Ventricular tachycardia secondary prevention

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-in Chief: Avirup Guha, M.B.B.S.[2]


There are several landmark trials which have shown some evidence-based secondary prevention measures for ventricular tachycardia.

Landmark Clinical Trials: Trials of Secondary Prevention of Sudden Cardiac Death

CASCADE(The Cardiac Arrest in Seatle Conventional Versus Amiodarone Drug Evaluation study)[1]

  • Strategy: Amiodarone vs conventional therapy in patients with/without AICD
  • Demographics: Total: 228 Amiodarone: 113 conventional antiarrhythmic drugs: 115(quinidine (n=33), procainamide (n = 26), combination therapy (n = 17), flecainide (n = 12). AICD: 105 (Amiodarone: 53, Conventional therapy: 52)
  • Mean EF: 35
  • Result: 13% more survival in patient population at the primary end point (total cardiac mortality, resuscitated cardiac arrest due to ventricular fibrillation, and syncopal Implanted defibrillator shocks) at the end of 6 years. (p=0.007). With AICD 16% survival more at the primary end point( shocks preceded by complete syncope)(p=0.032) conclusively showing superiority of Amidarone over convetional therapy in secondary prevention.

ESVEM (Electrophysiologic Study Versus Electrocardiographic Monitoring for Selection of Antiarrhythmic Therapy of Ventricular Tachyarrhythmias)[2][3]

  • Strategy: EP testing and Holter monitor of 7 antiarrhythmics (imipramine, mexiletine, procainamide, quinidine, sotalol, pirmenol, propafenone)
  • Demographics: 486 patients were randomized and 296 patients were eventually followed up.
  • Mean EF: 33% in all 296 and 34% in Sotalol group
  • Result: No difference between Holter- and EP-guided groups. Sotalol group had lowest recurrence rate of VT (risk ratio, 0.43; 95 percent confidence interval, 0.29 to 0.62; p<0.001), arrhythmic death (risk ratio, 0.50; 95 percent confidence interval, 0.26 to 0.96; P = 0.04), total death (risk ratio, 0.50; 95 percent confidence interval, 0.30 to 0.80; P = 0.004).

AVID (The Antiarrhythmics versus Implantable Defibrillators)[4]

  • Strategy: ICD vs medication either amiodarone or sotalol
  • Demographics: Total: 1016 ICD: 507 Medications (predominantly amiodarone): 509 (80% with ischemic heart disease)
  • Mean EF: 32 (inclusion<40)
  • Result: Relative risk reduction: 1-year: 39% ; 2-year: 27% ; 3-year: 31% (p = 0.02)

CIDS (Canadian Implantable Defibrillator Study)[5]

  • Strategy: ICD vs amiodarone
  • Demographics: Total: 659 ICD: 328 Amiodarone: 331 (82% with ischemic heart disease)
  • Mean EF: <35
  • Result: Relative risk reduction: 20% (p = 0.142)

CASH (Cardiac Arrest Study Hamburg)[6]

  • Strategy: ICD vs amiodarone vs beta blocker
  • Demographics: Total: 288 (74% with ischemic heart disease) ICD: 99 Amiodarone: 92 Metoprolol: 97
  • Mean EF: 45
  • Result: Relative risk reduction at 5 years: 23% (p = 0.081)

Landmark Clinical Trials: Trials of Primary Prevention of Sudden Cardiac Death

BHAT ( β-Blocker Heart Attack Trial)[7]

  • Strategy : multicenter, randomized, double-blind, and placebo-controlled trial designed to test whether the regular administration of propranolol hydrochloride to men and women who had experienced at least one myocardial infarction would result in a significant reduction in total mortality during a two- to four-year period.
  • Demographics: Total: 3837, Propanolol: 1916, Placebo: 1921 persons, five to 21 days after the infarction.
  • Mean EF:
  • Result: Total mortality during the average 25-month follow-up period was 7.2% in the propranolol group and 9.8% in the placebo group. Arteriosclerotic heart disease (ASHD) mortality was 6.2% in the propranolol group and 8.5% in the placebo group.

