Detection of the diastolic pathway, circuit morphology, and inducibility of human postinfarction ventricular tachycardia from mapping in sinus rhythm.
OBJECTIVE
The purpose of this study was to determine whether sinus rhythm activation maps could be used to detect the origin and characteristics of reentrant ventricular tachycardia in postinfarction patients.


METHODS
In each of 11 post-myocardial infarction patients, unipolar electrograms were acquired at 256 virtual endocardial sites using noncontact mapping. Electrograms were marked for activation time and mapped on a three-dimensional grid. Spatial differences in sinus rhythm activation time were correlated to isthmus characteristics and to activation through the diastolic pathway during tachycardia on the basis of the presence of contiguous lines of slow conduction and block.


RESULTS
Twenty tachycardia morphologies were analyzed. Fourteen sustained reentrant circuit morphologies occurred in nine patients, with dual morphologies having a shared isthmus occurring in five of nine patients. Dual morphologies were caused by changes in entrance-exit point location about a common isthmus. One transient circuit morphology of <10 beats occurred in three of nine patients also having sustained reentry. The estimated isthmus determined from sinus rhythm activation overlapped the diastolic pathway determined from tachycardia maps with 83.8% sensitivity and 89.2% specificity. The mean difference in sinus rhythm activation time across the isthmus border was larger in transient compared with sustained morphologies (32.8 +/- 9.5 ms vs. 22.8 +/- 1.8 ms), with smaller isthmus size (4.8 +/- 1.1 cm(2) vs. 10.0 +/- 1.1 cm(2); P < .05), narrower entrance-exit points (7.0 +/- 1.5 mm vs. 9.3 +/- 0.8 mm; P < .05), and greater activation time difference across them (16.3 +/- 3.5 ms vs. 10.1 +/- 1.0 ms; P < .05).


CONCLUSIONS
In post-myocardial infarction patients, the reentry isthmus can be localized in the endocardial border zone from sinus rhythm activation maps. Nonsustained reentry occurs when isthmus size is small and entrance-exit points are narrow and more electrically discontinuous.
Ciaccio
Edward J
EJ
Department of Pharmacology, Columbia University, New York, New York 10032, USA. ciaccio@columbia.edu
Chow
Anthony W
AW
Kaba
Riyaz A
RA
Davies
D Wyn
DW
Segal
Oliver R
OR
Peters
Nicholas S
NS
D018780:Body Surface Potential Mapping; D003971:Diastole; D005260:Female; D006329:Heart Conduction System / Q000503:physiopathology*; D006801:Humans; D008297:Male; D009203:Myocardial Infarction / Q000150:complications / Q000503:physiopathology*; D012680:Sensitivity and Specificity; D017180:Tachycardia, Ventricular / Q000175:diagnosis* / Q000209:etiology / Q000503:physiopathology*