Ventricular Tachycardia in Cardiac Sarcoidosis | Journal Scan
What are the characteristics of the arrhythmogenic substrate and outcomes of catheter ablation in patients with sarcoid-related ventricular tachycardia (VT)?
Cases of cardiac sarcoidosis were identified in a series of 435 patients with nonischemic cardiomyopathy referred for catheter ablation of sustained monomorphic VT, frequent premature ventricular contractions, or nonsustained VT from 1997 to 2014.
Twenty-one patients (5%) had cardiac sarcoidosis. Multiple inducible VTs were observed with a mechanism consistent with scar-mediated re-entry in all VTs. Voltage maps showed widespread and confluent right ventricular (RV) scarring. Left ventricular (LV) scarring was patchy with a predilection for the basal septum, anterior wall, and perivalvular regions. Epicardial RV scar overlayed and exceeded the region of corresponding endocardial scar. After procedures, ablation abolished at least one inducible VT in 90% and eliminated VT storm in 78% of patients; however, multiple residual VTs remained inducible. Failure to abolish all inducible VTs was due to septal intramural circuits or extensive RV scarring. Multiple procedure VT-free survival was 37% at 1 year, but VT control was achievable in the majority of patients with fewer antiarrhythmic drugs compared with preablation.
Patients with cardiac sarcoidosis and VT exhibit ventricular substrate characterized by confluent RV scarring and patchy LV scarring capable of sustaining a large number of re-entrant circuits. Catheter ablation is effective at terminating VT storm and eliminating ≥1 inducible VT in the majority of patients, but recurrences are common. Ablation in conjunction with antiarrhythmic drugs can help palliate VT in this high risk-population.
Patients with cardiac sarcoidosis and VT are very challenging to treat. First-line treatment is usually immunosuppression and antiarrhythmic drugs. When these therapies are ineffective, VT ablation is very appropriate. Unfortunately, in many patients, the arrhythmogenic substrate is capable of sustaining a large number of re-entrant VT circuits, and in most cases, a reduction in VT burden, rather than elimination of all VTs, is achieved with ablation. This study illustrates a very important point—delayed diagnosis of patients with cardiac sarcoidosis. Out of 21 patients in the series, six patients were not receiving immunosuppression prior to ablation, as the diagnosis was made after the electrophysiologic study, including two who had cardiac transplant granulomatous inflammation identified in the explanted heart, and four diagnosed immediately after ablation who were subsequently started on immunosuppressants. This highlights the need to investigate the arrhythmogenic substrate in patients with nonischemic cardiomyopathy and recurrent VT for possible treatable conditions with the use of advanced imaging such as cardiac magnetic resonance imaging and positron emission tomography.
Keywords: Tachycardia, Ventricular, Sarcoidosis, Catheter Ablation, Arrhythmias, Cardiac, Anti-Arrhythmia Agents, Cardiomyopathies, Immunosuppressive Agents, Ventricular Premature Complexes, Electrophysiologic Techniques, Cardiac
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