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Ann Thorac Surg 1995;60:422-425
© 1995 The Society of Thoracic Surgeons


Original Articles: Cardiovascular

Influence of Bypass Grafting to the Infarct Artery on Late Potentials in Coronary Operations

Yasushi Terada, MD, Toshio Mitsui, MD, Shounosuke Matsushita, MD, Naotaka Atsumi, MD, Tomoaki Jikuya, MD, Yuzuru Sakakibara, MD

Department of Cardiovascular Surgery, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Japan

Accepted for publication March 20, 1995.


    Abstract
 Top
 Footnotes
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
Background. Late potentials (LPs) after myocardial infarction identify the risk of arrhythmic events and sudden death, and the absence of anterograde flow in the infarct-causing occluded coronary artery frequently is associated with LPs on signal-averaged electrocardiography. The present study was designed to clarify the influence of revascularization of the infarct artery on the LPs in the late course after myocardial infarction.

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
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 Footnotes
 Abstract
 Introduction
 Patients and Methods
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 Comment
 References
 
See also page 425.

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
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 Footnotes
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
We studied 21 patients after myocardial infarction with positive late potentials who had at least one occluded infarct coronary artery (Table 1Go). The indication for coronary artery bypass grafting (CABG) was post–myocardial infarction angina.


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Table 1. . Clinical Profile
 
The infarct artery was identified by coronary angiographic evidence of a completely occluded coronary artery with evidence subendocardial or transmural (Q-wave) infarction at this site on electrocardiography. The left anterior descending artery was the infarct vessel in 6 of the 21 patients, the left circumflex in 1, the right coronary artery in 10, both left circumflex and right coronary artery in 2, both left anterior descending and right coronary artery in 1, and both left anterior descending artery and left circumflex in 1 (see Table 1Go).

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 {chi}2 test for categoric variables and Student's t test for continuous variables. A p value less than 0.05 was considered significant.


    Results
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 Footnotes
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
The positive late potentials disappeared soon after CABG in 13 patients, 10 of whom received grafts to all of the infarct arteries. The late potentials persisted in 8, who received no graft to the infarct artery (Table 2Go). The late potentials were still present a week after CABG in 4 patients, all of whom had no graft to the infarct right coronary artery.


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Table 2. . Late Potentials After Coronary Artery Bypass Grafting
 
There were 25 infarct arteries in the study patients, 13 of which were grafted (Table 3Go). Grafting of 12 of the infarct arteries eliminated the late potentials. Grafting of one infarct left anterior descending artery could not eliminate the late potentials in 1 patient, who received no graft to the infarct right coronary artery.


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Table 3. . Revascularization of Infarct Artery and Late Potentials
 
Between the patients with and without late potentials soon after CABG, there were no significant differences in aortic cross-clamp time (90.5 ± 37.5 versus 84.6 ± 40.2 minutes) and left ventricular function about 1 month after the operation (ejection fraction: 0.50 ± 0.14 versus 0.55 ± 0.18; end-diastolic pressure, 14.3 ± 2.7 versus 12.2 ± 5.1 mm Hg). There was no evidence of perioperative myocardial infarction.

Figure 1AGo 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 1BGo).



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Fig 1. . (A) Signal-averaged electrocardiogram of a 62-year-old man with three-vessel coronary artery disease with late potentials. The left anterior descending artery was occluded completely in segment 7. The darkened area represents RMS40 of the filtered QRS complex, from which the root mean square voltage was calculated. RMS40 is 14.3 µV, total filtered QRS duration is 96 ms, and low-amplitude signal duration under 40 µV is 41 ms. Note that RMS40 and the low- amplitude signal duration in signal-averaged electrocardiographic variables are abnormal and the late potentials are present. (B) Signal-averaged electrocardiogram of the patient soon after coronary artery bypass grafting with saphenous vein grafts to the right, the left anterior descending, and the left circumflex artery. RMS40 is 47.2 µV, total filtered QRS duration is 72 ms, and low-amplitude signal duration under 40 µV is 19 ms. Note that all signal-averaged electrocardiographic variables are normal, and the late potentials are absent.

 

    Comment
 Top
 Footnotes
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
This study showed that, even in the late course after myocardial infarction in all patients with positive late potentials, the late potentials could no longer be demonstrated postoperatively if the infarct-causing occluded coronary artery was grafted. The late potentials persisted in patients who received no graft to the infarct artery.

