I right ventricular outflow tract (RVOT) tachycardia is a well-described example of an adrenergically mediated form of ventricular tachycardia (VT).1 The mechanism responsible for RVOT VT is cyclic adenosine monophosphate-mediated triggered activity. A characteristic and identifying feature of this form of VT is termination in response to a bolus dose of adenosine, which is believed to be related to its antiadrenergic effects. This effect of adenosine on RVOT tachycardia may be mediated on at least 2 sites: (1) the cardiac myocyte,2 and (2) the presynaptic postganglionic sympathetic nerve fibers.3 Although continuous intravenous infusion of adenosine increases sympathetic nerve traffic,4 we have previously demonstrated that a bolus of adenosine results in a biphasic response of muscle sympathetic nerve activity (MSNA).3 An initial increase in MSNA is immediately followed by profound sympathetic withdrawal. We therefore sought to determine if adenosine’s antiarrhythmic effects mediated on RVOT VT were solely related to its direct antiadrenergic effects at the cardiac myocyte, or were also temporally related to its potentially synergistic suppressive effects on MSNA, consistent with a presynaptic postganglionic mechanism of action. • • • We studied 3 patients with RVOT tachycardia who were referred for diagnostic cardiac electrophysiologic study and ablation. All subjects gave informed written consent for a protocol approved by the institutional review board. These patients had the repetitive monomorphic form of RVOT tachycardia.5 This phenotype is characterized by frequent ventricular ectopy as well as multiple episodes of spontaneous sustained VT that increase in frequency and duration during infusion of isoproterenol. This permitted collection of multiple data points within each patient. Patient characteristics are listed in Table 1. All patients had sustained VT with left bundle branch block and inferior axis morphology that terminated with an intravenous bolus of adenosine. VT cycle length in these patients was between 360 and 400 ms. Two patients had structurally normal hearts, and the 1 patient with nearly incessant VT had decreased left ventricular function (ejection fraction 35%). Cardiac catheterization and echocardiography in this patient demonstrated no significant coronary artery or valvular disease and the etiology of the cardiomyopathy was believed to be related to the tachycardia. Subjects underwent continuous recording of 12lead electrocardiography, continuous noninvasive blood pressure monitoring (Finapres, Ohmeda, Louisville, Colorado), and monitoring of respiratory cycles and peroneal MSNA. Peripheral sympathetic nerve traffic was measured by direct microneurographic recordings of efferent MSNA as previously described.6 Bursts of MSNA throughout the entire recording were manually marked. The onset (ti) and offset (tf) points of each burst were identified. The area (A) of each burst was calculated as the sum of the voltage (relative to baseline) Vi Vf at all times t within the burst (ti t tf). A baseline recording of 2 minutes was obtained at the beginning of each study. Bursts during the entire recording period were manually annotated and the area A of each burst was calculated as previously described. From this baseline 2-minute recording, the average of all burst areas was calculated, Aavg. For each subsequent portion of the study, the total area of all bursts AT (where AT is the sum of A for each individual burst during time period T) was calculated. The number of normalized bursts occurring during time T is N AT/Aavg. The frequency of normalized bursts is N/T in units of bursts per second. Continuous noninvasive blood pressure was analyzed as systolic, diastolic, and mean pressures (mm Hg) throughout the recordings. Analysis of variance for repeated measures within subjects was used to determine the statistical significance of changes observed before, during, and after episodes of VT. All data were expressed as mean SD. A p value 0.05 was considered statistically significant. Consistent with the adrenergic-mediated mechanism of RVOT tachycardia, all patients demonstrated an increase in ventricular ectopy as well as sustained VT frequency during infusion of isoproterenol (mean dose 1.5 g/min). Sustained VT was also initiated or terminated with programmed stimulation. Antiadrenergic perturbations that terminated VT included adenFrom the Department of Medicine, Division of Cardiology, The New York Hospital–Cornell Medical Center, New York, New York. This study was supported in part by the Mary and David Hoar Fellowship from the New York Academy of Medicine, New York, New York; Grants R01 56139 and M01RR00047 from the National Institutes of Health, Bethesda, Maryland; the John C. Sable Memorial Heart Fund, Henrietta, New York; Maurice and Corinne Greenberg Arrhythmia Research Grant, New York, New York; and the Raymond and Beverly Sackler Foundation, New York, New York. Dr. Lerman’s address is: Division of Cardiology, The New York Hospital–Cornell Medical Center, 525 East 68th Street, Starr 4, New York, New York 10021. E-mail: blerman@mail.med.cornell.edu. Manuscript received June 12, 2002; revised manuscript received and accepted August 14, 2002.
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