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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-life threatening, 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.
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 life-threatening. 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
Drugs
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)
History:
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
Implantation:
• 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.
Advances
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.
Future
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
Future
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.