Diagnosis of high posterior infarction: Experimental study through the use of body surface isopotential maps

J. ELECTROCARDIOLOGY, 10 (3), 1977, 251-256

Diagnosis of High Posterior Infarction: Experimental Study through the Use of Body Surface Isopotential Maps BY SATORU SUGIYAMA, M.D., JUN-ICHI SUGENOYA, M.D., MASATOSHI WADA, M.D., NOBUO NIIMI, M.D., JUNJI TOYAMA, M.D. AND KAZUO YAMADA, M.D.

SUMMARY

The purpose of this study is to d e t e r m i n e if high posterior infarction, which is r a t h e r difficult to diagnose by conventional ECGs, can be easily diagnosed t h r o u g h the use of maps.

This investigation was designed to diagnose high posterior infarction easily t h r o u g h the use o f body surface isopotential maps. High posterior i nf a r ct i on was experimentally caused by ligation o f the br a nc h of the circumflex a r t e r y of the canine left c o r o n a r y artery. E a c h dog had a series of maps recorded before and f our weeks a f t e r experimentally induced myocardial infarction. The c o m m o n f e a t u r e s of maps in high posterior in f ar ctio n are: 1) The positive ar e a expanded into th e dorsal surface so slowly that, in the middle stage of the v e n t r i c u l a r depolarization, a large ar e a of the dorsal surface was still covered by the negative area. 2) F r o m the middle to the late stage, the absolute value o f the m i n i m u m significantly decreased and absolute potential of the dorsal surface also significantly decreased. In conclusion, we propose t h a t it is possible to d i a g n o s e high p o s t e r i o r i n f a r c t i o n t h r o u g h the use of maps.

MATERIALS AND METHODS Coronary artery occlusion: Seven mongrel dogs weighing from 8 to 12 kg were anesthetized with thiamylal sodium of 20 mg/kg and maintained with artificial respiration. Then the chest of each dog was opened by an incision at the left fifth intercostal space, and we selected a ligation site on the branch of the left circumflex artery to induce high posterior infarction. Four weeks after ligation, each heart was isolated for direct observation and myocardial infarction was confirmed by histological studies. In our previous study, 2 it was shown that openchest surgery itself has no significant effect on the maps. Recording and displaying maps: The procedure for recording and displaying maps has been repeated in detail previously. 1 To sum up, mapping was based on the record of unipolar lead electrocardiograms with the use of needle electrodes obtained from 85 lead points attached to each dog's chest surface (59 on the anterior and 26 dorsal). The dogs were in a supine position under anesthesia and artificial respiration. From these ECGs, through the use of a minicomputer system, a body surface isopotential map was obtained every 1.5 msec throughout the entire time course of the ventricular depolarization. All the dogs had two series of maps based on the ECGs recorded before and four weeks after the ligation. In all cases standard twelve-lead ECGs and McFee lead VCGs were also recorded pre- and post-infarction.

In our p r e v i o u s s t udi e s , 1-4 it has been shown t h a t body surface isopotential maps (referred to below as maps for short) are a useful method of detecting abnormal cardiac electrical phenomenon precisely. Other investigators' studies 5-1~ also suggest t h a t serial maps contain significant electrocardiographic i n f o r m a t i o n n o t p r e s e n t in t h e s t a n d a r d twelve lead electrocardiogram (ECG) or vectorcardiogram (VCG). Maps are becoming an indispensable procedure in the diagnosing of various cardiac diseases. From the Department of Circulation and Respiration, Research I n s t i t u t e of E n v i r o n m e n t a l Medicine, Nagoya University, Nagoya, Japan. Reprint requests to: Satoru Sugiyama, M.D., Department of Circulation and Respiration, Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusa-ku, Nagoya 464, Japan.

