We are IntechOpen, the world’s leading publisher of Open Access books Built by scientists, for scientists 6,300 170,000 190M Open access books available International authors and editors Downloads Our authors are among the 154 TOP 1% 12.2% Countries delivered to most cited scientists Contributors from top 500 universities Selection of our books indexed in the Book Citation Index in Web of Science™ Core Collection (BKCI) Interested in publishing with us? Contact [email protected] Numbers displayed above are based on latest data collected. For more information visit www.intechopen.com Chapter 5 Treatment of Ventricular Arrhythmias Wilbert S. Aronow Additional information is available at the end of the chapter http://dx.doi.org/10.5772/57545 1. Introduction The presence of 3 or more consecutive ventricular premature complexes (VPCs) on an elec‐ trocardiogram is ventricular tachycardia (VT) [1, 2]. VT is sustained if it lasts ≥30 seconds and nonsustained if its lasts <30 seconds [2]. Complex ventricular arrhythmias (VA) are VT or paired, multiform, or frequent VPCs. This author diagnoses frequent VPCs if there are an average of ≥30/hour on a 24-hour ambulatory electrocardiogram (AECG) or ≥6/minute on a 1-minute rhythm strip of an electrocardiogram (ECG) [2, 3]. Simple VA are infrequent VPCs and no complex forms. The prevalence of nonsustained VT diagnosed by 24-hour AECGs varied from 2% to 13% in older persons without cardiovascular disease [1, 4-7], was 9% in 385 older men and 8% in 806 older women with hypertension, valvular disease, or cardiomyopathy [7], and was 16% in 395 older men and 15% in 771 older women with coronary artery disease (CAD) [7]. The prevalence of complex VA in older persons in these studies varied from 16% to 50% in older persons without cardiovascular disease [1, 4-7], was 54% in older men and 55% in older women with hypertension, valvular disease, or cardiomyopathy [7], and was 69% in older men and 68% in older women with CAD [7]. In 104 older persons without cardiovascular disease, complex VA were present on 24-hour AECGs in 33% of persons and on 1-minute rhythm strips in 2% of persons [3]. In 843 older persons, with cardiovascular disease, complex VA were present on 24-hour AECGs in 55% of persons and on 1-minute rhythm strips in 4% of persons [3]. In persons with cardiovascular disease, those with an abnormal left ventricular (LV) ejection fraction [8], with echocardiographic LV hypertrophy [9], or with silent myocardial ischemia [10] have a higher prevalence of VT and of complex VA than those with normal LV ejection fraction, normal LV mass, and no myocardial ischemia. © 2014 Aronow; licensee InTech. This is a paper distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. 112 Cardiac Arrhythmias - Mechanisms, Pathophysiology, and Treatment 2. Prognosis of ventricular arrhythmias In the Baltimore Longitudinal Study of Aging, nonsustained VT or complex VA were not as‐ sociated with new coronary events at 10-year follow-up of 98 persons without heart disease [11]. In this study, exercise-induced nonsustained VT was not associated with new coronary events at 2-year follow-up in persons without heart disease [12]. At 5.6-year follow-up in this study, exer‐ cise-induced frequent or repetitive VPCs also were not associated with new coronary events in persons without heart disease [13]. Nonsustained VT or complex VA diagnosed by 24-hour AECGs were not associated with new coronary events at 2-year follow-up in 76 persons without heart disease [14] and were not associated with primary ventricular fibrillation (VF) or sudden cardiac death in 86 per‐ sons without heart disease [15]. Complex VA diagnosed by 24-hour AECGs or by 12-lead ECGs with 1-minute rhythm strips were also not associated with new coronary events at 39- month follow-up in 104 persons without heart disease [3]. Nonsustained VT or complex VA diagnosed by 24-hour AECGs were not associated with new coronary events at 45-month follow-up of 135 men and at 47-month follow-up of 297 women without cardiovascular dis‐ ease [7]. Because nonsustained VT or complex VA are not associated with new coronary events in persons without heart disease, asymptomatic nonsustained VT or complex VA in persons without heart disease should not be treated with antiarrhythmic drugs. Because simple VA in persons with heart disease are not associated with new coronary events [3, 7, 11, 14, 15], simple VA in older persons with heart disease should not be treated with antiarrhythmic drugs. However, patients with VT (sustained or nonsustained) or with complex VA associated with heart disease are at increased risk for developing new coronary events, primary VF, and sudden cardiac death [3, 7, 11, 14-19]. 