Ventricular tachycardia overview

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Ventricular tachycardia Microchapters
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Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Ventricular Tachycardia from other Disorders
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
Diagnostic Study of Choice
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
Chest X Ray
Echocardiography
Cardiac MRI
Other Diagnostic Tests
Treatment
Medical Therapy
Electrical Cardioversion
Ablation
Surgery
Primary Prevention
Secondary Prevention
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor-In-Chief: Sara Zand, M.D.[2] Cafer Zorkun, M.D., Ph.D. [3], Avirup Guha, M.B.B.S.[4]

Overview

Ventricular tachycardia is a tachycardia that originates in one of the ventricles of the heart. This is a potentially life-threatening arrhythmia because it may lead to ventricular fibrillation and sudden death. In 1906 Gallavardin discovered the reasons behind the cardiac instability which led to ventricular tachycardia, and put forth the idea that VT could convert into ventricular fibrillation. Thomas Lewis gave the first electrocardiographic description of ventricular tachycardia in 1909. It was first suggested in 1921 that coronary occlusion could be the main cause of ventricular tachycardia. Many advancements have been made in the diagnosis and management protocols of ventricular tachycardia since that time.Ventricular tachycardia refers to a rhythm with a heart rate in excess of 100 (and in some definitions 120) beats per minute that arises distal to the bundle of His. Ventricular tachycardia can be classified based on morphology and duration of tachyarrhythmia. The morphology of the QRS complexes on the ECG maybe monomorphic ventricular tachycardia or polymorphic ventricular tachycardia. In sustained VT duration of VT lasts > 30 sec or VT< 30 sec that needs to be terminated due to compromised hemodynamic. Nonsustained, or unsustained VT is more than 3 consecutive premature ventricular complexes with spontaneously termination. Bidirectional VT is a type of VT with beat to beat changing QRS frontal plane axis indicating of digoxin toxicity or catecholaminergic polymorphic VT. Torsades de pointed is a type of polymorphic VT in the setting of long QT interval which is characterized by twisting of the points, waxing and waning QRS amplitude, long-short sequence with long-coupling interval to the first VT beat, may be initiating after bradycardia such as high grade AV block. Ventricular flutter is explained as a regular ventricular arrhythmia with rate about 300 beat per minute (bpm), or cycle length 200 ms, sinusoidal monophorphic QRS complexes, without any isoelecterical interval between successive QRS complexes. Ventricular fibrillation is a rapid, grossly irregular electrical activity with variation in morphologic waveforms by ventricular rate >300bpm, cycle length <200 ms. VT/ VF storm is an electerical storm or cardiac instability due to ≥ 3 episodes of sustained VT, VF or shock delivery from ICD within 24 hours. The underlying mechanism of VT is due to automaticity arising in either the myocardium or in the distal conduction system. The most common underlying substrate for ventricular tachycardia is ischemic heart disease. Myocardial scarring from any process increases the likelihood of electrical reentrant circuits. These circuits generally include a zone where normal electrical propagation is slowed by the scar. Ventricular scar formation from a prior myocardial infarction (MI) is the most common cause of sustained monomorphic VT. The morphology of ventricular tachycardia often depends on its cause. VT in a structurally normal heart typically results from mechanisms such as triggered activity and enhanced automaticity. If VT is hemodynamically tolerated, the incessant tachyarrhythmia may cause a dilated cardiomyopathy. This may develop over a period of weeks to years and may resolve with successful suppression of the VT.Ischemic heart disease is a common cause of ventricular tachycardia. Other causes of ventricular tachycardia include congenital heart disease, valvular heart disease, dilated non-ischemic cardiomyopathy, sarcoidosis, infiltrative cardiomyopathy, inflammatory cardiomyopathy, and inherited channelopathies. In addition, illicit drug use with sympathetic activity such as cocaine and methamphetamine, and drugs with QT interval prolongation effect and also electrolyte disturbances such as hypokalemia, hypomagnesemia, and hypocalcemia may cause ventricular tachycardia. When wide QRS tachycardia is present on the ECG, it is necessary to rapidly differentiate whether it is caused by ventricular tachycardia (VT) or a supraventricular tachycardia (SVT) with aberrant conduction. While the ECG provides the most reliable data to distinguish VT from SVT with aberrant conduction, the clinical history and the age of the patient may also provide additional discriminatory information regarding the cause of the wide QRS tachycardia. While older patients with a prior history of myocardial infarction are more likely to have VT, young hemodynamically stable patients presenting with paroxysmal tachycardia are more likely to have SVT with aberrant conduction. Nevertheless, the primary tool to differentiate VT from SVT with aberrant conduction is the ECG. There are