This page has moved. Click here to view.


Primary and Secondary Prevention of Ventricular Arrhythmias 

Goals of Arrhythmia Therapy

Therapy for the treatment of cardiac arrhythmias should be instituted with only 2 goals in mind:

The prevention of sudden death.

The relief of intolerable symptoms.

In patients with non-lifethreatening, asymptomatic or only mildly symptomatic arrhythmias the best therapy is reassurance.

A given therapy is effective by:

Preventing arrhythmia occurrence/recurrence and/or 3) Converting a nontolerated to a tolerated arrhythmia

Terminating arrhythmias once they occur

Available Therapies

Drugs: Given chronically, prevent arrhythmia recurrence, and may limit the ability of an arrhythmia to remain sustained. In addition, in some cases drugs may slow an arrhythmia thereby rendering it better tolerated and non lifethreatening. Given acutely, terminate an existing arrhythmia.

Devices: Terminate existing arrhythmias. In the future they may be used to prevent arrhythmia recurrence.

Ablation: Prevent arrhythmia recurrence


Although the mainstay of therapy for years, antiarrhythmic agents have only limited efficacy m preventing ventricular tachycardia. Using electrophysiologic testing drugs suppress VT induction in at best 30% of patients. In a recent study (ESVEM) sotolol was effective in almost 40% of patients, this was far better than all other agents tested. Sotolol (Betapace) is a newly released Class III antiarrhythmic agent with significant beta adrenergic receptor blocking properties (approx. 1/4-1/10 that of propranolol). Class III activity (potassium channel blockade) leads to stabilization of both atrial and ventricular tissue. Therefore, sotolol has been shown to be effective for the treatment of both atrial and ventricular arrhythmias. Initial dose 80mg, watch for hypotension, bradycardia/heart block, heart failure. The chronic dose can be as low as 80rag BID, but usually is 160mg BID to 320 BID. The role of amiodarone will be discussed below.

Implantable Cardioverter/Defibrillators (ICD)


1947: First open chest electrical defibrillation (Beck)

1956: First closed chest electrical defibrillation (Zoll)

1980: First implantable defibrillator (Mirowski)

1985: First device approved by FDA

Today: >100,000 devices implanted

The standard device included:

An energy source (battery and large capacitor) and sensing mechanism

Rate sensing leads: epicardial (screw in) or endocardial (transvenous)

Defibrillating leads: 2 epicardial titanium mesh patches


Median sternotomy (if CABG also being performed)

Subxiphiod, subcostal or left lateral thoracotomy

In the operating room ventricular fibrillation is induced multiple times and the defibrillation threshold (DFF: energy required to reliably terminate ventricular fibrillation) is determined. Implantable cardioverter defibrillators (ICD) have clearly been shown to reduce the incidence of sudden death. In patients with a history of aborted sudden death the recurrence rate is 25-35%. In the same population, the ICD reduces this to 3-8% at 2years and 5-15% at 5 years.


Antitachycardia Pacing (ATP): Reentry is the most common mechanism responsible for clinical cardiac arrhythmias. For a reentrant rhythm to sustain the leading edge of the wavefront of activation must encounter excitable tissue. This area between the leading edge of activation and the tail of refractoriness is known as the excitable gap. By introducing a single or train of premature impulses the tissue in the excitable gap can be prexcited, rendering it refractory and terminating the tachycardia. Studies have shown that ventricular tachycardia can be terminated with antitachycardia pacing 70-90% of the time. Slower tachycardias are usually more amenable to ATP. However, there is a 3-20% risk of accelerating the tachycardia to a more poorly tolerated rhythm or ventricular fibrillation. For this reason antitachycardia devices should be used as part of a cardioverter/defibrillator. In many patients with well tolerated VT ATP can terminate VT with minimal or no symptoms.

Tiered Therapy: Devices have now been developed that have the capability of delivering antitachycardia pacing, low energy cardioversion, high energy defibrillation and backup bradycardia pacing. These devices allow for therapy to be tailored to different arrhythmias in the same patient.

