|
|
||||||||
Ann Thorac Surg 1995;60:422-425
© 1995 The Society of Thoracic Surgeons
Department of Cardiovascular Surgery, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Japan
Accepted for publication March 20, 1995.
| Abstract |
|---|
|
|
|---|
Methods. We studied 21 patients after myocardial infarction with positive LPs who had at least one occluded infarct coronary artery. We investigated the LPs on signal-averaged electrocardiograms on the day of elective coronary artery bypass grafting (CABG) and 1 week after CABG.
Results. There were 25 infarct arteries in the study patients, 13 of which were grafted. The positive LPs disappeared soon after CABG in 13 patients, 10 of whom had grafts to all of the infarct arteries. The LPs persisted in 8, who received no graft to the infarct artery. One week after CABG, the LPs were still present in 4, all of whom had no graft to the infarct right coronary artery.
Conclusions. In patients with positive LPs late after myocardial infarction, grafting to the infarct artery eliminated the LPs soon after CABG.
| Introduction |
|---|
|
|
|---|
Late potentials are low-amplitude, high-frequency signals in the terminal portion of the QRS complex identified on signal-averaged electrocardiography [13]. They are correlated with the risk of subsequent ventricular tachyarrhythmic events and sudden death in patients with myocardial infarction [46]. Early reperfusion of ischemic myocardium within a few hours of the onset of myocardial infarction is important because it can reduce mortality, which mainly is due to decreased ventricular tachyarrhythmias [79], and can improve left ventricular function [1012]. This is in concordance with the findings that late potentials are detected more frequently in survivors of infarction without residual anterograde flow in the infarct artery than those with anterograde flow [13].
This study investigated whether positive late potentials are influenced by elective bypass grafting to the infarct-causing occluded artery in the late course after myocardial infarction. The goal was to clarify, from an antiarrhythmic point of view, the influence of revascularization of the infarct artery on the late potentials.
| Patients and Methods |
|---|
|
|
|---|
|
Coronary artery bypass grafting was performed using standard techniques, which included cardiopulmonary bypass with moderate systemic hypothermia. Cold potassium crystalloid cardioplegia was used for myocardial protection in all patients. The operation consisted of single bypass grafting in 4, double grafting in 12, triple grafting in 4, and quadruple grafting in 1 patient.
Signal-averaged electrocardiography was performed using an ART 101-PC (Arrhythmia Research Technology, Inc, Austin, TX) immediately after the operation in the intensive care unit, and 1 week after the operation. In each patient, three silver-silver chloride electrodes were placed in the standard bipolar orthogonal X, Y, Z configuration. Signals were amplified, digitized, averaged, and filtered with a bidirectional high-pass digital filter [2] with a corner frequency of 40 Hz for low-cut filtering and 250 Hz for high-cut filtering. The noise level was reduced to less than 1.0 µV. A QRS vector magnitude was calculated as V = (X2 + Y2 + Z2)1/2. The root mean square voltage of the terminal 40 ms of the filtered QRS (RMS40), the duration of the filtered QRS, and the duration of the low-amplitude signal less than 40 µV in the terminal QRS were determined by a computer algorithm. A late potential was defined as the presence of an RMS40 less than 20 µV and a total filtered QRS duration more than 114 ms or a low-amplitude signal duration more than 38 ms as described by Lange and associates [13].
Patients who underwent emergency CABG and those who received antiarrhythmic therapy before the operation were not included in this study.
All data are reported as mean ± standard deviation. Differences between the two groups were compared with the
2 test for categoric variables and Student's t test for continuous variables. A p value less than 0.05 was considered significant.
| Results |
|---|
|
|
|---|
|
|
Figure 1A
shows the signal-averaged electrocardiogram of a 62-year-old man with three-vessel coronary artery disease with late potentials. Coronary angiography showed a 90% stenosis in segment 2 of the right coronary artery, a total occlusion in segment 7 of the left anterior descending artery, and a 75% stenosis in segment 11 of the left circumflex. Coronary artery bypass grafting was performed using saphenous vein grafts to the right coronary artery, the left anterior descending artery, and the obtuse marginal branch of the left circumflex artery. The late potentials vanished on the signal-averaged electrocardiogram on the day of CABG (Fig 1B
).