several findings that are more common in ventricular tachycardia, and there are also more sophisticated electrophysiologic algorithms such as the Brugada and Vereckei algorithms that can be used to distinguish VT from SVT with aberrant conduction. The diagnosis of VT is more likely if There is a history of myocardial infarction or structural heart disease, the electrical axis is -90 to -180 degrees (a “northwest” or “superior” axis), the QRS is > 140 msec, there is AV dissociation, there are positive or negative QRS complexes in all the precordial leads, and the morphology of the QRS complexes resembles that of a previous premature ventricular contraction (PVC). Common risk factors associated with VT/ VF include prior history of hypertension, Prior MI, ST-segment changes at presentation, chronic obstructive pulmonary disease. Risk factors of occurrence of VF before primary PCI in STEMI patients include alcohol consumption, preinfarction angina, anterior infarct location, complete coronary occlusion at the time of coronary angiography. Risk factors associated with VT/ VF after primary PCI include lower blood pressure, higher heart rate, poor coronary flow at the end of the procedure, incomplete resolution of ST elevation. Risk factors associated with monomorphic VT early after CABG include prior MI, ventricular scar, LV dysfunction, placement of a bypass graft across a noncollateralized occluded coronary vessel to a chronic infarct zone.Ventricular arrhythmia may include the range from triple premature ventricular contraction s (PVCs) to ventricular fibrillation. Clinical presentation varies from asymptomatic to cardiac arrest. Ventricular tachycardia can cause life-threatening or fatal hemodynamic compromise or it can degenerate into a life-threatening rhythm called ventricular fibrillation. Common complications of ventricular tachycardia include sudden cardiac death, cardiomyopathy, ventricular fibrillation, and infection related to ICD. The prognosis of ventricular tachycardia in patients largely depends upon the presence and severity of underlying cardiac disease. Mortality of ventricular tachycardia is higher in patients with coronary artery disease and presence of LV dysfunction. Prognosis is generally good in patients with right ventricular dysplasia, idiopathic ventricular tachycardia or ventricular fibrillation treated medically. Contrary to previous studies, VT or VF at any time after STEMI was associated with higher mortality rate within 90 days. Late VT or VF (after 48 hours of hospital admission) after STEMI was associated with a higher risk of death than early VT or VF (within 48 hours of hospital admission). ECG is the first diagnostic test that should be obtained in hemodynamically stable Ventricular tachycardia. For detection of tachyarrhythmia symptoms related exercise such as cathecolaminergic polymorphic VT, Exercise stress test is recommended. Findings on resting ECG associated with diagnosis of VT include evidence of structural hear disease such as prior MI or chamber enlargement, evidence of inherited arrhythmia disorders such as long QT syndrome, Brugada syndrome, arrhythmogenic right ventricular cardiomyopathy. QRS duration and conduction abnormality may have prognostic value in structural heart disease.The symptoms of ventricular tachycardia will depend on the ventricular rate, the duration of tachycardia, and the presence of underlying disease. In general, the symptoms include palpitations, lightheadedness, syncope, dyspnea, chest pain, cardiac arrest. Symptoms related to underlying heart disease include dyspnea at rest or on exertion, orthopnea, paroxysmal nocturnal dyspnea, chest pain, edema. Precipitating factors maybe exercise, or emotional stress. In patient presented with VT clinical history should be taken about coronary heart disease, valvular heart disease (mitral valve prolapse), congenital heart disease, thyroid disease, acute kidney injury, Chronic kidney disease, electrolyte abnormalities, stroke, embolic events, lung disease,epilepsy (arrhythmic syncope can be misdiagnosed as epilepsy), alcohol, illicit drug use, and use of over-the-counter medications causing QT prolongation and torsades de pointed. It is important to notify about the family history of SCD in first relatives, repetitive spontaneous pregnancy losses (concerning cardiac channelopathy), IHD, hypertrophic cardiomyopathy , dilated cardiomyopathy, ARVC, congenital heart disease, cardiac channelopathies( Long QT, Brugada, Short QT, CPVT), conduction disorders, pacemakers/ICDs, and Neuromuscular disease associated with cardiomyopathies (Muscular dystrophy, epilepsy).Physical examination should consist of a thorough cardiac exam, lung exam, and close monitoring of vital signs. Findings on physical exam may include hemodynamic instability, cannon a wave in jugolar venous pulsation, rales in lung fields, lower limbs edema, evidence of sternotomy scar due to previous CABG, and ICD pocket. Laboratory findings predicting sudden cardiac arrest and ventricular tachycardia include elevated level of Natriuretic peptides—B-type (BNP) or N-terminal pro-BNP as the marker of myocardial stress and fibrosis in heart failure disease, highly sensitive troponin T indicating cardiomyocyte injury, screening about hypokalemia, hypomagnesemia and also toxic level of digoxin, cocaine, tricyclic antidepressant.Finding