Endocardial Voltage Mapping to Evaluate RVOT Tachycardias
Abstract & Commentary
By John P. DiMarco, MD, PhD
Source: Corrado D, et al. Three-dimensional electroanatomical voltage mapping and histologic evaluation of myocardial substrate in right ventricular outflow tract tachycardia. J Am Coll Cardiol. 2008;51:731-739.
In this paper, corrado and colleagues describe the results of endocardial voltage mapping (EVM) and endomyocardial biopsy (EMB) in 27 patients with ventricular arrhythmias who were suspected to have a subtle manifestation of arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D). The patients were selected from a larger group of 89 consecutive patients with right ventricular outflow tract ventricular tachycardia (VT) (sustained or nonsustained ventricular tachycardia or frequent premature beats) studied in their laboratory. For all patients, the baseline evaluation included a history, a physical examination, laboratory tests, chest radiography, electrocardiography, Holter monitoring, signal averaged electrocardiography, exercise testing, echocardiography, and right and left ventricular cineangiography. All patients in this series had normal right and left ventricular cavity dimensions and function and, therefore, did not meet established criteria for the diagnosis of ARVC/D. However, 27 of the 89 patients included in this report were selected for further study because they had one or more of the following findings: family history of sudden death, presyncope, competitive athletic activity, QRS duration greater than 110 m/sec in the right precordial leads, late potentials on signal averaged electrocardiography, and inverted T waves in the inferior leads.
At the time of electrophysiologic study, patients underwent detailed EVM using the Biosense Webster CARTO system. Sites with local bipolar electrograms with an amplitude of less than 0.5 mV were considered to be electroanatomical scar tissue. Complete endocardial voltage maps were obtained in all patients. Patients in the series also underwent EMB of the right ventricle via the femoral vein using a long sheath technique. Samples were obtained from the anterior right free ventricular free wall abutting the ventricular septum. A final diagnosis of early ARVC/D was made on the basis of a significant amount of myocardial atrophy and fibrofatty tissue replacement. Electrophysiologic study was performed using both a ventricular stimulation protocol, as well as isoproterenol infusions. In selected patients with inducible sustained or frequent sustained ventricular tachycardia, or reproducible monomorphic ventricular ectopy, catheter ablation was attempted.
The study population consisted of 27 patients, including 15 men and 12 women. They ranged in age from 16 to 51 years. All patients had a clinical history of a left bundle branch block/inferior axis ventricular tachycardia pattern that had been sustained in 17 and nonsustained in 10. Endomyocardial biopsy showed significant myocardial atrophy and fibrofatty replacement consistent with ARVC/D in six patients, while no histologic abnormalities were found in the remaining 21. Electroanatomical voltage mapping was normal in 20 patients and abnormal in seven. The latter patients showed a mean of 1.4 discrete areas of electroanatomical scar tissue in the right ventricle. Five patients had electroanatomical scars in the anteroinfundibular region, whereas two patients had multiple areas of scar. Programmed ventricular stimulation induced one or more sustained ventricular tachycardias in six patients. Five of these six were in the abnormal EVM group. In the remaining 21 patients, isoproterenol was required to initiate arrhythmia. Catheter ablation was attempted in 20 of 27 patients and was acutely successful in 18 of 20 patients. During long-term follow-up, ventricular tachycardia recurred in 10 of 27 patients. The recurrence rate was 17% after successful catheter ablation and 78% in those with either no ablation or an unsuccessful attempt. Three patients, all of them in the abnormal EVM group, required ICD therapy because of life-threatening VT during follow-up. When patients with normal and abnormal EVM were compared, several differences were observed. Patients with abnormal EVM were more likely to manifest a prolonged right precordial QRS duration, VT inducibility with programmed stimulation, late potentials on signal averaged ECG, and histopathologic abnormalities on EMB.
Corrado et al conclude that an early form of ARVC/D may be difficult to distinguish from idiopathic right ventricular outflow tract tachycardia. Electroanatomical mapping to determine areas of low voltage scar is helpful in assessing prognosis in these patients.
Commentary
In patients with structurally normal hearts and ventricular arrhythmias, the most common site of origin is the right ventricular outflow tract, and the ECG typically shows a left bundle branch block pattern with an inferior axis. A similar ECG pattern during tachycardia may also be seen in patients with ARVC/D, and if the anatomic findings are subtle, differentiating between the normal heart VT, which has a benign prognosis and ARVC/D, which may be life-threatening, can be difficult. In this paper, a group of Italian investigators demonstrate the voltage mapping in the right ventricle may be very helpful for making this distinction. EVM is a relatively simple 3D mapping technique that is safe and fairly easy to perform. If the patient is to undergo a catheter ablation attempt, the voltage map is obtained as part of the procedure and can be easily examined. If drug therapy is planned, EVM should still be considered if the patient has any of the other high-risk test findings.
ARVC/D is more common in Northern Italy than in the United States, and more frequently occurs in a familial pattern. In the United States, most patients with apparently normal hearts and VT will not have ARVC/D, but it is important not to miss this diagnosis.
In this paper, corrado and colleagues describe the results of endocardial voltage mapping (EVM) and endomyocardial biopsy (EMB) in 27 patients with ventricular arrhythmias who were suspected to have a subtle manifestation of arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D).You have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
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