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Disappearance of electrocardiographic pattern of inferior wall myocardial infarction after aorta-coronary bypass surgery
Disappearance of electrocardiographic pattern of inferior wall myocardial infarction after aorta-coronary bypass surgery Three cases are presented showing the disappearance of electrocardiographic (ECG) evidence of old inferior wall myocardial infarction (M!) after aorta-coronary bypass surgery. Evidence is presented to suggest that the loss of Q waves may be the result of reperjusion of the ischemic myocardium (two cases) and the ,.cancelling effect" of a new perioperative myocardial damage upon the ECG evidence of an old myocardial infarction (one case). Q waves do not always indicate permanent myocardial scar formation; they are sometimes transient and reversible. Review of the literature provides further experimental and clinical evidences to suggest that surgical reperjusion of peri-infarction ischemic myocardium is an explanation for the ECG change. Pre- and postoperative angiographic and ventriculographic correlations are needed to further clarify the mechanism and clinical significance of such cases.
F. Bryan Kennedy, M.D., Andres R. Ticzon, M.D., Frederick C. Duffy, M.D., Linda R. Raymundo, M.D., and James W. Giacobine, M.D., Pittsburgh, Pa.
Long-standing pathological Q waves are usually an indication of previous myocardial infarction with a few exceptions; notably hypertrophic subaortic stenosis, myocardiopathy, Wolff-Parkinson-White syndrome, and left ventricular hypertrophy. Horan, Flowers, and Johnson' showed that "diagnostic" Q waves correlated with autopsy evidence of myocardial infarction in 79 percent of 1,184 hearts examined. More recent studies employing coronary arteriography and ventriculography showed a high correlation between Q waves and left ventricular focal asynergy. 2, 3 Previous experimental and clinical items of evidence suggest that "electrically silent" areas of myocardium, manifested as pathological Q waves in the surface ECG, may result from myocardial ischemia as well as myocardial necrosis.v 5 In ischemic cases, reperfusion From the Division of Cardiology and Department of Cardiovascular Surgery, St. Francis General Hospital, Pittsburgh, Pa. This work was supported in part by the Fraternal Order of Eagles Fund and the Health Research and Services Foundation, Pittsburgh, Pa. Received for publication Feb. 22, 1977. Accepted for publication April 14, 1977. Address for reprints: F. Bryan Kennedy, M.D., Division of Cardiology, St. Francis General Hospital, 45th St., off Penn Ave., Pittsburgh, Pa. 15201.
586
of the areas involved may be expected to result in the disappearance of the Q waves. In addition, focal block of the septal fibers of the left bundle branch conduction system may produce Q waves in Leads V 1 to V3 of the precordial leads, mimicking anteroseptal myocardial infarction. The Q waves may disappear upon restoration of conduction to the septal fibers." A recent study has demonstrated that some akinetic segments of myocardium (with corresponding pathological Q waves) show residual contractile ability when evaluated with the use of nitroglycerin. 7 Recent reports have shown the disappearance of significant Q waves in the precordial leads (usually Leads V 1 to V3) following aorta-coronary bypass graft surgery.v 9 The present report describes three cases showing the disappearance of long-standing Q waves in the inferior leads following coronary artery bypass surgery. The loss of Q waves is believed to result from reperfusion of the ischemic myocardium (two cases) and the development of the new anterolateral wall infarction and left anterior hemiblock (one case). Case reports CASE 1. P. N., a 59-year-old truck driver, had a 3 year history of dyspnea on exertion, substernal chest pain, and
Volume74 Number4 October, 1977
Loss of Q wave after coronary bypass
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Fig. 1. Twelve-lead electrocardiograms of Patient P. N" A, Preoperative tracing showing pathological Q waves in Leads II , III, and aY F consistent with old inferior wall myocardial infarction. B , Postoperative tracing showing disappearance of the Q waves. Also note the ST sagging in multiple leads and the more leftward axis postoperatively .