RESULTS All seven cases showed consistent common characteristics in t h e i r map pat t erns, so a typical case is presented below. F i g u r e 1 r e p r e s e n t s a case of a cardiac 251

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specimen where the whitish-colored region c o r r e s p o n d s to t h e i n f a r c t e d lesion. F i g u r e 2B i l l u s t r a t e s a s e q u e n c e of m a p s of this case. P r e - i n f a r c t i o n m a p s a r e also s h o w n (Fig. 2A) for e a s y c o m p a r i s o n . To i l l u s t r a t e t h e body s u r f a c e i s o p o t e n t i a l m a p , t h e m a p w a s cut a n d s e p a r a t e d a l o n g t h e r i g h t m i d - a x i l l a r y l i n e on t h e t h o r a c i c surface a n d w a s s p r e a d open. The shaded area illustrates the positive zone a n d t h e w h i t e a r e a t h e n e g a t i v e ~one. E a c h solid line i l l u s t r a t e s a n e q u i p o t e n t i a l line d r a w n a t a n i n t e r v a l of 0.4 mv, a n d t h e b r o k e n l i n e i l l u s t r a t e s t h e p o t e n t i a l of Wilson's central terminal, which may be called t h e zero line. (4-) i n d i c a t e s a m a x i m u m and (-) a minimum. In t h e p o s t - i n f a r c t i o n m a p (Fig. 2B), a t 6

Fig. 1. A cardiac specimen of a case of high posterior infarction. The whitish region corresponds to the infarcted lesion.

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J. ELECTROCARDIOLOGY, VOL. 10, NO. 3, 1977

HIGH POSTERIOR INFARCTION

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msec from the onset of ventricular depolarization, the positive area covered n e a r l y the whole anterior chest surface and the negative the dorsal surface. A m a x i m u m was present near the center of the anterior chest surface and a m i n i m u m on the upper dorsal as in the pre-infarction map (Fig. 2A). At 12 msec, in both maps, there appeared an irregularity of equipotential lines, which might be connected with the breakthrough of the electrical wave front to the right ventricular free wall. However, the map patterns did not resemble each other. That is, after infarction, unlike before infarction, the positive area did not expand far into the dorsal surface and nearly the whole of the dorsal surface was still covered by the negative area. The locations of the post-infarction m a x i m u m and m i n i m u m were s i m i l a r to t h o s e of preinfarction. d. ELECTROCARDIOLOGY, VOL. 10, NO. 3, 1977

At 18 msec, in the pre-infarction map, the negative area of the anterior chest surface was enlarged. The positive area occupied over h a l f the dorsal surface. The m i n i m u m was located near the center of the anterior chest and a m a x i m u m existed on the left anterior chest surface. On t h e o t h e r h a n d , in the postinfarction map, over h a l f the dorsal surface was still covered by the negative area. The time when over h a l f the dorsal surface (from the left mid-axillary line to the right midaxillary line) changed from negative to positive was 16.3 ___ 4.1 msec (mean ___ SD) in pre-infarction, meanwhile in post-infarction it was 22.3 _+4.9 msec. This time delay proved to be significant (P < 0.05, Student's T test). At 24 msec, the post-infarction negative area covering the dorsal surface was larger t h a n t h a t of p r e - i n f a r c t i o n , too. The m a x i m u m in the pre-infarction map was lo-

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cated on the dorsal; however, t h a t in the post-infarction map was still located in the left axillary region. The location of pre- and p o s t - i n f a r c t i o n m i n i m u m r e s e m b l e d each other. The potential of the post-infarction central position of the dorsal surface, which is shown by a filled circle in the post-infarction 24 msec map, was lower t h a n t h a t of preinfarction, and the potential of the m i n i m u m was lower t h a n t h a t of pre-infarction. At 30 msec, t h e m a p p a t t e r n of posti n f a r c t i o n w a s s i m i l a r to t h a t of preinfarction. To wit, the whole anterior chest surface was occupied by the negative area, the dorsal surface the positive. Standard twelve-lead electrocardiograms of this case and McFee lead scalar X,Y,Z are presented in Fig. 3A (pre-infarction) and in Fig. 3B (post-infarction). In comparing Fig. 3B with Fig. 3A, it may be seen t h a t there are scarcely any clear indications which allow easy diagnosis of high posterior infarction. To detect high posterior infarction through the use of maps, it is necessary to note not only the negative area of the dorsal surface but also the potential value of the m i n i m u m and maximum. Figure 4 shows the mean and s t a n d a r d e r r o r of t h e p o t e n t i a l of t h e m i n i m u m at 18, 21 and 24 msec, comparing pre- and post-infarction values. Significant decreases in m i n i m u m voltage are observed after infarction. Figure 5 shows the potential of the central position of the dorsal surface. Significant decreases in its voltage are observed after infarction. As mentioned above, the consistent features of high posterior infarction were as follows. 1) The positive area expanded into the dorsal surface so slowly that, in the middle s t a g e of t h e v e n t r i c u l a r d e p o l a r i z a t i o n , a large area of the dorsal surface was still covered by the negative area. 2) From the middle to the late stage, the absolute potential of the m i n i m u m significantly decreased and the absolute potential of the dorsal surface also significantly decreased. If we cannot gain any other data, we can diagnose high posterior infarction n o t i n g these features of maps.