|
| Comment |
|---|
|
|
|---|
Even late after myocardial infarction, the late potentials were influenced by the anterograde flow in the infarct artery that was obtained through the bypass graft. The presence of anterograde flow in the infarct artery restored within a few hours after infarction is associated with a low incidence of late potentials [13, 14]. Late potentials are thought to be the fragmented electrical activity caused by slowed and asynchronous conduction through ischemic myocardium [15], or to arise from border zone areas of myocardium in which normal myocardium is interspersed with fibrosis [3, 16]. Late after myocardial infarction, the coronary collateral vessels can not supply sufficient blood to the lesional subendocardium [17]. Anterograde perfusion of the infarct artery by the bypass graft may supply much blood flow to the ischemic myocardium so that the ischemic cells in the infarct area are electrically stable soon after CABG. We speculate that, in patients in whom late potentials were present after CABG, the ischemic myocardium may be persisting in the area of the ungrafted infarct artery. An alteration in remodeling of the infarction and the area adjacent to it may occur postoperatively.
As in previously published studies [5, 6, 13], infarct of the right coronary artery was associated with a high incidence of late potentials. Inferior myocardial infarction has a higher incidence of late potentials than anterior, because a particularly large amount of inferior myocardium with slow, fragmented intramyocardial conduction is required to create late potentials of sufficient magnitude [5, 6]. Late potentials identify the risk of subsequent arrhythmic events and sudden death in patients who have had myocardial infarction [46], so the revascularization of the infarct arteries, especially the occluded right coronary artery, may be important to produce an antiarrhythmic effect of CABG.
This study has certain limitations. First, there are no controls in this study. Ideally, we should have taken a control group of survivors of myocardial infarction without subjecting them to CABG and shown that their signal-averaged electrocardiographic findings were stable during a similar period of observation. Abnormalities in the signal-averaged electrocardiography are dynamic soon after acute myocardial infarction [4], and the interval from infarction to CABG was variable in the patients in this study. However, we studied the patients who underwent elective CABG at least several months after myocardial infarction. Second, the indication for revascularization of the infarct-related artery is not clear. The reason is that operative techniques varied by surgeon. If, in the surgeon's opinion, the vessel was small and noncritical, as in the case of a nondominant right coronary artery, the infarct right coronary artery was left ungrafted. With these limitations in mind, we conclude that in patients who have had myocardial infarction with positive late potentials, the late potentials disappear soon after CABG if the infarct-causing occluded vessel is grafted. The late potentials persist in patients who have no graft to the infarct artery.
| Footnotes |
|---|
|
|
|---|
| References |
|---|
|
|
|---|
Related Article
This article has been cited by other articles:
![]() |
Y. Terada Did the Global Myocardial Ischemia Produce an Influence On High-Frequency QRS Potentials? Ann. Thorac. Surg., October 1, 2005; 80(4): 1563 - 1564. [Full Text] [PDF] |
||||
![]() |
A. John, C. Glauner, M. A. Manoutcheri, V. Ziaukas, G. M. Mahesh, and H. Warnecke Aortic Valve Replacement with the Medtronic Freestyle Stentless Bioprosthesis Asian Cardiovasc Thorac Ann, September 1, 2004; 12(3): 213 - 217. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Matsushita, Y. Sakakibara, T. Imazuru, M. Noma, Y. Hiramatsu, O. Shigeta, T. Jikuya, and T. Mitsui High-frequency QRS potentials as a marker of myocardial dysfunction after cardiac surgery Ann. Thorac. Surg., April 1, 2004; 77(4): 1293 - 1297. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Gaudino, F. Alessandrini, F. Glieca, N. Luciani, C. Cellini, C. Pragliola, M. Morelli, F. Girola, and G. Possati Effect of surgical revascularization of a right coronary artery tributary of an infarcted nonischemic territory on the outcome of patients with three-vessel disease: A prospective randomized trial J. Thorac. Cardiovasc. Surg., February 1, 2004; 127(2): 435 - 439. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. Scharf, H. Redecker, F. Duru, R. Candinas, H. P. Brunner-La Rocca, A. Gerber, O. Bertel, M. I. Turina, and W. Kiowski Sudden cardiac death after coronary artery bypass grafting is not predicted by signal-averaged ECG Ann. Thorac. Surg., November 1, 2001; 72(5): 1546 - 1551. [Abstract] [Full Text] [PDF] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |