Precordial ST segment mapping. A sensitive technique for the evaluation of myocardial injury?

R J Capone, A S Most and P A Sydik Chest 1975;67;577-582 DOI 10.1378/chest.67.5.577 The online version of this article, along with updated information and services can be found online on the World Wide Web at: http://chestjournal.chestpubs.org/content/67/5/577

Chest is the official journal of the American College of Chest Physicians. It has been published monthly since 1935. Copyright1975by the American College of Chest Physicians, 3300 Dundee Road, Northbrook, IL 60062. All rights reserved. No part of this article or PDF may be reproduced or distributed without the prior written permission of the copyright holder. (http://chestjournal.chestpubs.org/site/misc/reprints.xhtml) ISSN:0012-3692

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Precordial ST Segment Mapping

A Sensitive Technique for the Evaluation
of Myocardial lniury?*
Robert J . Capone, M.D.,"" Albert S . Most, M.D.,t and Patricia A. Sydlik, M.A.:

Myocardial ischemic injury was created acutely in pigs by a closed-chest technique utilizing an intracoronary balloon occluder for the interruption of flow in the left anterior descending coronary artery and ST-segment elevation was followed over a two hour period using an 18 lead precordial map. In an experimental group of 10 animals, occtusion was carried out within the left anterior descending coronary artery 8.3 + 0.5 cm d i i to the origin of the main left coronary. Mean ST segment elevation (ST) showed a peak rise of 0.16 mV 10 minutes after occlusion. The balloon was moved proximally 1.6 t 0.2 cm giving a significant secondary rise of 0.16 mV within 5 minutes, despite indications of a generally small area of additional myocardial involvement, as judged

from anatomic distribution o additional vessek occhded f as well as a lack of significant change in hemodynamic parameters. In a control group of 5 additional pigs, a single distal occlusion at 6.4 f 0.9 cm from the origin of the main left coronary was produced by an identical technique. The ST rose to a peak of 0.20 mV at 15 minutes and was followed by a steady decline. Unlike the experimental group, no additional rise in ST was seen. The technique of precordial mapping thus appears to be a sensitive index of myocardial injury. In addition, it appears from this study that the magnitude of ST elevation is a direct reflection of the extent of myocardial injury.

he magnitude of ST segment elevation utilizing Ta precordial ECG multilead chest map has been considered an accurate, noninvasive technique for the evaluation of the extent of myocardial ischemic injury. While this technique has shown appropriate directional changes following a variety of pharmacologic and mechanical interventions intended to either limit or extend the boundaries of it has nevertheless been difficult to determine the sensitivity of this technique. This study was therefore undertaken to determine whether the technique of precordial ST segment mapping is sensitive enough to detect a small increase in the area of ischemic myocardial injury.

Farm-bred pigs, weighing between 91 and 128 lb, were anesthetized with sodium pentobarbital, 15 mg per pound N 'From the Department of Medicine, Section of Cardiology, Rhode Island Hospital, and the Division of Biological and Medical Sciences, Brown University, Providence, Rhode Island. "'Assistant Physician, Rhode Island Hospital; Assistant Professor of Medicine, Brown University. tAssociate Physician, Rhode Island Hospital; Assistant Professor of Medical Science, Brown University. :Research Assistant, Rhode Island Hospital. Reprint requests: Dr. Capone, Diuision of Cardidogy, @ode Island Hospital, Prouidence 02902

placed supine and tracheotomized to facilitate the treatment of potential drug-induced respiratory arrest (an infrequent complication during the induction of anesthesia in the pig). In addition to the standard limb leads, 18 electrodes were placed subcutaneously over the precordial area. There electrodes were arranged in a grid of four transverse rows and five longitudinal columns. The rows were spaced evenly from the first intercostal space to the xiphoid-sternal junction; the first column was placed at the right sternal border, the second at the left sternal border, and the three remaining columns spaced evenly between the left sternal border and the mid-axilla. The location of the left upper extremity in the pig prevented placement of the fourth and fifth column positions in row 4. EEG wire electrodes ( E45 silver disc electrodes, Grass Instrument Company) used for this purpose, were connected to a switch box which allowed the simultaneous recording of three ECG signals. ECGs were recorded at double standard (1.0 mV equal to 20 mm) at a paper speed of 25 mm per second on an 8-channel oscillographic ink recording system ( Hewlett-Packard, Model 7848A ) . ST-segment elevation was measured to the nearest 0.5 mm, using the TP segment as the isoelectric line, at a point LOO msec after the onset of the QRS. Those leads demonstrating a negative deflection were eliminated from the entire study, and the sum of positive ST-segment elevations divided by the number of leads was utilized to provide an average ST elevation (ST). These data were plotted at multiple recording periods both for each animal and as a mean for the entire group of ten animals. Femoral arterial blood pressure was monitored with a Statharn P23Db pressure transducer. A 7F Eppendorf catheter, introduced via the femoral vein and positioned in the pulmonary artery, was used in the