progressively decreasing exercise/work tolerance . Cardiovascular examination revealed a Grade 3/6 harsh systolic ejection murmur maximal at the third intercostal space at the left sternal border. Neither diastolic component nor gallop was noted. Pertinent laboratory investigation revealed a chest roentgenogram showing left ventricular enlargement with poststenotic dilatation of the ascending aorta . The standard twelve lead ECG revealed a pattern consistent with left ventricular hypertrophy and strain and old inferior wall myocardial infarction . Cardiac catheterization revealed a gradient of 85 mm. Hg across the aortic valve. Extensive calcification was noted in the aortic valve leaflets. Cinearteriography revealed stenosis in the proximal one third of the right coronary artery and severe stenosis in the proximal left anterior descending and circumflex coronary arteries, with good peripheral runoff. There was severe hypokinesis of the inferior wall and mild hypokinesis of the anterior wall of the left ventricle. The patient was discharged and readmitted on Nov. 2, 1975, for coronary artery bypass surgery. Fig. I, A shows the ECG on the second admission , which was unchanged from the tracing of the previous month. On Nov. 4 , 1975, the patient underwent aortic valve replacement and aortacoronary saphenous vein bypass grafts to the right and left anterior descending coronary arteries. The postoperative course was uneventful. The postoperative ECG on Nov. 7, 1975 (Fig. I, B) showed disappearance of the abnormal Q waves in the inferior leads. The postoperative vectorcardiogram (YCG) (Fig . 2) confirmed the absence of abnormal initial superior forces in the frontal plane . The patient was discharged on Nov. 14, 1975 in good condit ion and subsequent evaluat ion at 6 weeks and 3 months postoperativel y revealed a stable course. C A S E 2. A. K. , a 53-year-old construction engineer, was initially hospitalized in November, 1975, with acute chest
pain and dyspnea. Serial ECG's showed typical changes of acute inferior wall myocardial infarction with cardiac enzymes documentation. Fig. 3, A shows the ECG upon hospital discharge showing a stable pattern of inferior wall myocardial infarction . Subsequentl y, the patient continued to have moderate anginal chest pains and fatigue with minimal exertion . Fig . 3, B shows the ECG upon readmission on Jan. 18, 1976, for coronary arteriograph y. It is identical to the tracing of Dec. 9, 1975 (6 weeks before) . Coronary arteriography revealed severe narrowing in the midportion of the right main trunk and severe obstruct ion of the proximal left anterior descending coronary artery . In addition , there was complete occlusion of the circumflex branch of the left coronary artery proximal to the origin of the large obtuse marginal branch . Left ventricular angiography demonstrated an almost akinetic inferior wall and hypokinetic anterior wall of the left ventricle. On Jan . 19, 1976, triple aorta-coronary artery saphenous vein bypass grafts were placed into the involved arteries. The postoperative course was uneventful. The postoperative ECG of Jan. 21, 1976 (Fig. 3, C) showed disappearance of the inferior wall infarction Q waves. Similarly, the ECG upon hospital discharge (Fig. 3, D) showed no abnormal Q waves and the postoperative YCG showed no evidence of inferior wall myocardial infarction (Fig . 4). CASE 3. J. P" a 63-year-old retired man, had a history of previously documented inferior and anteroseptal myocardial infarction (1967) , He was hospitalized on Dec . 10, 1975 because of progressively increasing angina pectoris. The ECG (Fig. 5, A) showed evidence of old inferior and anteroseptal myocardial infarction . Coronary arteriography revealed total occlusion of the left anterior descending coronary artery and moderate stenosis of the left circumflex. The right coronary artery showed several areas of severe stenosis . He was discharged but readmitted on Feb. I, 1976, because of
588
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Fig. 2. Postoperative (Frank system) vectorcardiogram of Patient P. N. Left, X, Y, Z orthogonal leads tracings. Right. Top to bottom, frontal, transverse, and right sagittal planes, respectively. Note the normal initial QRS forces (arrows indicate direction) . increasing and persistent angina pectoris. The ECG (Fig. 5,
Discussion
On Feb. 2, 1976 the patient underwent aorta-coronary bypass surgery to the left anterior descending coronary artery. The postoperative ECG (Fig. 5, C) showed the disappearance of the inferior wall Q waves, replaced by a pattern of left anterior hemiblock . In addition , the precordial leads showed total Q-S complex across all precordial leads. The VCG (Fig . 6) was compatible with a previous extensive anterior and inferior wall myocardial infarction along with extreme left axis deviation consistent with left anterior hemiblock .
The significance of these cases is considered under the categories of (I) appearance and disappearance of transient Q waves and (2) disappearance of chronic Q waves. Transient Q waves. It is now well recognized that Q wave formation may be transient, especially following acute coronary insufficiency, 11 -14 Prinzmental variant angina," cardiopulmonary bypass;" and tachyar-
B) showed no change from the tracing of Dec. 10, 1975.
Volume 74 Number 4
Loss of Q wave after coronary bypass
October, 1977
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Fig. 3. Twelve-lead electrocardiograms from Patient A. K. A, Electrocardiogram obtained during initial admission showing changesconsistentwith inferolateral myocardial infarction. B, Electrocardiogram obtained6 weeks later showing essentially the samefindings. C andD, Postoperative electrocardiograms showingdisappearance of inferior wall Q waves. Also note that the wave abnormalities are not as pronounced. rhythmias .!? In these cases, Q wave formation is an expression of severe myocardial ischemia resulting in transient total failure of depolarization of myocardial cells. Such an area of ischemic myocardium becomes "electrically silent. " 15 , 16 With relief of ischemia, or improvement in myocardial perfusion, the QRS abnormalities disappear. As long ago as 1944, Bayley showed that Q waves appear within minutes after temporary coronary occlusion in the dog and are reversible. Perhaps transient ST-T changes associated with myocardial ischemia represent a milder form of ischemia . Disappearance of chronic Q waves. Our present report and two recent publicationsv 9 demonstrate the postoperative disappearance of chronic Q waves. In the
latter two the Q waves disappeared from the anterior precordial leads postoperatively, whereas in the present cases the disappearance of long-standing Q waves occurred in the inferior leads. This is an unexpected finding if such Q waves are evidence of actual myocardial scar formation. The major mechanisms which may explain such findings are: (I) development of a ventricular conduction disturbance, especially left bundle branch block, (2) new myocardial infarction resulting in a "realignment" of electromotive forces, 18.20 (3) gradual shrink age of an area of intarction,!" and (4) reperfusion of a chronically ischemic region of the myocardium . The first two mechanisms are well documented and understandable in ECO and VCO concepts. The third
590
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Kennedy et al.
