title: Relation between ventricular late endocardial activity during intraoperative endocardial mapping and low-amplitude signals within the terminal QRS complex on the signal-averaged surface electrocardiogram.
abstract: Noninvasive recording of ventricular late potentials and intraoperative endocardial mapping at 36 sites were performed in 24 patients with left ventricular aneurysm and drug-resistant sustained ventricular tachycardia due to coronary artery disease. Their mean age was 55 +/- 8 years. Mean ejection fraction was 28 +/- 12%. For detection of late potentials on the signal-averaged QRS complex, 3 different algorithms were used. Late potentials were found in 54, 67 and 67% of the patients, respectively. In patients with a late potential on the signal-averaged electrocardiogram (ECG), delayed local activation (greater than 40 ms beyond the QRS complex on the intraoperative surface ECG) was recorded at 5.5, 5.5 and 5.6 endocardial sites. In patients without a late potential, this type of delayed local activation was detected at 2.4, 1.1 and 0.9 of 36 endocardial sites, respectively (p less than 0.05; p less than 0.01; p less than 0.002). The mean delay of local endocardial activity was 38, 35 and 37 ms in patients with a late potential on the body surface recording versus 20, 19 and 11 ms, respectively, in patients without a late potential (p less than 0.05; p less than 0.05; p less than 0.002). There was no correlation between the duration or amplitude of the late potential, if present, and the number of endocardial sites exhibiting delayed activity (r = -0.23, r = -0.05, r = 0.21; correlation not significant for each) or the mean duration of the endocardial delayed activity (r = -0.25, r = -0.14, r = -0.07; correlation not significant for each). These results indicate that the presence of late potentials on the signal-averaged surface ECG is related to the mean duration of endocardial late activity as well as to the number of endocardial sites exhibiting a given degree of delayed activation. Thus, it is dependent on the mass of slowly activated tissue. However, a direct conclusion from the duration or the amplitude of a late potential to the amount of delayed activation or the extent of endocardial time delay does not seem possible.
authors.affiliation: Department of Cardiology and Angiology, Hospital of the University of Münster, Germany.
authors.forename: H J
authors.initials: HJ
authors.lastname: Schwarzmaier
authors.forename: U
authors.initials: U
authors.lastname: Karbenn
authors.forename: M
authors.initials: M
authors.lastname: Borggrefe
authors.forename: J
authors.initials: J
authors.lastname: Ostermeyer
authors.forename: G
authors.initials: G
authors.lastname: Breithardt
mesh_terms: D000465:Algorithms; D004562:Electrocardiography / Q000379:methods*; D004699:Endocardium / Q000503:physiopathology* / Q000601:surgery; D005260:Female; D006322:Heart Aneurysm / Q000209:etiology / Q000503:physiopathology* / Q000601:surgery; D006352:Heart Ventricles / Q000503:physiopathology / Q000601:surgery; D006801:Humans; D007430:Intraoperative Care / Q000379:methods*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications; D012044:Regression Analysis; D013610:Tachycardia / Q000209:etiology / Q000503:physiopathology* / Q000601:surgery; D014693:Ventricular Fibrillation / Q000209:etiology / Q000503:physiopathology* / Q000601:surgery