QRS alterations in body surface potential distributions during percutaneous transluminal coronary angioplasty in single-vessel disease

Journal of Elect'rocardiology Vol. 27 No. 4 1994

QRS A l t e r a t i o n s in B o d y Surface P o t e n t i a l Distributions During P e r c u t a n e o u s T r a n s l u m i n a l Coronary A n g i o p l a s t y in Single-vessel D i s e a s e

Istvfin Preda, MD, Reginald Nadeau, MD, Pierre Savard, PhD, Denis Hamel, MD, Donald Palisaitis, MD, Mohammad Shenasa, MD, and James Nasmith, MD

Abstract: Body surface QRS potentials were recorded with 63 chest leads in 20 patients with proximal single-vessel disease located on either the left anterior descending coronary artery (n = 10), the right coronary artery (n = 6), or the left circumflex coronary artery (n = 4) before, during, and after percutaneous transluminal coronary angioplasty. In each case, three consecutive inflations of relatively short duration (37 -+ 14 seconds) were carried out. Electrical activity was displayed as unipolar electrograms and body surface potential maps. The total QRS complex duration decreased in 14 of the 20 patients. Focal conduction disturbances were observed in six cases; all six had left anterior descending coronary artery occlusion and two were also accompanied by a clear shortening of the right epicardial breakthrough time. In these two cases, an initial activation loss seemed to be characteristic, whereas in the other four cases, a rather diffuse slowing of intraventricular conduction, especially during the terminal portion of the QRS, could be observed. Individual and group mean isointegral difference body surface potential maps (during-minus-before dilation) were considered valuable for the interpretation of localized changes in intraventricular conduction during percutaneous transluminal coronary angioplasty, and their individual variations could, at least partly, be explained by the presence or absence of collateral circulation. Two different hypotheses are suggested to account for the QRS complex shortening observed during short-term myocardial ischemic injury: ( 1) coronary artery occlusion delayed activation of the portion of the septal region that is normally activated early during the QRS, and/or (2) coronary artery occlusion increased the speed of propagation within the ventricles. Both of these hypotheses are discussed in light of earlier clinical and experimental results. Key words: percutaneous transluminal coronary angioplasty, myocardial ischemia, coronary occlusion, ECG changes, body surface potential mapping.

From the Research Center, H~pital du Sacrd-Coeur de Montreal, Department of Med&ine, Faculty of Medicine, and Ecole Polytechnique, Universit~ de Montrdal, Montreal (Quebec) Canada.

Supported by grants from the Medical Research Council of Canada. Reprint requests: R. Nadeau, MD, Research Centre, H6pital du Sacr6Coeur de Montreal, 5400 Gouin Boulevard West, Montreal, Quebec, Canada H4J 1C5.

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Journal of Electrocardiology Vol. 27 No. 4 October 1994

Electrocardiographic (ECG) r e c o r d i n g of b o d y surface p o t e n t i a l alterations p r o d u c e d b y s h o r t - t e r m myocardial ischemia provoked by percutaneous t r a n s l u m i n a l c o r o n a r y a n g i o p l a s t y (PTCA) provides a u n i q u e m o d e l of c o r o n a r y o c c l u s i o n i n h u m a n s , w i t h a fully defined c o r o n a r y a n a t o m y a n d k n o w n sites a n d d u r a t i o n s of occlusion. A l t e r a t i o n s i n b o t h d e p o l a r i z a t i o n a n d r e p o l a r i z a t i o n w e r e r e c e n t l y rep o r t e d a n d f o u n d to be specific 1-]3 for the o c c l u d e d c o r o n a r y artery, b u t relatively little a t t e n t i o n has b e e n paid to c h a n g e s at the very o n s e t of b a l l o o n inflation. Also, initial electrical instability i n acute m y o c a r d i a l i s c h e m i a is k n o w n to b e strongly related to the o c c u r r e n c e of m a j o r v e n t r i c u l a r a r r h y t h mias. ]4"~5 W i t h the e v a l u a t i o n of a series of b o d y surface m a p p i n g m e a s u r e m e n t s o b t a i n e d before, d u r i n g , a n d after b a l l o o n i n f l a t i o n o n p a t i e n t s w i t h single-vessel disease, w e tried to exploit all of the a d v a n t a g e s of the m e t h o d w i t h its h i g h t e m p o r a l a n d spatial r e s o l u t i o n . This series of b o d y surface p o t e n tial analyses are l i m i t e d to the c h a n g e s o b s e r v e d during depolarization.