on ECG associated with VT include: AV dissociation, atypical right bundle branch block or left bundle branch block characteristics, QRS> 140 ms for wide complex tachycardia with [[right bundle branch block pattern and QRS > 160 ms for wide complex tachycardia with left bundle branch block pattern, concordance or same polarity in all precordioal leads, rightward superior QRS axis.There are no x-ray findings associated with ventricular tachycardia. However, an x-ray may be helpful in the diagnosis underlying cause of ventricular tachycardia such as congestive heart failure, sternotomy suture, ICD wires and pocket.Echocardiography is an available and helpful modality for diagnosis and predicting the underlying causes of ventricular tachycardia and sudden cardiac arrest. Findings on an echocardiography include assessment of myocardial function, valvular structural and functional disease, congenital heart disease, cardiomyopathy, heart failure, prior MI.When structural heart disease is suspected in the context of ventricular tachycardia, it is necessary to have an accurate evaluation of the structure and function of the atria and ventricles. While echocardiography is the available modality, MRI is used when the assessment provided by echocardiography is not satisfactory. In addition, MRI seems to have an important role in the evaluation of suspected arrhythmogenic right ventricular cardiomyopathy because MRI provides a good assessment of the right ventricular structure, function, and fatty infiltration if present.Coronary angiography has an important role in diagnosis and treatment of myocardial ischemia-induced life-threatening VT, VF. Myocardial ischemia may induce recurrent polymorphic VT, or VF and is treatable by coronary revascularization. Evidence of ST segment elevation or early post resuscitated ECG changes suggestive of ischemia may lead to ventricular arrhythmia and sudden cardiac arrest and required urgent revascularization. In patients with low evidence of myocardial ischemia, coronary angiography is not recommended. For patients suspected anomalous origin of the coronary arteries leading SCA , coronary angiography is warranted.The mainstay of medical therapy in hemodynamic stable VT is suppression of tachyarrhythmia with antiarrhythmic medications such as amiodarone, sotalol, lidocaine, betablocker alongside with correction of hypokalemia, hypomagnesemia and hypocalcemia. In addition, treatment the underlying cause of VT including IHD or decompensated heart failure should be warranted. For treatment of unstable tachyarrhythmia (with chest pain, dyspnea, pulmonary edema, altered mental status), other than VF or pulselessVT, synchronized cardioversion should be warranted.In Synchronized cardioversion the amount of energy delivered is less than defibrillation and also the shock is delivered in different parts of the cardiac cycle. R-on -T phenomena may happen if the electrical defibrillated shock is delivered during the refractory period (on the latter part of T wave) which is vulnerable to induce VF. For prevention of this phenomena and monitoring R wave for each QRS complex for delivery of shock in cardiac cycle, the defibrillator is placed on synchronize mode. The recommendation energy for synchronized cardioversion is 50-200 jouls. Catheter ablation is useful for treating ventricular arrhythmia when drugs are ineffective. Monomorphic VT is a suitable target for ablation. Ablation can be used for polymorphic VT or VF if an initiating PVC focus or substrate is accessible. Cardiac surgery is rarely performed for treating ventricular tachycardia in case of highly symptomatic patients with failed antiarrhythmic medications or unsuccessful ventricular ablation. Inaccessible sites for ventricular ablation including area deep in the myocardium, beneath epicardial fat, or near the coronary arteries may lead to unsuccessful ablation. Surgical ablation of ventricular arrhythmia can be done during other surgical intervention such as placement of LVAD or at the time of left ventricular aneurysectomy which is a substrate for VT.Primary prevention strategy for heart failure patients with NYHA class II or III, and LVEF ≤35% at least 40 days after myocardial infarction is ICD implantation. In patients with LVEF ≤30% and prior MI and NYHA class I symptoms , ICD implantation was associated with survival benefit. Analysis of MADIT, MADIT-II, and SCD-HeFT showed survival benefit of ICD implantation for primary prevention of ventricular arrhythmia. There is not survival benefit of ICD implantation in patients with NYHA class IV heart failure.Secondary prevention strategies following SCA and unstable VT include ICD implantation, and medications. Based on meta-analysis of AVID trial implantation of ICD for secondary prevention of ventricular arrhythmia was superior to antiarrhythmic drugs in patients who survived of sudden cardiac arrest or unstable VT. Before ICD implantation, the reversible causes of ventricular arrhythmia including myocardial ischemia, electrolyte disturbance, proarrhythmic medication effect may be corrected. ICD implantation improved outcome in well-tolerated VT and structurally heart disease. Among patients with ischemia heart disease and syncope due to inducible sustained monomorphic VT, ICD is recommended even if there is not other criteria for primary prevention.

