustained ventricular tachycardia and ventricular fibrillation. British heart journal. 1989 Nov     [PubMed PMID: 2590589]


Somberg JC,Bailin SJ,Haffajee CI,Paladino WP,Kerin NZ,Bridges D,Timar S,Molnar J,Amio-Aqueous Investigators., Intravenous lidocaine versus intravenous amiodarone (in a new aqueous formulation) for incessant ventricular tachycardia. The American journal of cardiology. 2002 Oct 15     [PubMed PMID: 12372573]


Ochi RP,Goldenberg IF,Almquist A,Pritzker M,Milstein S,Pedersen W,Gobel FL,Benditt DG, Intravenous amiodarone for the rapid treatment of life-threatening ventricular arrhythmias in critically ill patients with coronary artery disease. The American journal of cardiology. 1989 Sep 15     [PubMed PMID: 2782249]


Pacifico A,Hohnloser SH,Williams JH,Tao B,Saksena S,Henry PD,Prystowsky EN, Prevention of implantable-defibrillator shocks by treatment with sotalol. d,l-Sotalol Implantable Cardioverter-Defibrillator Study Group. The New England journal of medicine. 1999 Jun 17     [PubMed PMID: 10369848]


Connolly SJ,Dorian P,Roberts RS,Gent M,Bailin S,Fain ES,Thorpe K,Champagne J,Talajic M,Coutu B,Gronefeld GC,Hohnloser SH,Optimal Pharmacological Therapy in Cardioverter Defibrillator Patients (OPTIC) Investigators., Comparison of beta-blockers, amiodarone plus beta-blockers, or sotalol for prevention of shocks from implantable cardioverter defibrillators: the OPTIC Study: a randomized trial. JAMA. 2006 Jan 11     [PubMed PMID: 16403928]


Antiarrhythmics versus Implantable Defibrillators (AVID) Investigators., A comparison of antiarrhythmic-drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias. The New England journal of medicine. 1997 Nov 27     [PubMed PMID: 9411221]


Connolly SJ,Hallstrom AP,Cappato R,Schron EB,Kuck KH,Zipes DP,Greene HL,Boczor S,Domanski M,Follmann D,Gent M,Roberts RS, 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. European heart journal. 2000 Dec     [PubMed PMID: 11102258]


Kuck KH,Cappato R,Siebels J,Rüppel R, Randomized comparison of antiarrhythmic drug therapy with implantable defibrillators in patients resuscitated from cardiac arrest : the Cardiac Arrest Study Hamburg (CASH). Circulation. 2000 Aug 15     [PubMed PMID: 10942742]


Buxton AE,Lee KL,Fisher JD,Josephson ME,Prystowsky EN,Hafley G, A randomized study of the prevention of sudden death in patients with coronary artery disease. Multicenter Unsustained Tachycardia Trial Investigators. The New England journal of medicine. 1999 Dec 16     [PubMed PMID: 10601507]


Moss AJ,Zareba W,Hall WJ,Klein H,Wilber DJ,Cannom DS,Daubert JP,Higgins SL,Brown MW,Andrews ML,Multicenter Automatic Defibrillator Implantation Trial II Investigators., Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. The New England journal of medicine. 2002 Mar 21     [PubMed PMID: 11907286]


Blomström-Lundqvist C,Scheinman MM,Aliot EM,Alpert JS,Calkins H,Camm AJ,Campbell WB,Haines DE,Kuck KH,Lerman BB,Miller DD,Shaeffer CW Jr,Stevenson WG,Tomaselli GF,Antman EM,Smith SC Jr,Alpert JS,Faxon DP,Fuster V,Gibbons RJ,Gregoratos G,Hiratzka LF,Hunt SA,Jacobs AK,Russell RO Jr,Priori SG,Blanc JJ,Budaj A,Burgos EF,Cowie M,Deckers JW,Garcia MA,Klein WW,Lekakis J,Lindahl B,Mazzotta G,Morais JC,Oto A,Smiseth O,Trappe HJ, ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias--executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias). Circulation. 2003 Oct 14     [PubMed PMID: 14557344]


Al-Khatib SM,Daubert JP,Anstrom KJ,Daoud EG,Gonzalez M,Saba S,Jackson KP,Reece T,Gu J,Pokorney SD,Granger CB,Hess PL,Mark DB,Stevenson WG, Catheter ablation for ventricular tachycardia in patients with an implantable cardioverter defibrillator (CALYPSO) pilot trial. Journal of cardiovascular electrophysiology. 2015 Feb     [PubMed PMID: 25332150]


Kuck KH,Schaumann A,Eckardt L,Willems S,Ventura R,Delacrétaz E,Pitschner HF,Kautzner J,Schumacher B,Hansen PS,VTACH study group., Catheter ablation of stable ventricular tachycardia before defibrillator implantation in patients with coronary heart disease (VTACH): a multicentre randomised controlled trial. Lancet (London, England). 2010 Jan 2     [PubMed PMID: 20109864]


van Diepen S,Girotra S,Abella BS,Becker LB,Bobrow BJ,Chan PS,Fahrenbruch C,Granger CB,Jollis JG,McNally B,White L,Yannopoulos D,Rea TD, Multistate 5-Year Initiative to Improve Care for Out-of-Hospital Cardiac Arrest: Primary Results From the HeartRescue Project. Journal of the American Heart Association. 2017 Sep 22     [PubMed PMID: 28939711]


Buick JE,Drennan IR,Scales DC,Brooks SC,Byers A,Cheskes S,Dainty KN,Feldman M,Verbeek PR,Zhan C,Kiss A,Morrison LJ,Lin S, Improving Temporal Trends in Survival and Neurological Outcomes After Out-of-Hospital Cardiac Arrest. Circulation. Cardiovascular quality and outcomes. 2018 Jan     [PubMed PMID: 29317455]


Sasson C,Rogers MA,Dahl J,Kellermann AL, Predictors of survival from out-of-hospital cardiac arrest: a systematic review and meta-analysis. Circulation. Cardiovascular quality and outcomes. 2010 Jan     [PubMed PMID: 20123673]


Rittenberger JC,Guyette FX,Tisherman SA,DeVita MA,Alvarez RJ,Callaway CW, Outcomes of a hospital-wide plan to improve care of comatose survivors of cardiac arrest. Resuscitation. 2008 Nov     [PubMed PMID: 18951113]


Ali B,Zafari AM, Narrative review: cardiopulmonary resuscitation and emergency cardiovascular care: review of the current guidelines. Annals of internal medicine. 2007 Aug 7     [PubMed PMID: 17679705]


Nallamothu BK,Guetterman TC,Harrod M,Kellenberg JE,Lehrich JL,Kronick SL,Krein SL,Iwashyna TJ,Saint S,Chan PS, How Do Resuscitation Teams at Top-Performing Hospitals for In-Hospital Cardiac Arrest Succeed? A Qualitative Study. Circulation. 2018 Jul 10     [PubMed PMID: 29986959]