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Further studies of the electrocardiographic effects of experimental myocardial lesions
Experimental andlaboratory
reports
Further studies of the electrocardiographic effects of experimental myocardial lesions J. A. Abildskov, M.D.* Robert S. Boyle, M.D. Salt Lake City, Utah
F
urther defintion of the mechanisms by which localized myocardial lesions alter the electrocardiogram is necessary to achieve the full utility of electrocardiographic records in the diagnosis of myocardial infarction. Information concerning the sequence of ventricular activation which is now available can be utilized in such investigations of the mechanisms of alteration of the QRS complex. Theoretical, experimental, and clinical studies in which the excitation sequence reported by Scher was so employed have been reported previously.1-3 In the previous experimental study, lesions were produced by the injection of a necrosing solution into the ventricular wall of dogs through the unopened chest. This procedure avoided the complex electrocardiographic effects of thoracotomy; however, little control of the location of the lesions was possible. In particular, lesions restricted to subepicardial and posterior basal portions of the left ventricle were not obtained in that study, and only one lesion restricted to the right ventricular wall was produced. In the present study, an open-chest preparation was employed, together with
measures designed to minimize the electrocardiographic effects of thoracotomy. With this preparation, the placement of lesions could be controlled more exactly than was possible in the previous experiments, and subepicardial, posterior basal, and right ventricular lesions were obtained. Materials and methods Experiments were performed on 12 dogs which ranged in weight from 10 to 26 kilograms, and which were anesthetized with pentobarbital. A total of 25 localized myocardial lesions was produced. Tracheotomy was performed and artificial respiration carried out using a respirator which could be halted at a fixed phase of the respiratory cycle. AII electrocardiograms were recorded within a few seconds after respiration was halted. The chest was opened with a mid-sternal incision extending from the xiphoid to a level near the base of the ventricles, and the chest wall was retracted only enough to permit placement of a needle at the desired site in the heart wall. This needle, through which a necrosing solution was to be injected, was inserted through the intact pericardium. Needles of 2O-gauge
From the Department of Internal Medicine, University of Utah College of Medicine, Salt Lake City, Utah. Received for publication March 5, 1964. This work was carried out during Dr. Abildskov’s tenure as Visiting Professor at the University of Uath, and was supported in part by the Utah Heart Association and the United States Public Health Service (Grant 5 Tl HE 5150). *Address: Department of Medicine, State University of New York, Upstate Medical Center. 766 Irving Ave., Syracuse, N. Y., 13210
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size were employed and were fitted with a flange which was held flush against the pericardium by a piano wire spring. The tips of the needles were occluded and injections were made through side openings located either 2 or 4 mm. distal to the flange. The needles were attached to plastic tubing, and the capacity of each needletubing system was calibrated so that sufficient necrosing solution to fill the system and deliver the desired amount to the myocardium could be injected. After placement of the needle, the chest cavity was packed with saline-soaked shredded polyurethane. The effects of this packing will be considered in the section on results. Electrocardiograms were recorded using an orthogonal lead system designed for the dog.4 The location of the center of the heart was estimated visually, and metal skin clips which served as electrodes were attached in appropriate relation to this point. The three leads from this system were recorded simultaneously from a multiple-beam cathode-ray oscilloscope on 35mm. film, using a film speed of 250 mm. per second. Lesions were produced by the injection of 0.2 cc. of 40 per cent formalin containing India ink. Lesions produced in this manner have been previously shown to result in electrocardiographic alterations, and microscopic study has indicated myocardial destruction confined to the area stained by the India ink.3 One to four lesions were produced in each experitnent. When multiple lesions were produced, the polyurethane packing was removed, the needle was placed at a new site, and the packing was replaced prior to obtaining the new control electrocardiogram. Post-lesion electrocardiograms were obtained 1 hour after the injection of formalin. Previous experience with lesions produced in this manner indicated that QRS alterations resulting from such lesions are usually complete and stable after this interval.2 The hearts were removed and fixed in formalin, after which they were sectioned transversely in a chamber with rigid guides for the cutting blade and the specimens, in order to yield sections with a uniform thickness of 5 mm. The location of lesions, including their relation to endocardial and
epicardial surfaces of the heart, was noted on frontal and horizontal plane diagrams of cardiac sections. The electrocardiograms were photographically enlarged to a scale of 1 mm. = 1 millisecond. Control and post-lesion records were compared by tracing each and superimposing the tracings. Identification of the proper time phase of control and postlesion records presented special problems which will be considered in the section on results. The electrocardiographic effects of each lesion were qualitatively compared to those which would be predicted on the basis of loss of tissue applied to the excitation sequence reported by Scher. In selected instances, electrocardiograms were derived from that excitation sequence before and after postulated areas of tissue destruction corresponding to actual lesions. The techniques employed in these derivations have been described in previous publications.1-3 Results
The reproducibility of electrocardiographic form with the techniques employed, the effects of packing the chest cavity, the identification of the time phase of control and post-lesion records, and the general characteristics of the lesions all require description prior to a presentation of the electrocardiographic effects of the lesions. Reproducibility. In 6 experiments, electrocardiograms were recorded under the sameconditions at intervals of 1 to 3 hours. No differences in the form of QRS complexes could be identified in these records. An example of these findings is shown in Fig. 1,A. These records were obtained 1 hour apart in an animal in which the opened chest was packed with salinesoaked polyurethane. Similar findings were made in the other 5 experiments in which reproducibility was examined. E$ect of Packing the chest cavity. The objective of packing the chest cavity with saline-soaked shredded polyurethane was to approximate the volume conductor properties of the intact chest. In 6 experiments, electrocardiograms were recorded prior to and after thoracotomy and after packing the chest as described. In these observations the cardiac center was con-
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Fig. 1. A, QRS complexes of electrocardiograms recorded 1 hour apart in a dog in which the opened chest was packed with saline-soaked shredded polyurethane. Superimposed tracings of these complexes are shown at the right of the figure and illustrate the reproducibility of QRS form under the conditions of the experiments reported. B, QRS complexes recorded before and after the chest was opened, and after packing of the open chest with saline-soaked shredded polyurethane.
sidered to be a point on the mid-sternal line, two intercostal spaces above the maximum cardiac impulse determined by palpation. The electrodes of the orthogonal leads system were placed in appropriate relation to this point with the chest closed and were replaced to approximate the same relation to the heart after the chest had been opened. As could be anticipated, the form of the prethoracotomy and post-thoracotomy records and those obtained after packing the chest cavity always differed. There was a consistent difference in the anteroposterior component of the QRS in prethoracotomy and post-thoracotomy records, with deflections in the 2 lead always being small in the post-thoracotomy records. Packing the chest cavity in the manner described had the consistent effect of increasing the amplitude of deflections in this lead. Examples of prethoracotomy and post-thoracotomy records and those obtained after
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packing the chest cavity are shown in Fig. 1,B. Time phase of control and post-lesion records. Since many of the lesions produced in this study altered only part of the QRS complex, the means by which the time phase of pte-lesion and post-lesion records was identified requites comment. Records associated with 17 of the lesions showed alterations of only the mid-temporal and terminal portions of the QRS complex. At least the initial one third of the QRS in all three orthogonal leads of pre-lesion and post-lesion records could be superimposed. In one experiment, alterations of the QRS were confined to the initial one third of the complex, and midtemporal and terminal portions of prelesion and post-lesion complexes could be superimposed. These findings provided reasonably certain identification of the proper time phase of those records. Identification of the absolute time phase of the records associated with the other 8 lesions was not so certain. In these cases the QRS form in at least two of the orthogonal leads of pre-lesion and post-lesion records could not be matched in any time phase relation. Thus, although the absolute time phase of these records could not be determined, it was certain that initial as well as later portions of the QRS complex had been altered.
Fig. 2. Cardiac lesions produced
sections showing in this study.
portions
of three
- ‘7 3”
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and Hoyle
El RV
PA 0 XX
00 X IV
x x
0
Q Subepicardial
X X
Lesions
X
x x
0
x
X
LV
O
;_I Right Ventricular
Lesions
Fig. 3. Approximate location of lesions produced in this study. Lesions at the sites indicated by circles altered initial as well as later portions of the QRS complex, whereas those at the other sites indicated altered only mid-temporal and terminal portions of the QRS.