x y
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Fig. 4. Vectorcardiogram (Frank system) of Patient A. K. Note the initial superior forces in the frontal and right sagittal planes. In the frontal plane the superiorforces lasted for 26 msec. and 0.17 mv. to the left of the' E point, which are within normal limits. mechanism would logically be a gradual process due to healing of an area of myocardial necrosis. Previous reports have demonstrated that if pathological Q waves gradually disappear following myocardial infarction, normalization usually occurs within the first year . 21, 22 The literature is inconclusive as to how soon after an infarction abnormal Q waves disappear owing to healing and shrinkage of fibrous tissue. It is suggested that in many cases of early disappearance of Q waves myocardial ischemia, rather than myocardial necrosis, was responsible for the QRS abnormalities.
The fourth mechanism to be considered in the disappearance of chronic pathological Q waves is that chronic ischemia, or an area of peri-infarction ischemia, may be responsible for the Q waves which disappear after successful bypass surgery. 9 We believe that this explanation applies to our Cases I and 2. Both patients had severe occlusive disease of the main right and circumflex coronary arteries which supplied the inferior left ventricular wall. In both cases venous bypass grafts were placed into the right coronary artery distal to the severe stenotic area, and in Case 2 a graft
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Loss of Q wave after coronary bypass
Number 4 October, 1977
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Fig. 5. Twelve-lead electrocardiograms of Patient J. P. A , Tracing obtained during initial admission showing changesconsistentwith previous old inferiorand anteroseptal myocardial infarction.B, Tracingobtained8 weeks later, unchanged from A . C, Postoperative electrocardiogram showing initial smaIl r waves in the inferior leads with development of abnormal left axis deviation and loss of R wavesin Leads V4-6 suggesting new anterolateral infarction (see text). was also placed into the obtuse marginal. Both patients had long-standing pathological Q waves in the inferior leads (II, III, aV F) which disappeared postoperatively. In neither case was there clinical or ECG evidence of a new infarction or bundle branch block. The loss of ECG evidence of myocardial infarction in Cases I and 2 is most likely the result of improved perfusion of a chronically ischemic zone of myocardium surrounding the area of actual old myocardial necrosis . Normal electrical activity was restored to the formerly "ischemic" area. De Pasquale, Burch, and Phillips" referred to a peri-infarction ischemic area as the zone of "myocardial percussion." It was not possible to repeat the coronary arteriography and ventriculography in the postoperative period in these cases. It would certainly be important to determine if the loss of corresponding Q waves is associated with evidence of improved wall motion in the areas previously showing asynergy in these cases. In addition, echocardiography and/or radioactive cardiac im-
aging done pre- and postoperatively would be helpful in the assessement of wall motion and myocardial function. In Case 3 the explanation for the loss of the pathological Q waves in the inferior leads is the "cancelling" of the changes due to the dominance of new anterolateral infarction effects which developed perioperatively. In this patient the severely diseased right coronary artery was considered unfit for a bypass graft. Consequently only a graft to the left anterior descending was performed. Intraoperatively he developed a new anterolateral infarction, resulting in new QRS changes and left anterior hemiblock. It is noteworthy that while initial R waves were seen in the inferior leads of the postoperative ECG, the VCG still showed evidence of the old inferior wall damage. Vectorcardiography performed pre- and postoperatively has proved useful in the evaluation of aorta-coronary bypass surgery. 23. 24 We recognized that new Q wave formation after coronary bypass surgery is a much more common event
592
Kennedy et
The Journal of
at.
Thoracic and Cardiovascular Surgery
x y
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~L Fig. 6. Postoperative (Frank system) vectorcardiogram Patient J. P. Note the evidence of extensive anterolateral and inferior wall infarction. There is total absence of anterior and inferior forces. Insert shows an enlargementof initial forces in the frontal plane. than its disappearance following surgery. The development of new Q waves postoperatively is usually an expression of new myocardial damage or the' 'unmasking" of an old infarction. to. 25, 26
Summary and conclusions 1. Two cases are presented demonstrating loss of pathological Q waves (inferior wall) after aortacoronary bypass surgery. It is suggested that this effect may be the result of improved perfusion to the periinfarction ischemic area of the myocardium.
2. One case demonstrates loss of abnormal Q waves due to the cancelling effect of a new peri operative infarction and intraventricular conduction abnormality. 3. Q wave formation should be looked upon as evidence of "electrically silent" myocardium, sometimes transient and sometimes reversible, following coronary bypass surgery. 4. It is unknown at this time if the disappearance of Q waves subsequent to improved perfusion of ischemic myocardium has long-term favorable prognostic significance. Perhaps this phenomenon is an indication
Volume 74 Number 4 October, 1977
that the previous myocardial infarction was small, or that there was a large ischemic area surrounding the infarction zone which was successfully reperfused. 5. The purpose of this report is to call attention to the loss of Q waves after coronary bypass surgery, and to stimulate performance of angiographic, ventriculographic, and noninvasive comparative studies pre- and postoperatively to clarify the mechanism and clinical significance of these findings. REFERENCES
2
3
4
5
6
7
8
9
10
II
Horan, L. 6., Flowers, N. c., and Johnson, J.: Significance of the Diagnostic Q Wave of Myocardial Infarction, Circulation 43: 428, 1971. Williams, R. A., Cohn, P. F., Vokonas, P. S., Young, E., Herman, M. V., and Gorlien, R.: Electrocardiographic, Arteriographic, and Ventriculographic Correlations in Transmural Myocardial Infarction, Am. J. Cardiol. 31: 595, 1973. Bodenheimer, M. M., Banka, V. S., and Helfant, R. H.: Q Waves and Ventricular Asynergy: Predictive Value and Hemodynamic Significance of Anatomic Location, Am. J. Cardiol. 35: 615, 1975. Gross, H., Rubin, I. L., Laufer, H., Bloomberg, A. E., Bujdoso, L., and Delman, A. J.: Transient Abnormal Q Waves in the Dog Without Myocardial Infarction, Am. J. Cardiol. 14: 669, 1964. DePasquale, N. P., Burch, G. E., and Phillips, J. H.: Electrocardiographic Alterations Associated With Electrically "Silent" Areas of Myocardium, Am. Heart J. 68: 697, 1964. Gambetta, M., and Childers, R. W.: Rate Dependent Right Precordial Q Waves "Septal Focal Block," Am. J. Cardiol. 32: 196, 1973. Banka, V. S., Bodenheimer, M. M., and Helfant, R. H.: Determinants of Reversible Asynergy. Effect of Pathological Q Waves, Coronary Collaterals, and Anatomic Location, Circulation 50: 714, 1974. Conde, C. A., Miller, J., Espinoza, 1., Donoso, E., and Dack, S.: Disappearance of Abnormal Q Waves after Aortocoronary Bypass Surgery, Am. J. Cardiol. 36: 889, 1975. Zeft, H. J., Friedberg, H. D., King, J. F., Manley, J. C., Huston, J. H., and Johnson, W. D.: Reappearance of Anterior QRS Forces After Coronary Bypass Surgery, Am. J. Cardiol. 36: 163, 1975. Bassan, M. M., Oatfield, R. Hoffman, I., Madoff, J., and Swan, H. J. c.: New Q Waves After Aortocoronary Bypass Surgery, N. Engl. J. Med. 290: 349, 1974. Rubin, I. L., Gross, H., and Vigliano E. M.: Transient Abnormal Q Waves During Coronary Insufficiency, Am. Heart J. 71: 254, 1966.
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12 Roesler, H., and Dressler, W.: Transient Electrocardiographic Changes Identical With Those of Acute Myocardial Infarction Accompanying Attacks of Angina Pectoris, Am. Heart J. 47: 520, 1954. 13 Haiat, R., and Chiche, P.: Transient Abnormal Q Waves in the Course of Ischemic Heart Disease, Chest 65: 140, 1974. 14 Haiat, R., Worthington, F. X., Castellanos, A., and Lemberg, L.: Unusual Normalization of the Electrocardiogram on the Sixth Day of Myocardial Infarction, J. Electrocardiol. 4: 363, 1971. 15 Miller, J., Conde, C. A., Donoso, E., and Dack, S.: Transient Q Waves in Prinzmetal's Angina, Am. J. Cardiol. 35: 691, 1975. 16 Klein, H. 0., Gross, H., and Rubin, I. L.: Transient Electrocardiographic Changes Simulating Myocardial Infarction During Open Heart Surgery, Am. Heart J. 79: 463, 1970. 17 Rubin, I. L., Gross, H., and Arbeit, S. R.: Transient Abnormal Q Waves During Bouts of Tachycardia, Am. J. Cardiol. 11: 659, 1963. 18 Bayley, R. H., and LaDue, 1. S.: Differentiation of the Electrocardiographic Changes Produced in the Dog by Prolonged Temporary Occlusion of a Coronary Artery From Those Produced by Postoperative Pericarditis, Am. Heart J. 28: 233, 1944. 19 Papas, M. P.: Disappearance of Pathological Q Waves After Cardiac Infarction, Br. Heart J. 20: 123, 1958. 20 Evans, W.: Cardiographic Contrecoup in the Course of Cardiac Infarction, Br. Heart J. 24: 713, 1963. 21 Anderssen, N., and Skjaeggestad, 0.: The Electrocardiogram in Patients with Previous Myocardial Infarction, Acta Med. Scand. 176: 123, 1964. 22. Kalbfleish, J., Shadaksharappa, K. S., Conrad, L. L., and Sarkar, N. K.: Disappearance of the Q Deflection Following Myocardial Infarction, Am. Heart J. 76: 193, 1968. 23 Benchimol, A., Promisloff, S. D., and Desser, K. B.: Electrovectorcardiographic Changes After Proximal Right Coronary Artery Venous Bypass Graft and Distal Endarterectomy, Am. 1. Cardiol. 30: 466, 1972. 24 Freidberg, D. H., Zeft, H. 1., Silverman, R. E., Tector, A. J., and Johnson, W. D.: Myocardial Infarction Following Coronary Surgery: Vectorcardiographic Assessment, Am. J. Cardiol. 31: 132, 1973. 25 Brewer, D., Bilbro, R., and Bartel, A.: Myocardial Infarction as a Complication of Coronary Bypass Surgery, Circulation 47: 58, 1973. 26 Espinoza, J., Lipski, J., Litwak, R., Donoso, E., and Dack, S.: New Q Waves After Coronary Artery Bypass Surgery for Angina Pectoris, Am. J. Cardiol. 33: 221, 1974.
F. Bryan Kennedy, M.D., Andres R. Ticzon, M.D., Frederick C. Duffy, M.D., Linda R. Raymundo, M.D., and James W. Giacobine, M.D., Pittsburgh, Pa.
Long-standing pathological Q waves are usually an indication of previous myocardial infarction with a few exceptions; notably hypertrophic subaortic stenosis, myocardiopathy, Wolff-Parkinson-White syndrome, and left ventricular hypertrophy. Horan, Flowers, and Johnson' showed that "diagnostic" Q waves correlated with autopsy evidence of myocardial infarction in 79 percent of 1,184 hearts examined. More recent studies employing coronary arteriography and ventriculography showed a high correlation between Q waves and left ventricular focal asynergy. 2, 3 Previous experimental and clinical items of evidence suggest that "electrically silent" areas of myocardium, manifested as pathological Q waves in the surface ECG, may result from myocardial ischemia as well as myocardial necrosis.v 5 In ischemic cases, reperfusion From the Division of Cardiology and Department of Cardiovascular Surgery, St. Francis General Hospital, Pittsburgh, Pa. This work was supported in part by the Fraternal Order of Eagles Fund and the Health Research and Services Foundation, Pittsburgh, Pa. Received for publication Feb. 22, 1977. Accepted for publication April 14, 1977. Address for reprints: F. Bryan Kennedy, M.D., Division of Cardiology, St. Francis General Hospital, 45th St., off Penn Ave., Pittsburgh, Pa. 15201.
586
of the areas involved may be expected to result in the disappearance of the Q waves. In addition, focal block of the septal fibers of the left bundle branch conduction system may produce Q waves in Leads V 1 to V3 of the precordial leads, mimicking anteroseptal myocardial infarction. The Q waves may disappear upon restoration of conduction to the septal fibers." A recent study has demonstrated that some akinetic segments of myocardium (with corresponding pathological Q waves) show residual contractile ability when evaluated with the use of nitroglycerin. 7 Recent reports have shown the disappearance of significant Q waves in the precordial leads (usually Leads V 1 to V3) following aorta-coronary bypass graft surgery.v 9 The present report describes three cases showing the disappearance of long-standing Q waves in the inferior leads following coronary artery bypass surgery. The loss of Q waves is believed to result from reperfusion of the ischemic myocardium (two cases) and the development of the new anterolateral wall infarction and left anterior hemiblock (one case). Case reports CASE 1. P. N., a 59-year-old truck driver, had a 3 year history of dyspnea on exertion, substernal chest pain, and
Volume74 Number4 October, 1977
Loss of Q wave after coronary bypass
V3
A , I
V4
Vs
587
v
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Fig. 1. Twelve-lead electrocardiograms of Patient P. N" A, Preoperative tracing showing pathological Q waves in Leads II , III, and aY F consistent with old inferior wall myocardial infarction. B , Postoperative tracing showing disappearance of the Q waves. Also note the ST sagging in multiple leads and the more leftward axis postoperatively .
progressively decreasing exercise/work tolerance . Cardiovascular examination revealed a Grade 3/6 harsh systolic ejection murmur maximal at the third intercostal space at the left sternal border. Neither diastolic component nor gallop was noted. Pertinent laboratory investigation revealed a chest roentgenogram showing left ventricular enlargement with poststenotic dilatation of the ascending aorta . The standard twelve lead ECG revealed a pattern consistent with left ventricular hypertrophy and strain and old inferior wall myocardial infarction . Cardiac catheterization revealed a gradient of 85 mm. Hg across the aortic valve. Extensive calcification was noted in the aortic valve leaflets. Cinearteriography revealed stenosis in the proximal one third of the right coronary artery and severe stenosis in the proximal left anterior descending and circumflex coronary arteries, with good peripheral runoff. There was severe hypokinesis of the inferior wall and mild hypokinesis of the anterior wall of the left ventricle. The patient was discharged and readmitted on Nov. 2, 1975, for coronary artery bypass surgery. Fig. I, A shows the ECG on the second admission , which was unchanged from the tracing of the previous month. On Nov. 4 , 1975, the patient underwent aortic valve replacement and aortacoronary saphenous vein bypass grafts to the right and left anterior descending coronary arteries. The postoperative course was uneventful. The postoperative ECG on Nov. 7, 1975 (Fig. I, B) showed disappearance of the abnormal Q waves in the inferior leads. The postoperative vectorcardiogram (YCG) (Fig . 2) confirmed the absence of abnormal initial superior forces in the frontal plane . The patient was discharged on Nov. 14, 1975 in good condit ion and subsequent evaluat ion at 6 weeks and 3 months postoperativel y revealed a stable course. C A S E 2. A. K. , a 53-year-old construction engineer, was initially hospitalized in November, 1975, with acute chest