Historical Perspective

In 1906 Gallavardin discovered the reasons behind the cardiac instability which leads to ventricular tachycardia, and put forth the idea that VT could convert into ventricular fibrillation. Thomas Lewis gave the first electrocardiographic description of ventricular tachycardia in 1909. It was first suggested in 1921 that coronary occlusion could the main cause of ventricular tachycardia. Many advancements have been made in the diagnosis and management protocols of ventricular tachycardia since that time.

Classification

Ventricular tachycardia refers to a rhythm with a heart rate in excess of 100 (and in some definitions 120) beats per minute that arises distal to the bundle of His. Ventricular tachycardia can be classified based on morphology and duration of tachyarrhythmia. The morphology of the QRS complexes on the ECG maybe (monomorphic ventricular tachycardiaor polymorphic ventricular tachycardia). In sustained VT duration of VT lasts > 30 sec or VT< 30 sec that needs to termination due to compromised hemodynamic. Nonsustained, or unsustained VT is more than 3 consecutive premature ventricular complexes with spontaneously termination. Bidirectional VT is a type of VT with beat to beat changing QRS frontal plane axis indicating of digoxin toxicity or catecholaminergic polymorphic VT.Torsades de pointed is a type of polymorphic VT in the setting of long QT interval which is characterized by twisting of the points, waxing and waning QRS amplitude, Long-short sequence with long-coupling interval to the first VT beat, maybe initiated after bradycardia such as high grade AV block.Ventricular flutter is explained as a regular ventricular arrhythmia with rate about 300 beat per minute (bpm), or cycle length 200 ms, sinusoidal monophorphic QRS complexes, Without any isoelecterical interval between successive QRS complexes. Ventricular fibrillation is a rapid, grossly irregular electrical activity with variation in morphologic waveforms by ventricular rate >300bpm, cycle length <200 ms. VT/ VF storm is an electerical storm or cardiac instability due to ≥ 3 episodes of sustained VT, VF or shock delivery from ICD within 24 hours.

