
Association of ventricular ectopy with nuclear scintigraphic perfusion defects during dipyridamole stress testing
Author(s) -
Rabin David L.,
Ali Amjad,
Barron John T.
Publication year - 1998
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.4960210207
Subject(s) - dipyridamole , medicine , perfusion , cardiology , thallium , ventricular tachycardia , stress testing (software) , inorganic chemistry , chemistry , computer science , programming language
Background and hypothesis : No information is available regarding the significance of ventricular ectopic activity induced during dipyridamole nuclear scintigraphic stress testing. This study tested the hypothesis that dipyridamole‐induced ventricular ectopy predicts a thallium‐201 or technetium‐99m sestamibi perfusion defect. Methods : A group of 186 consecutive patients with premature ventricular contractions and/or couplets occurring during dipyridamole stress testing (ventricular tachycardia did not occur) was compared with a control group of 194 patients without ventricular ectopy during dipyridamole stress testing. Results : The results indicated that ventricular ectopy induced during dipyridamole infusion occurred more frequently in patients demonstrating either a fixed or reversible perfusion defect on scintigraphic imaging (p <0.01). The higher frequency of perfusion defects in this group of patients was attributable to a higher frequency of “fixed” compared with “reversible” defects (p<0.05). This finding is consistent with the additional observation that ventricular ectopy induced by dipyridamole was associated with the presence of Q waves on the resting ECG (p<0.05). The positive and negative predictive values of the presence of ventricular ectopy in predicting a fixed myocardial perfusion defect were 59 and 54%, respectively. Conclusions : Ventricular ectopy induced during dipyridamole infusion suggests the presence of a fixed myocardial perfusion defect.