Catheter Ablation for Prevention of Ventricular Tachycardia

Usha B. Tedrow; William G. Stevenson


Abstract and Introduction


Patients with structural heart disease are at risk for life-threatening ventricular tachycardias (VTs). Implantable cardioverter-defibrillators (ICDs) can terminate VT, but often at the cost of traumatic shocks, syncope, or even exacerbation of underlying heart disease. Catheter ablation for VT can reduce the need for ICD therapies and is an increasingly important adjunct to the treatment of these patients.


Kuck et al. have reported encouraging data from the multicenter, prospective randomized VTACH trial,[1] in which a strategy of catheter ablation before cardioverter-defibrillator implantation was assessed in patients with hemodynamically stable ventricular tachycardia (VT) with associated prior myocardial infarction. The investigators found that prophylactic ablation prolonged the time to recurrence of VT or ventricular fibrillation, and reduced the incidence of implantable cardioverter-defibrillator (ICD) shocks and hospital admissions for cardiac causes when compared with ICD therapy without ablation.

ICDs terminate VT or ventricular fibrillation with a high degree of efficacy, aborting cardiac arrest, often within seconds. This benefit translates to improved survival, not only in patients who have been resuscitated from cardiac arrest, but also in other high-risk populations, such as patients with prior myocardial infarction and inducible VT or severely depressed ventricular function.[2,3] ICDs are also recommended for patients with structural heart disease and sustained VT that is hemodynamically stable.[2,3] However, the question remains—is an ICD enough? ICDs terminate ventricular arrhythmias, but do not prevent them. Many VTs are terminated by a painless burst of antitachycardia pacing before symptoms occur. Palpitations, presyncope, and occasionally syncope occur in some patients, particularly if multiple pacing attempts are required for termination. Other arrhythmias require shocks for termination; these are painful and reduce the patient's quality-of-life.[4,5]

For many years after the introduction of ICD therapy, patients who experienced a shock terminating an arrhythmia were reassured that all was well, and that the device was providing effective protection. It is now clear that such optimism is not always warranted. Patients who have depressed ventricular function (the vast majority of ICD recipients) who experience a therapy from their ICD have a greater risk of hospitalization for heart failure and death.[6,7] The explanation for this observation is not clear. Ventricular arrhythmia may be a marker for underlying disease progression; however, it has also been suggested that ICD shocks in particular could have an adverse effect on cardiac function.[8] Thus, for many patients, an ICD is not sufficient and additional therapies to prevent VT are needed. Antiarrhythmic drugs can reduce arrhythmia recurrences, but are incompletely effective. Drug toxicities are also a major limitation, particularly with the most effective drug, amiodarone.

Ventricular scars are a major source of substrate for ventricular arrhythmias. Scars causing VT contain myocyte bundles separated by fibrosis, resulting in slow conduction and heterogeneous recovery that facilitates re-entry. The resulting VT is typically monomorphic, with each QRS complex resembling the preceding and following complex. VT can degenerate to ventricular fibrillation as ischemia and hypotension develop, particularly in patients with impaired ventricular function. Although scars from a healed myocardial infarction are the most well-recognized cause, scar-related VT also occurs in patients with nonischemic dilated cardiomyopathies, arrhythmogenic right ventricular cardiomyopathy, and surgically repaired congenital heart disease. Scars can be identified as areas of fixed hypoperfusion on coronary perfusion imaging, delayed gadolinium enhancement on MRI, or absent metabolism on PET imaging. In the electrophysiology laboratory, scars can be identified as a region of low amplitude electrograms (Figure 1), facilitating the identification of potential re-entry circuit sites that can then be targeted for ablation with limited mapping, or without mapping during VT. This approach facilitates ablation when VT is hemodynamically unstable or when, as is often the case, a scar contains multiple potential re-entry circuits giving rise to several different VTs.

Figure 1.

A voltage map of the left ventricle viewed from the right anterior oblique projection. This map was created by moving a mapping catheter from point-to-point across the endocardial surface of the ventricle. Colors represent electrogram voltage: purple is normal, electrogram amplitude diminishes progressively below 1.5 mV from blue to green, to yellow to red. Ventricular scar is indicated by voltages less than 1.5 mV and unexcitable dense scar is marked in gray. A large septal infarct scar is present that supported multiple re-entry circuits causing recurrent ventricular tachycardias. Ablation sites (maroon circular tags) abolished ventricular tachycardia in this patient.

The anatomy of the scar is an important determinant of the ablation approach and the success of the procedure. Scars from a previous myocardial infarction often produce re-entry circuits that can be ablated from the endocardium. In cardiomyopathies, scar locations are more variable. Epicardial mapping and ablation—now routinely performed with percutaneous techniques in many laboratories—are often required. Intramural re-entry circuits that can not be ablated with these approaches also occur. Ablation within areas of scar is strategically attractive, as these regions are less likely to contribute to ventricular contraction, and thus ablation in the scar does not appear to depress ventricular function.[9]

Ablation has generally been reserved for patients with recurrent episodes of VT refractory to antiarrhythmic drug therapy.[4,10] Recurrent VT is eliminated by ablation in approximately half of patients who have experienced a myocardial infarction, and more than two-thirds experience a marked reduction in the frequency of VT episodes.[4] Procedure-related mortality is approximately 3% in such patient populations with ischemic heart disease,[4] and is largely caused by uncontrollable VT, which, in most cases, is likely to be a failure of the procedure rather than an adverse effect. Could the earlier use of ablation, before multiple recurrences of VT, improve outcomes and quality of life for patients receiving ICDs?

This question was addressed by Reddy and colleagues, who randomly assigned patients with prior myocardial infarction and hemodynamically unstable VT who were receiving an ICD, to ablation or to no ablation.[9] The addition of ablation led to a reduction in VT recurrences, with a favorable trend towards increased survival, but the study was not sufficiently powered to assess the impact on mortality. In this new analysis by Kuck and colleagues, 71% of patients who did not undergo ablation (n = 55) experienced a recurrence of VT by 2 years of follow-up and had a median of three ICD therapies per year.[1] By contrast, VT recurred in 53% of patients in the ablation group (n = 52). Ablation before device implantation also extended the time to recurrent VT from a median of 5.9 months to a median of 18.6 months (hazard ratio [HR] 0.61, 95% CI 0.37–0.99, P = 0.045), and increased the proportion of patients who survived free from cardiac hospitalization (67.4% versus 45.4%; HR 0.55, 95% CI 0.30–0.99, P = 0.044). Half of the patients who underwent ablation still experienced at least one recurrence of VT. There was no procedure-related mortality associated with ablation, but one patient suffered a transient cerebral ischemic attack. The trial did not, however, have sufficient power to assess an impact on mortality, and patient quality-of-life did not differ between the two treatment groups.[1]

These and other studies have demonstrated that catheter ablation has an important, and often life-saving, role for patients with frequent or incessant VT. We see many patients who suffer post-traumatic stress syndrome from ICD shocks due to VT that is subsequently abolished by catheter ablation. Earlier use of catheter ablation has the potential to greatly mitigate the impact of VT on these patients. The VTACH trial and other accumulated data support the use of catheter ablation, before multiple VT recurrences.[4] However, more research is needed before we will know if early use of ablation to reduce VT episodes will improve survival or other outcomes, warranting routine ablation before the first VT recurrence. Importantly, catheter ablation for VT should be undertaken in centers with expertise in the procedure, as center and operator experience are likely to affect risks, benefits, and patient outcomes.