Pathophysiology

The underlying mechanism of VT is due to automaticity arising in either the myocardium or in the distal conduction system. The most common underlying substrate for ventricular tachycardia is ischemic heart disease. Myocardial scarring from any process increases the likelihood of electrical reentrant circuits. These circuits generally include a zone where normal electrical propagation is slowed by the scar. Ventricular scar formation from a prior myocardial infarction (MI) is the most common cause of sustained monomorphic VT. The morphology of ventricular tachycardia often depends on its cause. VT in a structurally normal heart typically results from mechanisms such as triggered activity and enhanced automaticity. If VT is hemodynamically tolerated, the incessant tachyarrhythmia may cause a dilated cardiomyopathy. This may develop over a period of weeks to years and may resolve with successful suppression of the VT.

Causes

Ischemic heart disease is a common cause of ventricular tachycardia. Other causes of ventricular tachycardia include congenital heart disease, valvular heart disease, dilated non-ischemic cardiomyopathy, sarcoidosis, infiltrative cardiomyopathy, inflammatory cardiomyopathy, and inherited channelopathies. In addition, illicit drug use with sympathetic activity such as cocaine and methamphetamine, and drugs with QT interval prolongation effect and also electrolyte disturbances such as hypokalemia, hypomagnesemia, and hypocalcemia may cause ventricular tachycardia.

Differentiating Ventricular Tachycardia from other Disorders

When wide QRS tachycardia is present on the [[electrocardiogram] ECG, it is necessary to rapidly differentiate whether it is caused by ventricular tachycardia (VT) or a supraventricular tachycardia (SVT) with aberrant conduction. While the ECG provides the most reliable data to distinguish VT from SVT with aberrant conduction, the clinical history and the age of the patient may also provide additional discriminatory information regarding the cause of the wide QRS tachycardia. While older patients with a prior history of myocardial infarction are more likely to have VT, young hemodynamically stable patients presenting with paroxysmal tachycardia are more likely to have SVT with aberrant conduction. Nevertheless, the primary tool to differentiate VT from SVT with aberrant conduction is the ECG. There are several findings that are more common in ventricular tachycardia, and there are also more sophisticated electrophysiologic algorithms such as the Brugada and Vereckei algorithms that can be used to distinguish VT from SVT with aberrant conduction. The diagnosis of VT is more likely if: There is a history of myocardial infarction or structural heart disease, the electrical axis is -90 to -180 degrees (a “northwest” or “superior” axis), the QRS is > 140 msec, there is AV dissociation, there are positive or negative QRS complexes in all the precordial leads, and the morphology of the QRS complexes resembles that of a previous premature ventricular contraction (PVC).

Epidemiology and Demographics

VT is more prevalent among patients with coronary artery disease. Eldery patients are more commonly affected by ideopathic VT. Ideopathic VT is commonly observed in women.There is no racial predilection for VT.

Risk Factors

Common risk factors associated with VT/ VF include prior history of hypertension, Prior MI, ST-segment changes at presentation, chronic obstructive pulmonary disease. Risk factors of occurrence of VF before primary PCI in STEMI patients include alcohol consumption, preinfarction angina, anterior infarct location, complete coronary occlusion at the time of coronary angiography. Risk factors associated with VT/ VF after primary PCI include lower blood pressure, higher heart rate, poor coronary flow at the end of the procedure, incomplete resolution of ST elevation. Risk factors associated with monomorphic VT early after CABG include prior MI, ventricular scar, LV dysfunction, placement of a bypass graft across a noncollateralized occluded coronary vessel to a chronic infarct zone.

Screening

In a young patient with lone atrial fibrillation, short QT syndrome should be excluded. In a patient with a family history of sudden cardiac death a physical examination should be performed.

