CASE REPORTS
Electrophysiologic Effects of Acute Myocardial Infarction in Man
ISAAC WIENER, MD BRUCE MINDICH, MD JOEL KUPERSMITH, MD, FACC New York, New York
Six patients undergotng surgery for ischemlc heart disease were studied by means of epicardial electrodes affixed to the lefl ventricle. One patient who underwent triple coronary arterial bypass and plication of a left ventricular aneurysm had evidence of an acute myocardlal infarction 1 day after operation. A surface electrocardiogram and a bipolar electrogram from the lefl ventricle were recordad before and after development of the infarction. The bipolar electrogram showed a marked toss of voltage and delay of conduction that were not present in the patients who underwent surgery but did not sustain an acute myocardlal Infarction. Thus, any acute myocardlal infarction in conscious persons appears to be associated with areas of delayed epicardial action and dlmlnution of local vottage. This observatton suggests that the electrophysWogic mechanisms of infarction in man are slmllar to those of Infarction in the dog.
Most of our knowledge about the mechanisms of ventricular arrhythmias in acute myocardial infarction is derived from studies in the canine heart.’ In these studies, zones of infarction produced by coronary arterial ligation demonstrate slowing of conduction sufficient to permit the occurrence of reentrant arrhythmias. 24 The relevance of these studies to human myocardial infarction is unclear.5 Precise electrophysiologic data on acute infarction in man, particularly in conscious patients, is difficult to obtain. In this study, we made serial electrophysiologic recordings from the hearts of six patients who underwent surgery for ischemic heart disease, including one who had an acute myocardial infarction 1 day postoperatively. The observations suggest that the electrophysiologic changes similar to those seen in experimental myocardial infarction occur in infarction in conscious man. Methods
From the Division of Cardiology and Clinical Pharmacology, Department of Medicine, and the Division of Cardiothoracic Surgery, Department of Surgery, Mount Sinai School of Medicine of the city Universny of New York, New York, New York. This study was supported in part by grants HL 18801 and HL 10833 of the National Heart, Lung, and Blood Institute, U.S. Public Health Service, Bethesda, Maryfand; a &ant-in-Akl from the New York Heart Association, New Yak. New York; and a grant from the Heart Research Foundation. New York, New York. Manuscript received December 16.1977; revised manuscript received March 28, 1978, accepted March 29, 1978. Address for reprints: Joel Kupersmith. MD, Department of Medicine, Mount Sinai School of Medicine, Fifth Avenue and 100th Street, New York, New York 10029.
Six patients who underwent surgery for ischemic heart disease had bipolar electrodes for standby pacing placed on the left ventricle, in the distribution of the left anterior descending coronary artery. Bipolar electrograms were recorded from this electrode with an isolation unit on an Electronics for Medicine DR-8 research recorder with a filter frequency of 12 to 500 hertz at a paper speed of 100 mm/set. All recordings were made with the patient supine. Conduction intervals were measured from the earliest onset of the QRS complex in three simultaneously recorded standard electrocardiographic leads to the major deflection of the bipolar electrogram recorded from the left ventricle. A Vernier measuring device, with an accuracy of fl msec at recorded paper speed, was used for measurements. Recordings were performed 4 to 5 hours postoperatively and then during the following 6 days. Results Control patients: Five patients underwent coronary bypass surgery with grafts to the left anterior descending coronary artery and had an uncomplicated postoperative course. In these patients, the local electrograms showed no change in conduction time and a mean decrease in voltage of 44.0 f 11 percent from the
September 1978
The American Journal of CARDIOLOGY
Volume 42
513
ELECTROPHYSIOLOGYOF HUMAN INFARCTION-WIENER
ET AL.