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determination of cardiac output, either as the site of injection for cardio-green dye, or as a sampling site for mixed venous blood in a Fick determination. In the former, blood was withdrawn using standard techniques from the femoral artery and outputs calculated by a cardiac output computer (Lexington Instruments); in the latter, mixed venous and arterial bloods were withdrawn simultaneously with expired air collected in Douglas bags. Arterial blood gases were monitored to assess the adequacy of ventilation. Animals were rejected from the study if initial P a was less than 80 mm Hg. If evidence of hypoxia developed during a study, supplemental oxygen was given to maintain the level of oxygenation between 80 and 90 mm Hg.
Occlusion Technique

the fluoroscope screen just prior to and immediately after its withdrawal to a proximal position. This distance was measured and the fluoroscopic magnification calculated at the end of each study. The distance between the two occluding positions could then be calculated, and by direct measurement from the known proximal occlusion site, the position of the initial, more distal site determined.

The right internal carotid artery was isolated and an 8 F thin-walled Lehman catheter (U.S.Catheter & Instrument Company No. 5400), shortened to 50 cm,was introduced and guided fluoroscopically into the left anterior descending coronary artery (LAD). Dilute x-ray contrast material was injected to verify its position. A 3 F embolectomy catheter (Edwards Laboratories) was then passed through the 8 F catheter and positioned in the distal LAD, (left anterior descending coronary artery). The larger 8 F catheter was then withdrawn into the aorta, the balloon on the embolectomy catheter inflated with radiographic contrast material, and its expansion visualized fluoroscopically. Balloon expansion was maintained thereafter by closing the catheter lumen. Protocol Fifteen animals were studied. Control measurements of the precordial map, arterial blood gases, cardiac output, as well as calculation of heart rate and blood pressure were made. Following the occlusion, these were repeated at 5, 10, 15, 30, and 4 minutes, with cardiac output repeated only . 5 at 10 and 45 minutes. At the end of the first hour followinn occlusion. measurements including cardiac output were again taken. The animals were divided i t two groups: Group A consisting of five anino mals, which received no additional intervention; and Group B consisting of ten animals, in which a small extension of the initial myocardial injury was created by moving the occluder to a more proximal position in the LAD. A sequence of measurements identical to those made during the first hour were again taken during this second hour. AU animals m i v e d heparin, 0.3 m g h g IV at the time of introduction of the carotid catheter. To prevent serious ventricular arrhythmias, each animal was given lidocaine, 100 mg IV by bolus, prior to the positioning of the occluding catheter, followed by a constant infusion ( 2 to 4 mg/min) for the duration of the study. At the end of the second hour, the animal was s a d c e d , the chest opened via a left lateral thoracotomy, and the position of the i d a t e d balloon-occluder marked on the myocardium. The balloon was then deflated and removed, the heart excised, and the appearance of the area subserved by the occluded vessel noted. At this point, the left coronary artery was opened longitudinally beginning at its ostium and continuing into the left anterior descending as far as possible. The ostia of all branches of the LAD were noted, as well as their distribution (septa1 vs diagonal) and size. The distance of the h a l proximal occlusion, as observed from the ostium of the main left coronary artery, was measured. The anatomic location of the distal occlusion was determined by marking the position of the occluding balloon on

Data concerning the animal and type of occlusion is summarized in Table 1. For Group B the location of both occluders, determined as previously described, is indicated for each animal; the mean distance of the initial occlusion from the ostium of the main left coronary artery was 8.3 + 0.5 cm, and the mean interocclusion or pullback distance 1.6 k 0.2 cm. When the hearts were examined in situ at the termination of the study, the exocardial surface was seen to be normal in color and appearance. The location of the balloon-occluder was within the main LAD in all animals with the exception of no. 8, in which the occluder was located in a major diagonal branch. Subsequent examination of the coronary artery distribution and correlation with the calculated pullback distance indicated
Table
1 S u m m a r y of Anatomic Data on Pigs Studied

