Approach
Avoidance of behavioural factors associated with coronary artery disease (CAD) and left ventricular dysfunction is useful to prevent the most common causes of ventricular arrhythmia. Likewise, aggressive management of conditions that predispose to CAD and myocardial infarction (MI) (e.g., hypertension, hyperlipidaemia, diabetes mellitus) would be expected to reduce the subsequent risk of ventricular tachycardia (VT).
In special cases such as hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy (ARVC), and long QT syndrome type 1, patients should be counselled to avoid significant physical exertion. See Hypertrophic cardiomyopathy and Long QT syndrome for more information.
It is important to distinguish ventricular arrhythmia patients with underlying structural heart disease from those with idiopathic VT, which is associated with a good prognosis, rarely progressing to cardiac arrest.
Idiopathic VT (although defined as occurring in the absence of structural heart disease, known genetic disorder, drug toxicity, or electrolyte imbalance) is identifiable by electrophysiological (EP) testing. Therefore, in the case of ventricular tachycardias, idiopathic VT refers to a specific sub-type of tachycardias that can be defined by arrhythmia mechanism. This is different from tachycardias with no identifiable cause, in which the patient would have no signs of a definitive cause for the VT or signs of an idiopathic VT.
Treatment for identifiable reversible cause of VT such as ischaemia, MI, toxicity, drug overdose
In patients with a reversible cause of VT such as active ischaemia, recent MI, or drug toxicity or overdose, management includes treatment of the underlying cause of the VT in addition to the arrhythmia itself.[1] Until the reversible cause of VT has been corrected, an implantable cardioverter defibrillator (ICD) should not be considered.
Haemodynamically unstable sustained VT
Detailed discussion on CPR and defibrillation, in the advanced cardiac life support (ACLS) algorithm for the management of haemodynamically unstable VT in the setting of cardiac arrest such as pulseless VT and ventricular fibrillation (VF), is beyond the scope of this topic.[29][30][31] American Heart Association: guidelines for CPR and emergency cardiovascular care Opens in new window See Cardiac arrest.
Cardioversion is essential for the acute treatment of patients with haemodynamically unstable VT (symptomatic or severely hypotensive VT).[1] Left untreated, these conditions frequently culminate in death; rapid recognition and initiation of appropriate treatment may provide the only hope for the patient's survival.
Synchronised cardioversion should be considered before attempting anti-arrhythmic drug therapy in patients who have syncope, presyncope, and/or hypotension.
The anti-arrhythmic medications amiodarone and lidocaine can be used as adjunctive therapy.
Torsades de pointes
Torsades de pointes, a specific type of polymorphic VT characterised by a twisting appearance around the baseline, occurs in the setting of QT prolongation due to either the congenital or the acquired forms of the long QT syndrome. Torsades de pointes should be treated as any other form of VT according to the ACLS protocol. If the patient is haemodynamically unstable, immediate defibrillation should be performed. There should be special recognition of the fact that hypokalaemia and hypomagnesaemia are frequently associated with torsades de pointes, and empiric administration of magnesium should be considered. Offending drugs should be withdrawn and electrolyte deficiencies should be treated aggressively. An up-to-date list of drugs is available through research centres. CredibleMeds: Arizona Center for Education and Research on Therapeutics Opens in new window Intravenous magnesium sulfate should be administered. Additionally, overdrive pacing and isoprenaline infusion may be useful adjunctively in this arrhythmia as they reduce the QT interval.[30][31]
Catecholaminergic polymorphic VT
Medical therapy for catecholaminergic polymorphic VT, an inherited arrhythmia syndrome with high risk of VT, includes the use of beta-blockers for both acute and chronic treatment.[27][32] ICD insertion is needed in patients with recurrent syncope despite beta-blockers, or those who are survivors of cardiac arrest. However, ICDs should not be implanted without concomitant beta-blocker therapy as ICD shocks will increase catecholamine surge, potentially leading to a vicious cycle of ventricular arrhythmias and ICD shocks. Left cardiac sympathetic denervation appears to be effective, but has only been tested on small cohorts, and is not universally available.[33] In addition, flecainide, which acts to block the RyR2 channel, prevents RyR2-mediated premature calcium release and suppresses triggered beats. However, there are limited data showing its effectiveness in humans.[34][35] Other treatment strategies have been proposed, including a stepwise addition of alternative treatment options, such as calcium-channel blockers and flecainide, to beta-blockers in patients who do not respond sufficiently or who cannot tolerate beta-blockers.[27]
Haemodynamically stable non-idiopathic sustained VT
Anti-arrhythmic medications are useful in the acute management of VT that is asymptomatic and associated with normal blood pressure. Before initiating anti-arrhythmic drug therapy for a VT, it is important to be confident in the diagnosis and to make sure that the patient is not experiencing supraventricular tachycardia (SVT) with aberrant conduction. Conversely, the diagnosis of SVT with aberrancy should also be made carefully, as certain medications (e.g., verapamil, diltiazem) can exacerbate the clinical situation by worsening the patient’s haemodynamic status if the actual arrhythmia is VT.