pain and dyspnea. Serial ECG's showed typical changes of acute inferior wall myocardial infarction with cardiac enzymes documentation. Fig. 3, A shows the ECG upon hospital discharge showing a stable pattern of inferior wall myocardial infarction . Subsequentl y, the patient continued to have moderate anginal chest pains and fatigue with minimal exertion . Fig . 3, B shows the ECG upon readmission on Jan. 18, 1976, for coronary arteriograph y. It is identical to the tracing of Dec. 9, 1975 (6 weeks before) . Coronary arteriography revealed severe narrowing in the midportion of the right main trunk and severe obstruct ion of the proximal left anterior descending coronary artery . In addition , there was complete occlusion of the circumflex branch of the left coronary artery proximal to the origin of the large obtuse marginal branch . Left ventricular angiography demonstrated an almost akinetic inferior wall and hypokinetic anterior wall of the left ventricle. On Jan . 19, 1976, triple aorta-coronary artery saphenous vein bypass grafts were placed into the involved arteries. The postoperative course was uneventful. The postoperative ECG of Jan. 21, 1976 (Fig. 3, C) showed disappearance of the inferior wall infarction Q waves. Similarly, the ECG upon hospital discharge (Fig. 3, D) showed no abnormal Q waves and the postoperative YCG showed no evidence of inferior wall myocardial infarction (Fig . 4). CASE 3. J. P" a 63-year-old retired man, had a history of previously documented inferior and anteroseptal myocardial infarction (1967) , He was hospitalized on Dec . 10, 1975 because of progressively increasing angina pectoris. The ECG (Fig. 5, A) showed evidence of old inferior and anteroseptal myocardial infarction . Coronary arteriography revealed total occlusion of the left anterior descending coronary artery and moderate stenosis of the left circumflex. The right coronary artery showed several areas of severe stenosis . He was discharged but readmitted on Feb. I, 1976, because of
588
The Journal of Thoracic and Cardiovascular Surgery
Kennedy et al.
-
- 1- -
t-
t -
x
y
z t-
>
E .....
500msec pn
Fig. 2. Postoperative (Frank system) vectorcardiogram of Patient P. N. Left, X, Y, Z orthogonal leads tracings. Right. Top to bottom, frontal, transverse, and right sagittal planes, respectively. Note the normal initial QRS forces (arrows indicate direction) . increasing and persistent angina pectoris. The ECG (Fig. 5,
Discussion
On Feb. 2, 1976 the patient underwent aorta-coronary bypass surgery to the left anterior descending coronary artery. The postoperative ECG (Fig. 5, C) showed the disappearance of the inferior wall Q waves, replaced by a pattern of left anterior hemiblock . In addition , the precordial leads showed total Q-S complex across all precordial leads. The VCG (Fig . 6) was compatible with a previous extensive anterior and inferior wall myocardial infarction along with extreme left axis deviation consistent with left anterior hemiblock .
The significance of these cases is considered under the categories of (I) appearance and disappearance of transient Q waves and (2) disappearance of chronic Q waves. Transient Q waves. It is now well recognized that Q wave formation may be transient, especially following acute coronary insufficiency, 11 -14 Prinzmental variant angina," cardiopulmonary bypass;" and tachyar-
B) showed no change from the tracing of Dec. 10, 1975.
Volume 74 Number 4
Loss of Q wave after coronary bypass
October, 1977
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Fig. 3. Twelve-lead electrocardiograms from Patient A. K. A, Electrocardiogram obtained during initial admission showing changesconsistentwith inferolateral myocardial infarction. B, Electrocardiogram obtained6 weeks later showing essentially the samefindings. C andD, Postoperative electrocardiograms showingdisappearance of inferior wall Q waves. Also note that the wave abnormalities are not as pronounced. rhythmias .!? In these cases, Q wave formation is an expression of severe myocardial ischemia resulting in transient total failure of depolarization of myocardial cells. Such an area of ischemic myocardium becomes "electrically silent. " 15 , 16 With relief of ischemia, or improvement in myocardial perfusion, the QRS abnormalities disappear. As long ago as 1944, Bayley showed that Q waves appear within minutes after temporary coronary occlusion in the dog and are reversible. Perhaps transient ST-T changes associated with myocardial ischemia represent a milder form of ischemia . Disappearance of chronic Q waves. Our present report and two recent publicationsv 9 demonstrate the postoperative disappearance of chronic Q waves. In the
latter two the Q waves disappeared from the anterior precordial leads postoperatively, whereas in the present cases the disappearance of long-standing Q waves occurred in the inferior leads. This is an unexpected finding if such Q waves are evidence of actual myocardial scar formation. The major mechanisms which may explain such findings are: (I) development of a ventricular conduction disturbance, especially left bundle branch block, (2) new myocardial infarction resulting in a "realignment" of electromotive forces, 18.20 (3) gradual shrink age of an area of intarction,!" and (4) reperfusion of a chronically ischemic region of the myocardium . The first two mechanisms are well documented and understandable in ECO and VCO concepts. The third
590
The Journal of Thoracic and Cardiovascular Surgery
Kennedy et al.
x y
z
>
E
500 msec
Fig. 4. Vectorcardiogram (Frank system) of Patient A. K. Note the initial superior forces in the frontal and right sagittal planes. In the frontal plane the superiorforces lasted for 26 msec. and 0.17 mv. to the left of the' E point, which are within normal limits. mechanism would logically be a gradual process due to healing of an area of myocardial necrosis. Previous reports have demonstrated that if pathological Q waves gradually disappear following myocardial infarction, normalization usually occurs within the first year . 21, 22 The literature is inconclusive as to how soon after an infarction abnormal Q waves disappear owing to healing and shrinkage of fibrous tissue. It is suggested that in many cases of early disappearance of Q waves myocardial ischemia, rather than myocardial necrosis, was responsible for the QRS abnormalities.
