Ventricular tachycardia

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Ventricular tachycardia
Other namesV-tach, [1] Vtach, VT
Lead II rhythm ventricular tachycardia Vtach VT (cropped).JPG
A run of ventricular tachycardia as seen on a rhythm strip
Specialty Cardiology
Symptoms Lightheadedness, palpitations, chest pain, shortness of breath, Decreased level or total loss of consciousness [2]
Complications Cardiac arrest, ventricular fibrillation [2] [3]
TypesNon-sustained (NSVT), sustained [2]
Causes Coronary heart disease, aortic stenosis, cardiomyopathy, electrolyte problems, heart attack [2] [3]
Diagnostic method Electrocardiogram [2]
Differential diagnosis Supraventricular tachycardia with aberrancy, ventricular pacing, ECG artifact [4]
Prevention Implantable cardiac defibrillator, calcium channel blockers, amiodarone [2]
Treatment Procainamide, cardioversion, cardiopulmonary resuscitation [2] [5]
Frequency~7% of people in cardiac arrest [2]

Ventricular tachycardia (V-tach or VT) is a cardiovascular disorder in which fast heart rate occurs in the ventricles of the heart. [3] Although a few seconds of VT may not result in permanent problems, longer periods are dangerous; and multiple episodes over a short period of time are referred to as an electrical storm. [3] [6] [7] Short periods may occur without symptoms, or present with lightheadedness, palpitations, shortness of breath, chest pain, and decreased level of consciousness. [2] Ventricular tachycardia may lead to coma and persistent vegetative state due to lack of blood and oxygen to the brain. Ventricular tachycardia may result in ventricular fibrillation (VF) and turn into cardiac arrest. [2] [3] This conversion of the VT into VF is called the degeneration of the VT. It is found initially in about 7% of people in cardiac arrest. [2]

Contents

Ventricular tachycardia can occur due to coronary heart disease, aortic stenosis, cardiomyopathy, electrolyte imbalance, or a heart attack. [2] [3] Diagnosis is by an electrocardiogram (ECG) showing a rate of greater than 120 beats per minute and at least three wide QRS complexes in a row. [2] It is classified as non-sustained versus sustained based on whether it lasts less than or more than 30 seconds. [2] The term ventricular arrhythmia refers to the group of abnormal cardiac rhythms originating from the ventricle, which includes ventricular tachycardia, ventricular fibrillation, and torsades de pointes. [2]

In those who have normal blood pressure and strong pulse, the antiarrhythmic medication procainamide may be used. [2] Otherwise, immediate cardioversion is recommended, preferably with a biphasic DC shock of 200 joules. [2] In those in cardiac arrest due to ventricular tachycardia, cardiopulmonary resuscitation (CPR) and defibrillation is recommended. [5] Biphasic defibrillation may be better than monophasic. [5] While waiting for a defibrillator, a precordial thump may be attempted (However reserved to those who have the prior experience of doing so) in those on a heart monitor who are seen going into an unstable ventricular tachycardia. [5] In those with cardiac arrest due to ventricular tachycardia, survival is about 75%. [2] An implantable cardiac defibrillator or medications such as calcium channel blockers or amiodarone may be used to prevent recurrence. [2]

Signs and symptoms

While a few seconds may not result in problems, longer periods are dangerous. [3] Short periods may occur without symptoms or present with lightheadedness, palpitations, shortness of breath, chest pain, or unconsciousness. [2] Ventricular tachycardia may turn into ventricular fibrillation and can result in cardiac arrest. [2] [3]

Cause

Ventricular tachycardia can occur due to coronary heart disease, aortic stenosis, cardiomyopathy, electrolyte problems (e.g., low blood levels of magnesium or potassium), inherited channelopathies (e.g., long-QT syndrome), catecholaminergic polymorphic ventricular tachycardia, arrhythmogenic right ventricular dysplasia, alcohol withdrawal syndrome (typically following atrial fibrillation), or a myocardial infarction. [2] [3]

Pathophysiology

The morphology of the tachycardia depends on its cause and the origin of the re-entry electrical circuit in the heart.[ citation needed ]

In monomorphic ventricular tachycardia, the shape of each heart beat on the ECG looks the same because the impulse is either being generated from increased automaticity of a single point in either the left or the right ventricle, or due to a reentry circuit within the ventricle. The most common cause of monomorphic ventricular tachycardia is scarring of the heart muscle from a previous myocardial infarction (heart attack). This scar cannot conduct electrical activity, so there is a potential circuit around the scar that results in the tachycardia. This is similar to the re-entrant circuits that are the cause of atrial flutter and the re-entrant forms of supraventricular tachycardia. Other rarer congenital causes of monomorphic VT include right ventricular dysplasia, and right and left ventricular outflow tract VT.[ citation needed ]

