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Ventricular Arrhythmias

State of the Art
Published:August 12, 2013DOI:https://doi.org/10.1016/j.ccl.2013.07.007

      Keywords

      Key points

      • Wide complex tachycardia in patients with structural heart disease is most likely ventricular tachycardia (VT), but the 12-lead electrocardiogram should be systematically analyzed for confirmation.
      • Direct current cardioversion or infusion of intravenous amiodarone, procainamide, or lidocaine is usually successful for acutely terminating VT.
      • A combination of β-blockers and amiodarone is the most effective medical treatment for preventing recurrent VT after implantable cardioverter-defibrillator placement.
      • Catheter ablation is an effective treatment of recurrent VT despite antiarrhythmic therapy, but success rates vary depending on the mechanism and substrate of VT.
      • Electrical storm that continues despite defibrillation, β-blockade, and antiarrhythmics may respond to general anesthesia, left stellate ganglion blockade, hemodynamic support, or catheter ablation.

      Introduction

      Epidemiology of Ventricular Arrhythmias

      Sudden cardiac death (SCD) accounts for approximately 300,000 deaths in the United States per year and in most cases is the final result of ventricular tachycardia (VT) or ventricular fibrillation (VF).
      • Myerburg R.J.
      • Kessler K.M.
      • Castellanos A.
      Sudden cardiac death: epidemiology, transient risk, and intervention assessment.
      Ventricular arrhythmias must be recognized and treated promptly because of the high risk of acute mortality. In patients in the cardiac intensive care unit, 8% have episodes of nonsustained VT, 2% develop sustained VT, and 5% are treated for VF.
      • Ting P.
      • Chua T.S.
      • Wong A.
      • et al.
      Trends in mortality from acute myocardial infarction in the coronary care unit.
      SCD is a significant cause of long-term mortality in ischemic heart disease, accounting for 22% of all causes of death.
      • Jokhadar M.
      • Jacobsen S.J.
      • Reeder G.S.
      • et al.
      Sudden death and recurrent ischemic events after myocardial infarction in the community.
      Nonischemic conditions associated with VT, VF, and SCD include genetic conditions, cardiomyopathies, and idiopathic VT in structurally normal hearts. VT and VF can be challenging to manage, particularly if they recur despite initial therapy. The diversity of pharmacotherapy, devices, catheter ablation techniques, and other interventions increases the complexity of management.

      Prognostic Significance

      Sustained VT and VF have a high acute mortality and adversely affect long-term prognosis despite treatment. Even asymptomatic nonsustained VT confers higher long-term mortality if programmed stimulation induces sustained VT.
      • Buxton A.E.
      • Lee K.L.
      • DiCarlo L.
      • et al.
      Electrophysiologic testing to identify patients with coronary artery disease who are at risk for sudden death.
      VT or VF within 48 hours of the onset of an acute myocardial infarction (MI), although it significantly increases in-hospital mortality, does not adversely affect long-term prognosis.
      • Hohnloser S.H.
      • Kuch K.H.
      • Dorian P.
      • et al.
      Prophylactic use of an implantable cardioverter-defibrillator after acute myocardial infarction.
      VT or VF immediately after cardiac surgery not only increases in-hospital mortality
      • Pires L.A.
      • Hafley G.E.
      • Lee K.L.
      • et al.
      Prognostic significance of nonsustained ventricular tachycardia identified postoperatively after coronary artery bypass grafting in patients with left ventricular dysfunction.
      but also worsens long-term prognosis.
      • El-Chami M.F.
      • Sawaya F.J.
      • Kilgo P.
      • et al.
      Ventricular arrhythmia after cardiac surgery: incidence, predictors, and outcomes.