Characteristics of the lesions. Although standard amounts of formalin solution were injected, the size and shape of the resulting lesions varied. The irregular shape of the lesions makes it difficult to specify their size, but their location within certain areas was noted. These locations will be described, together with the electrocardiographic effects of the lesions. Examples of the lesions produced are shown in Fig. 2. Electrocardiographic effects of subepicardial lesions in the left ventricle. Eleven lesions restricted to the subepicardial one half of the left ventricular wall were produced. The approximate location of these lesions is indicated in the diagram in Fig. 3,A. Three of the lesions which were located near the interventricular septum, and which are indicated by circles in the diagram, altered initial as well as midtemporal and terminal portions of the QRS complex. The other 8 subepicardial lesions of the left ventricle altered on11 mid-temporal and terminal portions of the QRS. The direction of QRS alterations with relation to the location of individual lesions was variable. This was consistent with the expected effects of loss of subepicardial tissue and with available information concerning the ventricular excitation sequence. With all localized myocardial lesions, the form of the QRS complex is determined b> the activation pattern in uninvolved portions of the ventricles. In the case of subendocardial and intramural lesions, the
widespread extent of the excitation process at the time the area of the lesion would normally have been activated often leads to marked displacement of the heart vector away from the location of the lesion. The magnitude of the heart vector may be either increased or decreased by the presence of the lesion.’ With subepicardial lesions, the activation process existing at the moment the area of the lesion would normally have been excited is less extensive. This leads to a less marked displacement of the heart vector than is often the case with lesions in other locations. A more regular effect of decreasing the magnitude of the heart vector is also to be expected with subepicardial lesions. The effect of a decrease in magnitude of the heart vector may exceed that of displacement of the vector with respect to an individual lead axis. As an exatnple of such an effect, it is possible that an anterior wall subepicardial lesion may actually result in a decreased posterior component of ventricular activation. These considerations seem to be adequate to account for the variability in the direction of alteration of the QRS which occurred with subepicardial lesions. The changes in the QRS complex which resulted from subepicardial lesions were small relative to those which often occurred with similar lesions in intramural and subendocardial areas in a previous study.2 The relatively small QRS alterations in the present study were consistent with simple loss of tissue as the mechanism of the alterations. The theoretical effects of subepicardial lesions derived from the excitation sequence reported b, Scher were also small. These results are illustrated in Fig. 4. In A of that figure the effects of a subepicardial lesion in the apical portion of the anterolateral left ventricular wall are shown. The oscilloscopic traces shown are the control and postlesion XY 2 leads. Superimposed tracings of the QRS portions of these records are shown at the right of the figure, with the control form indicated by solid and the post-lesion form by dotted lines. The QRS alterations associated with this lesion were confined to mid-temporal and terminal portions of the QRS complex and include alteration of the slope of the de-
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scending limb of the R wave in leads X and Y. Fig. 4,B shows the effects of one of the 3 subepicardial lesions located near the interventricular septum which altered initial as well as terminal portions of the QRS complex. All three orthogonal leads were altered by this lesion, with the most marked effect being a decreased amplitude of both Q and R deflections in the Z lead. The theoretical effects of a lesion of the subepicardial anterior wall are illustrated in Fig. 4,C. Leads X and Z shown were derived from the excitation sequence reported by Scher. The control form of these derived leads is shown by a solid line, and the form of the leads derived after a postulated lesion at the site illustrated are shown by the dotted lines. The effects of the lesion were confined to mid-temporal and terminal portions of the QRS and consist of slight alterations in the peak amplitude and slope of the R waves. BASAL LEFT VENTRICULAR LESIONS. Two transmural lesions were produced in the posterior wall of the left ventricle near its base. Despite their transmural extent these lesions altered only mid-temporal and terminal portions of the QRS complex. Both lesions decreased the amplitude of the I?. wave in lead Z, reflecting a decreased posterior component of ventricular excitation, and decreased the amplitude of an S wave in lead Y, reflecting a decreased superior component of activation. Both of these effects are consistent with simple loss of tissue in the posterior and basal portions of the heart. RIGHT VENTRICULAR LESIONS. Right ventricular lesions were produced at the approximate sites indicated in the diagram in Fig. 3,B. Ten of these lesions were transmural, and 2 were restricted to the subepicardial one half of the ventricular thickness. Lesions at the sites indicated by circles in the diagram altered initial portions of the QRS complex, and all but one of these also altered mid-temporal and terminal portions of the complex. Lesions at the other sites indicated altered only mid-temporal and terminal portions of the QRS complex. As is evident from the diagram, 4 of the lesions which altered early portions of the QRS complex were located in the right lateral wall of the ven-
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tricle, and one was located near the interventricular septum. These findings are consistent with Scher’s excitation sequence data, which indicates early activation of the right ventricular wall in both of these areas. The magnitude of QRS alterations due to right ventricular lesions was small and qualitatively consistent with the expected effects of right ventricular lesions, as shown in Fig. 5. In Fig. .5,/I, the effects of a lesion in the
Fig. 4. A, QRS complexes of electrocardiograms before and after production of a subepicardial lesion in the apical portion of the anterolateral left ventricular wall. In the tracings of the QRS complexes shown on the right-hand side of the figure, the control form is indicated by the solid line, and the post-lesion form by the dotted line. Only midtemporal and terminal portions of the complex were altered by this lesion. B, QRS complexes before and after production of a subepicardial left ventricular lesion near the interventricular septum. As illustrated by the tracings on the right-hand side of the figure, initial as well as later portions of the complex were altered by this lesion. C, QRS complexes in X and Z leads derived from the excitation sequence reported by Scher are shown as solid lines. The theoretical effects of the subepicardial lesion illustrated are shown by the dotted traces.