Polymorphic ventricular tachycardia, on the other hand, is most commonly caused by abnormalities of ventricular muscle repolarization. The predisposition to this problem usually manifests on the ECG as a prolongation of the QT interval. QT prolongation may be congenital or acquired. Congenital problems include long QT syndrome and catecholaminergic polymorphic ventricular tachycardia. Acquired problems are usually related to drug toxicity or electrolyte abnormalities, but can occur as a result of myocardial ischemia. Class III anti-arrhythmic drugs such as sotalol and amiodarone prolong the QT interval and may in some circumstances be pro-arrhythmic. Other relatively common drugs including some antibiotics and antihistamines may also be a danger, in particular in combination with one another. Problems with blood levels of potassium, magnesium and calcium may also contribute. High-dose magnesium is often used as an antidote in cardiac arrest protocols.[ citation needed ]

Diagnosis

The diagnosis of ventricular tachycardia is made based on the rhythm seen on either a 12-lead ECG or a telemetry rhythm strip. It may be very difficult to differentiate between ventricular tachycardia and a wide-complex supraventricular tachycardia in some cases. In particular, supraventricular tachycardias with aberrant conduction from a pre-existing bundle branch block are commonly misdiagnosed as ventricular tachycardia. Other rarer phenomena include Ashman beats and antidromic atrioventricular re-entry tachycardias.[ citation needed ]

Various diagnostic criteria have been developed to determine whether a wide complex tachycardia is ventricular tachycardia or a more benign rhythm. [8] [9] In addition to these diagnostic criteria, if the individual has a history of a myocardial infarction, congestive heart failure, or recent angina, the wide complex tachycardia is much more likely to be ventricular tachycardia. [10]

The proper diagnosis is important, as the misdiagnosis of supraventricular tachycardia when ventricular tachycardia is present is associated with worse prognosis. This is particularly true if calcium channel blockers, such as verapamil, are used to attempt to terminate a presumed supraventricular tachycardia. [11] Therefore, it is wisest to assume that all wide complex tachycardia is VT until proven otherwise.[ citation needed ]

ECG features of Ventricular Tachycardia in addition to the increased Heart rate are:

  1. A wide QRS Complex (because the ectopics for the generation of the cardiac impulse originates in the Ventricular Myocyte and propagated via the intermyocyte conduction, which is a delayed conduction)
  2. A Josephson's sign where there is the notch in the downsloping of the S wave near its nadir (considered very specific for the VT).
  3. Capture beats (normal QRS complex in between when the Heart pick up the sinus rhythm from the impulses generated by the SA node), fusion beats (due to the fusion of the Abnormal and the Normal QRS complexes) which has a unique morphology.
  4. Positive or negative concordance.
  5. Extreme Axis deviation or NORTH WEST axis (axis between -90 and +180 degrees)

Classification

Normal sinus top, ventricular tachycardia bottom Ventricular Tachycardia.png
Normal sinus top, ventricular tachycardia bottom
12 lead electrocardiogram showing a run of monomorphic ventricular tachycardia (VT) Electrocardiogram of Ventricular Tachycardia.png
12 lead electrocardiogram showing a run of monomorphic ventricular tachycardia (VT)

Ventricular tachycardia can be classified based on its morphology:[ citation needed ]

Another way to classify ventricular tachycardias is the duration of the episodes: Three or more beats in a row on an ECG that originate from the ventricle at a rate of more than 120 beats per minute constitute a ventricular tachycardia.[ citation needed ]

A third way to classify ventricular tachycardia is on the basis of its symptoms: Pulseless VT is associated with no effective cardiac output, hence, no effective pulse, and is a cause of cardiac arrest (see also: pulseless electrical activity [PEA]). In this circumstance, it is best treated the same way as ventricular fibrillation (VF), and is recognized as one of the shockable rhythms on the cardiac arrest protocol. Some VT is associated with reasonable cardiac output and may even be asymptomatic. The heart usually tolerates this rhythm poorly in the medium to long term, and patients may certainly deteriorate to pulseless VT or to VF.[ citation needed ]