3. Medical therapy Underlying causes of complex VA should be treated, if possible. Therapy of congestive heart failure (CHF), digitalis toxicity, hypokalemia, hypomagnesemia, hypertension, LV dysfunc‐ tion, LV hypertrophy, myocardial ischemia by anti-ischemic drugs such as beta blockers or by coronary revascularization, hypoxia, and other conditions may abolish or decrease com‐ plex VA. Persons should not smoke or drink alcohol and should avoid drugs that may cause or increase complex VA. CAD should be treated with aspirin [20-23], with beta blockers [23-28], with angiotensin- converting enzyme (ACE) inhibitors [23, 28-33], and with 3-hydroxy-3-methylglutaryl coen‐ zyme A reductase inhibitors (statins) [23, 34-40] unless there are contraindications to these Treatment of Ventricular Arrhythmias 113 http://dx.doi.org/10.5772/57545 drugs. The serum low-density lipoprotein (LDL) cholesterol level should be reduced ≥ 50% by high-dose statins (atorvastatin 40to 80 mg daily or rosuvastatin 20 to 40 mg daily) [40]. Age-related physiologic changes may affect absorption, distribution, metabolism, and excre‐ tion of cardiovascular drugs [41]. Numerous physiologic changes with aging affect pharma‐ codynamics with alterations in end-organ responsiveness to cardiovascular drugs [41]. Drug interactions between antiarrhythmic drugs and other cardiovascular drugs are common [41]. There are also important drug-disease interactions [41]. Class I antiarrhythmic drugs have an unacceptable proarrhythmia rate in patients with heart disease and should be avoided. Class III antiarrhythmic drugs should also be used with caution in patients with heart disease since multiple factors may increase proarrhythmia. Except for beta blockers, all antiarrhythmic drugs may cause torsades de pointes (VT with polymorphous appearance associated with prolonged QT interval). Class I antiarrhythmic drugs are sodium channel blockers. Class Ia antiarrhythmic drugs have intermediate channel kinetics and prolong repolarization. These drugs include quini‐ dine, procainamide, and disopyramide. Class Ib antiarrhythmic drugs have rapid channel kinetics and slightly shorten repolarization. These drugs include lidocaine, mexilitine, tocai‐ nide, and phenytoin. Class Ic drugs have slow channel kinetics and have little effect on repo‐ larization. These drugs include encainide, flecainide, moricizine, propafenone, and lorcainide. None of the Class I antiarrhythmic drugs have been found in controlled, clinical trials to reduce sudden cardiac death, total cardiac death, or total mortality. The International Mexilitine and Placebo Antiarrhythmic Coronary Trial (IMPACT) was a prospective, double-blind, randomized study in survivors of myocardial infarction (MI) in whom 317 persons were randomized to mexilitine and 313 persons to placebo [42]. At 1-year follow-up, mortality was 7.6% for mexilitine-treated patients versus 4.8% for placebo-treated patients [42]. The Cardiac Arrhythmia Suppression Trial (CAST) I was a prospective, double-blind, randomized study in survivors of MI with asymptomatic or mildly symptomatic VA in which 730 patients were randomized to encainide or flecainide and 725 patients to placebo [43]. Adequate suppression of VA by encainide or flecainide was needed before randomiza‐ tion. Despite adequate suppression of VA, at 10-month follow-up, encainide and flecainide significantly increased mortality from arrhythmia or cardiac arrest 3.6 times and significant‐ ly increased total mortality 2.5 times[43). Older age increased the likelihood of adverse events, including death, in patients treated with encainide and flecainide[44]. CAST II was a prospective, double-blind, randomized study in survivors of MI with asymp‐ tomatic or mildly symptomatic VA in which 581 patients were randomized to moricizine and 574 patients to placebo. [45]. Adequate suppression of VA by moricizine was required before randomization. At 18-month follow-up, the mortality from arrhythmia or cardiac ar‐ rest was 8.4% for patients treated with moricizine and 7.3% for patients treated with placebo [45]. The 2-year survival rate was 81.7% for patients treated with moricizine and 85.6% for patients treated with placebo [45]. Older age increased the likelihood of adverse events, in‐ cluding death, in patients receiving moricizine [44]. 