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Fig. 5. A, QRS complexes from an experiment in which a lesion in the right lateral portion of the right ventricular wall was produced. r’s shown by the superimposed tracings of these complexes, initial as well as later portions of the complex were altered by this lesion. B, QRS complexes from an experiment in which a lesion in the anterior portion of the right ventricle was produced. Only midtemporal and terminal portions of the complex were altered.
right lateral portion of the right ventricular wall which altered both initial and terminal portions of the QRS are shown. The effects of a lesion in the frank anterior wall of the right ventricle which altered only midtemporal and terminal portions of the QRS complex are shown in Fig. 5,B. Discussion
The result with most significance to the electrocardiographic diagnosis of myocardial infarction was the finding that many lesions confined to the subepicardial half of the left ventricular wall, and even transmural lesions in the posterior basal wall, altered only mid-temporal and terminal portions of the QRS complex. Such alterations would not be recognized as the result of localized lesions by standards which require abnormalities of the initial portion of the QRS, such as pathologic Q waves. The finding that most subepicardial lesions did not alter initial portions of the QRS complex is not consistent with reported evidence that activation of only
subepicardial portions of the ventricles contributes to the form of QRS complexes.” ,Another finding which is relevant to diagnostic use of the electrocardiogram in the recognition of localized lesions was the small magnitude and the variable direction of alterations produced by subepicardial lesions. It seems likely that most lesions in this location would not be recognized by current electrocardiographic standards and techniques. Another finding of interest was that the electrocardiographic effects of subepicardial lesions near the interventricular septum differed from those of similar lesions elsewhere in the left ventricle. Lesions near the septum altered initial as well as later portions of the QRS complex. Such alterations which extended over the entire duration of the QRS complex may have been the result of a conduction disorder of the per-infarction block t\-pe, as well as of simple loss of tissue. -These findings are compatible with, although they do not prove, intramural extension of the specialized conduction system near the interventricular septum. Some lesions in the right lateral wall of the right ventricle and in the right ventricle near the interventricular septum also altered early as will as late portions of the QRS complex. There are a number of features of the present study which limit its significance. As in previous studies of localized myocardial lesions, it is impossible to exclude factors other than the lesions themselves which may have contributed to electrocardiographic alterations. The necessity of conducting these experiments with the chest open definitely limits the significance of the results, even though “normal” volume conductor properties of the thorax were partially restored by the procedure of packing the chest cavity. The variability of the size and shape of the lesions also limits the conclusions which can be drawn from the findings, and the variability of the form of the control records constitutes a similar limitation. Despite the shortcomings of the study, the results appear to be a further step in the definition of the electrocardiographic effects of localized lesions and their mechanism.
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Summary The electrocardiographic effects of 25 chemically produced myocardial lesions in dogs were studied. Eleven of these were restricted to the subepicardial half of the left ventricular wall, 2 were located in the posterior basal portion of the left ventricle, and 12 were located in the right ventricular wall. Eight of the 11 subepicardial left ventricular lesions altered only mid-temporal and terminal portions of the QRS complex. The other 3 lesions were all located near the interventricular septum and altered early as well as later portions of the QRS. The 2 lesions of the posterior basal left ventricular wall altered only mid-temporal and terminal portions of the QRS complex. Right ventricular lesions in the right lateral wall near the base and those near the interventricular septum altered early as well as late portions of the QRS complex. Other right ventricular lesions altered only mid-temporal and terminal portions of the QRS. The significance of these findings may be summarized as follows: (1) Lesions in a variety of locations cannot be recognized by electrocardiographic standards which require abnormalities of the initial portion of the QRS complex. (2) Recognition of
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the relatively small and variable electrocardiographic effects of subepicardial, posterior basal, and right ventricular lesions may require modification of current clinical electrocardiographic techniques and standards for the diagnosis of myocardial infarction (3) The finding that most subepicardial lesions did not alter initial portions of the QRS is not consistent with reported evidence that activation of only subepicardial portions of the heart contributes to the form of QRS deflections. REFERENCES 1. Jacobson, E. D., Rush, S., Zinberg, S., and Abildskov, J. A.: The effect of infarction on the magnitude and orientation of electrical events in the heart, AM. HEART J. 58:863,1959. 2. Abildskov, J. A., Wilkinson, R. S., Vincent, W. A., and Cohen, W.: An experimental study of the electrocardiographic effects of localized myocardial lesions, Am. J. Cardiol. 8:485, 1961. 3. Wilkinson, R. S., Schaefer, J. A., and Abildskov, J. A.: Observations on the electrocardiographic and pathologic features of myocardial infarction in man, Am. J. Cardiol. 11:24, 1963. 4. McFee, R., and Parungao, A.: An orthogonal lead system for clinical electrocardiography, AM. HEART J. 62:93, 1961. 5. Kennamer, R., Bernstein, J. L., Maxwell, M. H., Prinzmetal, M., and Shaw, C. L.: Studies on the mechanism of ventricular activity. V. Intramural depolarization potentials in the normal heart, with a consideration of currents of injury in coronary artery disease, AM. HEART J. 46:379, 1953.