Occasionally in ventricular tachycardia, supraventricular impulses are conducted to the ventricles, generating QRS complexes with normal or aberrant supraventricular morphology (ventricular capture). Or, those impulses can be merged with complexes that are originated in the ventricle and produce a summation pattern (fusion complexes). [13]

Less common is ventricular tachycardia that occurs in individuals with structurally normal hearts. This is known as idiopathic ventricular tachycardia and in the monomorphic form coincides with little or no increased risk of sudden cardiac death. In general, idiopathic ventricular tachycardia occurs in younger individuals diagnosed with VT. While the causes of idiopathic VT are not known, in general it is presumed to be congenital, and can be brought on by any number of diverse factors.[ citation needed ]

Treatment

Therapy may be directed either at terminating an episode of the abnormal heart rhythm or at reducing the risk of another VT episode. The treatment for stable VT is tailored to the specific person, with regard to how well the individual tolerates episodes of ventricular tachycardia, how frequently episodes occur, their comorbidities, and their wishes. Individuals with pulseless VT or unstable VT are hemodynamically compromised and require immediate electric cardioversion to shock them out of the VT rhythm. [14]

Cardioversion

If a person still has a pulse, it is usually possible to terminate the episode using electric cardioversion. [15] This should be synchronized to the heartbeat if the waveform is monomorphic if possible, in order to avoid degeneration of the rhythm to ventricular fibrillation. [15] An initial energy of 100J is recommended. [15] If the waveform is polymorphic, then higher energies and an unsynchronized shock should be provided (also known as defibrillation). [15]

Defibrillation

A person with pulseless VT is treated the same as ventricular fibrillation with high-energy (360J with a monophasic defibrillator, or 200J with a biphasic defibrillator) unsynchronised cardioversion (defibrillation). [15] They will be unconscious.

The shock may be delivered to the outside of the chest using the two pads of an external defibrillator, or internally to the heart by an implantable cardioverter-defibrillator (ICD) if one has previously been inserted.[ citation needed ]

An ICD may also be set to attempt to overdrive pace the ventricle. Pacing the ventricle at a rate faster than the underlying tachycardia can sometimes be effective in terminating the rhythm. If this fails after a short trial, the ICD will usually stop pacing, charge up and deliver a defibrillation grade shock.[ citation needed ]

Medication

For those who are stable with a monomorphic waveform the medications procainamide or sotalol may be used and are better than lidocaine. [16] Evidence does not show that amiodarone is better than procainamide. [16]

As a low magnesium level in the blood is a common cause of VT, magnesium sulfate can be given for torsades de pointes or if a low blood magnesium level is found/suspected.[ citation needed ]

Long-term anti-arrhythmic therapy may be indicated to prevent recurrence of VT. Beta-blockers and a number of class III anti-arrhythmics are commonly used, such as the beta-blockers carvedilol, metoprolol, and bisoprolol, and the Potassium-Channel-Blockers amiodarone, dronedarone, bretylium, sotalol, ibutilide, and dofetilide. Angiotensin-converting-enzyme (ACE) inhibitors and aldosterone antagonists are also sometimes used in this setting. [17]

Invasive treatment

An ICD (implantable cardioverter defibrillator ) is more effective than drug therapy for prevention of sudden cardiac death due to VT and VF, but does not prevent these rhythm from happening.

Catheter ablation is a potentially definitive treatment option for those with recurrent VT. [18] Remote magnetic navigation is one effective method to do the procedure. [19]

In the past, ablation was often not considered until pharmacological options had been exhausted, often after the patient had developed substantial morbidity from recurrent episodes of VT and ICD shocks. Antiarrhythmic medications can reduce the frequency of ICD therapies, but have efficacy varies and side effects can be significant. Advances in technology and understanding of VT substrates now allow ablation of multiple and unstable VTs with acceptable safety and efficacy, even in patients with advanced heart disease. [20]

Related Research Articles

<span class="mw-page-title-main">Cardiac arrest</span> Sudden failure of heart beat

Cardiac arrest, also known as sudden cardiac arrest, is when the heart suddenly and unexpectedly stops beating. As a result, blood cannot properly circulate around the body and there is diminished blood flow to the brain and other organs. When the brain does not receive enough blood, this can cause a person to lose consciousness. Coma and persistent vegetative state may result from cardiac arrest. Cardiac arrest is also identified by a lack of central pulses and abnormal or absent breathing.

