Mechanisms underlying different surface ECG morphologies of recurrent monomorphic ventricular tachycardia and their modification by procainamide.
BACKGROUND
Distinct surface ECG morphologies (ECGMs), from one episode to the next, of recurrent monomorphic ventricular tachycardia (VT) in the same patient complicate endocardial catheter mapping and the success of ablative therapy. This study investigates the incidence and mechanisms of multiple ECGMs during recurrent monomorphic VTs in a canine model of experimental myocardial infarction (MI).


RESULTS
Computerized ECG analysis and simultaneous endocardial and epicardial activation mapping with a 64 bipolar electrode array were used to analyze the relation between site of VT origin, local activation sequence, and surface ECGM in 72 VT episodes induced in 9 of 17 dogs with experimental MI. Pairwise comparisons of all VTs induced in the same animal were done in drug-free state (47 VTs) and after intravenous procainamide (25 VTs). In drug-free state, VT pairs with similar surface ECGMs manifested endocardial breakthrough sites (BSs) within a distance < 10 mm in 46 (100%) of 46 VT pairs compared to 43 (45%) of 95 VT pairs with different surface ECGMs (P < 0.0001). Of all 89 VT pairs with endocardial BSs within < 10 mm, similar endocardial activation patterns were found in 34 (74%) of 46 pairs with similar ECGMs in contrast to 6 (14%) of 43 pairs with different ECGMs (P < 0.001). Similar comparisons of VT pairs induced after intravenous procainamide administration showed that the endocardial BSs were located within < 10 mm in 9 (75%) of 12 VT pairs with similar and in 17 (49%) of 95 with different surface ECGMs, respectively (P = NS).


CONCLUSIONS
In the same heart, similar surface ECGMs of recurrent VT are highly predictive of closely spaced endocardial BSs in drug-free state, but not after procainamide administration. Nearly half of the VTs with different surface ECGMs still originate from closely spaced endocardial BSs but commonly manifest a change in the endocardial activation spread from this site. Thus, assumptions about different mechanisms and sites of VT origin based on different surface ECGMs should be made with caution.
Osswald
S
S
Harvard Medical School, Massachusetts General Hospital, Boston 02114, USA.
Wilber
D J
DJ
Lin
J L
JL
Du
D
D
Holden
H B
HB
Ruskin
J N
JN
Garan
H
H
D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000008:administration & dosage*; D004285:Dogs; D004562:Electrocardiography / Q000187:drug effects*; D007275:Injections, Intravenous; D009203:Myocardial Infarction / Q000503:physiopathology*; D011342:Procainamide / Q000008:administration & dosage*; D014693:Ventricular Fibrillation / Q000188:drug therapy / Q000503:physiopathology*
D000889:Anti-Arrhythmia Agents; D011342:Procainamide