The fourth mechanism to be considered in the disappearance of chronic pathological Q waves is that chronic ischemia, or an area of peri-infarction ischemia, may be responsible for the Q waves which disappear after successful bypass surgery. 9 We believe that this explanation applies to our Cases I and 2. Both patients had severe occlusive disease of the main right and circumflex coronary arteries which supplied the inferior left ventricular wall. In both cases venous bypass grafts were placed into the right coronary artery distal to the severe stenotic area, and in Case 2 a graft
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Loss of Q wave after coronary bypass
Number 4 October, 1977
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Fig. 5. Twelve-lead electrocardiograms of Patient J. P. A , Tracing obtained during initial admission showing changesconsistentwith previous old inferiorand anteroseptal myocardial infarction.B, Tracingobtained8 weeks later, unchanged from A . C, Postoperative electrocardiogram showing initial smaIl r waves in the inferior leads with development of abnormal left axis deviation and loss of R wavesin Leads V4-6 suggesting new anterolateral infarction (see text). was also placed into the obtuse marginal. Both patients had long-standing pathological Q waves in the inferior leads (II, III, aV F) which disappeared postoperatively. In neither case was there clinical or ECG evidence of a new infarction or bundle branch block. The loss of ECG evidence of myocardial infarction in Cases I and 2 is most likely the result of improved perfusion of a chronically ischemic zone of myocardium surrounding the area of actual old myocardial necrosis . Normal electrical activity was restored to the formerly "ischemic" area. De Pasquale, Burch, and Phillips" referred to a peri-infarction ischemic area as the zone of "myocardial percussion." It was not possible to repeat the coronary arteriography and ventriculography in the postoperative period in these cases. It would certainly be important to determine if the loss of corresponding Q waves is associated with evidence of improved wall motion in the areas previously showing asynergy in these cases. In addition, echocardiography and/or radioactive cardiac im-
aging done pre- and postoperatively would be helpful in the assessement of wall motion and myocardial function. In Case 3 the explanation for the loss of the pathological Q waves in the inferior leads is the "cancelling" of the changes due to the dominance of new anterolateral infarction effects which developed perioperatively. In this patient the severely diseased right coronary artery was considered unfit for a bypass graft. Consequently only a graft to the left anterior descending was performed. Intraoperatively he developed a new anterolateral infarction, resulting in new QRS changes and left anterior hemiblock. It is noteworthy that while initial R waves were seen in the inferior leads of the postoperative ECG, the VCG still showed evidence of the old inferior wall damage. Vectorcardiography performed pre- and postoperatively has proved useful in the evaluation of aorta-coronary bypass surgery. 23. 24 We recognized that new Q wave formation after coronary bypass surgery is a much more common event
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~L Fig. 6. Postoperative (Frank system) vectorcardiogram Patient J. P. Note the evidence of extensive anterolateral and inferior wall infarction. There is total absence of anterior and inferior forces. Insert shows an enlargementof initial forces in the frontal plane. than its disappearance following surgery. The development of new Q waves postoperatively is usually an expression of new myocardial damage or the' 'unmasking" of an old infarction. to. 25, 26
Summary and conclusions 1. Two cases are presented demonstrating loss of pathological Q waves (inferior wall) after aortacoronary bypass surgery. It is suggested that this effect may be the result of improved perfusion to the periinfarction ischemic area of the myocardium.