Transvenous implantation (nonthoractomy lead system): In the initial transvenous devices energy was delivered between a coil electrode in the right ventricle, coronary sinus or superior vena cava and a subcutaneous patch or electrode array. Adequate defibrillation thresholds could be achieved in 80-95% of patients. This approach is associated with lower morbidity/mortality of implantation, is easier to remove/replace, and avoids thoracotomy in patient who may require future CABG/valve surgery. Transvenous implantation has become the approach of choice. Devices can now be implanted in the pectoral region (similar to a standard pacemaker) and involve only a single endocardial lead. The most recent devices allow shock energy to be delivered from a coil in the Right Ventricle to the ICD can itself ("active can") removing the need for additional endocardial leads or subcutaneous arrays or patches. Adequate DFTs can be achieved in close to 100% of cases.


Avoid inappropriate therapy: dual chamber sensing (2 devices now available)

Dual chamber pacing (DDDR device just released)

Hemodynamic guided therapy

Lower DFT's: various energy delivery

Smaller size

Lower cost

Ablation of Ventricular Tachycardia

Idiopathic VT

Ventricular tachycardia in patients with no underlying structural heart disease or precipitating factors (ie, electrolyte disturbances) has been labeled idiopathic. Although the prognosis is excellent with a very low incidence of sudden death, patients can be severely symptomatic. Patients often present with repetitive bursts of nonsustained tachycardia or occasional episodes of sustained tachycardia. This disorder can be divided into 2 groups:

Right ventricular outflow tract tachycardia

Idiopathic left ventricular tachycardia

These tachycardias appear to arise from focal areas in the right ventricle (outflow tract) and left ventricle (inferior, posterior septum), making than ideal targets for catheter ablation. Cure can be achieved in close to 90% of patients undergoing attempted ablation.

Bundle Branch Reentrant Tachycardia

Bundle branch reentrant tachycardia (BBRT) is a macroreentrant rhythm involving the His-Purkinje system. Most commonly activation proceeds down the right bundle, across the interventricular septum, and up the left bundle. This rhythm disturbance appears to be more common than previously thought. In recent studies 6-18% of patients undergoing EP study for sustained ventricular tachycardia or sudden death were found to have bundle branch reentrant tachycardia (BBRT). Patients with BBRT have dilated left ventricles with poor function, and a interventricular conduction delay or bundle branch block pattern on ECG. Due to their poor LV function and usually rapid tachycardia these patients most often present with syncope or sudden death. Drugs are not usually effective for this disorder, However catheter ablation has proven to be very efficacious. By ablating the right bundle, a critical component of the tachycardia circuit is severed and the tachycardia is cured

Ventricular Tachycardia in Patients with Coronary Artery Disease

Ventricular tachycardia in patients with underlying coronary artery disease is thought to be due to reentry in the border zone of infarcted and normal tissue. Current mapping techniques make it difficult to accurately determine and localize components of this reentrant circuit. This has lead to limited success in performing catheter ablative procedures in these patients. A recent report demonstrated encouraging results a series of 17 patients with hemodynamically stable ventricular tachycardia. Using a variety of mapping techniques (pace mapping, entrainment mapping, activation mapping) and radiofrequency energy, they achieved an 80% acute success rate. At present catheter ablation can only be performed in patients with hemodynamically tolerated ventricular tachycardia, to allow for adequate mapping. It is best used in patients with: recurrent, well tolerated VT, frequent ICD discharges due to a particular VT morphology: and incessant ventricular tachycardia not responsive to antiarrhythmic medication


Sudden Death Prevention

Primary Prevention

Patients surviving acute myocardial infarction and those with idiopathic cardiomyopathies are at risk for sudden cardiac death. Studies of the use of a variety of agents in these patients populations to try and prevent sudden death have been discouraging. Therapy has lead to no change in outcome or even an adverse outcome. The only exception has been beta blockers in post MI patients. This is in part due to the application of therapy to a group of patients at low or at best moderate risk.

As with any therapy, the risk/benefit ratio should be considered carefully prior to instituting antiarrhythmic therapy. Not only should the efficacy and proarrhythmic potential of an agent be considered, but also potential gains to the population being treated.