CAST (The Cardiac Arrhythmia Suppression Trial)[8][9]

  • Strategy: Suppression of ventricular ectopy after a myocardial infarction reduces the incidence of sudden death, patients in whom ventricular ectopy could be suppressed with encainide, flecainide, or moricizine were randomly assigned to receive either active drug or placebo
  • Demographics: Total: 1498 patients,Encainide+Placebo: 857(432 to active drug and 425 to placebo), Flecainide+Placebo: 641 (323 to active drug and 318 to placebo).
  • Mean EF: ≤40%
  • Result: 89 patients had died: 59 of arrhythmia (43 receiving drug vs. 16 receiving placebo; P = 0.0004), 22 of nonarrhythmic cardiac causes (17 receiving drug vs. 5 receiving placebo; P = 0.01), and 8 of noncardiac causes (3 receiving drug vs. 5 receiving placebo). Almost all cardiac deaths not due to arrhythmia were attributed to acute myocardial infarction with shock (11 patients receiving drug and 3 receiving placebo) or to chronic congestive heart failure (4 receiving drug and 2 receiving placebo). There were no differences between the patients receiving active drug and those receiving placebo in the incidence of nonlethal disqualifying ventricular tachycardia, proarrhythmia, syncope, need for a permanent pacemaker, congestive heart failure, recurrent myocardial infarction, angina, or need for coronary-artery bypass grafting or angioplasty.

CHF-STAT (Congestive heart failure: Survival trial of antiarrhythmic therapy)[10]

  • Demographics: Total: 674, Amiodarone: 336, Placebo: 338
  • Strategy: to determine whether Amiodarone can reduce overall mortality in patients with congestive heart failure and asymptomatic ventricular arrhythmias.
  • Mean EF: ≤40%, ≥10 PVCs/hr
  • Result: The rate of sudden death was 15% in the Amiodarone group and 19% in the placebo group in Ischemic Cardiomyopathy group (P=0.43). Reduction in overall mortality among the patients with nonischemic cardiomyopathy who received Amiodarone (P =0.07).

SWORD (The Survival With Oral d-Sotalol trial)[11]

  • Strategy: whether d-sotalol, could reduce all-cause mortality in patients with Left ventricular dysfunction after myocardial infarction .
  • Demographics: Total : 3121, d-Sotalol : 1549, placebo : 1572
  • Mean EF: 40%
  • Result: Mortality : d-sotalol: 78 deaths (5.0%), Placebo: 48 deaths (3.1%) (relative risk 1.65 [95% CI 115–2.36], p=0.006). Presumed arrhythmic deaths (relative risk 1.77 [1.15–2.74], p=0.008). The effect was greater in patients with a left ventricular ejection fraction of 31–40% than in those with lower (≤30%) ejection fractions (relative risk 4.0 vs 1.2, p=0.007).

MADIT I (Multicenter Automatic Defibrillator Implantation Trial)[12]

  • Strategy: Conventional medical therapy vs ICD in patients with clinical NSVT and inducible VT during EPS that is not suppressible with procainamide
  • Demographics: Medical therapy: 101 ICD arm: 95
  • Mean EF: 35
  • Result: RR reduction in mortality in favor of ICD; 95% CI: 0.26-0.82; p = 0.009

GESICA (the Gruppo de Estudo de la Sobrevida en la Insuficiencia Cardiaca en Argentina)[13]

  • Strategy: To determine the prognostic value of nonsustained ventricular tachycardia (NSVT) in total mortality in severe congestive heart failure (CHF) and predictive value of NSVT as a marker for sudden death or death due to progressive heart failure.
  • Demographics: Total: 516, NSVT: 173 (33.5%), No NSVT: and 343 (66.5
  • Mean EF:
  • Result: Efficacy Study: Mortality - NSVT: 87(50.3%) No NSVT: (30.9%) (RR = 1.69 (95% confidence interval [CI], 1.27 to 2.24; P<.0002; Cox proportional hazard analysis was 1.62 (95% CI, 1.22 to 2.16; P<.001)). Sudden death – No NSVT: 8.7%, NSVT: 23.7% (RR, 2.77; 95% CI, 1.78 to 4.44; P<.001). Progressive heart failure death – No NSVT: 17.5%, NSVT: 20.8% (P=.22). Couplets prediction of total all-cause mortality: RR, 1.81; 95% CI, 1.22 to 2.66; P<.002 ; sudden death: RR, 3.37; 95% CI, 1.57 to 7.25; P<.0005. Couplets±NSVT prediction of sudden death: RR, 10.1; 95% CI, 1.91 to 52.7; P<.01.