<span class="mw-page-title-main">Electrocardiography</span> Examination of the hearts electrical activity

Electrocardiography is the process of producing an electrocardiogram, a recording of the heart's electrical activity through repeated cardiac cycles. It is an electrogram of the heart which is a graph of voltage versus time of the electrical activity of the heart using electrodes placed on the skin. These electrodes detect the small electrical changes that are a consequence of cardiac muscle depolarization followed by repolarization during each cardiac cycle (heartbeat). Changes in the normal ECG pattern occur in numerous cardiac abnormalities, including:

<span class="mw-page-title-main">Artificial cardiac pacemaker</span> Medical device

An artificial cardiac pacemaker, commonly referred to as simply a pacemaker, is an implanted medical device that generates electrical pulses delivered by electrodes to one or more of the chambers of the heart. Each pulse causes the targeted chamber(s) to contract and pump blood, thus regulating the function of the electrical conduction system of the heart.

<span class="mw-page-title-main">Cardioversion</span> Conversion of a cardiac arrhythmia to a normal rhythm using an electrical shock or medications

Cardioversion is a medical procedure by which an abnormally fast heart rate (tachycardia) or other cardiac arrhythmia is converted to a normal rhythm using electricity or drugs. Synchronized electrical cardioversion uses a therapeutic dose of electric current to the heart at a specific moment in the cardiac cycle, restoring the activity of the electrical conduction system of the heart. Pharmacologic cardioversion, also called chemical cardioversion, uses antiarrhythmia medication instead of an electrical shock.

<span class="mw-page-title-main">Defibrillation</span> Treatment for life-threatening cardiac arrhythmias

Defibrillation is a treatment for life-threatening cardiac arrhythmias, specifically ventricular fibrillation (V-Fib) and non-perfusing ventricular tachycardia (V-Tach). A defibrillator delivers a dose of electric current to the heart. Although not fully understood, this process depolarizes a large amount of the heart muscle, ending the arrhythmia. Subsequently, the body's natural pacemaker in the sinoatrial node of the heart is able to re-establish normal sinus rhythm. A heart which is in asystole (flatline) cannot be restarted by a defibrillator; it would be treated only by cardiopulmonary resuscitation (CPR) and medication, and then by cardioversion or defibrillation if it converts into a shockable rhythm.

<span class="mw-page-title-main">Tachycardia</span> Heart rate exceeding normal resting rate

Tachycardia, also called tachyarrhythmia, is a heart rate that exceeds the normal resting rate. In general, a resting heart rate over 100 beats per minute is accepted as tachycardia in adults. Heart rates above the resting rate may be normal or abnormal.

<span class="mw-page-title-main">Ventricular fibrillation</span> Rapid quivering of the ventricles of the heart

Ventricular fibrillation is an abnormal heart rhythm in which the ventricles of the heart quiver. It is due to disorganized electrical activity. Ventricular fibrillation results in cardiac arrest with loss of consciousness and no pulse. This is followed by sudden cardiac death in the absence of treatment. Ventricular fibrillation is initially found in about 10% of people with cardiac arrest.

<span class="mw-page-title-main">Automated external defibrillator</span> Portable electronic medical device

An automated external defibrillator or automatic electronic defibrillator (AED) is a portable electronic device that automatically diagnoses the life-threatening cardiac arrhythmias of ventricular fibrillation (VF) and pulseless ventricular tachycardia, and is able to treat them through defibrillation, the application of electricity which stops the arrhythmia, allowing the heart to re-establish an effective rhythm.

<span class="mw-page-title-main">Wolff–Parkinson–White syndrome</span> Medical condition

Wolff–Parkinson–White syndrome (WPWS) is a disorder due to a specific type of problem with the electrical system of the heart involving an accessory pathway able to conduct electrical current between the atria and the ventricles, thus bypassing the atrioventricular node. About 60% of people with the electrical problem developed symptoms, which may include an abnormally fast heartbeat, palpitations, shortness of breath, lightheadedness, or syncope. Rarely, cardiac arrest may occur. The most common type of irregular heartbeat that occurs is known as paroxysmal supraventricular tachycardia.

<span class="mw-page-title-main">Implantable cardioverter-defibrillator</span> Medical device

An implantable cardioverter-defibrillator (ICD) or automated implantable cardioverter defibrillator (AICD) is a device implantable inside the body, able to perform defibrillation, and depending on the type, cardioversion and pacing of the heart. The ICD is the first-line treatment and prophylactic therapy for patients at risk for sudden cardiac death due to ventricular fibrillation and ventricular tachycardia.