For example:

Population: Patients at risk of sudden cardiac death (SCD) i.e. 5% risk (higher than current patients post MI).

Drug: 80% efficacy, 5% proarrhythmic potential (far better than any available agent)

Sample population: 1,000 patients

5% at risk = 50 patients 95% not at risk = 950 patients

80% helped = 40 patients 5% proarrhythmia = 48 patients

Despite a very effective, safe agent more patients would be harmed than helped. Therefore, therapy should be limited to the only selected patients at highest risk. The difficulty is identifying these patients.

Risk of Sudden Death Post Myocardial Infarction

The risk of SCD post MI has been estimated to be 2-10%/year. There has been a trend towards a lower risk most likely due to aggressive revascularization (Thrombolytics, PTCA/Stenting, and CABG) and an increased use of Beta Blocking agents. Therefore the risk for all post MI patients is relatively low and empiric treatment of this cohort is unwarranted. Attempts have been made to better select patients at higher risk.

Noninvasive Risk Stratification

A variety of tests have been used to try and select patients at risk. Unfortunately, as can be seen below, this tests offer good negative predictive accuracy (NPA) but poor positive predictive accuracy (PPA).

Test                                       PPA (%)                     NPA (%)

Signal Averaged ECG            17                                81

R-R Variability                       17                                77

VPC> 1O/hour                      16                                82

NSVT                                   15                                 97

Mean R-R <750msec            13                                 97

EF <40%                               10                                75

Farrell, JACC, 1991


Test                                  Specificity                     Sensitivity                 PPA (%)                         NPA (%)

EF <40%                          57                                 61                           12                                      94

NSVT on Holter               44                                 73                           13                                      93

+S AECG                         69                                 62                           15                                      95

EF/NSVT                         21                                 85                             12                                    92

EF/SAECG                       36                                 83                             17                                    93

NSVT/SAECG 38 89 25 93

EF/NSVT/SAECG 21 94 25 93

Steinberg, AJC 1992

Based on some of these non invasive risk stratifiers studies have been performed to test a variety of agents in preventing post MI sudden death. Uniformly these studies have found no difference, or a worse outcome, in patients receiving antiarrhythmics as compared to placebo

Suppression of VPCs Post MI (no improvement in survival for any agent below)

Tocainide: Ryden, AHJ 1980 Mexiletine: Chamberlain, Lancet 1980 Quinidine: Bloomfeld, NEJM 1971 Jones, AJC 1974

Disopyramide:Jennings, Lancet 1976

Procainamide: Koch, NEJM 1969 Kosowsky, Circ 1973

Suppression of VPC's Post MI in patients with depressed LV function

Sword: d-Sotolol (stopped, increased mortality in treatment arm)

CAST 1: Encainide, Flecainide (stopped, increased mortality in treatment arm) CAST 2: Moricacine (stopped, increased mortality in treatment arm)


Recently studies have demonstrated a beneficial effect of low dose amiodarone for the prevention of sudden death post MI. A meta analysis of the randomized trials to date of amiodarone vs. placebo has shown a 29% reduction in mortality. The results of 2 large studies designed to evaluate this issue were recently reported (Lancet 1997:349).

Canadian Amiodarone Myocardial Infarction Arrhythmia Trial (CAMIAT):

1,200 patients post MI with >10 PVC's/hour and NSVT on 24hr holter.

Amiodarone 10mg/kg x 2Wks with eventual reduction to 200mg/day vs. placebo

Results: 46% of death were arrhythmic

SCD/aborted SCD decreased in amiodarone arm (6 vs. 3.3%, p=0.003)

No improvement in all cause mortality at 1.7yr follow-up

Significant reduction in cardiac mortality in amio + Beta Blocker group

European Myocardial Infarction Arrhythmia Trial (EMIAT):

1,500 patients post MI with EF_<40%

Amiodarone 800rag/day x 2Wks with eventual reduction to 200rag/day vs. placebo Results: No improvement in total mortality

35% reduction in arrhythmic deaths in amio arm (7 vs. 4%, p=0.05) Significant reduction in cardiac deaths in amio + Beta Blocker grou

The role of electrophysiologic testing has also been evaluated to better select patients at risk post MI.