Natural History, Complications and Prognosis

Ventricular arrhythmia may include the range from triple premature ventricular contraction s (PVCs) to ventricular fibrillation. Clinical presentation varies from asymptomatic to cardiac arrest. Ventricular tachycardia can cause life-threatening or fatal hemodynamic compromise or it can degenerate into a life-threatening rhythm called ventricular fibrillation. Common complications of ventricular tachycardia include sudden cardiac death, cardiomyopathy, ventricular fibrillation, and infection related to ICD. The prognosis of ventricular tachycardia in patients largely depends upon the presence and severity of underlying cardiac disease. Mortality of ventricular tachycardia is higher in patients with coronary artery disease and presence of LV dysfunction. Prognosis is generally good in patients with right ventricular dysplasia, idiopathic ventricular tachycardia or ventricular fibrillation treated medically. Contrary to previous studies, VT or VF at any time after STEMI was associated with higher mortality rate within 90 days. Late VT or VF (after 48 hours of hospital admission) after STEMI was associated with a higher risk of death than early VT or VF (within 48 hours of hospital admission).

Diagnosis

Diagnostic study of choice

ECG is the first diagnostic test that should be obtained in hemodynamically stable Ventricular tachycardia. For detection of tachyarrhythmia symptoms related exercise such as cathecolaminergic polymorphic VT, Exercise stress test is recommended. Findings on resting ECG associated with diagnosis of VT include evidence of structural hear disease such as prior MI or chamber enlargement, evidence of inherited arrhythmia disorders such as long QT syndrome, Brugada syndrome, arrhythmogenic right ventricular cardiomyopathy. QRS duration and conduction abnormality may have prognostic value in structural heart disease.

History and Symptoms

The symptoms of ventricular tachycardia will depend on the ventricular rate, the duration of tachycardia, and the presence of underlying disease. In general, the symptoms include palpitations, lightheadedness, syncope, dyspnea, chest pain, cardiac arrest. Symptoms related to underlying heart disease include dyspnea at rest or on exertion, orthopnea, paroxysmal nocturnal dyspnea, chest pain, edema. Precipitating factors maybe exercise, or emotional stress. In patient presented with VT clinical history should be taken about coronary heart disease, valvular heart disease (mitral valve prolapse), congenital heart disease, thyroid disease, acute kidney injury, chronic kidney disease, electrolyte abnormalities, stroke, embolic events, lung disease,epilepsy (arrhythmic syncope can be misdiagnosed as epilepsy), alcohol, illicit drug use, and use of over-the-counter medications causing QT prolongation and torsades de pointed. It is important to notify about the family history of SCD in first relatives, repetitive spontaneous pregnancy losses (concerning cardiac channelopathy), IHD, hypertrophic cardiomyopathy , dilated cardiomyopathy, ARVC, congenital heart disease, cardiac channelopathies( Long QT, Brugada, Short QT, CPVT), conduction disorders, pacemakers/ICDs, and Neuromuscular disease associated with cardiomyopathies (Muscular dystrophy, epilepsy).

Physical Examination

Physical examination should consist of a thorough cardiac exam, lung exam, and close monitoring of vital signs. Findings on physical exam may include hemodynamic instability, cannon a wave in jugular venous pulsation, rales in lung fields, lower limbs edema, evidence of sternotomy scar due to previous CABG, and ICD pocket.

Laboratory Findings

Serial cardiac enzymes, serum electrolytes as well as calcium, magnesium and phosphate levels, should be obtained. A toxicology screen should also be obtained to assess for illicit drugs as the cause of the VT, as well as levels of medications that may have caused the VT.

Electrocardiogram

Finding on ECG associated with VT include: AV dissociation, atypical right bundle branch block or left bundle branch block characteristics, QRS> 140 ms for wide complex tachycardia with [[right bundle branch block pattern and QRS > 160 ms for wide complex tachycardia with left bundle branch block pattern, concordance or same polarity in all precordioal leads, rightward superior QRS axis.

Chest X Ray

There are no x-ray findings associated with ventricular tachycardia. However, a chest x-ray may be helpful in the diagnosis underlying cause of ventricular tachycardia such as congestive heart failure, sternotomy suture, ICD wires and pocket.

Echocardiography

Echocardiography is an available and helpful modality for diagnosis and predicting the underlying causes of ventricular tachycardia and sudden cardiac arrest. Findings on an echocardiography include assessment of myocardial function, valvular structural and functional disease, congenital heart disease, cardiomyopathy, heart failure, prior MI.