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
 Top
 Footnotes
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
Address reprint requests to Dr Terada, Department of Cardiovascular Surgery, Institute of Clinical Medicine, University of Tsukuba, Tsukuba-shi, Ibaraki-ken 305, Japan.


    References
 Top
 Footnotes
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 

  1. Berbari EJ, Scherlag BJ, Hope RR, Lazzara R. Recording from the body surface of arrhythmogenic ventricular activity during the ST segment. Am J Cardiol 1987;41:697–702.
  2. Simson MB. Use of signals in the terminal QRS complex to identify patients with ventricular tachycardia after myocardial infarction. Circulation 1981;64:235–42.[Abstract/Free Full Text]
  3. Winters SL, Stewart D, Targonski A, Gomes JA. Role of signal-averaging of the surface QRS complex in selecting patients with nonsustained ventricular tachycardia and high grade ventricular arrhythmias for programmed ventricular stimulation. J Am Coll Cardiol 1988;12:1481–7.[Abstract]
  4. McGuire M, Kuchar D, Gains J, Sammel N, Thorburn C. Natural history of late potentials in the first ten days after acute myocardial infarction and relation to early ventricular arrhythmias. Am J Cardiol 1988;61:1187–90.[Medline]
  5. Gomes JA, Mehra R, Barreca P, El-Sherif N, Hariman R, Holtzman R. Quantitative analysis of the high frequency components of the signal-averaged QRS complex in patients with acute myocardial infarction: a prospective study. Circulation 1985;72:105–11.[Abstract/Free Full Text]
  6. Kuchar DL, Thorburn CW, Sammel NL. Late potentials detected after myocardial infarction: natural history and prognostic significance. Circulation 1986;74:1280–9.[Abstract/Free Full Text]
  7. Gruppo Italiano per lo Studio della Streptochinasi Nell' Infarto Miocardico (GISSI). Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Lancet 1986;1:397–401.[Medline]
  8. Cigarroa RG, Lange RA, Hillis LD. Prognosis after acute myocardial infarction in patients with and without anterograde coronary blood flow. Am J Cardiol 1989;64:155–60.[Medline]
  9. Kersschot IE, Brugada P, Ramentol M, et al. Effects of early reperfusion in acute myocardial infarction on arrhythmias induced by programmed stimulation: a prospective, randomized study. J Am Coll Cardiol 1986;7:1234–42.[Abstract]
  10. Guerci AD, Gerstenblith G, Brinker JA, et al. A randomized trial of intravenous tissue plasminogen activator for acute myocardial infarction with subsequent randomization to elective coronary angioplasty. N Engl J Med 1987;317:1613–8.[Abstract]
  11. White HD, Norris RM, Brown MA, et al. Effect of intravenous streptokinase on left ventricular function and early survival after myocardial infarction. N Engl J Med 1987;317:850–5.[Abstract]
  12. I.S.A.M. Study Group. A prospective trial of intravenous streptokinase in acute myocardial infarction (I.S.A.M.). Mortality, morbidity, and infarct size at 21 days. N Engl J Med 1986;314:1465–71.[Abstract]
  13. Lange RA, Cigarroa RG, Wells PJ, Kremers MS, Hillis LD. Influence of anterograde flow in the infarct artery on the incidence of late potentials after acute myocardial infarction. Am J Cardiol 1990;65:554–8.[Medline]
  14. Gang ES, Lew AS, Hong M, Wang FZ, Siebert CA, Peter T. Decreased incidence of ventricular late potentials after successful thrombolytic therapy for acute myocardial infarction. N Engl J Med 1989;321:712–6.[Abstract]
  15. Simson MB, Untereker WJ, Spielman SR, et al. Relation between late potentials on the body surface and directly recorded fragmented electrograms in patients with ventricular tachycardia. Am J Cardiol 1983;51:105–12.[Medline]
  16. Gardner PI, Ursel PC, Fenoglio JJ, Wit AL. Electrophysiologic and anatomic basis for fractional electrograms recorded from healed myocardial infarcts. Circulation 1985;72:596–611.[Abstract/Free Full Text]
  17. Cox JL, Pass HI, Oldham HN, Wechsler AS, Sabiston DC Jr. Coronary collateral circulation during stress and the effects of aorto-coronary bypass grafts. J Thorac Cardiovasc Surg 1976;71:540–4.[Abstract]

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