114 Cardiac Arrhythmias - Mechanisms, Pathophysiology, and Treatment Aronow et al [46] performed a prospective study in 406 persons with heart disease (58% with prior MI) and asymptomatic complex VA diagnosed by 24-hour AECGs. The preva‐ lence of nonsustained VT was 20%. The prevalence of an abnormal ejection fraction was 32%. The incidence of adverse effects causing cessation of drug was 48% for quinidine and 55% for procainamide. At 24-month follow-up, the incidences of sudden cardiac death, total cardiac death, and of total death were not significantly different in persons treated with qui‐ nidine or procainamide or with no antiarrhythmic drug [46]. The incidence of total mortality was 65% for persons treated with quinidine or procainamide and 63% for persons treated with no antiarrhythmic drug. Quinidine or procainamide did not decrease sudden cardiac death, total cardiac death, or total death in comparison with no antiarrhythmic drug in older patients with ischemic or nonischemic heart disease, abnormal or normal LV ejection frac‐ tion, and presence versus absence of VT [46]. Moosvi et al [47] performed a retrospective analysis of the effect of empiric antiarrhythmic therapy in 209 resuscitated out-of-hospital cardiac arrest patients with CAD. Of the 209 pa‐ tients, 48 received quinidine, 45 received procainamide, and 116 received no antiarrhythmic drug. The 2-year sudden death survival was 69% for quinidine-treated patients, 69% for pro‐ cainamide-treated patients, and 89% for patients treated with no antiarrhythmic drug [47]. The 2-year total survival was 61% for quinidine-treated patients, 57% for procainamide- treated patients, and 71% for patients treated with no antiarrhythmic drug [47]. Hallstrom et al [48] performed a retrospective analysis of the effect of antiarrhythmic drug use in 941 patients resuscitated from prehospital cardiac arrest attributable to VF between 1970 and 1985. Quinidine was given to 19% of patients, procainamide to 18% of patients, be‐ ta blockers to 28% of patients, and no antiarrhythmic drug to 39% of patients. There was a 17% increased incidence of death or recurrent cardiac arrest in patients treated with quini‐ dine or procainamide versus no antiarrhythmic drug. Survival was 57% worse for patients treated with procainamide than for patients treated with quinidine [48]. A meta-analysis of 6 double-blind studies of 808 patients with chronic atrial fibrillation who underwent direct-current cardioversion to sinus rhythm showed that the mortality at one year was higher in patients treated with quinidine (2.9%) than in patients treated with place‐ bo (0.8%) [49]. Of 1, 330 patients in the Stroke Prevention in Atrial Fibrillation Study, 127 were receiving quinidine, 57 procainamide, 15 disopyramide, 34 flecainide, 20 encainide, and 7 amiodarone [50]. The adjusted relative risk of cardiac mortality was 1.8 times higher and the adjusted relative risk of arrhythmic death was 2.1 times higher in patients receiving antiarrhythmic drugs [50]. In patients with a history of CHF, the adjusted relative risk of cardiac death was 3.3 times higher and the adjusted relative risk of arrhythmic death was 5.8 times higher in patients receiving antiarrhythmic drugs[50]. Morganroth and Goin [51] performed a meta-analysis of 4 randomized, double-blind con‐ trolled trials lasting 2 to 12 weeks in which quinidine (n=502) was compared with flecainide (n=141), mexiletine (n=246), tocainide (n=67), and propafenone (n=53) in the treatment of complex VA. There was an increased risk of mortality in patients treated with quinidine compared with patients treated with the other antiarrhythmic drugs (absolute risk increase = 1.6%) [51]. Treatment of Ventricular Arrhythmias 115 http://dx.doi.org/10.5772/57545 Teo et al [52] analyzed 59 randomized controlled trials of 23, 229 patients that investigated use of Class I antiarrhythmic drugs after MI. The Class I drugs investigated included quini‐ dine, procainamide, disopyramide, imipramine, moricizine, lidocaine, tocainide, phenytoin, mexiletine, aprindine, encainide, and flecainide. Mortality was 14% higher in patients re‐ ceiving Class I antiarrhythmic drugs than in patients receiving no antiarrhythmic drugs. None of the 59 studies demonstrated that use of a Class I antiarrhythmic drug decreased mortality in postinfarction patients [52].On the basis of these data, no Class I antiarrhythmic drugs should be used for the treatment of VT or complex VA. Calcium channel blockers are not useful in treatment of complex VA. Although verapamil can terminate a left septal fascicular VT, hemodynamic collapse can occur if intravenous ve‐ rapamil is given to patients with the more common forms of reentry VT. Teo et al [52] ana‐ lyzed randomized controlled trials of 20, 342 patients that investigated the use of calcium channel blockers after MI. Mortality was insignificantly 4% higher in patients receiving cal‐ cium channel blockers than in patients receiving no antiarrhythmic drugs [52]. On the basis of these data, no calcium channel blockers should be used in the treatment of VT or complex VA. Teo et al [52] analyzed 55 randomized controlled trials comprising 53, 268 patients that in‐ vestigated use of beta blockers after MI. Mortality was significantly reduced 19% in patients receiving beta blockers [52]. The decrease in mortality after MI in persons treated with beta blockers was due to both a reduction in sudden cardiac death and recurrent MI [24-27, 53]. The Beta Blocker Heart Attack Trial was a double-blind, randomized study of 3, 290 patients after MI [53-55]. At 25-month follow-up, propranolol decreased sudden cardiac death by 28% in patients with complex VA and by 16% in patients without complex VA. Propranolol significantly reduced total mortality by 34% in patients aged 60 to 69 years (p=0.01) and in‐ significantly reduced total mortality by 19% in patients aged 30 to 59 years [53-55]. Beta blockers decrease complex VA including VT [55-57]. Beta blockers also increase VF threshold in animal models and have been found to decrease VF in patients with acute MI [58] A randomized, double-blind, placebo-controlled study of propranolol in high-risk sur‐ vivors of acute MI at 12 Norwegian hospitals showed a 52% significant reduction in sudden cardiac death in patients treated with propranolol for 1 year [58]. Beta blockers decrease myocardial oxygen demand and myocardial ischemia, which may re‐ duce the likelihood of VF. Stone et al [59] showed by 48-hour AECGs in 50 patients with sta‐ ble angina pectoris that propranolol, but not diltiazem or nifedipine, caused a significant decrease in mean number of episodes of myocardial ischemia and in mean duration of myo‐ cardial ischemia compared with placebo. Beta blockers also decrease sympathetic tone, in‐ crease vagal tone, and stabilize cardiac membrane potentials which reduces the likelihood of VF. In addition, beta blockers are antithrombotic [60] and may prevent atherosclerotic pla‐ que rupture [61]. In the retrospective study by Hallstrom et al [48] in 941 patients resuscitated from prehospi‐ tal cardiac arrest attributed to VF, beta blockers were given to 28% of patients and no antiar‐ rhythmic drug to 39% of patients. At 108-month follow-up, patients treated with beta 116 Cardiac Arrhythmias - Mechanisms, Pathophysiology, and Treatment blockers had a significant 38% decreased incidence of death or recurrent cardiac arrest com‐ pared to patients treated with no antiarrhythmic [48]. Aronow et al [62] performed a prospective study in 245 persons with heart disease (64% with prior MI and 36% with hypertensive heart disease) and complex VA diagnosed by 24- hour AECGs and a LV ejection fraction ≥40%. Nonsustained VT occurred in 32% of patients. Silent myocardial ischemia occurred in 33% of patients. Of 245 patients, 123 were random‐ ized to propranolol and 122 to no antiarrhythmic drug. Follow-up was 29 months. Propra‐ nolol was stopped because of adverse effects in 14 of 123 patients (11%). Follow-up 24-hour AECGs were obtained at a median of 6 months in 91% of patients treated with propranolol and in 89% of patients treated with no antiarrhythmic drug [62]. Proprano‐ lol was significantly more effective than no antiarrhythmic drug in reducing VT >90% (71% versus 25% of patients) and in decreasing the average number of VPCs/hour >70% (71% ver‐ sus 25% of patients) [62]. The prevalence of silent myocardial ischemia on follow-up 24-hour AECGs was insignificantly higher on no antiarrhythmic drug. However, silent ischemia was significantly abolished by propranolol, with 37% of patients with silent ischemia on their baseline 24-hour AECGs having no silent ischemia on their follow-up 24-hour AECGs [62]. Multivariate Cox regression analyses showed that propranolol caused a 47% significant re‐ duction in sudden cardiac death, a 37% significant decrease in total cardiac death, and a 20% insignificant decrease in total death [62]. Univariate Cox regression analysis showed that among patients taking propranolol, suppression of complex VA caused a 33% insignificant reduction in sudden cardiac death, a 27% insignificant decrease in total cardiac death, and a 30% insignificant reduction in total death [63]. Among patients taking propranolol, abolition of silent myocardial ischemia caused a 70% significant decrease in sudden cardiac death, a 70% significant reduction in total cardiac death, and a 69% significant decrease in total death [63]. There was also a circadian distribution of sudden cardiac death or fatal MI with the peak incidence occurring from 6 AM to 12 PM (peak hour was 8 AM and a secondary peak occur‐ red around 7 PM) in patients treated with no antiarrhythmic drug [64] Propranolol abolish‐ ed this circadian distribution of sudden cardiac death or fatal MI [64]. In this study, propranolol markedly decreased the circadian variation of complex VA [65] and abolished the circadian variation of myocardial ischemia [66]. In a retrospective analysis of data from the CAST study, Kennedy et al [67] showed that 30% of patients with a LV ejection fraction ≤40% were receiving beta blockers. Patients on beta blockers had a significant decrease in all-cause mortality of 43% at 30 days, of 46% at 1 year, and of 33% at 2 years [67]. Patients treated with beta blockers had a significant reduction in arrhythmic death or cardiac arrest of 66% at 30 days, of 53% at 1 year, and of 36% at 2 years [67]. Multivariate analysis showed that beta blockers were an independent factor for de‐ creasing arrhythmic death or cardiac arrest by 40%, for reducing all-cause mortality by 33%, and for decreasing new or worsened CHF by 32% [67]. Treatment of Ventricular Arrhythmias 117 http://dx.doi.org/10.5772/57545 ACE inhibitors have been shown to cause a significant reduction in complex VA in patients with CHF in some studies [68, 69] but not in other studies [70, 71]. ACE inhibitors have also been shown to reduce sudden cardiac death in some studies of patients with CHF [32, 72]. ACE inhibitors should be given to reduce total mortality in older and younger patients with CHF [30, 32, 72, 73], an anterior MI [31], an MI with a LV ejection fraction ≤40% [28, 29, 32], and in all patients with atherosclerotic cardiovascular disease [23, 33]. ACE inhibitors should be used to treat patients with CHF with abnormal LV ejection fraction [30, 32, 72, 73] or with normal LV ejection fraction [74, 75]. On the basis of available data, ACE inhibitors should be used to treat patients with VT or complex VA associated with CHF, an anterior MI, an MI with LV systolic dysfunction, or atherosclerotic cardiovascular disease if there are no contraindications to use of ACE inhibi‐ tors. Beta blockers should be used in addition to ACE inhibitors in treating these patients. Class III antiarrhythmic drugs are potassium channel blockers which prolong repolarization manifested by an increase in QT interval on the electrocardiogram. These drugs suppress VA by increasing the refractory period. However, prolonging cardiac repolarization and re‐ fractory period can trigger afterdepolarizations and resultant torsade de pointes. In the Survival With Oral d-Sotalol (SWORD) Trial, 3, 121 survivors of MI with a LV ejection fraction ≤40% were randomized to d-sotalol, a pure potassium channel blocker with no beta blocking activity, or to double-blind placebo [76]. At 148-day follow-up, mortality was 5.0% in patients treated with d-sotalol versus 3.1% in patients treated with placebo [76]. Pre‐ sumed arrhythmic deaths accounted for the 77% increased mortality (relative risk = 1.77; 95% CI, 1.15 to 2.74) [76]. Studies comparing the effect of d, l-sotalol, a Class III antiarrhythmic drug with beta block‐ ing activity, versus placebo or beta blockers in patients with VT or complex VA have not been performed. In a study of 1, 486 patients with prior MI, compared with placebo, d, l- sotalol did not reduce mortality in patients followed for 1 year [77]. In the Electrophysiologic Study versus Electrocardiographic Monitoring (ESVEM) study of 486 patients, Holter monitor-guided therapy significantly predicted antiarrhythmic drug ef‐ ficacy more often than did the electrophysiologic study in patients with sustained VT or sur‐ vivors of cardiac arrest (77% versus 45% of patients) [78]. However, there was no significant difference in the success of drug therapy selected by the two methods in preventing recur‐ rences of ventricular tachyarrhythmias. In the ESVEM study, d, l-sotalol was more effective than the other 6 antiarrhythmic drugs [imipramine, mexiletine, pirmenol, procainamide, propafenone, and quinidine] used in re‐ ducing recurrence of arrhythmia, death from arrhythmia, death from cardiac causes, and death from any cause [79]. However, 7 of 10 episodes of torsade de pointes during this study occurred in patients receiving d, l-sotalol [79]. In 481 patients with VT, d, l-sotalol caused torsade de pointes (12 patients) or an increase in VT episodes (11 patients) in 23 pa‐ tients (4.9%) [80]. Women had a significantly higher risk for drug-induced VF. On the basis of available data, use of beta blockers is recommended over the use of d, l-sotalol in treating patients with VT or complex VA associated with heart disease. 118 Cardiac Arrhythmias - Mechanisms, Pathophysiology, and Treatment Amiodarone is very effective in suppressing VT and complex VA associated with heart dis‐ ease [81-83]. However, the incidence of adverse effects from amiodarone approaches 90% af‐ ter 5 years of therapy [84]. In the Cardiac Arrest in Seattle: Conventional Versus Amiodarone Drug Evaluation study, the incidence of pulmonary toxicity was 10% at 2 years in patients receiving an amiodarone dose of 158 mg daily [81]. Amiodarone can also cause cardiac adverse effects, gastrointestinal adverse effects including hepatitis, hyperthyroidism, hypothyroidism, and neurologic, dermatologic, and ophthalmologic adverse effects. A double-blind study randomized 674 patients with CHF and complex VA to amiodarone or placebo [82]. Compared with placebo, amiodarone significantly decreased the number of episodes of VT and the frequency of complex VA. Twenty-seven percent of patients discon‐ tinued amiodarone in this study. At 2-year follow-up, survival was not different in patients treated with amiodarone or placebo [82]. The Canadian Amiodarone Myocardial Infarction Arrhythmia Trial (CAMIAT) randomized 1, 202 survivors of MI with nonsustained VT or complex VA to amiodarone or placebo [83] Early permanent discontinuation of amiodarone for reasons other than adverse events oc‐ curred in 36% of patients taking this drug [83]. At 1.8-year follow-up, amiodarone caused no significant reduction in mortality [83]. The European Myocardial Infarction Amiodarone Trial (EMIAT) randomized 1, 486 survi‐ vors of MI with a LV ejection fraction ≤40% to amiodarone or placebo [85]. Early permanent discontinuation of amiodarone occurred in 38.5% of patients taking this drug. At 21-month follow-up, mortality was similar in patients treated with amiodarone or with placebo [85]. In the Sudden Cardiac Death in Heart Failure Trial (SCD-HEFT), 2, 521 patients with New York Heart Association (NYHA) class II or III CHF due to ischemic or nonischemic heart disease, a LV ejection fraction of 35% or less, and a mean QRS duration on the resting ECG of 120 msec were randomized to placebo, amiodarone, or an automatic implantable cardi‐ overter-defibrillator (AICD) [86]. At 45.5-month median follow-up, compared with placebo, amiodarone insignificantly increased mortality by 6% [86]. At 45.5-month median follow-up, compared with placebo, AICD therapy significantly