Cardiac MRI

When structural heart disease is suspected in the context of ventricular tachycardia, it is necessary to have an accurate evaluation of the structure and function of the atria and ventricles. While echocardiography is the available modality, MRI is used when the assessment provided by echocardiography is not satisfactory. In addition, MRI seems to have an important role in the evaluation of suspected arrhythmogenic right ventricular cardiomyopathy because MRI provides a good assessment of the right ventricular structure, function, and fatty infiltration if present.

Coronary angiography

Coronary angiography has an important role in diagnosis and treatment of myocardial ischemia-induced life-threatening VT, VF. Myocardial ischemia may induce recurrent polymorphic VT, or VF and is treatable by coronary revascularization. Evidence of ST segment elevation or early post resuscitated ECG changes suggestive of ischemia may lead to ventricular arrhythmia and sudden cardiac arrest and required urgent revascularization. In patients with low evidence of myocardial ischemia, coronary angiography is not recommended. For patients suspected anomalous origin of the coronary arteries leading SCA , coronary angiography is warranted.

Treatment

Medical therapy

The mainstay of medical therapy in hemodynamic stable VT is suppression of tachyarrhythmia with antiarrhythmic medications such as amiodarone, sotalol, lidocaine, betablocker alongside with correction of hypokalemia, hypomagnesemia and hypocalcemia. In addition, treatment the underlying cause of VT including IHD or decompensated heart failure should be warranted.

Electrical Cardioversion

For treatment of unstable tachyarrhythmia (with chest pain, dyspnea, pulmonary edema, altered mental status), other than VF or pulselessVT, synchronized cardioversion should be warranted.In Synchronized cardioversion the amount of energy delivered is less than defibrillation and also the shock is delivered in different parts of the cardiac cycle. R-on -T phenomena may happen if the electrical defibrillated shock is delivered during the refractory period (on the latter part of T wave) which is vulnerable to induce VF. For prevention of this phenomena and monitoring R wave for each QRS complex for delivery of shock in cardiac cycle, the defibrillator is placed on synchronize mode. The recommendation energy for synchronized cardioversion is 50-200 jouls.

Catheter ablation

Catheter ablation is useful for treating ventricular arrhythmia when drugs are ineffective. Monomorphic VT is a suitable target for ablation. Ablation can be used for polymorphic VT or VF if an initiating PVC focus or substrate is accessible.

Surgery

Cardiac surgery is rarely performed for treating ventricular tachycardia in case of highly symptomatic patients with failed antiarrhythmic medications or unsuccessful catheter ablation. Inaccessible sites for ventricular ablation including area deep in the myocardium, beneath epicardial fat, or near the coronary arteries may lead to unsuccessful ablation. Surgical ablation of ventricular arrhythmia can be done during other surgical intervention such as placement of LVAD or at the time of left ventricular aneurysectomy which is a substrate for VT.

Primary prevention

Primary prevention strategy for heart failure patients with NYHA class II or III, and LVEF ≤35% at least 40 days after myocardial infarction is ICD implantation. In patients with LVEF ≤30% and prior MI and NYHA class I symptoms , ICD implantation was associated with survival benefit. Analysis of MADIT, MADIT-II, and SCD-HeFT showed survival benefit of ICD implantation for primary prevention of ventricular arrhythmia. There is not survival benefit of ICD implantation in patients with NYHA class IV heart failure.

Secondary prevention

Secondary prevention strategies following SCA and unstable VT include ICD implantation, and medications. Based on meta-analysis of AVID trial implantation of ICD for secondary prevention of ventricular arrhythmia was superior to antiarrhythmic drugs in patients who survived of sudden cardiac arrest or unstable VT. Before ICD implantation, the reversible causes of ventricular arrhythmia including myocardial ischemia, electrolyte disturbance, proarrhythmic medication effect may be corrected. ICD implantation improved outcome in well-tolerated VT and structurally heart disease. Among patients with ischemia heart disease and syncope due to inducible sustained monomorphic VT, ICD is recommended even if there is not other criteria for primary prevention.

References

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