reports
Further studies of the electrocardiographic effects of experimental myocardial lesions J. A. Abildskov, M.D.* Robert S. Boyle, M.D. Salt Lake City, Utah
F
urther defintion of the mechanisms by which localized myocardial lesions alter the electrocardiogram is necessary to achieve the full utility of electrocardiographic records in the diagnosis of myocardial infarction. Information concerning the sequence of ventricular activation which is now available can be utilized in such investigations of the mechanisms of alteration of the QRS complex. Theoretical, experimental, and clinical studies in which the excitation sequence reported by Scher was so employed have been reported previously.1-3 In the previous experimental study, lesions were produced by the injection of a necrosing solution into the ventricular wall of dogs through the unopened chest. This procedure avoided the complex electrocardiographic effects of thoracotomy; however, little control of the location of the lesions was possible. In particular, lesions restricted to subepicardial and posterior basal portions of the left ventricle were not obtained in that study, and only one lesion restricted to the right ventricular wall was produced. In the present study, an open-chest preparation was employed, together with
measures designed to minimize the electrocardiographic effects of thoracotomy. With this preparation, the placement of lesions could be controlled more exactly than was possible in the previous experiments, and subepicardial, posterior basal, and right ventricular lesions were obtained. Materials and methods Experiments were performed on 12 dogs which ranged in weight from 10 to 26 kilograms, and which were anesthetized with pentobarbital. A total of 25 localized myocardial lesions was produced. Tracheotomy was performed and artificial respiration carried out using a respirator which could be halted at a fixed phase of the respiratory cycle. AII electrocardiograms were recorded within a few seconds after respiration was halted. The chest was opened with a mid-sternal incision extending from the xiphoid to a level near the base of the ventricles, and the chest wall was retracted only enough to permit placement of a needle at the desired site in the heart wall. This needle, through which a necrosing solution was to be injected, was inserted through the intact pericardium. Needles of 2O-gauge
From the Department of Internal Medicine, University of Utah College of Medicine, Salt Lake City, Utah. Received for publication March 5, 1964. This work was carried out during Dr. Abildskov’s tenure as Visiting Professor at the University of Uath, and was supported in part by the Utah Heart Association and the United States Public Health Service (Grant 5 Tl HE 5150). *Address: Department of Medicine, State University of New York, Upstate Medical Center. 766 Irving Ave., Syracuse, N. Y., 13210
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size were employed and were fitted with a flange which was held flush against the pericardium by a piano wire spring. The tips of the needles were occluded and injections were made through side openings located either 2 or 4 mm. distal to the flange. The needles were attached to plastic tubing, and the capacity of each needletubing system was calibrated so that sufficient necrosing solution to fill the system and deliver the desired amount to the myocardium could be injected. After placement of the needle, the chest cavity was packed with saline-soaked shredded polyurethane. The effects of this packing will be considered in the section on results. Electrocardiograms were recorded using an orthogonal lead system designed for the dog.4 The location of the center of the heart was estimated visually, and metal skin clips which served as electrodes were attached in appropriate relation to this point. The three leads from this system were recorded simultaneously from a multiple-beam cathode-ray oscilloscope on 35mm. film, using a film speed of 250 mm. per second. Lesions were produced by the injection of 0.2 cc. of 40 per cent formalin containing India ink. Lesions produced in this manner have been previously shown to result in electrocardiographic alterations, and microscopic study has indicated myocardial destruction confined to the area stained by the India ink.3 One to four lesions were produced in each experitnent. When multiple lesions were produced, the polyurethane packing was removed, the needle was placed at a new site, and the packing was replaced prior to obtaining the new control electrocardiogram. Post-lesion electrocardiograms were obtained 1 hour after the injection of formalin. Previous experience with lesions produced in this manner indicated that QRS alterations resulting from such lesions are usually complete and stable after this interval.2 The hearts were removed and fixed in formalin, after which they were sectioned transversely in a chamber with rigid guides for the cutting blade and the specimens, in order to yield sections with a uniform thickness of 5 mm. The location of lesions, including their relation to endocardial and
epicardial surfaces of the heart, was noted on frontal and horizontal plane diagrams of cardiac sections. The electrocardiograms were photographically enlarged to a scale of 1 mm. = 1 millisecond. Control and post-lesion records were compared by tracing each and superimposing the tracings. Identification of the proper time phase of control and postlesion records presented special problems which will be considered in the section on results. The electrocardiographic effects of each lesion were qualitatively compared to those which would be predicted on the basis of loss of tissue applied to the excitation sequence reported by Scher. In selected instances, electrocardiograms were derived from that excitation sequence before and after postulated areas of tissue destruction corresponding to actual lesions. The techniques employed in these derivations have been described in previous publications.1-3 Results
The reproducibility of electrocardiographic form with the techniques employed, the effects of packing the chest cavity, the identification of the time phase of control and post-lesion records, and the general characteristics of the lesions all require description prior to a presentation of the electrocardiographic effects of the lesions. Reproducibility. In 6 experiments, electrocardiograms were recorded under the sameconditions at intervals of 1 to 3 hours. No differences in the form of QRS complexes could be identified in these records. An example of these findings is shown in Fig. 1,A. These records were obtained 1 hour apart in an animal in which the opened chest was packed with salinesoaked polyurethane. Similar findings were made in the other 5 experiments in which reproducibility was examined. E$ect of Packing the chest cavity. The objective of packing the chest cavity with saline-soaked shredded polyurethane was to approximate the volume conductor properties of the intact chest. In 6 experiments, electrocardiograms were recorded prior to and after thoracotomy and after packing the chest as described. In these observations the cardiac center was con-
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Fig. 1. A, QRS complexes of electrocardiograms recorded 1 hour apart in a dog in which the opened chest was packed with saline-soaked shredded polyurethane. Superimposed tracings of these complexes are shown at the right of the figure and illustrate the reproducibility of QRS form under the conditions of the experiments reported. B, QRS complexes recorded before and after the chest was opened, and after packing of the open chest with saline-soaked shredded polyurethane.