FIGURE 1. Twelve lead electrocardiograms. A, 4 hours postoperatively. The tracing is unchanged from the preoperative electrocardiogram. B. first postoperative day. Note new Ct waves, S-T elevation and upr@ht T waves in IIIanda”F. leads I and aVL and S-T depression in leads II,
first recording 4 hours postoperatively to the 6th postoperative day; these findings are similar to those reported by others.6
Electrophysiologic findings in a patient with acute myocardialinfarction: The patient was a 42 year old woman
with angina pectoris that was intractable despite pharmacologic therapy. Coronary arteriography revealed severe triple vessel disease with a Friesinger score of 13, relatively poor runoff and poor left ventricular function. At operation, diffuse scarring of the apicolateral area and a small apical aneurysm were noted. Three coronary bypass grafts, including one to the left anterior descending coronary artery, were constructed, and the apical aneurysm was plicated. During surgery, a bipolar electrode was placed on the left ventricle in an area adjacent to the middle third of the left anterior descending coronary artery. When cardiopulmonary bypass was discontinued, the patient’s condition was hemodynamically unstable; an intraaorticballoon pump was inserted,and stable blood pressure and cardiac output were maintained. The electrocardiogram 4 hours postoperatively (Fig. 1A) was unchanged from the preoperative tracing, and the bipolar electrogram recorded from the left ventricle (Fig. 2A) showed an,amplitude of 2.7 mv and a conduction interval of 19 msec. The next morning (postoperative day l), the patient became hypotensive while on the intraaortic balloon pump, and dopamine, 16 pg/kg/per min, was required to maintain a stable blood pressure and cardiac output. The surface electrocardiogram (Fig. 1B) showed new S-T elevation and new Q waves in leads I and aVL. The left ventricular electrogram (Fig. 2B) showed a 92 percent loss of voltage to 0.2 mv and an increase of the conduction interval to 28 msec. By postoperative day 2 administration of dopamine had been discontinued, but lidocaine therapy (2 mg/min) was started for ventricular arrhythm@. The electrocardiogram showed evolution of a lateral acute myocardial infarction, and local left ventricular activation time was further delayed to 33 msec (Fig. 1C). On day 3, both lidocaine therapy and the intraaortic balloon
514
September 1979
The Amorkan
Journal ol CARDDLGGY
pump were discontinued. The electrocardiogram was unchanged, and the left ventricularelectrogram (Fig. 1D) showed further delay in local activation to 36 msec. After this, the patient had no other complications. The left ventricular electrogram recorded 6 days postoperatively (Fig. 1E) showed a further decrease in voltage to 0.08 mv and shortening of the local conduction interval to 30 msec.
Discussion Previous electrophysiologic studies on human myocardial infarction: Studies on intramyocardial conduction in man are difficult to perform.7 Using epicardial mapping during open heart surgery, Daniel et aL8 demonstrated delayed epicardial activation over zones of chronic infarction. Kaiser et a1.,g using electrophysiologic mapping during open heart surgery, localized the infarct zone in a patient with acute myocardial infarction. Unipolar recordingsrevealedQ waves, and bipolar electrograms demonstrated low voltage and increased duration. Local activation time was not evaluated and, because no recordings were made before the development of infarction, change in local activation caused by the infarction could not, be evaluated. Sung et aL6 studied left ventricular bipolar electrograms in patients before and after coronary bypass surgery. In 13 of 19 patients, the voltage of the bipolar electrogram increased immediately after grafting. During the first 5 days postoperatively, the voltage of the electrogram decreased in 16 of 19 patients, with no change in local activation time. In our control patients, the first recordings were made several hours postoperatively, and the results were consistent with those of Sung et al.6 In their study, three patients had a perioperative
Volume 42
infarc-
ELECTROPHYSIOLOGY OF HUMAN INFARCTION-WIENER
r r /-
ET AL.
I
T
lmv
lmv
+f
4 -
1
/-V-U-* -30
FIGURE 2. Standard electrocardiographic leads I, II and 111with simultaneous bipolar electrogram recorded from the left ventricle (I-V). A, 4 hours postoperatively, heart rate is 89 beats/min. Conductii interval from the onset of the QRS complex to ths maximal deflection of the bipolar electrogram is 19 msec. Voltage of electrogram is 2.7 mv. B, first postoperative day. Note ti new Q wave and S-T elevation in lead I. Heart rate is 120 beaWmin. The conduction interval is 28 msec and voltage of the bipolar electrogram is 0.2 mv. C, second postoperative day. There is atrial pacing to a heart rate of 91 beats/min. The conduction interval is 33 msec, and voltage of the bipolar electrogram is 0.25 mv. D, third postoperative day. There is atrial pacing to a heart rate of 93 beatslmin. The conductii interval is 36 msec, and voltage of the blpolar electrqam is 0.15 mv. E, sixth po&operative day. Heart rate is 103 beatslmin. The conduction interval is 30 msec, and voltage of the bipolar elecWgram Is 0.08 mv.
