Fig. S. Management of sustained monomorphic VT in patients with structural heart disease.

Secondary Prevention Identification of Reversible Triggers

Because the management of patients with ischemic and nonischemic heart disease varies considerably, the initial evaluation of patients presenting with sustained mono-morphic ventricular tachycardia (SMVT) should include an evaluation for CAD and underlying cardiomyopathy or valvular disorders (Fig. 5). The clinical history should be carefully inspected, and potential triggers should be identified and treated. These triggers include adverse drug effects, electrolyte abnormalities, and ischemia. The proarrhythmic effects of antiarrhythmic drugs are well-known. Drugs can have an adverse effect on the electrophysiologic properties of the reentrant circuit converting NSVT into sustained episodes. Digitalis toxicity manifests in a wide variety of rhythm and conduction disturbances, including VT. VT caused by digitalis toxicity should be recognized because treating the toxicity will effectively terminate VT. This tachycardia typically arises from the fascicles (fascicular tachycardia); and therefore demonstrates a right bundle-branch block (RBBB) morphology with a left superior or right inferior frontal axis when originating from the left posterior or left anterior fascicle, respectively. Rarely, the frontal axis can alternate between left superior and right inferior on a beat-to-beat basis (bi-directional VT) when the VT originates alternately from each fascicle (Fig. 6). Patients can be highly sensitive to potassium levels. A drop in serum potassium

Bidirectional Digoxin
Fig. 6. 12-lead ECG recording of bidirectional VT in a patient with digitalis toxicity. Note the RBBB morphology (arrow) and alternating frontal axis (arrowheads). AV dissociation is evident in the V1 rhythm strip.

may aggravate ventricular arrhythmias by enhancing the binding of digoxin at the level of the Na-K ATPase molecule. Residual ischemia in an area of prior infarction may adversely affect a circuit, resulting in VT. Patients who present with ischemia, VT, and reduced ventricular function should be evaluated for revascularization in an attempt to reduce the ischemic burden, improve ventricular function, and improve survival (38,39). Importantly, the presence of monomorphic VT implies a fixed anatomic substrate for the arrhythmia. Although it may be important to reverse any potential triggers that may result in frequent arrhythmic recurrences, treating the triggers alone does not necessarily eliminate the risk of potentially life-threatening arrhythmia recurrences. Monomorphic VT must be managed with treatment that can effectively alter the anatomic substrate or stop an arrhythmia with appropriate pacing or shock therapy.

Hemodynamically Intolerable VT

The mode of presentation and left ventricular function are important determinants of the aggressiveness of therapy. Any patient who presents with hemodynamically intolerable VT (cardiac arrest, syncope) should be considered for device therapy. Substrate modification techniques serve only an adjunctive role to the ICD.

The Role of Antiarrhythmic Drug Therapy

Drug therapy has a limited role in patients with hemodynamically intolerable VT, serving an adjunctive role to the ICD. Before the AVID trial was published, the CASCADE (Cardiac Arrest in Seattle: Conventional Versus Amiodarone Drug Evaluation) trial was conducted to determine whether empiric amiodarone therapy was more effective than guided (electrophysiologic or electrocardiographic-monitored) antiarrhythmic therapy in reducing mortality of sudden-cardiac-death survivors (40). A total of 228 enrolled patients were randomized either to empiric amiodarone therapy (113) or guided antiarrhythmic therapy (115). Eight-two percent of the patients had CAD. Survival free of cardiac death or sustained ventricular arrhythmias was significantly lower for the amiodarone group (78% vs 52% at 2 yr, 52% vs 36% at 4 yr, 41% vs 29% at 6 yr, (p = 0.001). Although amiodarone was more effective than guided antiarrhythmic therapy, overall mortality remained high.

In 1997, Haverkamp et al. published a trial evaluating the role of d,1-sotalol in patients with inducible VT, VF, or aborted sudden death (41). Enrolled patients were treated with sotalol and underwent programmed ventricular stimulation to document effective suppression of inducibility by sotalol. Only 57% (227) of 396 enrolled patients had effective arrhythmia suppression. Actuarial total survival rates were 94% at 1 yr and 86% at 3 yr. Although oral sotalol can be effective in suppressing ventricular tachyarrhythmias, sudden cardiac death still occurred in a considerable proportion of the study population.

In 1999, Pacifico et al. published a multicenter, double-blinded, placebo-controlled trial demonstrating that sotalol therapy was associated with a lower risk of death and delivery of first shocks from an ICD compared to placebo (risk reduction: 40%, (p = 0.001) (42).

The Role of Catheter Ablative Therapy

At present, only patients with monomorphic VT are candidates for catheter ablation. The standard approach to arrhythmic localization requires induction of the arrhythmia and mapping during the tachycardia to pinpoint the appropriate site for ablation. This standard approach cannot be used in patients with rapid VT that is not tolerated hemodynamically. Voltage-mapping techniques to define the anatomic substrate in conjunction with pace-mapping to regionalize the area of interest have been applied to VT which is not mappable. Linear lesions which cross the densely scarred myocardium through the border zone to normal myocardium appear very effective in treating patients with hemodynamically intolerable VT (Fig. 7).

The Role of ICD Therapy

The introduction of the ICD into the armamentarium of available treatment options for VT has raised questions about its effectiveness compared to antiarrhythmic drug therapy in reducing mortality. The CASH (Cardiac Arrest Study Hamburg) trial compared antiarrhythmic therapy (metoprolol, amiodarone, and propafenone) to ICD therapy in mortality reduction of sudden-cardiac-death survivors (43). After baseline clinical testing, enrolled patients were randomized to one of the four regimens. Almost one-half of the patients had CAD. At an interim analysis, propafenone was associated with an increase in mortality, resulting in early termination of the propafenone arm. The final results of the trial were recently published (43a). The total mortality in the ICD group was 23% lower than in the combined amiodarone and metoprolol groups, although this did not reach statistical significance.

In 1997, the larger AVID (Antiarrhythmics Versus Implantable Defibrillator) trial was published comparing antiarrhythmic therapy to ICD in patients with either resusci-

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