      Immediate considerations

      In patients with suspected VT, rapid but accurate recognition of the rhythm is imperative. Although treating hemodynamic instability is the first priority in patient care, hemodynamic instability does not confirm the diagnosis of VT. Wide complex tachycardia in patients with a history of coronary artery disease or structural heart disease is most likely VT; even so, the 12-lead electrocardiogram (ECG) must be systematically analyzed to reach the correct diagnosis. Other aspects of evaluating patients with VT are described in Table 1.
      Table 1Initial assessment of a patient with VT
      EvaluationAssessmentGoal
      Vital signsHemodynamic stabilityIf hemodynamically unstable, treat with urgent DCCV or defibrillation
      12-lead ECGTachycardia diagnosisDifferentiate VT from SVT with aberrancy; determine VT exit site
      HistorySymptoms (eg, chest pain indicating ongoing ischemia)Identify cause and triggers
      Current medicationsAntiarrhythmics, digoxin, QTc-prolonging medicationsIdentify pharmacologic contribution to a proarrhythmic state
      Family historyFamily history of SCDDetermine risk of inherited predisposition to SCD
      Physical examinationCanon A wavesIndicate AV dissociation
      Murmurs, sternotomy scarIndicate existing structural heart disease
      Laboratory testsElectrolytes, creatinine, troponin, thyroid-stimulating hormone, toxicology assaysIdentify metabolic, ischemic, or pharmacologic contributions to a proarrhythmic state
      ImagingChest roentgenography, echocardiographyIndicated in all patients with VT to assess for structural heart disease
      Coronary angiographyIndicated if VT occurs secondary to ischemia
      Computed tomography, magnetic resonance imagingIndicated in special cases when particular cardiomyopathies are suspected
      Abbreviations: A, atrial; AV, atrioventricular; DCCV, direct current cardioversion; QTc, corrected QT interval.
      Noncardiac artifact obscuring a narrow complex rhythm must be excluded. Then, the QRS complexes can be classified as monomorphic (constant in form) or polymorphic (variable in form). Polymorphic VT also requires analysis of the preceding rhythm. In the setting of a prolonged corrected QT interval (QTc), polymorphic VT is consistent with torsades de pointe (TdP)
      • Krikler D.M.
      • Curry P.V.
      Torsade de pointes, an atypical ventricular tachycardia.
      and usually initiates with a short cycle length after a prolonged cardiac cycle.
      • Kay G.N.
      • Plumb V.J.
      • Arciniegas J.G.
      • et al.
      Torsade de pointes: the long-short initiating sequence and other clinical features: observations in 32 patients.
      Several ECG features, summarized in Fig. 1, differentiate monomorphic VT from supraventricular tachycardia (SVT) with aberrant conduction. Particularly useful for differentiating VT from SVT with aberrancy are the validated criteria developed by Brugada and colleagues,
      • Brugada P.
      • Brugada J.
      • Mont L.
      • et al.
      A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex.
      which are 98.7% sensitive and 96.5% specific for VT and 96% sensitive and 98.7% specific for SVT with aberrancy. Fig. 2 shows the application of these criteria to an ECG showing VT.
      • Absence of an RS complex in the precordial leads: 100% specific for VT
      • RS interval (beginning of R to trough of S) greater than 100 milliseconds: 98% specific for VT
      • Atrioventricular dissociation: 98% specific for VT
      • Apply morphologic criteria to V1 and V6. If both leads are consistent with VT, then VT is diagnosed; otherwise, the rhythm is classified as SVT with aberrancy.
      Figure thumbnail gr1
      Fig. 1Criteria for diagnosing a wide QRS complex tachycardia as VT. AV, atrioventricular; LBBB, left bundle branch block; RBBB, right bundle branch block.
      Figure thumbnail gr2
      Fig. 212-lead ECG showing monomorphic VT. This ECG shows a regular monomorphic tachycardia with a wide QRS of 160 milliseconds and an atypical QRS morphology in the precordial leads. The Brugada criteria can be applied. Step 1: There is an R wave in V1, so continue to step 2. Step 2: the longest RS interval in a precordial lead is slightly more than 100 milliseconds in V5 and is thus consistent with VT, even although no atrioventricular dissociation (step 3) is visible. Step 4: R is greater than R′ in V1, and S is greater than R in V6, meeting morphologic criteria for VT in V1 and V6.
      After morphologic criteria are applied, SVT conducting through an accessory pathway remains difficult to distinguish from VT, even with additional criteria.
      • Steurer G.
      • Gürsoy S.
      • Frey B.
      • et al.
      The differential diagnosis on the electrocardiogram between ventricular tachycardia and preexcited tachycardia.
      The ECG is also useful for determining the exit site of VT
      • Segal O.R.
      • Chow A.W.
      • Wong T.
      • et al.
      A novel algorithm for determining endocardial VT exit site from 12-lead surface ECG characteristics in human, infarct-related ventricular tachycardia.
      and for distinguishing endocardial from epicardial origin.
      • Berruezo A.
      • Mont L.
      • Nava S.
      • et al.
      Electrocardiographic recognition of the epicardial origin of ventricular tachycardias.

      Nonpharmacologic therapeutic modalities

      External Defibrillation and Cardioversion

      Early defibrillation with a rectilinear biphasic automatic external defibrillator improves initial success of defibrillation for out-of-hospital VF arrest.
      • Morrison L.J.
      • Dorian P.
      • Long J.
      • et al.
      Out-of-hospital cardiac arrest rectilinear biphasic to monophasic dampened sine defibrillation waveforms with advanced life support intervention trial (ORBIT).
      Thus, national guidelines recommend early biphasic defibrillation for VF followed by epinephrine and amiodarone administration if the patient is difficult to defibrillate.
      • Zipes D.P.
      • Camm A.J.
      • Borggrede M.
      • et al.
      ACC/AHA/ESC 2006 guidelines 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 and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society.
      In VT, direct current cardioversion (DCCV) must be synchronized, because a shock occurring in a partially repolarized ventricle precipitates VF. In polymorphic VT, defibrillation is required, because synchronization is usually not possible. For comfort, hemodynamically stable conscious patients should be sedated before synchronized DCCV.
      • Biphasic waveform defibrillation improves initial success of defibrillation.
      • In VT, unsynchronized DCCV can precipitate VF.

      Implantable Cardioverter-Defibrillator and Pacing

      Numerous trials have shown the importance of implantable cardioverter-defibrillator (ICD) placement in high-risk patients to prevent SCD.
      • Moss A.J.
      • Hall J.
      • Cannom D.S.
      • et al.
      Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia.
      • Moss A.J.
      • Zareba W.
      • Hall J.
      • et al.
      Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction.
      • Bardy G.H.
      • Lee K.L.
      • Mark D.B.
      • et al.
      Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure.
      • Kadis A.
      • Dyer A.
      • Daubert J.P.
      • et al.
      Prophylactic defibrillator implantation in patients with nonischemic dilated cardiomyopathy.
      The ICD treats but does not prevent recurrent VT. Because ICD shocks cause significant discomfort, inappropriate shocks should be acutely stopped by placing a magnet over the device while awaiting reprogramming. The ICD also can perform antitachycardia pacing, which creates a paced wavefront that collides with the VT wavefront and terminates it.
      • ICD implantation significantly reduces mortality from SCD in high-risk patients.
      • Inappropriate ICD therapy can be halted by applying a magnet over the device.

      Left Cardiac Sympathetic Denervation

      Left stellate ganglion resection completely removes sympathetic input to the heart. It effectively prevents VT that recurs despite β-blockade in long QT syndrome (LQTS),
      • Schwartz P.J.
      • Priori S.G.
      • Cerrone M.
      • et al.
      Left cardiac sympathetic denervation in the management of high-risk patients affected by the long-QT syndrome.
      catecholaminergic polymorphic VT (CPVT), and other types of VT.
      • Coleman M.A.
      • Bos M.
      • Johnson J.N.
      • et al.
      Videoscopic left cardiac sympathetic denervation for patients with recurrent ventricular fibrillation/malignant ventricular arrhythmia syndromes besides congenital long-QT syndrome.
      Stellate ganglion blockade with lidocaine injection is feasible in unstable patients with electrical storm (ES).
      • Nademanee K.
      • Taylor R.
      • Bailey W.E.
      • et al.
      Treating electrical storm: sympathetic blockade versus advanced cardiac life support–guided therapy.

      Radiofrequency Catheter Ablation

      Catheter ablation techniques are rapidly advancing. VT is mapped by entrainment, pacing, or an electroanatomic system that determines catheter position in a magnetic field.
      • Nademanee K.
      • Kosar E.M.
      A nonfluoroscopic catheter-based mapping technique to ablate focal ventricular tachycardia.
      Radiofrequency current ablates the endocardium identified as part of the reentry circuit.
      • Stevenson W.G.
      • Kahn H.
      • Sager P.
      • et al.
      Identification of reentry circuit sites during catheter mapping and radiofrequency ablation of ventricular tachycardia late after myocardial infarction.
      Another technique, substrate ablation, identifies slow conduction zones around myocardial scars and isolated potentials; these areas are ablated to prevent VT.
      • Arenal A.
      • Hernandez J.
      • Calvo D.
      • et al.
      Safety, long-term results, and predictors of recurrence after complete endocardial ventricular tachycardia substrate ablation in patients with previous myocardial infarction.
      The 24-month rate of freedom from recurrent VT or VF after catheter ablation is 48% to 88% in recent trials.
      • Delacrétaz E.
      • Brenner R.
      • Schaumann A.
      • et al.
      Catheter ablation of stable ventricular tachycardia before defibrillator implantation in patients with coronary heart disease (VTACH): an on-treatment analysis.
      • Reddy V.Y.
      • Reynolds M.R.
      • Neuzil P.
      • et al.
      Prophylactic catheter ablation for the prevention of defibrillator therapy.
      VT from the left ventricular endocardium can be ablated via either transseptal access from the left atrium or retrograde arterial access through the aortic valve. If a patient fails endocardial ablation or has an epicardial site of VT origin, epicardial ablation can be performed through percutaneous pericardial access or surgical thoracotomy.
      • Della Bella P.
      • Brugada J.
      • Zeppenfeld K.
      • et al.
      Epicardial ablation for ventricular tachycardia: a European multicenter study.
      Rarely, if both endocardial and epicardial ablation fail or are not possible, ethanol injection in distal coronary arteries may successfully ablate midmyocardial sites; but this technique should be reserved for refractory cases because of the low success rate and risk of complications from the ethanol-induced infarction.
      • Tokuda M.
      • Sobieszczyk P.
      • Eisenhauer A.C.
      • et al.
      Transcoronary ethanol ablation for recurrent ventricular tachycardia after failed catheter ablation: an update.
      Intracardiac echocardiography is integrated with electroanatomic mapping, reducing fluoroscopy time.
      • Khaykin Y.
      • Skanes A.
      • Whaley B.
      • et al.
      Real-time integration of 2D intracardiac echocardiography and 3D electroanatomical mapping to guide ventricular tachycardia ablation.
      Cryoablation can be performed to reduce the risk of permanent damage when ablation is performed near a coronary artery or the phrenic nerve.
      • Di Biase L.
      • Al-Ahamad A.
      • Santeangeli P.
      • et al.
      Safety and outcomes of cryoablation for ventricular tachyarrhythmias: results from a multicenter experience.
      Potential complications include a 2.8% risk of thrombosis, which increases with more extensive ablations but is reduced by irrigated catheters, antiplatelet medications, intraprocedural anticoagulation, and intracardiac echocardiography.
      • Zhou L.
      • Keane D.
      • Reed G.
      • et al.
      Thromboembolic complications of cardiac radiofrequency catheter ablation: a review of the reported incidence, pathogenesis, and current research directions.
      There is a 1% risk of perforation and pericardial tamponade during endocardial ablation
      • Tokuda M.
      • Kojodjojo P.
      • Epstein L.M.
      • et al.
      Outcomes of cardiac perforation complicating catheter ablation of ventricular arrhythmias.
      and 3.4% during epicardial ablation.
      • Della Bella P.
      • Brugada J.
      • Zeppenfeld K.
      • et al.
      Epicardial ablation for ventricular tachycardia: a European multicenter study.
      Intracardiac echocardiography
      • Ren J.F.
      • Marchlinski F.E.
      Early detection of iatrogenic pericardial effusion: importance of intracardiac echocardiography.
      and fluoroscopic evaluation of the cardiac silhouette
      • Nanthakumar K.
      • Kay G.N.
      • Plumb V.J.
      • et al.
      Decrease in fluoroscopic cardiac silhouette excursion precedes hemodynamic compromise in intraprocedural tamponade.
      are important means of early detection of an accumulating pericardial effusion during ablation. If a large effusion develops, or if epicardial ablation is performed, a pericardial drain is placed until it drains less than 20 mL over 4 to 6 hours. Anticoagulation postprocedure is initiated for patients requiring extensive ablation, patients with atrial fibrillation or severely reduced ejection fraction, or patients who have a hemodynamic support or ventricular assist device (VAD). Antiarrhythmic medications are continued unless the patient experiences marked adverse effects from them. Intensive care unit admission postprocedure is recommended for patients requiring a prolonged procedure (>6 hours), patients requiring an intra-aortic balloon pump or a percutaneous hemodynamic support device such as an Impella (Abiomed, Danvers, MA), patients with a pericardial drain, patients with recurrent VT after unsuccessful ablation, and patients with significant fluid overload after a procedure.

      Pharmacotherapy

      Intravenous Medications for Acute Management

      Procainamide blocks both sodium and potassium channels, slowing and terminating VT. As a negative inotrope, it can cause hypotension; therefore, it is recommended for stable VT in patients with normal systolic function. Lidocaine is a sodium channel blocker that is potentially effective for VT during acute ischemia. Amiodarone has a complex mechanism of action and is superior to lidocaine for treating shock-resistant VF
      • Dorian P.
      • Cass D.
      • Schwartz B.
      • et al.
      Amiodarone as compared with lidocaine for shock-resistant ventricular fibrillation.
      and VT refractory to procainamide.
      • Leak D.
      • Eydt J.N.
      Control of refractory cardiac arrhythmias with amiodarone.
      It shows significant long-term thyroid, pulmonary, and hepatic toxicities, which should be considered before initiating long-term oral therapy. Table 2 lists the recommended dosing and acute adverse effects of these medications.
      • Procainamide is preferred for pharmacologic cardioversion of stable VT in patients with normal systolic function.
      • Lidocaine is useful for VT during acute ischemia; it does not cause QTc prolongation.
      • Amiodarone is the most effective antiarrhythmic for VT but requires time to load.
      Table 2Acute and maintenance dosing of intravenous antiarrhythmic medications
      AntiarrhythmicDosingAcute Adverse Reactions
      ProcainamideLoad: 17 mg/kg

      Maximum rate: 50 mg/min

      Maintenance: 1–4 mg/min
      Hypotension

      Hold if QRS prolongs >50%
      LidocaineLoad: 1–3 mg/kg

      Rate: 20–50 mg/min

      Maintenance: 1–4 mg/min
      Reduce dose in heart failure

      Monitor for neurotoxicity: delirium, seizures, or paresthesias
      AmiodaroneLoad: 150 mg over 10 min if blood pressure is normal; 300 mg over 19 min if hypotensive

      Maintenance: 1 mg/min for 6 h, then 0.5 mg/min for 18 h
      Caution in cardiogenic shock

      TdP is rare

      Use with pacing if patient is severely bradycardic

      Long-Term Oral Therapy

      In a randomized controlled trial of sotalol, amiodarone with β-blockers, or β-blockers alone, amiodarone with a β-blocker (metoprolol, carvedilol, or bisoprolol) significantly reduced defibrillator shocks more than sotalol or β-blockers alone.
      • Connolly S.J.
      • Dorian P.
      • Roberts R.S.
      • et al.
      Comparison of beta blockers, amiodarone plus beta blockers, or sotalol for prevention of shocks from implantable cardioverter defibrillators: the OPTIC study: a randomized trial.
      There was no significant mortality difference, and in patients receiving amiodarone, 5% experienced pulmonary adverse events and 5.7% developed thyroid abnormalities. β-Blockers by themselves reduce SCD in patients with MI
      • Piccini J.P.
      • Hraniztky P.M.
      • Kilaru R.
      • et al.
      Relation of mortality to failure to prescribe beta blockers acutely in patients with sustained ventricular tachycardia and ventricular fibrillation following acute myocardial infarction.
      and improve survival in patients with treated VT or VF.
      • Exner D.V.
      • Reiffel J.A.
      • Epstein A.E.
      • et al.
      Beta-blocker use and survival in patients with ventricular fibrillation or symptomatic ventricular tachycardia: the antiarrhythmics versus implantable defibrillators (AVID) trial.
      • A combination of β-blockers and amiodarone is the most successful long-term medical strategy for reducing defibrillator shocks.
      • β-blockers improve survival in patients after VT or VF is treated.
      Although right ventricular outflow tract (RVOT) and left ventricular outflow tract (LVOT) VT are typically sensitive to diltiazem and verapamil,
      • Gill J.S.
      • Ward D.E.
      • Camm A.J.
      Comparison of verapamil and diltiazem in the suppression of idiopathic ventricular tachycardia.
      giving calcium channel blockers acutely during VT when the mechanism of VT is unknown is contraindicated because of the risk of hemodynamic collapse.
      • Zipes D.P.
      • Camm A.J.
      • Borggrede M.
      • et al.
      ACC/AHA/ESC 2006 guidelines 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 and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society.
      Other oral antiarrhythmics may suppress VT that recurs despite treatment with sotalol or amiodarone with β-blockers. Mexiletine is a sodium channel blocker that counteracts the sodium channel gain-of-function mutation in LQTS type 3. Quinidine has a significant side effect profile but may be particularly effective in Brugada syndrome. Flecainide and other class 1C sodium channel blockers are associated with increased mortality in patients with coronary artery disease.
      • Epstein A.E.
      • Hallstrom A.P.
      • Rogers W.J.
      • et al.
      Mortality following ventricular arrhythmia suppression by encainide, flecainide, and moricizine after myocardial infarction.
      However, flecainide can be used in VT associated with structurally normal hearts.
      • Gill J.S.
      • Mehta D.
      • Ward D.E.
      • et al.
      Efficacy of flecainide, sotalol, and verapamil in the treatment of right ventricular tachycardia in patients without overt cardiac abnormality.
      Dofetilide and ranolazine are not approved to treat ventricular arrhythmias but have significantly reduced recurrent VT and VF in small studies.
      • Baquero G.A.
      • Banchis J.E.
      • Depalma S.
      • et al.
      Dofetilide reduces the frequency of ventricular arrhythmias and implantable cardioverter defibrillator therapies.
      • Bunch T.J.
      • Mahapatra S.
      • Murdock D.
      • et al.
      Ranolazine reduces ventricular tachycardia burden and ICD shocks in patients with drug-refractor ICD shocks.

      VT in patients with structural heart disease

      VT in Patients with Acute MI

      Acute MI significantly increases the risk for VT and VF. Ischemia prolongs the QTc and can trigger polymorphic VT.
      • Wolfe C.L.
      • Nibley C.
      • Bahndari A.
      • et al.
      Polymorphous ventricular tachycardia associated with acute myocardial infarction.
      Acutely, polymorphic VT requires defibrillation, because it is unlikely to allow hemodynamic stability. The patient should then receive urgent coronary reperfusion and other evidence-based therapies for MI. Both lidocaine and amiodarone are used for VT; neither is clearly superior to the other.
      • Piccini J.P.
      • Schulte P.J.
      • Pieper K.S.
      • et al.
      Antiarrhythmic drug therapy for sustained ventricular arrhythmias complicating acute myocardial infarction.
      Lidocaine should not be used prophylactically in patients with MI.
      • Zipes D.P.
      • Camm A.J.
      • Borggrede M.
      • et al.
      ACC/AHA/ESC 2006 guidelines 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 and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society.
      Neither long-term antiarrhythmics nor ICD placement are required for VT during acute MI.
      • Hohnloser S.H.
      • Kuch K.H.
      • Dorian P.
      • et al.
      Prophylactic use of an implantable cardioverter-defibrillator after acute myocardial infarction.

      VT in Revascularized Patients with Ischemic Cardiomyopathy

      Numerous trials show that ICD implantation decreases mortality in patients with ischemic cardiomyopathy at high risk.
      • Moss A.J.
      • Hall J.
      • Cannom D.S.
      • et al.
      Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia.
      • Moss A.J.
      • Zareba W.
      • Hall J.
      • et al.
      Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction.
      • Bardy G.H.
      • Lee K.L.
      • Mark D.B.
      • et al.
      Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure.
      In patients with VT occurring 1 month or more after MI, recurrence can be successfully prevented with catheter ablation before initiation of long-term antiarrhythmics.
      • Reddy V.Y.
      • Reynolds M.R.
      • Neuzil P.
      • et al.
      Prophylactic catheter ablation for the prevention of defibrillator therapy.
      • Kuck K.H.
      • Schaumann A.
      • Eckardt L.
      • et al.
      Catheter ablation of stable ventricular tachycardia before defibrillator implantation in patients with coronary heart disease (VTACH): a multicentre randomized controlled trial.
      • Catheter ablation of VT before initiation of long-term antiarrhythmic therapy is reasonable in patients with sustained VT and a previous MI.

      VT in Patients with Nonischemic Cardiomyopathy

      The mechanisms of VT in nonischemic cardiomyopathy are diverse, including bundle branch reentry, reentry around fibrosis, activation around focal inflammation (as in sarcoidosis), and epicardial involvement. Acutely, VT should be treated with DCCV and amiodarone, because most other antiarrhythmics are negative inotropes. VT with a typical bundle branch block should be evaluated for bundle branch reentry tachycardia, because ablation of the right bundle branch successfully treats bundle branch reentry.
      • Balasundaram R.
      • Rao H.B.
      • Kalavakolanu S.
      • et al.
      Catheter ablation of bundle branch reentrant ventricular tachycardia.
      Catheter ablation for recurrent VT in patients with dilated cardiomyopathy, arrhythmogenic right ventricular dysplasia (ARVD), hypertrophic cardiomyopathy, or cardiac sarcoidosis is associated with variable success rates.
      • Arya A.
      • Bode K.
      • Piorkowski C.
      • et al.
      Catheter ablation of electrical storm due to monomorphic ventricular tachycardia in patients with nonischemic cardiomyopathy: acute results and its effect on long-term survival.
      • Philips B.
      • Madhavan S.
      • James C.
      • et al.
      Outcomes of catheter ablation of ventricular tachycardia in arrhythmogenic right ventricular dysplasia/cardiomyopathy.
      • Santangeli P.
      • Di Biase L.
      • Lakkireddy D.
      • et al.
      Radiofrequency catheter ablation of ventricular arrhythmias in patients with hypertrophic cardiomyopathy: safety and feasibility.
      • Jefic D.
      • Joel B.
      • Good E.
      • et al.
      Role of radiofrequency catheter ablation of ventricular tachycardia in cardiac sarcoidosis: report from a multicenter registry.
      • Catheter ablation of VT in nonischemic cardiomyopathy has variable success rates depending on the mechanism and substrate of VT.

      VT in Patients After Cardiac Surgery

      VT and VF occur in some patients immediately after coronary artery bypass grafting and valvular surgeries. Sympathetic stimulation, electrolyte abnormalities, ischemia from vein graft closure, atrial dysrhythmias, injury from cannulation, and preexisting substrate all contribute to initiation of VT. Prophylactic amiodarone prevents both atrial arrhythmias and VT,
      • Mitchell L.B.
      • Exner D.V.
      • Wyse D.G.
      • et al.
      Prophylactic oral amiodarone for the prevention of arrhythmias that begin early after revascularization, valve replacement, or repair.
      although no mortality benefit has been shown.
      • Aasbo J.D.
      • Lawrence A.T.
      • Krishnan K.
      • et al.
      Amiodarone prophylaxis reduces major cardiovascular morbidity and length of stay after cardiac surgery: a meta-analysis.
      VT after cardiac surgery increases both in-hospital and long-term mortality,
      • El-Chami M.F.
      • Sawaya F.J.
      • Kilgo P.
      • et al.
      Ventricular arrhythmia after cardiac surgery: incidence, predictors, and outcomes.
      but ICD placement is not indicated.
      • Bigger J.T.
      Prophylactic use of implanted cardiac defibrillators in patients at high risk for ventricular arrhythmias after coronary-artery bypass graft surgery.
      • Amiodarone prophylaxis reduces postoperative VT and VF.