EMIAT (The European Myocardial Infarct Amiodarone Trial)[14]

  • Strategy: Amiodarone effect on reduction of mortality in patients of myocardial infarction with impaired ventricular function, irrespective of whether they had ventricular arrhythmias.
  • Demographics: Total: 1486, Amiodarone : 743, Placebo : 743
  • Mean EF: <40%
  • Result: Amiodarone group, there was a 35% risk reduction (95% CI 0–58, p=0.05) in arrhythmic deaths.

CAMIAT (The Cardiac Arrhythmia Suppression Trial)[15]

  • Strategy: To assess the effect of amiodarone on the risk of resuscitated ventricular fibrillation or arrhythmic death among survivors of myocardial infarction with frequent or repetitive VPDs (≥10 VPDs per h or ≥1 run of ventricular tachycardia).
  • Demographics: Total : 1202, Amiodarone : 606, Placebo: 596
  • Mean EF:
  • Result: Efficacy Analysis: resuscitated ventricular fibrillation or arrhythmic death – Placebo : 31 (6.0%) Amiodarone : 15 (3.3%) (relative-risk reduction 48.5% [95% CI 4.5 to 72.2], p=0.016). Intention-to-treat analysis: primary outcome events Placebo : 24 (6.9%) Amiodarone : 15 (4.5 (38.2% [95% CI –2.1 to 62.6], p=0.029). The absolute-risk reductions were greatest among patients with congestive heart failure or a history of myocardial infarction.

CABG-PATCH (Coronary Artery Bypass Graft (CABG) Patch Trial)[16]

  • Strategy: CAD patients undergoing CABG with abnormal signal averaged ECG randomized to ICD or control group
  • Demographics: ICD epicardial: 446 Control arm: 45 Total: 900 30days and revascularization > 90 days) randomized 3:2 to ICD vs conventional medical therapy ICD: 42 Conventional medical therapy: 490
  • Mean EF: 30
  • Result: 31% RR reduction in favor of ICD; 95% CI: 0.51-0.93; p = 0.16

MUSTT (the Multicenter Unsustained Tachycardia Trial)[17]

  • Strategy: Electrophysiologically guided antiarrhythmic therapy would reduce the risk of sudden death among patients with coronary artery disease, a left ventricular ejection fraction of 40 percent or less, and asymptomatic, unsustained ventricular tachycardia
  • Demographics: 704 patients who underwent randomization, 351 were assigned to receive electrophysiologically guided therapy and 353 were assigned to receive no antiarrhythmic therapy.
  • Mean EF: LVEF <40% + NSVT
  • Result: Efficacy Study: Cardiac Arrest or Death from Arrhythmia - EP guided therapy = 25% no antiarrhythmic therapy = 32% (RR=0.73, CI=0.53-0.99). Cardiac arrest or death from arrhythmia - Treatment with Defibrillators vs w/o Defibrillator Treatment (RR=0.24; CI=0.13-0.45; P<0.001).

MADIT II (Multicenter Automatic Defibrillator Implantation Trial - II)[18]

  • Strategy: To evaluate the effect of an implantable defibrillator on survival in patients with reduced left ventricular function after myocardial infarction are at risk for life threatening ventricular arrhythmias.
  • Demographics: Total: 1232, ICD: 742, Conventional Medical Therapy: 490 patients
  • Mean EF: ≤30% >10 PVCs/hr or couplets
  • Result: Efficacy Study: Mortality – Conventional Medical Therapy: 19.8%, ICD: 14.2%(HR 0.69 (95 CI= 0.51-0.93, P=0.016).

AMIOVIRT (Amiodarone versus Implantable Defibrillator)[19]

  • Strategy: Nonischemic dilated cardiomyopathy patients with nonsustained VT, randomized to ICD vs amiodarone
  • Demographics: ICD: 51 Amiodarone: 52 Total: 103
  • Mean EF: 35
  • Result: No significant difference in survival

DEFINITE (Defibrillators in Non-Ischemic Cardiomyopathy Treatment Evaluation)[20]

  • Strategy: Nonischemic dilated cardiomyopathy patients with nonsustained VT, randomized to ICD vs standard medical therapy
  • Demographics: Singlechamber ICD: 229 Standard medical therapy: 229 Total: 458 120 ms) in both ischemic and nonischemic causes 1520 randomized in 1:2:2 ratio to receive optimum pharmacological therapy, biventricular pacemaker alone or biventricular pacemaker defibrillator
  • Mean EF: 35
  • Result: Combined end point of hospitalization and death reduced by the pacemaker alone 34% (p = 0.002) and pacemaker-ICD by 40% (p = 0.001). Secondary end point all-cause mortality reduced by defibrillator by RR-36% (p = 0.003) but not by pacemaker alone. RR: 24% (p = 0.059)

DINAMIT (Defibrillator in Acute Myocardial Infarction Trial)[21]

  • Strategy: Benefit of an ICD early after an MI within 6-40 days towards reduction of mortality when compared with medical therapy
  • Demographics: ICD: 332 Control: 342 Total: 674
  • Mean EF: 35
  • Result: 62 deaths in the ICD group and 58 in the control group (p = 0.66; CI: 0.76-1.55). Arrhythmic causes were less in the ICD group but nonarrhythmic causes were significantly higher and thus overall mortality was not significantly different

COMPANION (The Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure trial )[22]

  • Strategy: Prophylactic cardiac-resynchronization therapy in the form of biventricular stimulation with a pacemaker with or without a defibrillator would reduce the risk of death and hospitalization among patients with advanced chronic heart failure and intraventricular conduction delays.
  • Demographics: Total: 1520, Optimal Pharmacologic Therapy: 308, Cardiac- Resynchronization Therapy: Pacemaker=617, Pacemaker– Defibrillator=595
  • Mean EF: Ischemic or nonischemic CM NYHA Class III-IV QRS ≥120 msec
  • Result: Efficacy Study: Pacemaker group - Primary end point mortality reduction (hazard ratio, 0.81; P=0.014), Pacemaker–defibrillator group (hazard ratio, 0.80; P=0.01). Primary end point mortality reduction: 34% - Pacemaker group (P<0.002), 40% - Pacemaker–Defibrillator group (P<0.001). Secondary end point mortality reduction: 24% - Pacemaker group (P=0.059), 36% - Pacemaker–Defibrillator group (P=0.003).

SCD-HeFT (Sudden Cardiac Death in Heart Failure Trial)[23]

  • Strategy: To assess prognostic effect of ICD vs amiodarone vs placebo in class II and III heart failure regardless of etiology.
  • Demographics: Conventional therapy and placebo: 847 Conventional therapy and amiodarone: 845 Conventional therapy and single lead, shock only ICD: 829 Total: 2521
  • Mean EF: 35 (ischemic etiology patients 52% and nonischemic etiology 48%)
  • Result: Amiodarone and placebo outcome were comparable. ICD arm absolute risk reduction: 7.2% after 5 years; RR: 23% (p = 0.007)

MADIT-CRT(Multicenter automatic defibrillator implantation trial-cardiac resynchronization therapy)[24]

  • Strategy: To determine whether cardiac-resynchronization therapy (CRT) with biventricular pacing would reduce the risk of death or heart-failure events in patients with mild cardiac symptoms, a reduced ejection fraction, and a wide QRS complex.
  • Demographics: Total: 1820, CRT + ICD = 1089, ICD alone = 731
  • Mean EF: <30%
  • Result: Efficacy study: CRT-ICD primary end point mortality = 17.2%, ICD-only group = 25.3% HR=0.66; 95% CI = 0.52-0.84, p=0.001.


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  21. Hohnloser SH, Kuck KH, Dorian P, Roberts RS, Hampton JR, Hatala R; et al. (2004). "Prophylactic use of an implantable cardioverter-defibrillator after acute myocardial infarction". N Engl J Med. 351 (24): 2481–8. doi:10.1056/NEJMoa041489. PMID 15590950. Review in: ACP J Club. 2005 May-Jun;142(3):58
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  24. Moss AJ, Hall WJ, Cannom DS, Klein H, Brown MW, Daubert JP; et al. (2009). "Cardiac-resynchronization therapy for the prevention of heart-failure events". N Engl J Med. 361 (14): 1329–38. doi:10.1056/NEJMoa0906431. PMID 19723701.