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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:

1) The prevention of sudden death.

2) The relief of intolerable symptoms.

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

A given therapy is effective by:

1) Preventing arrhythmia occurrence/recurrence and/or

3) Converting a non-tolerated to a tolerated arrhythmia

2) Terminating arrhythmias once they occur

Available Therapies

1) 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-life-threatening. Given acutely, terminate an existing arrhythmia.

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

3) Ablation: Prevent arrhythmia recurrence

Drugs

Although the mainstay of therapy for years, antiarrhythmic agents have only limited efficacy in preventing tachycardia. Using electrophysiologic testing drugs suppress VT induction in at best 30% of patients. In a recent study (ESVEM) sotalol was effective in almost 40% of patients, this was far better than all other agents tested. Sotalol (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, sotalol 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)

The standard device includes:

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

Implantation:

Median sternotomy (if CABG also being performed)

Subxiphoid, subcostal or left lateral thoracotomy

In the operating room ventricular fibrillation is induced multiple times and the defibrillation threshold (DFT: 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.

Advances

Antitachycardia Pacing (ATP): Reentry is the most common mechanism responsible for clinical cardiac arrhythmias. For a Re-entrant 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 pre-excited, rendering it refractory and terminating the tachycardia. Studies have shown that it 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. 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 (non-thoracotomy lead, system): In the initial transvenous devices energy was delivered between a coil electrode in the right ventricle, coronary sinus or superior vena cava.