According to the American Heart Association (AHA), intravenous adenosine can be considered to aid in treatment and diagnosis when the cause of the regular, monomorphic rhythm cannot be determined.[31] Other anti-arrhythmic drugs may also be considered in the acute management of stable VT. The AHA recommends intravenous procainamide or intravenous amiodarone.[31] Intravenous procainamide has been shown to be more efficacious than intravenous amiodarone in terminating wide complex tachycardia (67% vs. 38%, respectively; P = 0.026), and was associated with fewer adverse events.[36] However, procainamide may be more pro-arrhythmic and should be used with caution in the setting of baseline QT prolongation.[31]
Patients not responsive to initial anti-arrhythmic therapy:
Synchronised electrical cardioversion is another important treatment for haemodynamically tolerated sustained (monomorphic) VT. Among patients who fail an initial attempt at synchronised cardioversion, anti-arrhythmic medications such as amiodarone or lidocaine may be administered prior to additional attempts at cardioversion.
Synchronised cardioversion should be considered before attempting anti-arrhythmic drug therapy in patients who have syncope, presyncope, frequent palpitations, or hypotension (particularly those with symptoms of diminished cerebral perfusion), even if they have apparently stable haemodynamic parameters.
Initial management of haemodynamically stable idiopathic VT
There are several distinct entities of VT that occur in the absence of structural heart disease. Idiopathic VT occurs in the absence of apparent structural heart disease (e.g., ischaemia, prior infarction, cardiomyopathy, ARVC, left ventricular non-compaction, and valvular or other disorders of the myocardium), known channelopathy (e.g., long QT syndrome, Brugada syndrome, catecholaminergic polymorphic VT, short QT syndrome), drug toxicity, or electrolyte imbalance. These VTs are; however, identifiable through EP testing and response to certain medications.
Idiopathic VT requires specific treatment, and consultation with an electrophysiologist is recommended.
Specific types of idiopathic VT characteristically respond to specific medications, a feature that is useful for diagnostic as well as therapeutic purposes. Idiopathic outflow tract VT (which typically arises from the right ventricular outflow tract, but which may also arise from other regions including the left ventricular outflow tract) demonstrates one of several characteristic ECG morphologies. This arrhythmia is due to cyclic-AMP-mediated triggered activity that results in delayed after-depolarisations and can therefore be terminated with a bolus of adenosine. Outflow tract tachycardia may also respond to beta-adrenergic blockade, calcium-channel blockers, or to vagal manoeuvres.
Fascicular VT, a common form of idiopathic VT due to a re-entrant circuit involving part of either the left anterior or left posterior fascicle, characteristically responds to verapamil, but the drug should be only be used with extreme caution due to the risk of hypotension and haemodynamic collapse if given to other forms of VT. Cases of idiopathic VT refractory to adenosine or verapamil can be treated with other anti-arrhythmic medications (lidocaine, amiodarone); if the arrhythmia persists, synchronised electrical cardioversion should be considered.[31]
Earlier use of cardioversion may be warranted in patients who are highly symptomatic (particularly with symptoms of diminished cerebral perfusion) despite apparently stable haemodynamics. Among patients who fail an initial attempt at synchronised cardioversion, additional anti-arrhythmic medications such as amiodarone or lidocaine may be administered prior to additional attempts at cardioversion.
Subsequent management of haemodynamically stable idiopathic VT
For patients with idiopathic VT and mild-to-moderate symptoms (rare palpitations that do not interfere with daily activities), beta-blockers or calcium-channel blockers usually provide sufficient treatment. Catheter ablation is also reasonable as first-line therapy in patients with mild-to-moderate symptoms who prefer not to take medications.[37] It is a matter of patient preference in deciding between medications and ablation in this setting.
In patients with moderate-to-severe symptoms (syncope, presyncope, or frequent, disabling palpitations) or with associated cardiomyopathy, catheter ablation of VT should be considered as first-line therapy. Catheter ablation is also indicated in patients in whom beta-blockers and/or calcium-channel blockers are ineffective or poorly tolerated.[37]
Anti-arrhythmic agents, including class I drugs (mexiletine, flecainide, and propafenone) and class III agents (amiodarone and sotalol), may be used in patients who fail therapy with beta-blockers and/or calcium-channel blockers and who are not candidates for catheter ablation due to medical co-morbidity or reluctance to undergo the procedure, or in whom catheter ablation is ineffective.[38] In patients with idiopathic VT, ICD therapy is not recommended as a first-line treatment.
Medication choice is usually based on individual patient/physician preference. In some cases, a beta-blocker or calcium-channel blocker will suffice, whereas in other cases catheter ablation of the arrhythmia is curative.[38]
Medications such as flecainide, sotalol, and amiodarone may be employed as second-line therapy for patients with idiopathic VT who have refractory symptoms and who fail therapy with beta-blockers or catheter ablation.
