The Changes of Ventricular Activation Time According to Acute Myocardial Ischemia.
10.4070/kcj.2001.31.3.317
- Author:
Seong Wook HAN
;
Yoon Nyun KIM
;
Ki Young KIM
;
Chang Wook NAM
;
Kee Sik KIM
;
Kwon Bae KIM
- Publication Type:Original Article
- MeSH:
Action Potentials;
Angina, Stable;
Angina, Unstable;
Electrocardiography;
Endocardium;
Female;
Humans;
Ischemia;
Male;
Middle Aged;
Myocardial Infarction;
Myocardial Ischemia*;
Pericardium;
Thoracic Surgery, Video-Assisted
- From:Korean Circulation Journal
2001;31(3):317-326
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND AND OBJECTIVES: In acute myocardial ischemia, the conduction velocity of action potential is decreased by several electrophysiological and physical factors. The ventricular activation time(VAT) is a time duration of electrical impulse propagating from endocardium to epicardium. The goal of this study is to determine whether the reduction in conduction velocity in acute myocardial ischemia can lead a change in VAT. MATERIALS AND METHOD: Thirty patient, 18 males and 12 females, who had received percutaneous balloon coronary angioplasty(PTCA) were enrolled. The mean age was 59 years old. A twelve lead surface electrocardiogram(ECG) were obtained before, during, 1 minute, 5 minutes, and 10 minutes after the PTCA as digitized data by using Cardiolab EP 4.1 program. The magnitude of the QRS wave was amplified 3 to 4 folds and the speed was increased to 200mm/sec in order to get the VAT easily and accurately. The data was the mean of three consecutive VATs. The number of vessel treated with PTCA included left anterior descending artery(12), left circumflex artery(9), and right coronary artery(9). Among twelve chronic stable angina, sixteen unstable angina, and two acute myocardial infarction patients, twenty six had single and four had two vessel diseases. RESULTS: The significant increase in VAT during PTCA compared to that before PTCA was observed in eight of 12 leads. In addition, the significant decrease in VAT of 1, 5, and 10 minutes after PTCA compared to that during PTCA were noted. Furthermore, 10 minutes after PTCA, VAT decreased significantly compared to that before PTCA. The leads did not show a significant change of VAT depending on target vessels. The ECG of 16 patients showed changes of the ST segment during PTCA. The changes of VAT were not related to the ST segment change. CONCLUSION: The conduction delay from endocardium to epicardium in acute myocardial ischemia was presented as a prolongation of VAT in surface ECG. In addition, the conduction delay was recovered within 5 minutes after relief of ischemia. Therefore, the changes of VAT can possibly be used as one of the noninvasive parameters of myocardial ischemia.