DISCUSSION The diagnosis of high posterior infarction is difficult because there appear no abnormal Q waves in standard twelve-lead ECG. Diagnostic criteria using the VCG have been proposed by m a n y investigators. 11-13 These criteria are useful to a degree, but as Ha and coworkers 14 pointed out, it remains a difficult problem to distinguish between posterior infarcJ. ELECTROCARDIOLOGY, VOL. 10, NO. 3, 1977

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tion and normal variation. The difficulty of diagnosing high posterior infarction lies in the fact t h a t there are no lead points on the dorsal surface in the standard twelve-lead ECG and only one lead point in the McFee lead VCG. To wit, there is hardly any inform a t i o n available from the dorsal surface. Since the dorsal surface is a greater distance from the heart t h a n the anterior surface, the ECG potential recorded on the dorsal surface is reduced and its QRS deflection is usually small. Moreover, Q waves, that is, minus deflection of early QRS, appear even in recordings of the normal heart. The scarcity of information resulting from these factors makes it extremely difficult to detect cardiac events which are projected to the dorsal surface. Thus, t h e use of body surface isopotential maps, which have m a n y lead points on the dorsal surface as well as the anterior, have an advantage in catching electrical events t h a t are projected on the dorsal surface. Maps, as their name implies, provide a presentation of body surface potential distributions over the entire t r u n k surface. Areas of positive and negative potentials apparently associate with major wave fronts within the heart. Noting the distribution of positive and negative areas in each stage and the transformation of the area, we can estimate the electrical cardiac phenomenon. The locations and potentials of m a x i m a and m i n i m a and the movement of the m a x i m a and minima also provide us with considerable information about cardiac wave fronts. Since a positive area results from the approach of an electrical wave front, if the wave fronts are impaired in any way, the shape of the positive area will change. In the case of high posterior infarction, since a considerable part of the posterior free wall is infarcted, the electromotive force which exists in the posterior wall is smaller t h a n t h a t of pre-infarction. Therefore the approach of the wave fronts toward the dorsal is so impaired t h a t the expansion rate of the positive area on the dorsal surface is very slow, and the time when positive area covers over h a l f the dorsal surface is delayed. This accounts for the delayed appearance on the d o r s a l s u r f a c e of t h e p o s t - i n f a r c t i o n maximum. Taking into consideration the fact t h a t some of posterior wall is free from infarction and t h a t the posterior wall excites later t h a n anterior wall as whole, it is understandable t h a t the positive area covers the dorsal surface at the late stage, but t h a t the positive potential of the dorsal surface decreased. Negative area results from the movement of an electrical front away from the observation point. Since the wave fronts t h a t proceed toward the dorsal decline because of posterior J. ELECTROCARDIOLOGY, VOL. 10, NO. 3, 1977

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infarction, the negative area of the anterior chest is comparatively small (Fig. 2B) and the potential of the m i n i m u m t h a t appears on the anterior surface decreases. Since it is at the early late stage of ventricular depolarization t h a t the excitation of the posterior wall is greatest, it is at this stage t h a t the change in map patterns is most obvious. Acknowledgment: We would like to express our appreciation to Mr. John H. Haig of the Language Center, Nagoya University for reading previous drafts of this paper and giving us numerous suggestions concerning language and style.

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11. HUGENHOLTZ, P.G, FORKNER, C E, JR, AND LEVINE, H D: A clinical appraisal of the vectorcardiogram in myocardial infarction. II. The Frank system. Circulation 24:825, 1961 12. HOFFMAN,I, TAYMOR,R C, MORRIS, M H AND KITTELL, I: Quantitative criteria for the diagnosis of dorsal infarction using the Frank vectorcardiogram. Am Heart J 70:295, 1965

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J. ELECTROCARDIOLOGY, VOL. 10, NO. 3, 1977