Study                            n                         %Inducible                         Events (Inducible)                     Events (Noninducible)

Buxton                         62                         39                                     25%                                             10%

Klein                            40                        42                                     47%                                               4%

Gomes                          56                       15                                     30%                                               5%

Zheultin                         57                       46                                     15%                                                 0%

Wilber 100 43 43% 6%

As with noninvasive testing a negative test predicts a good outcome, but although the risk is higher in inducible patients the majority of patients will not have an event. Non randomized trials have suggested that inducible patients do better with treatment (Wilber NEJM 1988). No completed trial has compared treatment to placebo in this cohort of patients.

The Multicenter Unsustained Tachycardia Trial (MUSST)

This trail is designed to hopefully answer the question of how to treat the above noted patients. Asymptomatic patients post MI with depressed LV function (<35%) and NSVT undergo EP testing. If none inducible they are followed in a prospective registry on standard post MI medications, but no antiarrhythmic therapy. If sustained VT is induced they are randomized to standard EP guided antiarrhythmic therapy (including ICD if not suppressed by drags) or no antiarrhythmic therapy. Patients in the treated group did better than those without treatment, however the survival advantages was due to the patients who received ICDs. The patients treated with medications did as poorly as those receiving no specific antiarrhythmic therapy. (ACC 1999).


I96 asymptomatic patients post MI with depressed LV function (<35%) and NSVT who had inducible sustained VT that was not suppressed by procainamide in the EP lab. Patients randomized to ICD or EP guided therapy/amiodarone. Trial terminated due to significant reduction in mortality in the ICD group. The majority of non ICD patients were on amiodarone and significantly more ICD patients were on beta blockers. (Moss NEJM 1996).

CABG Patch

900 patients with depressed LV function (EF 35%) and a positive signal averaged ECG undergoing coronary artery bypass surgery were randomized to ICD or standard non antiarrhythmic therapy. There was no difference in mortality between the groups (24% control vs. 27% ICD).

Sudden Death Prevention in Patients with Heart Failur


A South American study evaluating the efficacy of low dose amiodarone in patients with congestive heart failure. The majority of patients had non ischemic dilated cardiomyopathy. There was a significant reduction in mortality in the amiodarone group.


A VA cooperative study evaluating the efficacy of low dose amiodarone in patients with congestive heart failure. There was no improvement in overall survival in the entire population. However in patients with non ischemic dilated cardiomyopathy the was a reduction of mortality in the amiodarone group.

Sudden Cardiac Death/Heart Failure Trial (SCDHFF)

Comparing ICD therapy to Amiodarone to standard heart failure medications in patients with depressed LV function and clinical heart failure. This study has just begun enrollment.

Secondary Prevention


228 patients with SCD or poorly tolerated VT randomized to amiodarone or other standard antiarrhythmic medications. There was a decreased mortality in the amiodarone group.

Canadian Implantable Defibrillator Study (CIDS)

Ongoing trial with planned enrollment of 650 patients comparing ICD to amiodarone in patients with SCD or poorly tolerated VT.

Cardiac Arrest Study of Hamburg (CASH)

Ongoing trial with planned enrollment of 600 patients comparing ICD to amiodarone to metoprolol to propafanone in patients with SCD or poorly tolerated VT. The propafanone arm was terminated due to excessive mortality. The remainder of the trial is ongoing.

Antiarrhythmics vs. Implantable Defibrillators Trial (AVID)

644 patients with SCD or poorly tolerated VT randomized to ICD amiodarone or EP guided sotolol therapy. The trial was terminated due to improved survival in the ICD group (27% reduction in mortality at 2 years). Again the ICD group had a higher use of beta blockers.

Of note, subgroup analysis of AVID, CIDS and CASH revealed that there was no benefit for the ICD over amiodarone in patients with ejection fractions greater than 35%.