sidered to be a point on the mid-sternal line, two intercostal spaces above the maximum cardiac impulse determined by palpation. The electrodes of the orthogonal leads system were placed in appropriate relation to this point with the chest closed and were replaced to approximate the same relation to the heart after the chest had been opened. As could be anticipated, the form of the prethoracotomy and post-thoracotomy records and those obtained after packing the chest cavity always differed. There was a consistent difference in the anteroposterior component of the QRS in prethoracotomy and post-thoracotomy records, with deflections in the 2 lead always being small in the post-thoracotomy records. Packing the chest cavity in the manner described had the consistent effect of increasing the amplitude of deflections in this lead. Examples of prethoracotomy and post-thoracotomy records and those obtained after
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packing the chest cavity are shown in Fig. 1,B. Time phase of control and post-lesion records. Since many of the lesions produced in this study altered only part of the QRS complex, the means by which the time phase of pte-lesion and post-lesion records was identified requites comment. Records associated with 17 of the lesions showed alterations of only the mid-temporal and terminal portions of the QRS complex. At least the initial one third of the QRS in all three orthogonal leads of pre-lesion and post-lesion records could be superimposed. In one experiment, alterations of the QRS were confined to the initial one third of the complex, and midtemporal and terminal portions of prelesion and post-lesion complexes could be superimposed. These findings provided reasonably certain identification of the proper time phase of those records. Identification of the absolute time phase of the records associated with the other 8 lesions was not so certain. In these cases the QRS form in at least two of the orthogonal leads of pre-lesion and post-lesion records could not be matched in any time phase relation. Thus, although the absolute time phase of these records could not be determined, it was certain that initial as well as later portions of the QRS complex had been altered.
Fig. 2. Cardiac lesions produced
sections showing in this study.
portions
of three
- ‘7 3”
Abildskov
and Hoyle
El RV
PA 0 XX
00 X IV
x x
0
Q Subepicardial
X X
Lesions
X
x x
0
x
X
LV
O
;_I Right Ventricular
Lesions
Fig. 3. Approximate location of lesions produced in this study. Lesions at the sites indicated by circles altered initial as well as later portions of the QRS complex, whereas those at the other sites indicated altered only mid-temporal and terminal portions of the QRS.