Animal

Vessel Occluded

Distal Pullback Location Distance (cm) (cm)

Vessels Occluded by Pullback

Croup A (n =5) Single Occlusion Mean (of 5) 5 SEM Range

-

LAD

* .9 (4.0-8.5)
7 8.5 5.5 9.2 9.1 7.8 11.8 7.3 9.5 7.9 8.3 0.5 1.5 1.3 1.0 2.0 1.2 2.0 1.9 1.3 1.1 2.9 1.6 0.2 1 Sm Sept 2 Sm Diag 2 Sm Sept 2 Sm Diag 6 Sm Sept 1 Sm Diag 2 Sm Sept 2 Sm Diag 2 Sm Sept 2 Sm Diag 2 Sm Sept 3 Sm Diag Small Secondary Diagonals 1 Sm Sept 1 Sm Diag 1 Major Sept 1 Sm Diag

6.4

Croup B (n = 10) Occlusion with Extension 1 2 3 4 5 6 7 8 9 10 Mean f SEM LAD LAD LAD LAD LAD LAD LAD Diagonal LAD LAD

Diag=diagonal branches of the left anterior deacending coronary artery (LAD); Sept=septal branches of the LAD; Sm =small

578 CAPONE, MOST, SYDLIK

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ANIMAL * 9 Initial Occlusion 9 . 5 c m Pull Bock I.lcm

TlME (Minutes)

20

40

60

80

100

120

TlME

(Minutes)

FIGURE The mean ST segment elevation for ten animals, 2. sustaining both an initial distal and subsequent more proximal coronary occlusion (Group B). This rise from control is significant (p<.01) for the entire period of occlusion. Following the pullback occlusion (arrow), the secondary rise is significant when compared to the 80 minute value for the next 30 minutes (p<.01). C=control; NS=non-significant, Values are expressed as mean 2 standard error of the mean.

FIGURE The mean ST segment elevation of animal no. 9 1. ( Group B ) after initial distal and subsequent more proximal coronary occlusion. After control ( C ) an initial distal occlusion is created and ST followed for one hour, at which time the balloon occluder is moved 1.1 cm more proximally along the left anterior descending coronary artery. This pullback is accompanied by an abrupt rise of ST.

that, with the exception of animal no. 8, the initial distal occlusion occurred in the main LAD. The septa1 and diagonal branches located between the two occlusions are listed in Table 1. Except for animals nos. 3 and 10, these branches were small in size and number. The precordial map for animal no. 9 is presented as a typical example of the information obtained (Fig 1 ) . Following the initial occlusion at a distance of 9.5 cm from the left main coronary ostium, ST rises 0.20 mV to a peak at 15 minutes after occlusion, and then falls .08 mV by the end of the first hour. Following a pullback of 1.1 cm, ST rises 0.19 mV, peaks at 10 minutes, and falls 0.13 mV by the end of the hour following pullback. For Group B, the mean distance of the initial occlusion from the ostium of the main left coronary artery was 8.3 + 0.5 (Table 1 ) . ST elevation for this entire group (Fig 2 ) rises 0.16 mV within 10 minutes to a peak and falls 0.07 mV by the end of the first hour; after the pullback, ST rises 0.16 mV to a peak at 5 minutes and falls 0.14 mV one hour after pullback. The rise from control is statistically significant ( p <.01) for the entire initial occlusion. Following the pullback occlusion, the secondary rise in ST was significantly elevated ( p <.01) for the next 30 minutes. In Group A (Table 1), the mean distance of the occlusion from the ostium of the main left coronary artery was 6.4 cm. This resulted in a signifiCHEST, 67: 5, MAY, 1975

cant rise of ST (Fig 3 ) of 0.21 mV to the peak, occurring at 15 minutes. This rise is greater than that seen during the experimental group occlusions, and is consistent with the more proximal location of the occlusion when compared to the initial occlusion of the Group B. Following the peak, there is a downward trend of ST. Hemodynamic parameters followed in the control and experimental groups are indicated in Figure 4. Tests for significance were carried out comparing each observation with the preceding control. In order to allow comparisons between Groups A and B, those observations in Group A made during the second hour use the one-hour value for comparison. In the extension group (Group B), there appears to be an upward trend for mean heart rate and a downward trend for mean arterial pres-

TlME (Minutes) FIGURE3. The mean ST segment elevation for five animals sustaining only an initial coronary occlusion (Croup A). The initial rise from control is significant ( p < .01) followed by a downward trend which remains elevated ( p < .05) when compared to control ( C ) . Values are expressed as mean k standard error of the mean.