2. One case demonstrates loss of abnormal Q waves due to the cancelling effect of a new peri operative infarction and intraventricular conduction abnormality. 3. Q wave formation should be looked upon as evidence of "electrically silent" myocardium, sometimes transient and sometimes reversible, following coronary bypass surgery. 4. It is unknown at this time if the disappearance of Q waves subsequent to improved perfusion of ischemic myocardium has long-term favorable prognostic significance. Perhaps this phenomenon is an indication
Volume 74 Number 4 October, 1977
that the previous myocardial infarction was small, or that there was a large ischemic area surrounding the infarction zone which was successfully reperfused. 5. The purpose of this report is to call attention to the loss of Q waves after coronary bypass surgery, and to stimulate performance of angiographic, ventriculographic, and noninvasive comparative studies pre- and postoperatively to clarify the mechanism and clinical significance of these findings. REFERENCES
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Horan, L. 6., Flowers, N. c., and Johnson, J.: Significance of the Diagnostic Q Wave of Myocardial Infarction, Circulation 43: 428, 1971. Williams, R. A., Cohn, P. F., Vokonas, P. S., Young, E., Herman, M. V., and Gorlien, R.: Electrocardiographic, Arteriographic, and Ventriculographic Correlations in Transmural Myocardial Infarction, Am. J. Cardiol. 31: 595, 1973. Bodenheimer, M. M., Banka, V. S., and Helfant, R. H.: Q Waves and Ventricular Asynergy: Predictive Value and Hemodynamic Significance of Anatomic Location, Am. J. Cardiol. 35: 615, 1975. Gross, H., Rubin, I. L., Laufer, H., Bloomberg, A. E., Bujdoso, L., and Delman, A. J.: Transient Abnormal Q Waves in the Dog Without Myocardial Infarction, Am. J. Cardiol. 14: 669, 1964. DePasquale, N. P., Burch, G. E., and Phillips, J. H.: Electrocardiographic Alterations Associated With Electrically "Silent" Areas of Myocardium, Am. Heart J. 68: 697, 1964. Gambetta, M., and Childers, R. W.: Rate Dependent Right Precordial Q Waves "Septal Focal Block," Am. J. Cardiol. 32: 196, 1973. Banka, V. S., Bodenheimer, M. M., and Helfant, R. H.: Determinants of Reversible Asynergy. Effect of Pathological Q Waves, Coronary Collaterals, and Anatomic Location, Circulation 50: 714, 1974. Conde, C. A., Miller, J., Espinoza, 1., Donoso, E., and Dack, S.: Disappearance of Abnormal Q Waves after Aortocoronary Bypass Surgery, Am. J. Cardiol. 36: 889, 1975. Zeft, H. J., Friedberg, H. D., King, J. F., Manley, J. C., Huston, J. H., and Johnson, W. D.: Reappearance of Anterior QRS Forces After Coronary Bypass Surgery, Am. J. Cardiol. 36: 163, 1975. Bassan, M. M., Oatfield, R. Hoffman, I., Madoff, J., and Swan, H. J. c.: New Q Waves After Aortocoronary Bypass Surgery, N. Engl. J. Med. 290: 349, 1974. Rubin, I. L., Gross, H., and Vigliano E. M.: Transient Abnormal Q Waves During Coronary Insufficiency, Am. Heart J. 71: 254, 1966.
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12 Roesler, H., and Dressler, W.: Transient Electrocardiographic Changes Identical With Those of Acute Myocardial Infarction Accompanying Attacks of Angina Pectoris, Am. Heart J. 47: 520, 1954. 13 Haiat, R., and Chiche, P.: Transient Abnormal Q Waves in the Course of Ischemic Heart Disease, Chest 65: 140, 1974. 14 Haiat, R., Worthington, F. X., Castellanos, A., and Lemberg, L.: Unusual Normalization of the Electrocardiogram on the Sixth Day of Myocardial Infarction, J. Electrocardiol. 4: 363, 1971. 15 Miller, J., Conde, C. A., Donoso, E., and Dack, S.: Transient Q Waves in Prinzmetal's Angina, Am. J. Cardiol. 35: 691, 1975. 16 Klein, H. 0., Gross, H., and Rubin, I. L.: Transient Electrocardiographic Changes Simulating Myocardial Infarction During Open Heart Surgery, Am. Heart J. 79: 463, 1970. 17 Rubin, I. L., Gross, H., and Arbeit, S. R.: Transient Abnormal Q Waves During Bouts of Tachycardia, Am. J. Cardiol. 11: 659, 1963. 18 Bayley, R. H., and LaDue, 1. S.: Differentiation of the Electrocardiographic Changes Produced in the Dog by Prolonged Temporary Occlusion of a Coronary Artery From Those Produced by Postoperative Pericarditis, Am. Heart J. 28: 233, 1944. 19 Papas, M. P.: Disappearance of Pathological Q Waves After Cardiac Infarction, Br. Heart J. 20: 123, 1958. 20 Evans, W.: Cardiographic Contrecoup in the Course of Cardiac Infarction, Br. Heart J. 24: 713, 1963. 21 Anderssen, N., and Skjaeggestad, 0.: The Electrocardiogram in Patients with Previous Myocardial Infarction, Acta Med. Scand. 176: 123, 1964. 22. Kalbfleish, J., Shadaksharappa, K. S., Conrad, L. L., and Sarkar, N. K.: Disappearance of the Q Deflection Following Myocardial Infarction, Am. Heart J. 76: 193, 1968. 23 Benchimol, A., Promisloff, S. D., and Desser, K. B.: Electrovectorcardiographic Changes After Proximal Right Coronary Artery Venous Bypass Graft and Distal Endarterectomy, Am. 1. Cardiol. 30: 466, 1972. 24 Freidberg, D. H., Zeft, H. 1., Silverman, R. E., Tector, A. J., and Johnson, W. D.: Myocardial Infarction Following Coronary Surgery: Vectorcardiographic Assessment, Am. J. Cardiol. 31: 132, 1973. 25 Brewer, D., Bilbro, R., and Bartel, A.: Myocardial Infarction as a Complication of Coronary Bypass Surgery, Circulation 47: 58, 1973. 26 Espinoza, J., Lipski, J., Litwak, R., Donoso, E., and Dack, S.: New Q Waves After Coronary Artery Bypass Surgery for Angina Pectoris, Am. J. Cardiol. 33: 221, 1974.