Characteristics of the lesions. Although standard amounts of formalin solution were injected, the size and shape of the resulting lesions varied. The irregular shape of the lesions makes it difficult to specify their size, but their location within certain areas was noted. These locations will be described, together with the electrocardiographic effects of the lesions. Examples of the lesions produced are shown in Fig. 2. Electrocardiographic effects of subepicardial lesions in the left ventricle. Eleven lesions restricted to the subepicardial one half of the left ventricular wall were produced. The approximate location of these lesions is indicated in the diagram in Fig. 3,A. Three of the lesions which were located near the interventricular septum, and which are indicated by circles in the diagram, altered initial as well as midtemporal and terminal portions of the QRS complex. The other 8 subepicardial lesions of the left ventricle altered on11 mid-temporal and terminal portions of the QRS. The direction of QRS alterations with relation to the location of individual lesions was variable. This was consistent with the expected effects of loss of subepicardial tissue and with available information concerning the ventricular excitation sequence. With all localized myocardial lesions, the form of the QRS complex is determined b> the activation pattern in uninvolved portions of the ventricles. In the case of subendocardial and intramural lesions, the
widespread extent of the excitation process at the time the area of the lesion would normally have been activated often leads to marked displacement of the heart vector away from the location of the lesion. The magnitude of the heart vector may be either increased or decreased by the presence of the lesion.’ With subepicardial lesions, the activation process existing at the moment the area of the lesion would normally have been excited is less extensive. This leads to a less marked displacement of the heart vector than is often the case with lesions in other locations. A more regular effect of decreasing the magnitude of the heart vector is also to be expected with subepicardial lesions. The effect of a decrease in magnitude of the heart vector may exceed that of displacement of the vector with respect to an individual lead axis. As an exatnple of such an effect, it is possible that an anterior wall subepicardial lesion may actually result in a decreased posterior component of ventricular activation. These considerations seem to be adequate to account for the variability in the direction of alteration of the QRS which occurred with subepicardial lesions. The changes in the QRS complex which resulted from subepicardial lesions were small relative to those which often occurred with similar lesions in intramural and subendocardial areas in a previous study.2 The relatively small QRS alterations in the present study were consistent with simple loss of tissue as the mechanism of the alterations. The theoretical effects of subepicardial lesions derived from the excitation sequence reported b, Scher were also small. These results are illustrated in Fig. 4. In A of that figure the effects of a subepicardial lesion in the apical portion of the anterolateral left ventricular wall are shown. The oscilloscopic traces shown are the control and postlesion XY 2 leads. Superimposed tracings of the QRS portions of these records are shown at the right of the figure, with the control form indicated by solid and the post-lesion form by dotted lines. The QRS alterations associated with this lesion were confined to mid-temporal and terminal portions of the QRS complex and include alteration of the slope of the de-
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scending limb of the R wave in leads X and Y. Fig. 4,B shows the effects of one of the 3 subepicardial lesions located near the interventricular septum which altered initial as well as terminal portions of the QRS complex. All three orthogonal leads were altered by this lesion, with the most marked effect being a decreased amplitude of both Q and R deflections in the Z lead. The theoretical effects of a lesion of the subepicardial anterior wall are illustrated in Fig. 4,C. Leads X and Z shown were derived from the excitation sequence reported by Scher. The control form of these derived leads is shown by a solid line, and the form of the leads derived after a postulated lesion at the site illustrated are shown by the dotted lines. The effects of the lesion were confined to mid-temporal and terminal portions of the QRS and consist of slight alterations in the peak amplitude and slope of the R waves. BASAL LEFT VENTRICULAR LESIONS. Two transmural lesions were produced in the posterior wall of the left ventricle near its base. Despite their transmural extent these lesions altered only mid-temporal and terminal portions of the QRS complex. Both lesions decreased the amplitude of the I?. wave in lead Z, reflecting a decreased posterior component of ventricular excitation, and decreased the amplitude of an S wave in lead Y, reflecting a decreased superior component of activation. Both of these effects are consistent with simple loss of tissue in the posterior and basal portions of the heart. RIGHT VENTRICULAR LESIONS. Right ventricular lesions were produced at the approximate sites indicated in the diagram in Fig. 3,B. Ten of these lesions were transmural, and 2 were restricted to the subepicardial one half of the ventricular thickness. Lesions at the sites indicated by circles in the diagram altered initial portions of the QRS complex, and all but one of these also altered mid-temporal and terminal portions of the complex. Lesions at the other sites indicated altered only mid-temporal and terminal portions of the QRS complex. As is evident from the diagram, 4 of the lesions which altered early portions of the QRS complex were located in the right lateral wall of the ven-
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tricle, and one was located near the interventricular septum. These findings are consistent with Scher’s excitation sequence data, which indicates early activation of the right ventricular wall in both of these areas. The magnitude of QRS alterations due to right ventricular lesions was small and qualitatively consistent with the expected effects of right ventricular lesions, as shown in Fig. 5. In Fig. .5,/I, the effects of a lesion in the
Fig. 4. A, QRS complexes of electrocardiograms before and after production of a subepicardial lesion in the apical portion of the anterolateral left ventricular wall. In the tracings of the QRS complexes shown on the right-hand side of the figure, the control form is indicated by the solid line, and the post-lesion form by the dotted line. Only midtemporal and terminal portions of the complex were altered by this lesion. B, QRS complexes before and after production of a subepicardial left ventricular lesion near the interventricular septum. As illustrated by the tracings on the right-hand side of the figure, initial as well as later portions of the complex were altered by this lesion. C, QRS complexes in X and Z leads derived from the excitation sequence reported by Scher are shown as solid lines. The theoretical effects of the subepicardial lesion illustrated are shown by the dotted traces.