      VT in Patients with VADs

      Increasing numbers of patients with advanced heart failure are being supported with VADs. In these patients, VT and VF cause hemodynamic instability from right heart failure, reducing left ventricular preload, which can cause a suction event. Catheter ablation in patients with a VAD is feasible; mapping has shown that VT originates from the scar in 75% of patients and less commonly from the inflow cannula site.
      • Cantillon D.J.
      • Bianoc C.
      • Wazni O.M.
      • et al.
      Electrophysiologic characteristics and catheter ablation of ventricular tachyarrhythmias among patients with heart failure on ventricular assist device support.
      • VT in patients with a VAD comes predominantly from the preexisting substrate rather than from the inflow cannula site.

      VT in Patients After Orthotopic Heart Transplantation

      VT in orthotopic heart transplant recipients is rare, and acute rejection must be ruled out. β-Blockers should be used cautiously after heart transplantation because of the risk of sinus node dysfunction.
      • Stecker E.C.
      • Strelich K.R.
      • Chugh S.S.
      • et al.
      Arrhythmias after orthotopic heart transplantation.
      Amiodarone, lidocaine, and mexiletine have been used for VT in heart transplant patients.
      • Kertesz N.J.
      • Towbin J.A.
      • Clunie S.
      • et al.
      Long-term follow-up of arrhythmias in pediatric orthotopic heart transplant recipients: incidence and correlation with rejection.
      • Rejection must be ruled out in patients with orthotopic heart transplantation and VT.

      VT in Patients with Congenital Heart Disease

      Any congenital anomaly involving the ventricles predisposes patients to VT, especially tetralogy of Fallot, transposition of the great arteries, single ventricle, and congenital aortic stenosis. The predominant mechanism is reentry around fibrosis and surgical scar, which is responsive to catheter ablation.
      • Ventura A.
      • Soriano L.
      • Lopez M.
      Ventricular tachycardia ablation in repaired tetralogy of Fallot.

      VT in patients with structurally normal hearts

      VT in Patients with Brugada Syndrome

      Brugada syndrome is diagnosed by coved ST segment increase in leads V1 to V3 either spontaneously or provoked by sodium channel blockade. Fig. 3 shows an ECG consistent with Brugada syndrome. Impaired sodium channel function prolongs the epicardial action potential, reversing the direction of repolarization and predisposing the ventricle to reentry. Isoproterenol prevents recurrent VT by increasing calcium current and should be titrated to increase the heart rate by 20% and to normalize the ST segments.
      • Ohgo T.
      • Okamura H.
      • Noda T.
      • et al.
      Acute and chronic management in patients with Brugada syndrome associated with electrical storm of ventricular fibrillation.
      Quinidine prevents recurrent VF by normalizing the direction of repolarization.
      • Berne P.
      • Brugada J.
      Brugada syndrome 2012.
      • In patients with Brugada syndrome presenting with VT, isoproterenol infusion should be initiated after DCCV and titrated until the ST segments normalize.
      Figure thumbnail gr3
      Fig. 312-lead ECG showing coved ST segment elevation in leads V1 to V3 in a patient with Brugada syndrome.

      VT in Patients with TdP

      TdP is polymorphic VT in the setting of a prolonged QTc in which a premature ventricular depolarization follows a prolonged cardiac cycle, as in Fig. 4.
      • Kay G.N.
      • Plumb V.J.
      • Arciniegas J.G.
      • et al.
      Torsade de pointes: the long-short initiating sequence and other clinical features: observations in 32 patients.
      TdP can be secondary to electrolyte abnormalities, bradyarrhythmias, or medication effects. After defibrillation, temporarily pacing faster than the intrinsic rate prevents long-short cycles from occurring, and pacing is more successful than isoproterenol and lidocaine in preventing recurrent TdP.
      • Kay G.N.
      • Plumb V.J.
      • Arciniegas J.G.
      • et al.
      Torsade de pointes: the long-short initiating sequence and other clinical features: observations in 32 patients.
      Drugs that prolong the QTc must be discontinued, and potassium and magnesium levels must be maintained in normal ranges.
      • Pacing prevents recurrent TdP while awaiting clearance of offending medications.
      Figure thumbnail gr4
      Fig. 412-lead ECG showing the initiation of TdP with a long-short sequence occurring in the setting of a prolonged QT interval.

      VT in Patients with Congenital LQTS

      Congenital LQTS is caused by one of many mutations affecting repolarization. β-Blockers are an essential therapy for most types, and mexiletine is useful in LQTS type 3. Treatment of VT in LQTS requires pacing after DCCV; isoproterenol in patients with LQTS is potentially harmful and can precipitate recurrent VT. Permanent pacemaker placement may be required in LQTS to allow the use of adequate doses of β-blockers.
      • Khan I.A.
      • Gowda R.M.
      Novel therapeutics for treatment of long-QT syndrome and torsade de pointes.
      Left stellate ganglion resection is 91% effective for preventing recurrent VT.
      • Schwartz P.J.
      • Priori S.G.
      • Cerrone M.
      • et al.
      Left cardiac sympathetic denervation in the management of high-risk patients affected by the long-QT syndrome.
      • β-blockade combined with pacing prevents recurrent VT in LQTS.