tion, but their electrograms showed no change in conduction interval, and the changes in amplitude did not differ from those in patients without infarction. The authors attributed this finding to the fact that the electrodes did not lie in the zone of the infarction as predicted by the electrocardiogram. Changes in left ventricular electrogram: Our patient clearly had an acute myocardial infarction on the first postoperative day. The left ventricular electrodes, which appeared to be in or near the infarct zone, demonstrated a marked loss of voltage and considerable slowing of activation. The further delay on day 2 may have been related to the evolution of the infarction, the withdrawal of dopamine or the administration of lidocaine.lO The delay of activation on day 3 may have represented ischemia related to discontinuation of the intraaortic balloon pump. By day 6 voltage continued to decrease, but epicardial activation time, although still delayed, was shorter than previously. None of these changes occurred in our patients who underwent coronary bypass surgery but did not sustain infarction. Overall, the delay in activation and loss of voltage in the patient with acute infarction are similar to those occurring after ligation of a canine coronary artery. Possible limitations of study: There are certain limitations to these observations. Only one patient with infarction was observed. Although postoperative myo-
cardial infarction is not rare, the electrocardiographic changes of infarction are almost always present in the first electrocardiogram recorded in the recovery room.ll It is thus quite unusual to be able to obtain a baseline electrogram after surgery but before the occurrence of infarctiqn. The patient who had infarction also had plication of a left ventricular aneurysm. The control recording after surgery indicates that it is quite unlikely that the changes were secondary to plication of the aneurysm. Although dislodgment of the electrodes might explain our findings, this also appears unlikely because dislodgment was not seen in any of the control cases and would have had to occur precisely at the time of infarction. It is possible that the electrodes were located in the periinfarction zone rather than within the infarct itself. For clinical reasons, multiple interventions were often performed simultaneously. A change in heart rate occurred on day 2, but the changes in conduction intervalpersistedwhen,the heart rate returned to baseline level. Although the total delay in epicardial activation was considerable, the delay demonstrated in these recordings did not extend beyond the refractory period of the ventiicle and by itself would not be sufficient for reentry to occur (although our electrodes may not have been in the zone of maximal conduction delay). Implications: Acute myocardial infarction in conscious persons appears to be associated with areas of delayed epicardial activation and diminution of local
September 1979
The Amerkan
Journal of CARDIDLDGY
Volume 42
515
ELECTROPHYSIOLOGY
OF HUMAN INFARCTION-WIENER
ET AL
voltage. As far as we know, this observation has not been made before, and it suggests that the electrophysiologic mechanisms of infarction in man are similar to those of
infarction in the dog. This delay in epicardial activation may be important in the pathogenesis of reentrant ventricular arrhythmias.
References 1. Wit AL, Bigger JT: Possible electrophysiological mechanisms for lethal arrhythmias accompanying myocardial ischemia and infarction. Circulation 51, 52:Suppl lll:lll-96-111-115, 1975 2. Waldo AL, Kaiser 0: A study of ventricular arrhythmias associated with acute myocardial infarction in the canine heart. Circulation 47:1222-1228, 1973 3. Scherlag B, El-Sherlf N, Hope R, et al: Characterization and localization of ventricular arrhythmias resulting from myocardial ischemia and infarction. Circ Res 35372-383, 1974 4. Bolneau JP, Cox JL: Slow ventricular activation in acute myocardial infarction. A source of re-entrant premature ventricular contractions. Circulation 48:702-713, 1973 5. Forzard H: Validity of myocardial infarction models. Circulation 51, 52:Suppl lll:lll-131-111-138, 1975 6. Bung RJ, Bassett AL, Thurer RJ, et al: Effects of coronary bypass
516
September 1978
The American Journal ol CARDIOLOGY
7. 8.
9.
10.
11.
surgery on the electrical activity of revascularized myocardium. J Thorac Cardiovasc Surg 73:269-277, 1977 Kupersmlth J: Electrophysiologic mapping during open heart surgery. Prog Cardiovasc Dis 19:167-202, 1976 Danlel T, Bolneau J, Sablston D: Comparison of human ventricular activation with canine model in chronic myocardial infarction. Circulation 44:74-89, 1971 Kaiser GA, Waldo AL, Bowman FO, et al: The use of ventricular electrograms in operation for coronary artery disease and its complications. Ann Thorac Surg 10:153-162, 1970 Kupersmlth J, Antman E, Hoffman BF: In vivo electrophysiologic effects of lidocaine in canine acute myocardial infarction. Circ Res 36:84-91, 1975 Brewer D, Bilbro R, Bartel A: Myocardial infarction as a complication of coronary bypass surgery. Circulation 4758-64, 1973
Volume 42
Electrophysiologic Effects of Acute Myocardial Infarction in Man
ISAAC WIENER, MD BRUCE MINDICH, MD JOEL KUPERSMITH, MD, FACC New York, New York
Six patients undergotng surgery for ischemlc heart disease were studied by means of epicardial electrodes affixed to the lefl ventricle. One patient who underwent triple coronary arterial bypass and plication of a left ventricular aneurysm had evidence of an acute myocardlal infarction 1 day after operation. A surface electrocardiogram and a bipolar electrogram from the lefl ventricle were recordad before and after development of the infarction. The bipolar electrogram showed a marked toss of voltage and delay of conduction that were not present in the patients who underwent surgery but did not sustain an acute myocardlal Infarction. Thus, any acute myocardlal infarction in conscious persons appears to be associated with areas of delayed epicardial action and dlmlnution of local vottage. This observatton suggests that the electrophysWogic mechanisms of infarction in man are slmllar to those of Infarction in the dog.
Most of our knowledge about the mechanisms of ventricular arrhythmias in acute myocardial infarction is derived from studies in the canine heart.’ In these studies, zones of infarction produced by coronary arterial ligation demonstrate slowing of conduction sufficient to permit the occurrence of reentrant arrhythmias. 24 The relevance of these studies to human myocardial infarction is unclear.5 Precise electrophysiologic data on acute infarction in man, particularly in conscious patients, is difficult to obtain. In this study, we made serial electrophysiologic recordings from the hearts of six patients who underwent surgery for ischemic heart disease, including one who had an acute myocardial infarction 1 day postoperatively. The observations suggest that the electrophysiologic changes similar to those seen in experimental myocardial infarction occur in infarction in conscious man. Methods
From the Division of Cardiology and Clinical Pharmacology, Department of Medicine, and the Division of Cardiothoracic Surgery, Department of Surgery, Mount Sinai School of Medicine of the city Universny of New York, New York, New York. This study was supported in part by grants HL 18801 and HL 10833 of the National Heart, Lung, and Blood Institute, U.S. Public Health Service, Bethesda, Maryfand; a &ant-in-Akl from the New York Heart Association, New Yak. New York; and a grant from the Heart Research Foundation. New York, New York. Manuscript received December 16.1977; revised manuscript received March 28, 1978, accepted March 29, 1978. Address for reprints: Joel Kupersmith. MD, Department of Medicine, Mount Sinai School of Medicine, Fifth Avenue and 100th Street, New York, New York 10029.
Six patients who underwent surgery for ischemic heart disease had bipolar electrodes for standby pacing placed on the left ventricle, in the distribution of the left anterior descending coronary artery. Bipolar electrograms were recorded from this electrode with an isolation unit on an Electronics for Medicine DR-8 research recorder with a filter frequency of 12 to 500 hertz at a paper speed of 100 mm/set. All recordings were made with the patient supine. Conduction intervals were measured from the earliest onset of the QRS complex in three simultaneously recorded standard electrocardiographic leads to the major deflection of the bipolar electrogram recorded from the left ventricle. A Vernier measuring device, with an accuracy of fl msec at recorded paper speed, was used for measurements. Recordings were performed 4 to 5 hours postoperatively and then during the following 6 days. Results Control patients: Five patients underwent coronary bypass surgery with grafts to the left anterior descending coronary artery and had an uncomplicated postoperative course. In these patients, the local electrograms showed no change in conduction time and a mean decrease in voltage of 44.0 f 11 percent from the
September 1978
The American Journal of CARDIOLOGY
Volume 42
513
ELECTROPHYSIOLOGYOF HUMAN INFARCTION-WIENER
ET AL.
FIGURE 1. Twelve lead electrocardiograms. A, 4 hours postoperatively. The tracing is unchanged from the preoperative electrocardiogram. B. first postoperative day. Note new Ct waves, S-T elevation and upr@ht T waves in IIIanda”F. leads I and aVL and S-T depression in leads II,
first recording 4 hours postoperatively to the 6th postoperative day; these findings are similar to those reported by others.6
Electrophysiologic findings in a patient with acute myocardialinfarction: The patient was a 42 year old woman
with angina pectoris that was intractable despite pharmacologic therapy. Coronary arteriography revealed severe triple vessel disease with a Friesinger score of 13, relatively poor runoff and poor left ventricular function. At operation, diffuse scarring of the apicolateral area and a small apical aneurysm were noted. Three coronary bypass grafts, including one to the left anterior descending coronary artery, were constructed, and the apical aneurysm was plicated. During surgery, a bipolar electrode was placed on the left ventricle in an area adjacent to the middle third of the left anterior descending coronary artery. When cardiopulmonary bypass was discontinued, the patient’s condition was hemodynamically unstable; an intraaorticballoon pump was inserted,and stable blood pressure and cardiac output were maintained. The electrocardiogram 4 hours postoperatively (Fig. 1A) was unchanged from the preoperative tracing, and the bipolar electrogram recorded from the left ventricle (Fig. 2A) showed an,amplitude of 2.7 mv and a conduction interval of 19 msec. The next morning (postoperative day l), the patient became hypotensive while on the intraaortic balloon pump, and dopamine, 16 pg/kg/per min, was required to maintain a stable blood pressure and cardiac output. The surface electrocardiogram (Fig. 1B) showed new S-T elevation and new Q waves in leads I and aVL. The left ventricular electrogram (Fig. 2B) showed a 92 percent loss of voltage to 0.2 mv and an increase of the conduction interval to 28 msec. By postoperative day 2 administration of dopamine had been discontinued, but lidocaine therapy (2 mg/min) was started for ventricular arrhythm@. The electrocardiogram showed evolution of a lateral acute myocardial infarction, and local left ventricular activation time was further delayed to 33 msec (Fig. 1C). On day 3, both lidocaine therapy and the intraaortic balloon
514
September 1979
The Amorkan
Journal ol CARDDLGGY
pump were discontinued. The electrocardiogram was unchanged, and the left ventricularelectrogram (Fig. 1D) showed further delay in local activation to 36 msec. After this, the patient had no other complications. The left ventricular electrogram recorded 6 days postoperatively (Fig. 1E) showed a further decrease in voltage to 0.08 mv and shortening of the local conduction interval to 30 msec.
Discussion Previous electrophysiologic studies on human myocardial infarction: Studies on intramyocardial conduction in man are difficult to perform.7 Using epicardial mapping during open heart surgery, Daniel et aL8 demonstrated delayed epicardial activation over zones of chronic infarction. Kaiser et a1.,g using electrophysiologic mapping during open heart surgery, localized the infarct zone in a patient with acute myocardial infarction. Unipolar recordingsrevealedQ waves, and bipolar electrograms demonstrated low voltage and increased duration. Local activation time was not evaluated and, because no recordings were made before the development of infarction, change in local activation caused by the infarction could not, be evaluated. Sung et aL6 studied left ventricular bipolar electrograms in patients before and after coronary bypass surgery. In 13 of 19 patients, the voltage of the bipolar electrogram increased immediately after grafting. During the first 5 days postoperatively, the voltage of the electrogram decreased in 16 of 19 patients, with no change in local activation time. In our control patients, the first recordings were made several hours postoperatively, and the results were consistent with those of Sung et al.6 In their study, three patients had a perioperative
Volume 42
infarc-
ELECTROPHYSIOLOGY OF HUMAN INFARCTION-WIENER
r r /-
ET AL.
I
T
lmv
lmv
+f
4 -
1
/-V-U-* -30
FIGURE 2. Standard electrocardiographic leads I, II and 111with simultaneous bipolar electrogram recorded from the left ventricle (I-V). A, 4 hours postoperatively, heart rate is 89 beats/min. Conductii interval from the onset of the QRS complex to ths maximal deflection of the bipolar electrogram is 19 msec. Voltage of electrogram is 2.7 mv. B, first postoperative day. Note ti new Q wave and S-T elevation in lead I. Heart rate is 120 beaWmin. The conduction interval is 28 msec and voltage of the bipolar electrogram is 0.2 mv. C, second postoperative day. There is atrial pacing to a heart rate of 91 beats/min. The conduction interval is 33 msec, and voltage of the bipolar electrogram is 0.25 mv. D, third postoperative day. There is atrial pacing to a heart rate of 93 beatslmin. The conductii interval is 36 msec, and voltage of the blpolar electrqam is 0.15 mv. E, sixth po&operative day. Heart rate is 103 beatslmin. The conduction interval is 30 msec, and voltage of the bipolar elecWgram Is 0.08 mv.