<span class="mw-page-title-main">Short QT syndrome</span> Medical condition

Short QT syndrome (SQT) is a very rare genetic disease of the electrical system of the heart, and is associated with an increased risk of abnormal heart rhythms and sudden cardiac death. The syndrome gets its name from a characteristic feature seen on an electrocardiogram (ECG) – a shortening of the QT interval. It is caused by mutations in genes encoding ion channels that shorten the cardiac action potential, and appears to be inherited in an autosomal dominant pattern. The condition is diagnosed using a 12-lead ECG. Short QT syndrome can be treated using an implantable cardioverter-defibrillator or medications including quinidine. Short QT syndrome was first described in 2000, and the first genetic mutation associated with the condition was identified in 2004.

<span class="mw-page-title-main">Supraventricular tachycardia</span> Abnormally fast heart rhythm

Supraventricular tachycardia (SVT) is an umbrella term for fast heart rhythms arising from the upper part of the heart. This is in contrast to the other group of fast heart rhythms – ventricular tachycardia, which start within the lower chambers of the heart. There are four main types of SVT: atrial fibrillation, atrial flutter, paroxysmal supraventricular tachycardia (PSVT), and Wolff–Parkinson–White syndrome. The symptoms of SVT include palpitations, feeling of faintness, sweating, shortness of breath, and/or chest pain.

<span class="mw-page-title-main">AV nodal reentrant tachycardia</span> Medical condition

AV-nodal reentrant tachycardia (AVNRT) is a type of abnormal fast heart rhythm. It is a type of supraventricular tachycardia (SVT), meaning that it originates from a location within the heart above the bundle of His. AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia. It is more common in women than men. The main symptom is palpitations. Treatment may be with specific physical maneuvers, medications, or, rarely, synchronized cardioversion. Frequent attacks may require radiofrequency ablation, in which the abnormally conducting tissue in the heart is destroyed.

Premature atrial contraction (PAC), also known as atrial premature complexes (APC) or atrial premature beats (APB), are a common cardiac dysrhythmia characterized by premature heartbeats originating in the atria. While the sinoatrial node typically regulates the heartbeat during normal sinus rhythm, PACs occur when another region of the atria depolarizes before the sinoatrial node and thus triggers a premature heartbeat, in contrast to escape beats, in which the normal sinoatrial node fails, leaving a non-nodal pacemaker to initiate a late beat.

Pediatric advanced life support (PALS) is a course offered by the American Heart Association (AHA) for health care providers who take care of children and infants in the emergency room, critical care and intensive care units in the hospital, and out of hospital. The course teaches healthcare providers how to assess injured and sick children and recognize and treat respiratory distress/failure, shock, cardiac arrest, and arrhythmias.

The following outline is provided as an overview of and topical guide to cardiology, the branch of medicine dealing with disorders of the human heart. The field includes medical diagnosis and treatment of congenital heart defects, coronary artery disease, heart failure, valvular heart disease and electrophysiology. Physicians who specialize in cardiology are called cardiologists.

<span class="mw-page-title-main">Junctional ectopic tachycardia</span> Medical condition

Junctional ectopic tachycardia (JET) is a rare syndrome of the heart that manifests in patients recovering from heart surgery. It is characterized by cardiac arrhythmia, or irregular beating of the heart, caused by abnormal conduction from or through the atrioventricular node. In newborns and infants up to 6 weeks old, the disease may also be referred to as His bundle tachycardia or congenital JET.

A wearable cardioverter defibrillator (WCD) is a non-invasive, external device for patients at risk of sudden cardiac arrest (SCA). It allows physicians time to assess their patient's arrhythmic risk and see if their ejection fraction improves before determining the next steps in patient care. It is a leased device. A summary of the device, its technology and indications was published in 2017 and reviewed by the EHRA Scientific Documents Committee.

<span class="mw-page-title-main">Arrhythmia</span> Group of medical conditions characterized by irregular heartbeat

Arrhythmias, also known as cardiac arrhythmias, are irregularities in the heartbeat, including when it is too fast or too slow. A resting heart rate that is too fast – above 100 beats per minute in adults – is called tachycardia, and a resting heart rate that is too slow – below 60 beats per minute – is called bradycardia. Some types of arrhythmias have no symptoms. Symptoms, when present, may include palpitations or feeling a pause between heartbeats. In more serious cases, there may be lightheadedness, passing out, shortness of breath, chest pain, or decreased level of consciousness. While most cases of arrhythmia are not serious, some predispose a person to complications such as stroke or heart failure. Others may result in sudden death.