      VT in Patients with CPVT

      CPVT occurs when a mutant ryanodine receptor allows calcium to leak into the cytoplasm and cause delayed afterdepolarizations. β-Blockers are essential but may not prevent recurrent VT in all patients, and many patients require an ICD.
      • Marks A.R.
      Sudden unexplained death caused by cardiac ryanodine receptor (RyR2) mutations.
      Left stellate ganglion resection is particularly effective for preventing recurrent VT.
      • Coleman M.A.
      • Bos M.
      • Johnson J.N.
      • et al.
      Videoscopic left cardiac sympathetic denervation for patients with recurrent ventricular fibrillation/malignant ventricular arrhythmia syndromes besides congenital long-QT syndrome.

      VT in Patients with Idiopathic VT

      VT occurring in the absence of structural heart disease, metabolic or pharmacologic provocation, or ion channel dysfunction is considered idiopathic. Idiopathic VT most commonly originates in the RVOT or LVOT and is suppressed by diltiazem or verapamil.
      • Gill J.S.
      • Ward D.E.
      • Camm A.J.
      Comparison of verapamil and diltiazem in the suppression of idiopathic ventricular tachycardia.
      Structural heart disease (particularly ARVD causing right ventricular VT) must be carefully excluded. Catheter ablation is often successful in treating recurrent VT. Idiopathic VT rarely causes hemodynamic compromise or SCD and is unlikely to present to the cardiac intensive care unit.
      • Patients with RVOT VT should be evaluated to exclude ARVD.

      ES

      ES is defined as 3 or more episodes of VT or VF within 24 hours; electrical stability deteriorates rapidly, causing high mortality. A diversity of substrates and triggers can cause ES, and no single therapy is effective in all patients. VT refractory to 1 antiarrhythmic may be suppressed by another. After DCCV or defibrillation, amiodarone infusion is typically begun,
      • Dorian P.
      • Cass D.
      • Schwartz B.
      • et al.
      Amiodarone as compared with lidocaine for shock-resistant ventricular fibrillation.
      • Leak D.
      • Eydt J.N.
      Control of refractory cardiac arrhythmias with amiodarone.
      to which a sodium channel blocker can be added if VT recurs. β-Blockade with esmolol, metoprolol, or propranolol can be titrated as blood pressure tolerates. In patients unable to tolerate β-blockade, sympathetic input to the heart can be blocked centrally with general anesthesia such as propofol
      • Mulpuru S.K.
      • Patel D.V.
      • Wilbur S.L.
      • et al.
      Electrical storm and termination with propofol therapy: a case report.
      and peripherally with injection of the left stellate ganglion with lidocaine.
      • Nademanee K.
      • Taylor R.
      • Bailey W.E.
      • et al.
      Treating electrical storm: sympathetic blockade versus advanced cardiac life support–guided therapy.
      In some patients, percutaneous hemodynamic support with Impella (Abiomed, Danvers, MA) or TandemHeart (CardiacAssist, Pittsburgh, PA) is necessary.
      • Abuissa H.
      • Roshan J.
      • Lim B.
      • et al.
      Use of the Impella microaxial blood pump for ablation of hemodynamically unstable ventricular tachycardia.
      Fig. 5 shows Impella placement. Catheter ablation is successful for terminating ES in 48% of patients after the first ablation and in 84% after multiple attempts.
      • Kozeluhova M.
      • Peichl P.
      • Cihak R.
      • et al.
      Catheter ablation of electrical storm in patients with structural heart disease.
      Fig. 6 shows an algorithm for treating ES.
      Figure thumbnail gr5
      Fig. 5Use of an Impella device for percutaneous hemodynamic support in a patient with intractable VT. The arrow indicates the tip of the Impella catheter within the left ventricle. A defibrillator lead is also seen in the right ventricular apex.
      Figure thumbnail gr6
      Fig. 6Therapeutic protocol for treating ES. IV, intravenous.

      Summary

      VT and VF commonly occur in the cardiac intensive care unit but have many potential causes. Acutely, synchronized DCCV or pharmacologic cardioversion likely terminate VT, but definitive treatment is complex. Determining the cause, correcting reversible causes, and defining the substrate are the goals of initial evaluation. ICD programming, β-blockers, antiarrhythmics, and catheter ablation should be considered to prevent recurrence. For patients with ES, additional modalities, including general anesthesia, left stellate ganglion blockade, hemodynamic support, and additional catheter ablation, may be considered.

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