reduced all-cause mortality by 23%, with an absolute reduction in mortality of 7.2% after 5 years [86]. Since amiodarone has not been found to reduce mortality in patients with VT or complex VA associated with MI or CHF and has a very high incidence of toxicity, beta blockers should be used rather than amiodarone in treating these patients. A meta-analysis of 10 randomized trials showed that the use of beta blockers significantly reduced 2-year mortali‐ ty in patients receiving AICD therapy [87]. In a study of 965 patients with AICDs, at 32- month mean follow-up, use of beta blockers significantly reduced all-cause mortality by 46%, whereas use of amiodarone or sotalolol did not affect mortality [88]. During 33-month mean follow-up of 1, 038 patients with AICDs, use of beta blockers significantly reduced ap‐ propriate AICD shocks [89]. Use of amiodarone plus a beta blocker was not more effective than beta blocker therapy alone in reducing AICD shocks for any reason [89]. In this study, use of sotalol did not reduce appropriate AICD shocks [89]. Treatment of Ventricular Arrhythmias 119 http://dx.doi.org/10.5772/57545 4. Invasive intervention If patients have life-threatening recurrent VT or VF resistant to antiarrhythmic drugs, inva‐ sive intervention should be performed. Patients with critical coronary artery stenosis and se‐ vere myocardial ischemia should undergo coronary artery bypass graft surgery to reduce mortality [90]. In the Coronary Artery Bypass Graft (CABG) Patch Trial, there was no evi‐ dence of improved survival among patients with CAD, LV ejection fraction <36%, and an abnormal signal-averaged electrocardiogram undergoing complete coronary revasculariza‐ tion in whom an AICD was implanted prophylactically at the time of elective coronary ar‐ tery bypass graft surgery [91]. Surgical ablation of the arhythmogenic focus in patients with life-threatening ventricular ta‐ chyarrhythmias can be curative. This treatment includes aneurysectomy or infarctectomy and endocardial resection with or without adjunctive cryoablation based on activation map‐ ping in the operating room [92-94]. However, the perioperative mortality rate is high. En‐ doaneurysmorrhaphy with a pericardial patch combined with mapping-guided subendocardial resection frequently cures recurrent VT with a low operative mortality and improvement of LV systolic function [95]. Radiofrequency catheter ablation of VT has been beneficial in the therapy of selected patients with arrhythmogenic foci of monomorphic VT [96-98]. Catheter ablation has been effectively used to treat patients with right ventricular outflow tract VT and LV fascicular VT. Prophylactic VT ablation should be considered be‐ fore implantation of an AICD in patients with stable VT, prior MI, and reduced LV ejection fraction [99]. 4.1. Automatic implantable cardioverter-defibrillator However, the AICD is the most effective treatment for patients with life-threatening VT or VF. [93-110]. The Multicenter Automatic Defibrillator Implantation Trial (MADIT) random‐ ized 196 patients, with a prior MI, a LV ejection fraction ≤35%, a documented episode of asymptomatic nonsustained VT, and inducible nonsuppressible ventricular tachyarrhyth‐ mia on electrophysiologic study to an AICD or conventional medical therapy [100]. At 27- month follow-up, patients receiving an AICD had a 54% significant reduction in mortality [100]. In the Antiarrhythmics versus Implantable Defibrillators (AVID) Trial, 1, 016 patients were randomized to an AICD or class III antiarrhythmic drug therapy [101]. Forty-five percent of patients had been resuscitated from near-fatal VF. The other 55% of patients had sustained VT with syncope or sustained VT with a LV ejection fraction ≤40% and symptoms suggest‐ ing severe hemodynamic compromise due to the arrhythmia (near-syncope, CHF, and angi‐ na pectoris). The 1-year survival was 89.3% for patients who had the AICD versus 82.3% for patients treated with drug therapy (39% reduction by AICD) [101]. The 2-year survival was 81.6% for patients who had the AICD versus 74.7% for patients treated with drug therapy (27% reduction by AICD) [101]. The 3-year survival was 75.4% for patients who had the AICD versus 64.1% for patients treated with drug therapy (31% reduction by AICD) [101].