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Mechanism‐Specific Effects of Adenosine on Ventricular Tachycardia
Author(s) -
LERMAN BRUCE B.,
IP JAMES E.,
SHAH BINDI K.,
THOMAS GEORGE,
LIU CHRISTOPHER F.,
CIACCIO EDWARD J.,
WIT ANDREW L.,
CHEUNG JIM W.,
MARKOWITZ STEVEN M.
Publication year - 2014
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1111/jce.12510
Subject(s) - medicine , adenosine , cardiology , ventricular tachycardia , tachycardia , anesthesia
Mechanism Specific Effects of Adenosine on VT Introduction There is no universally accepted method by which to diagnose clinical ventricular tachycardia (VT) due to cAMP‐mediated triggered activity. Based on cellular and clinical data, adenosine termination of VT is thought to be consistent with a diagnosis of triggered activity. However, a major gap in evidence mitigates the validity of this proposal, namely, defining the specificity of adenosine response in well‐delineated reentrant VT circuits. To this end, we systematically studied the effects of adenosine in a model of canine reentrant VT and in human reentrant VT, confirmed by 3‐dimensional, pace‐ and substrate mapping. Methods and Results Adenosine (12 mg [IQR 12–24]) failed to terminate VT in 31 of 31 patients with reentrant VT due to structural heart disease, and had no effect on VT cycle length (age, 67 years [IQR 53–74]); ejection fraction, 35% [IQR 20–55]). In contrast, adenosine terminated VT in 45 of 50 (90%) patients with sustained focal right or left outflow tract tachycardia. The sensitivity of adenosine for identifying VT due to triggered activity was 90% (95% CI, 0.78–0.97) and its specificity was 100% (95% CI, 0.89–1.0). Additionally, reentrant circuits were mapped in the epicardial border zone of 4‐day‐old infarcts in mongrel dogs. Adenosine (300–400 μg/kg) did not terminate sustained VT or have any effect on VT cycle length. Conclusion These data support the concept that adenosine's effects on ventricular myocardium are mechanism specific, such that termination of VT in response to adenosine is diagnostic of cAMP‐mediated triggered activity.