Substrate modification techniques include antiarrhythmic drug therapy, catheter and surgical ablative therapy (e.g., encircling ventriculotomy or subendocardial resection). Antiarrhythmic drug therapy functionally modifies the substrate by affecting the electro-physiologic properties of ventricular tissue, prolonging refractoriness and preventing reentry or suppressing automaticity. Catheter and surgical ablation physically disrupt the substrate for VT by either local tissue destruction with radiofrequency energy or excision of critical ventricular sites. Although device therapy does not prevent recurrent episodes of VT or VF, the implantable cardioverter defibrillator (ICD) can effectively terminate ventricular tachyarrhythmias when they occur.
Selection of an antiarrhythmic compound for patients with ventricular tachyarrhythmias depends upon several factors: 1) type of arrhythmia; 2) underlying cardiac substrate; 3) left ventricular function; and 4) comorbid diseases, which may be affected by a particular drug or may influence drug metabolism. For VT that occurs without structural heart disease, beta-blockers are standard treatment for RVOT tachycardias (Fig. 1), and verapamil often effectively treats idiopathic left ventricular tachycardias arising from the mid-inferior septum (Fig. 2). Type 1A (e.g., procainamide or quinidine), 1B (e.g., mexiletine), 1C (e.g., propafenone or flecainide) and Type 3 (amiodarone or sotalol) antiarrhythmic drug therapy have been used to successfully prevent recurrent infarct-related VT; and all may be appropriate in patients with an ICD. Because many of these patients have depressed left ventricular function, amiodarone is frequently considered a first-line agent. The results of the AVID study strongly suggest that antiarrhythmic drug therapy alone is inadequate treatment for any patient with structural heart disease who presents with VF or hemodynamically intolerable VT (3). Anti-arrhythmic therapy is currently being used as an important adjuvant therapy to the ICD to prevent frequent, symptomatic VT and to control supraventricular arrhythmias. When used primarily as adjuvant therapy coupled with an ICD, any of the Type 1 and 3 antiarrhythmic agents may be appropriate. Selection of antiarrhythmic therapy is frequently based upon the side-effect profile of the particular drug.
Catheter ablative therapy has replaced surgical ablative therapy in the management of frequent, recurrent, drug-refractory VT. The desire to avoid surgical mortality and the success of catheter-based ablation has enabled it to become the standard approach to ablative therapy (4). Catheter ablative therapy typically involves the delivery of radiofrequency energy to ventricular sites crucial for the initiation and/or propagation of VT. Selected areas of ventricular tissue are destroyed by local heating. The ideal VT for catheter ablation has the following features: 1) the tachycardia is easily and reproducibly inducible with programmed stimulation or burst pacing; 2) the tachycardia is associated with a discrete scar (MI) or a structurally normal heart; 3) the VT is monomorphic, with only one tachycardia morphology observed both clinically and in the electrophysiology laboratory; and 4) the tachycardia is well-tolerated hemodynamically. Examples include RVOT tachycardias, idiopathic left ventricular tachycardias, and hemodynamically tolerable infarct-related VT. Bundle-branch reentrant VT is another form of VT that can be successfully treated by ablating the right or left bundle branch, a critical limb of the macroreentrant circuit which involves the His-Purkinje system (Fig. 3). Patients with VT that arises from nonischemic cardiomyopathies are generally more difficult to ablate. Techniques are being developed which target the anatomic substrate for VT. These techniques will undoubtedly extend the clinical applicability of catheter ablation to patients with multiple VT morphologies and VT, which is not mappable using standard mapping techniques. Patients with PVT or VF are not typically candidates for ablative therapy; an important exception is patients with WPW in whom cardiac arrest results from extremely rapid, pre-excited AF or atrial flutter. In these patients, successful ablation of the accessory pathway is curative, and primary therapy for VF is not indicated. Risks of catheter ablation include local complications related to venous and arterial cannulation (bleeding, infection, pseudo-aneurysm formation, thrombosis), cardiac perforation, and stroke.
Implantable Cardioverter-Defibrillator (ICD) Therapy
The first human ICD implantation was performed in 1980 (5). The first ICD systems consisted of both a bulky generator implanted in the abdomen and an epicardial lead system which required an open thoracotomy for implantation. The leads were subcutane-ously tunneled to the generator. Implantation required surgical expertise, and was associated with significant morbidity and mortality. ICD implantation has since become simpler and safer. Improvements in capacitor design have allowed for a significant decrease in generator size, and still provides adequate shock energies. Current generators can be implanted subcutaneously in the pectoral region, and improvements in lead design have allowed the development of a non-thoracotomy endocardial system, which
BASELINE- AFIB BUNDLE-BRANCH
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