Patients at high risk for VT or with history of sustained VT/cardiac arrest without identifiable reversible cause: ICD
ICD implantation is the recommended initial treatment/preventative measure for patients at high risk of developing a malignant ventricular arrhythmia, for:
High-risk patients who have not yet experienced a sustained arrhythmia (primary prevention)[39][40]
Patients who have survived an episode of sustained VT or VF and who have no identifiable reversible cause for VT/cardiac arrest.[41][42][43]
Patients at high risk for VT for which ICD implantation is the recommended initial treatment/preventive measure include those with:
Ischaemic cardiomyopathy (left ventricular ejection fraction [LVEF] ≤35%) and mild-to-moderate congestive heart failure symptoms (New York Heart Association class II or III symptoms)
Ischaemic cardiomyopathy with LVEF ≤30%
Ischaemic cardiomyopathy (LVEF ≤40%) with non-sustained VT and inducible sustained VT during EP testing
Non-ischaemic cardiomyopathy (LVEF ≤35% and New York Heart Association class II or III symptoms)
Hypertrophic cardiomyopathy (HCM) with high-risk features such as family history of sudden death from HCM; massive left ventricular hypertrophy (wall thickness ≥30 mm); unexplained syncope; left ventricular systolic dysfunction; left ventricular apical aneurysm; extensive late gadolinium enhancement on cardiovascular magnetic resonance imaging; or frequent, longer, and faster runs of non-sustained VT.[8][9] Other clinical features that are utilised in calculating sudden cardiac death risk in HCM include age, left atrial diameter, left ventricular outflow tract obstruction, and exercise blood pressure response.
Congenital arrhythmia syndromes, including symptomatic patients with long QT syndrome and Brugada syndrome.
ICDs are highly effective in terminating sustained ventricular arrhythmias. These devices provide a continuous monitor for the cardiac rhythm and the capability of terminating VT by overdrive pacing and/or cardioversion/defibrillation. Multiple clinical trials have shown the ICDs to be more effective than anti-arrhythmic medications in reducing total mortality for cardiac arrest survivors, especially in the setting of coronary artery disease. It is understood that ICD programming can affect not only frequency of ICD therapies (including anti-tachycardia pacing and ICD shocks) but also inappropriate therapies (i.e., those for rhythms other than ventricular tachyarrhythmias) and mortality rates.[44][45] It should be emphasised that these trials excluded patients with reversible causes of cardiac arrest, including toxic/metabolic abnormalities, trauma, and acute ischaemia. ICD implantation is not indicated in such cases when correction of the disorder is considered feasible and likely to substantially reduce the risk of recurrence.
Although an invasive procedure, ICD implantation is associated with a procedural mortality of only 0.02%. The long-term risks of ICD therapy include device malfunction, infection, and/or inappropriate shocks. Risk factors for infection include comorbid conditions such as diabetes and chronic obstructive pulmonary disease, as well as oral anticoagulation therapy and corticosteroid use. Measures such as antibiotic prophylaxis and good patient education on wound care can help reduce risk.[46] ICD shocks can be painful and if frequent may impair the patient's quality of life.[41][42][43][47]
Traditionally, ICDs have been implanted with a transvenous lead. However, a subcutaneous ICD, where the ICD lead remains extravascular, is also an option. An approved version involves an ICD lead tunnelled subcutaneously near the inferior border of the left rib cage and then up along the sternum, with the ICD generator located in the left axillary region.[19] Another extravascular ICD, involving a lead placed under the sternum, is being investigated.[20]
All currently available ICDs are capable of responding to arrhythmias in a tiered fashion. Transvenous ICDs are capable of anti-bradycardia pacing, anti-tachycardia pacing for VT, low-energy cardioversion for VT, and high-energy defibrillation for VF. ICDs detect arrhythmias primarily on the basis of heart rate. Thus, they will not intervene in the case of VT below the programmed rate and may inappropriately intervene in the case of supraventricular arrhythmias with a rapid ventricular response.
Appropriate use guidelines are available with respect to ICD implantation for both primary and secondary prevention, including use of cardiac resynchronisation devices.[48][49]
Adjunctive therapies in high-risk patients already implanted with an ICD or for whom ICD therapy is not an option
Anti-arrhythmic drugs may be useful as adjunctive therapies for high-risk patients already implanted with an ICD or for whom ICD therapy is not an option.[7] However, it should be emphasised that with the notable exception of beta-blockers, randomised trials have shown that currently available oral anti-arrhythmic drugs do not prolong life when used chronically in the treatment of life-threatening ventricular arrhythmias and sudden death.[7] Some anti-arrhythmic medications may not be appropriate for patients with structural heart disease because they have negative inotropic properties and may increase the risk of VT. It is important to be aware that amiodarone can increase defibrillation thresholds and, therefore, potentially impair ICD function.[50]
Catheter ablation may also be used as a palliative measure in patients with structural heart disease experiencing recurrent episodes of VT. Catheter ablation has also been shown to decrease appropriate ICD therapies, including ICD shocks.[37][51][52]
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