tion, but their electrograms showed no change in conduction interval, and the changes in amplitude did not differ from those in patients without infarction. The authors attributed this finding to the fact that the electrodes did not lie in the zone of the infarction as predicted by the electrocardiogram. Changes in left ventricular electrogram: Our patient clearly had an acute myocardial infarction on the first postoperative day. The left ventricular electrodes, which appeared to be in or near the infarct zone, demonstrated a marked loss of voltage and considerable slowing of activation. The further delay on day 2 may have been related to the evolution of the infarction, the withdrawal of dopamine or the administration of lidocaine.lO The delay of activation on day 3 may have represented ischemia related to discontinuation of the intraaortic balloon pump. By day 6 voltage continued to decrease, but epicardial activation time, although still delayed, was shorter than previously. None of these changes occurred in our patients who underwent coronary bypass surgery but did not sustain infarction. Overall, the delay in activation and loss of voltage in the patient with acute infarction are similar to those occurring after ligation of a canine coronary artery. Possible limitations of study: There are certain limitations to these observations. Only one patient with infarction was observed. Although postoperative myo-
cardial infarction is not rare, the electrocardiographic changes of infarction are almost always present in the first electrocardiogram recorded in the recovery room.ll It is thus quite unusual to be able to obtain a baseline electrogram after surgery but before the occurrence of infarctiqn. The patient who had infarction also had plication of a left ventricular aneurysm. The control recording after surgery indicates that it is quite unlikely that the changes were secondary to plication of the aneurysm. Although dislodgment of the electrodes might explain our findings, this also appears unlikely because dislodgment was not seen in any of the control cases and would have had to occur precisely at the time of infarction. It is possible that the electrodes were located in the periinfarction zone rather than within the infarct itself. For clinical reasons, multiple interventions were often performed simultaneously. A change in heart rate occurred on day 2, but the changes in conduction intervalpersistedwhen,the heart rate returned to baseline level. Although the total delay in epicardial activation was considerable, the delay demonstrated in these recordings did not extend beyond the refractory period of the ventiicle and by itself would not be sufficient for reentry to occur (although our electrodes may not have been in the zone of maximal conduction delay). Implications: Acute myocardial infarction in conscious persons appears to be associated with areas of delayed epicardial activation and diminution of local
September 1979
The Amerkan
Journal of CARDIDLDGY
Volume 42
515
ELECTROPHYSIOLOGY
OF HUMAN INFARCTION-WIENER
ET AL
voltage. As far as we know, this observation has not been made before, and it suggests that the electrophysiologic mechanisms of infarction in man are similar to those of
infarction in the dog. This delay in epicardial activation may be important in the pathogenesis of reentrant ventricular arrhythmias.
References 1. Wit AL, Bigger JT: Possible electrophysiological mechanisms for lethal arrhythmias accompanying myocardial ischemia and infarction. Circulation 51, 52:Suppl lll:lll-96-111-115, 1975 2. Waldo AL, Kaiser 0: A study of ventricular arrhythmias associated with acute myocardial infarction in the canine heart. Circulation 47:1222-1228, 1973 3. Scherlag B, El-Sherlf N, Hope R, et al: Characterization and localization of ventricular arrhythmias resulting from myocardial ischemia and infarction. Circ Res 35372-383, 1974 4. Bolneau JP, Cox JL: Slow ventricular activation in acute myocardial infarction. A source of re-entrant premature ventricular contractions. Circulation 48:702-713, 1973 5. Forzard H: Validity of myocardial infarction models. Circulation 51, 52:Suppl lll:lll-131-111-138, 1975 6. Bung RJ, Bassett AL, Thurer RJ, et al: Effects of coronary bypass
516
September 1978
The American Journal ol CARDIOLOGY
7. 8.
9.
10.
11.
surgery on the electrical activity of revascularized myocardium. J Thorac Cardiovasc Surg 73:269-277, 1977 Kupersmlth J: Electrophysiologic mapping during open heart surgery. Prog Cardiovasc Dis 19:167-202, 1976 Danlel T, Bolneau J, Sablston D: Comparison of human ventricular activation with canine model in chronic myocardial infarction. Circulation 44:74-89, 1971 Kaiser GA, Waldo AL, Bowman FO, et al: The use of ventricular electrograms in operation for coronary artery disease and its complications. Ann Thorac Surg 10:153-162, 1970 Kupersmlth J, Antman E, Hoffman BF: In vivo electrophysiologic effects of lidocaine in canine acute myocardial infarction. Circ Res 36:84-91, 1975 Brewer D, Bilbro R, Bartel A: Myocardial infarction as a complication of coronary bypass surgery. Circulation 4758-64, 1973
Volume 42