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TlME (Minutes)

loor i
~-Y--+*f--+ ----?--%+-----{ 5
y -e-MA P.
5

50

T---I
CO.

3
2

TIME (Minutes)

FIGURE ( A and B ) . Hemodynarnic 4 parameters for animals having a single distal occlusion (Croup A), and for those having a distal coronary occlusion with extension (Group B)-ie followed, at 60 minutes, by a more proximal occlusion (vertical arrow). COZcardiac output; HR=heart rate; MAP=mean atrial pressures.

sure. There are, however, no significant differences demonstrated for the heart rate rise; arterial pressure is significantly lower (p<.05) only at 105 minutes (92 I+ 11 compared to 114 2 9 at 60 min), well after the peak of the ST rise and at a time when the ST is not significantly different from 60 minute value. Cardiac output gradually fell during the study, although no significant differences can be shown when compared to the control prior to the more proximal occlusion ( p > .05). In Group A, no significance could be demonstrated *th regard to heart rate or arterial pressure. Cardiac output was not significantly depressed ( p >.05) during the second hour after occlusion, when compared to the 60 minute value.

Previous studies using a mapping technique for the evaluation of ST elevation at multiple precordial recording sites during myocardial ischemic injury have correlated the sum of the ST elevation (H ST) with the extent of myocardial damage.14 The studies have demonstrated that hypotension as well as agents known to increase cardiac work and
580 CAPONE, MOST, SYDLIK

consequently myocardial oxygen need, may increase 8ST; agents known to decrease cardiac work decrease 8ST.'s3 A serial examination of 14 patients with acute myocardial infarction, using similar techniques, has shown a subsequent rise of 9ST to correlate with biochemical evidence of extension of the infarction in 8.4 Nevertheless, the actual sensitivity of this new, noninvasive index of myocardial injury remains unproved. This study was therefore devised to demonstrate the sensitivity of the technique by examining the efled on the precordial map of a small controlled extension of myocardial infarction in the closed-chest animal. Pigs were chosen as the experimental animal because of the similarity of their coronary supply to the left ~ e n t r i c l e , the atrioventricular node,' and ~.~ the similarity of the size and type of collateral circ u l a t i ~ nto man. ~.~ Inflation of the balloon occluding catheter with radiographic contrast material makes both catheter and balloon easily seen fluoroscopically, permitting the degree of balloon expansion to be easily controlled, and providing accurate localization on the fluoroscopic screen of the two points of occlusion.
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Since the course of the left anterior descending coronary in its mid- to distal portion produces little if any foreshortening when the supine animal is viewed fluoroscopically in the PA projection, accurate assessment of the distance between the two occlusion sites is possible. When combined with post-mortem examination, the anatomic site of occlusion and the caliber and distribution of the vessels serving the area undergoing infarct extension can be readily determined. The actual distances on the LAD between distal and proximal occlusions varied little in the animals studied and, with the exception of animals nos. 3 and 10, include a few small septal and diagonal branches (Table 1 ) . Nevertheless, a distinct and abrupt rise of ST could be found shortly after the creation of the more proximal occlusion. The new ST elevation was statistically sigdcant, remaining so for the next 30 minutes (Fig 2 ) . While this second rise resembled, in general, that seen after the initial occlusion, it reached peak sooner ( 16.5 + 3.9 min) than the initial peak ( 10.0 & 2.5 min, P < .01), perhaps reflecting accelerated injury to myocardium already rendered ischemic by the initial occlusion. Heart rate and arterial pressure have been demonstrated to affect the level of ST elevation during In epicardial r n a p ~ i n g . ~ this study, these parameters have not varied significantly during the period of infarct extension. While there does appear to have been a gradual fall in mean arterial pressure during this extension period, this does not appear to have adversely influenced the ST since it was associated with the return of ST to baseline, to a level which, at 45 minutes, is not significantly different from that observed before the infarct extension. Cardiac output, while dropping significantly during the initial occlusion, likewise fails to fall significantly during the period of infarct extension. It therefore seems unlikely that changes in heart rate, arterial pressure, or cardiac output are responsible in themselves for the ST elevations appearing during the infarct extension period. A correlation has been shown between depressed levels of myocardial creatine phosphokinase and the degree of ST segment elevation over the epicardial surface of those areas8 Precordial mapping, however, has not been shown to define clearly a similar area of cellular injury. This report, along with previous epicardial mapping studies (see references), does support the inference that a larger area of cellular injury is reflected by a greater degree of ST segment elevation. In this study, eight of the ten animals in Group B had distal occlusions with small pullback distances. The LAD branches
CHEST, 67: 5, MAY, 1975