<span class="mw-page-title-main">Rhythm interpretation</span>

Rhythm interpretation is an important part of healthcare in Emergency Medical Services (EMS). Trained medical personnel can determine different treatment options based on the cardiac rhythm of a patient. There are many common heart rhythms that are part of a few different categories, sinus arrhythmia, atrial arrhythmia, ventricular arrhythmia. Rhythms can be evaluated by measuring a few key components of a rhythm strip, the PQRST sequence, which represents one cardiac cycle, the ventricular rate, which is the rate at which the ventricles contract, and the atrial rate, which is the rate at which the atria contract.

References

  1. ↑ "Ventricular tachycardia: MedlinePlus Medical Encyclopedia". medlineplus.gov. Retrieved 29 May 2019.
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  3. 1 2 3 4 5 6 7 8 9 "Types of Arrhythmia". NHLBI. July 1, 2011. Archived from the original on 7 June 2015. Retrieved 7 September 2016.
  4. ↑ B Garner, J; M Miller, J (April 2013). "Wide Complex Tachycardia - Ventricular Tachycardia or Not Ventricular Tachycardia, That Remains the Question". Arrhythmia & Electrophysiology Review. 2 (1): 23–29. doi:10.15420/aer.2013.2.1.23. PMC   4711501 . PMID   26835036.
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  6. ↑ Eifling M, Razavi M, Massumi A. "The evaluation and management of electrical storm". Texas Heart Institute Journal 2011; 38: 111–121
  7. ↑ Bains, Kavin, Janfaza, David, Flaherty, Devon, et al. "Sympathetic Blockade for the Management of Refractory Ventricular Tachycardia: A Case Report". A&A Practice 2021;15(4):e01456. doi : 10.1213/XAA.0000000000001456.
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  11. ↑ Stewart RB, Bardy GH, Greene HL (June 1986). "Wide complex tachycardia: misdiagnosis and outcome after emergent therapy". Annals of Internal Medicine. 104 (6): 766–71. doi:10.7326/0003-4819-104-6-766. PMID   3706928.
  12. 1 2 John, RM; Tedrow, UB; Koplan, BA; Albert, CM; Epstein, LM; Sweeney, MO; Miller, AL; Michaud, GF; Stevenson, WG (October 2012). "Ventricular arrhythmias and sudden cardiac death". Lancet. 380 (9852): 1520–9. doi:10.1016/S0140-6736(12)61413-5. PMID   23101719. S2CID   11558991.
  13. ↑ "Answer to diagnostic dilemma: EKG". The American Journal of Medicine. 108 (6): 512–3. 15 April 2000. doi: 10.1016/s0002-9343(00)00373-9 . PMID   10781791.
  14. ↑ Kasper, D. (2012). "The Tachyarrhythmias". In Harrison's Principles of Internal Medicine (18th ed., Vol. 2, pp. 1892–1893). New York: McGraw-Hill, Medical Pub. Division.
  15. 1 2 3 4 5 Link, MS; Atkins, DL; Passman, RS; Halperin, HR; Samson, RA; White, RD; Cudnik, MT; Berg, MD; Kudenchuk, PJ; Kerber, RE (2 November 2010). "Part 6: electrical therapies: automated external defibrillators, defibrillation, cardioversion, and pacing: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care". Circulation. 122 (18 Suppl 3): S706–719. doi: 10.1161/CIRCULATIONAHA.110.970954 . PMID   20956222.
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  17. ↑ Compton, Steven J. MD, FACC, FACP, FHRS https://emedicine.medscape.com/article/159075-overview Ret. Nov. 17 2017.
  18. ↑ Aliot EM, Stevenson WG, Almendral-Garrote JM, et al. (June 2009). "EHRA/HRS Expert Consensus on Catheter Ablation of Ventricular Arrhythmias: developed in a partnership with the European Heart Rhythm Association (EHRA), a Registered Branch of the European Society of Cardiology (ESC), and the Heart Rhythm Society (HRS); in collaboration with the American College of Cardiology (ACC) and the American Heart Association (AHA)". Europace. 11 (6): 771–817. doi: 10.1093/europace/eup098 . PMID   19443434.
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  20. ↑ Wissner E, Stevenson WG, Kuck KH (June 2012). "Catheter ablation of ventricular tachycardia in ischaemic and non-ischaemic cardiomyopathy: where are we today? A clinical review". European Heart Journal. 33 (12): 1440–1450. doi: 10.1093/eurheartj/ehs007 . PMID   22411192. S2CID   17525941.
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