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Fig. 5. A, QRS complexes from an experiment in which a lesion in the right lateral portion of the right ventricular wall was produced. r’s shown by the superimposed tracings of these complexes, initial as well as later portions of the complex were altered by this lesion. B, QRS complexes from an experiment in which a lesion in the anterior portion of the right ventricle was produced. Only midtemporal and terminal portions of the complex were altered.
right lateral portion of the right ventricular wall which altered both initial and terminal portions of the QRS are shown. The effects of a lesion in the frank anterior wall of the right ventricle which altered only midtemporal and terminal portions of the QRS complex are shown in Fig. 5,B. Discussion
The result with most significance to the electrocardiographic diagnosis of myocardial infarction was the finding that many lesions confined to the subepicardial half of the left ventricular wall, and even transmural lesions in the posterior basal wall, altered only mid-temporal and terminal portions of the QRS complex. Such alterations would not be recognized as the result of localized lesions by standards which require abnormalities of the initial portion of the QRS, such as pathologic Q waves. The finding that most subepicardial lesions did not alter initial portions of the QRS complex is not consistent with reported evidence that activation of only
subepicardial portions of the ventricles contributes to the form of QRS complexes.” ,Another finding which is relevant to diagnostic use of the electrocardiogram in the recognition of localized lesions was the small magnitude and the variable direction of alterations produced by subepicardial lesions. It seems likely that most lesions in this location would not be recognized by current electrocardiographic standards and techniques. Another finding of interest was that the electrocardiographic effects of subepicardial lesions near the interventricular septum differed from those of similar lesions elsewhere in the left ventricle. Lesions near the septum altered initial as well as later portions of the QRS complex. Such alterations which extended over the entire duration of the QRS complex may have been the result of a conduction disorder of the per-infarction block t\-pe, as well as of simple loss of tissue. -These findings are compatible with, although they do not prove, intramural extension of the specialized conduction system near the interventricular septum. Some lesions in the right lateral wall of the right ventricle and in the right ventricle near the interventricular septum also altered early as will as late portions of the QRS complex. There are a number of features of the present study which limit its significance. As in previous studies of localized myocardial lesions, it is impossible to exclude factors other than the lesions themselves which may have contributed to electrocardiographic alterations. The necessity of conducting these experiments with the chest open definitely limits the significance of the results, even though “normal” volume conductor properties of the thorax were partially restored by the procedure of packing the chest cavity. The variability of the size and shape of the lesions also limits the conclusions which can be drawn from the findings, and the variability of the form of the control records constitutes a similar limitation. Despite the shortcomings of the study, the results appear to be a further step in the definition of the electrocardiographic effects of localized lesions and their mechanism.
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Summary The electrocardiographic effects of 25 chemically produced myocardial lesions in dogs were studied. Eleven of these were restricted to the subepicardial half of the left ventricular wall, 2 were located in the posterior basal portion of the left ventricle, and 12 were located in the right ventricular wall. Eight of the 11 subepicardial left ventricular lesions altered only mid-temporal and terminal portions of the QRS complex. The other 3 lesions were all located near the interventricular septum and altered early as well as later portions of the QRS. The 2 lesions of the posterior basal left ventricular wall altered only mid-temporal and terminal portions of the QRS complex. Right ventricular lesions in the right lateral wall near the base and those near the interventricular septum altered early as well as late portions of the QRS complex. Other right ventricular lesions altered only mid-temporal and terminal portions of the QRS. The significance of these findings may be summarized as follows: (1) Lesions in a variety of locations cannot be recognized by electrocardiographic standards which require abnormalities of the initial portion of the QRS complex. (2) Recognition of
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the relatively small and variable electrocardiographic effects of subepicardial, posterior basal, and right ventricular lesions may require modification of current clinical electrocardiographic techniques and standards for the diagnosis of myocardial infarction (3) The finding that most subepicardial lesions did not alter initial portions of the QRS is not consistent with reported evidence that activation of only subepicardial portions of the heart contributes to the form of QRS deflections. REFERENCES 1. Jacobson, E. D., Rush, S., Zinberg, S., and Abildskov, J. A.: The effect of infarction on the magnitude and orientation of electrical events in the heart, AM. HEART J. 58:863,1959. 2. Abildskov, J. A., Wilkinson, R. S., Vincent, W. A., and Cohen, W.: An experimental study of the electrocardiographic effects of localized myocardial lesions, Am. J. Cardiol. 8:485, 1961. 3. Wilkinson, R. S., Schaefer, J. A., and Abildskov, J. A.: Observations on the electrocardiographic and pathologic features of myocardial infarction in man, Am. J. Cardiol. 11:24, 1963. 4. McFee, R., and Parungao, A.: An orthogonal lead system for clinical electrocardiography, AM. HEART J. 62:93, 1961. 5. Kennamer, R., Bernstein, J. L., Maxwell, M. H., Prinzmetal, M., and Shaw, C. L.: Studies on the mechanism of ventricular activity. V. Intramural depolarization potentials in the normal heart, with a consideration of currents of injury in coronary artery disease, AM. HEART J. 46:379, 1953.