between the two occlusions in this subgroup were small in number and size. The mean highest ST elevation at any one observation period for this group following reocclusion, was 0.34 + 0.04 mV. The remaining two animals, nos. 3 and 10, had extensions which from an anatomic analysis were larger in size: animal 3, having many branches arising from a short but proximal pullback distance; and animal 10, having a long pullback area, including a major septal branch. Peak ST elevations of 0.61 and 0.57 mV for animals nos. 3 and 10 respectively, were clearly outside the range of the other eight. There does, then, seem to be a correlation between the size of the area of extension and the magnitude of the ST elevation, paralleling observations made during other, epicardial mapping studies. Quantification of the actual mass of myocardium involved in the extension, while of major interest, was not within the scope of this study. However, the lack of significant hemodynamic changes, the anatomically distal location of the occlusions, along with the small size and numbers of vessels further occluded in order to create the extension, all indicate that the infarct extension does indeed involve a small mass of myocardium. That this small area of additional infarction results in a major elevation of the mean ST segment, statistically different from a control group of animals having no extension, is indicative of the sensitive nature of this technique. While it examines the effect of two episodes of myocardial injury closely related in time, it is in basic agreement with the clinical study of P. R. Reid and associates,4 which indicated that precordial mapping in humans sustaining an acute myocardial infarction was s&ciently sensitive to detect an extension of the original infarction which did not affect immediate prognosis. It is, therefore, quite possible that precordial mapping can detect minimal myocardial inchemic injury of interest for statistical and research purposes, but which is below the threshold of clinical usefulness. Additional studies correlating the magnitude of the precordial ST segment elevations with the actual mass of injured myocardium would provide important clinical and investigative information.
ACKNOWLEDGMENT: We acknowled e the technical assistanoe of Carl Bruno, Wade Choke, a Thomas DeVo n ! as well as the skilled secretarial help of Carol White Kathleen Mahoney.
1 Maroko PR, Libby P, Covell JW, et al: Precordial STsegment elevation mapping: An atraumatic method for

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assessing alterations in the extent of myocardial ischemic injury. Am J Cardiol29:223-230,1974 2 Maroko PR, Bernstein EF, Libby P, et al: Effects of intraaortic balloon counterpulsation on the severity of myocardial ischemic injury following acute coronary occlusion. Circulation 45: 1150-1159,1972 3 Maroko PR, Braunwald E: Modification of myocardial infarction size after coronary occlusion. AM Int Med 79: 720-733, 1973 4 Reid PR, Taylor DR, Kelly DT, et al: Myocardial infarction extension detected by precordial ST-segment mapping. N Engl J Med 290: 123-128,1974

5 Lumb GD. Hardv LB: Collateral circulation and survival related to gradual occlusion of the right coronary artery in the pig. Circulation 27:717-721, 1963 6 Blumgart HL, Zoll PM, Freedberg AS, et al: The experimental production of intracoronary arterial anastomoses and their functional significance. Circulation 1: 10-27, 1950 7 Lumb G, Singletary H: Blood supply to the atrioventricular node and bundle of His: A comparative study in pig, dog and man. Am J Pathol41:65-75,1962 8 Maroko P, Kiekshus JF, Sobel BE, et al: Factors influencing infarct size following experimental coronary artery occlusions. Circulation 43:67-83, 1971

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Precordial ST segment mapping. A sensitive technique for the evaluation of myocardial injury? R J Capone, A S Most and P A Sydik Chest 1975;67; 577-582 DOI 10.1378/chest.67.5.577 This information is current as of January 15, 2012
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