Modified VT 45%
No Inducible VT
Acute Effect of VT ablation in 108 patients
Acute Effect of VT ablation in 108 patients
patient. Ablation abolished all inducible monomorphic tachycardias in 33% patients, tachycardias were inducible but modified in 45% of patients, and the procedure failed to abolish targeted, inducible tachycardias in 22% of patients (Fig. 6). During mean follow-ups ranging from 12-18 mo, 66% of patients remained free of recurrent tachycardia and 34% suffered one or more tachycardia recurrences. Spontaneous tachycardia recurred more frequently in patients whose arrhythmia substrate was modified, as opposed to those with no inducible tachycardia at the end of the procedure—but less often than in patients whose tachycardia was not altered by ablation. Sudden death occurred in 2.8% of patients—the majority of patients in all three series had implantable cardioverter defibrillators (ICDs).
Of the 180 patients reported in these four series, complications occurred in 10%; the most frequent were: atrioventricular (AV) block caused by ablation in the region of the conduction system, complications of arterial access, and pericardial effusion without tamponade (60-63) (Fig. 6). Procedure-related mortality was 1%. In a recent multicenter trial of catheter ablation using a saline-cooled ablation catheter in 146 patients (82% with prior MI), procedural mortality was 2.7% and the risk of stroke was 2.7% (64). When extensive lesions have been created in ventricular scar, anticoagulation with warfarin is recommended, although the efficacy and optimal duration of this therapy has not been established (65). Chronic warfarin therapy is a reasonable consideration for many of these patients because of associated severe ventricular dysfunction. These procedures are relatively difficult, as indicated by the average procedure duration of 4.8 h and fluoroscopy time of 56 min in the multicenter study (64). During follow-up, the major cause of mortality is heart failure, with a mortality of approx 10% over the following 12-18 mo (60-64). The high risk of heart failure is not unexpected, given the antecedant history of heart failure and depressed ventricular function in this patient population. However, damage to the adjacent contracting myocardium outside the infarct, or injury to the aortic or mitral valves, are procedural complications that could exacerbate heart failure. Attention to restriction of ablation lesions to regions of the infarct is prudent. As noted previously, sudden death is rare, but the majority of patients have ICDs.
Control of frequent, symptomatic shocks from an ICD has emerged as a major reason for catheter ablation in patients with VT after MI (63,66). In the year following defibrillator implantation, 60% of patients will be hospitalized again, usually for control of recurrent arrhythmias. Addition of an antiarrhythmic drug is required in more than 25% of patients. Catheter ablation can allow control of recurrent arrhythmias, avoiding drug toxicity and the adverse impact of many drugs—particularly amiodarone, on defibrillation threshold. Antiarrhythmic drugs can also slow the rate of spontaneous VT, making discrimination of VT from sinus tachycardia more difficult and leading to inappropriate defibrillator therapies. Because VT is usually associated with depressed ventricular function and a risk of sudden death, catheter ablation does not replace the need for an ICD in most patients. In some patient populations, the risk of sudden death may be acceptably low, and successful ablation may be adequate therapy (60). Ablation should be considered reasonable initial therapy for incessant VT, and can be life-saving in this situation (67,68).
In right ventricular dysplasia, portions of the right ventricle are replaced by fibrous or fatty tissue (69). Scar-related reentry circuits occur, giving rise to tachycardias that usually have a LBBB-like configuration. When involvement is sufficient to produce detectably depressed right ventricular function, the success of ablation is variable (70,71). Individual tachycardias can often be targeted and ablated, but other tachycardias can recur later, possibly related to progression of the disease process. We usually reserve ablation as a palliative therapy to control frequent episodes of tachycardia. Although the right ventricle can be quite thinned, the risk of perforation during mapping does not appear to be substantially increased, but reported series are small.
In patients with idiopathic nonischemic causes of cardiomyopathy, the mechanisms of sustained monomorphic VT are more diverse. Scar-related reentry is most common, but bundle-branch reentry and focal automaticity also occur (10,68). Discrete regions of scarring are often identified based on electrograms. Scar-related VT also occurs in patients with cardiac sarcoidosis (5), scleredema (72), Chagas' disease (73), and late after repair of tetralogy of Fallot (74-76). Experience with ablation is confined to small series and case reports. Results are somewhat similar to those for patients with prior MI; multiple tachycardias are not rare, but reduction in number of episodes and termination of incessant tachycardia can often be achieved.
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