Materials and Methods

w e r e 1 1 m e n a n d 9 w o m e n w i t h a m e a n age of 5 5 years (range, 4 3 - 6 5 years). All of the p a t i e n t s h a d single-vessel disease w i t h m o r e t h a n 70% n a r r o w i n g i n the p r o x i m a l third of the left a n t e r i o r d e s c e n d i n g (LAD) c o r o n a r y artery (10 p a t i e n t s ) , right c o r o n a r y artery (RCA) (6 patients), or left circumflex (LCX) c o r o n a r y artery (4 patients). No p a t i e n t h a d n a r r o w i n g of m o r e t h a n 50% of o t h e r c o r o n a r y arteries. N o n e of the p a t i e n t s h a d a p r e v i o u s m y o c a r d i a l infarction, b u n d l e b r a n c h block, or v e n t r i c u l a r hypert r o p h y , b u t 13 h a d h y p o k i n e s i a i n the Segment perfused b y the target c o r o n a r y artery. D o m i n a n c e of c o r o n a r y c i r c u l a t i o n , existence a n d g r a d i n g of coron a r y collateral flow, 16-19 as well as the basic p a r a m eters of left v e n t r i c u l a r diastolic a n d systolic f u n c t i o n , w e r e carefully n o t e d . All p a t i e n t s gave w r i t t e n i n f o r m e d c o n s e n t for c o r o n a r y a n g i o g r a p h y , a n g i o p l a s t y , a n d b o d y surface p o t e n t i a l m a p p i n g recordings. P e r c u t a n e o u s t r a n s l u m i n a l c o r o n a r y a n g i o p l a s t y w a s p e r f o r m e d via the f e m o r a l a p p r o a c h u s i n g s t a n d a r d protocol, 2° a n d the p a t i e n t s received 5,000 IU h e p a r i n a n d 50 m g n i t r o g l y c e r i n via c o n t i n u o u s i n t r a v e n o u s i n f u s i o n before i n t r o d u c i n g the balloon.

Acquisition of ECGs

Table 1 s h o w s the m a i n clinical a n d h e m o d y n a m i c characteristics of the p a t i e n t s w h o u n d e r w e n t elective PTCA a n d w e r e a n a l y z e d i n this study. There

D u r i n g PTCA, t h e surface ECG leads I, II, a n d aVF, as well as i n t r a a o r t i c a n d i n t r a c o r o n a r y pressures, w e r e displayed o n a m u l t i c h a n n e l oscilloscope a n d

T a b l e 1. M a i n Clinical a n d Hemodynamic Characteristics of the Single-vessel PTCA Patients

Patient No.

Age/ Sex (years)

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20

56/M 55/F 48/F 59/M 53/M 56/M 64/M 52/M 61/F 43/M 59/F 46/M 45/F 54/M 64/F 60/M 63/F 65/F 58/F 45/M

Vessel

Narrowing (%) Preoperative/ Postoperative

Collateral Circulation

LAD LAD LAD LAD LAD LAD LAD LAD LAD LAD RCA RCA RCA RCA RCA RCA LCX LCX LCX LCX

90/10 90/05 98/20 90/0 85/10 90/10 90/70 98/10 98/40 80/20 70/0 90/10 80/40 70/20 95/10 90/0 95/30 80/70 80/10 80/70

Balanced Right Right Right Right Right Right Right Balanced Right Right Right Right Right Right Right Balanced Right Left Right

LVEDP (mmHg)

R-L+ R-L+ R-L +

L-R + L-R + L-R + +

Preoperative/ During

LV Wall Motion

Duration (seconds)

21/26 5/20 5/13 8/15 8/13 25/25 15/30 17/22 23/24 11/21 15/18 15/18 7/25 9/28 16/32 15/16 6/10 5/8 11/25 8/12

n AL hypokinesis n AL hypokinesis AL hypokinesis AL hypokinesis AL + A hypokinesis AL + A hypokinesis n n n AL hypokinesis n PI hypokinesis n PB hypokinesis AL hypokinesis AL hypokinesis PB hypokinesis AL hypokinesis

36 28 30 36 23 35 33 60 28 24 38 25 29 30 66 50 43 45 30 56

PTCA, percutaneous transluminal coronary angioplasty; LAD, left anterior descending coronary artery; RCA, right coronary artery; LCX, left circumflex coronary artery; R-L, right-to-left coronary collaterals; L-R, left-to-right coronary collaterals; LVEDP, left ventricular end-diastolic pressure; LV, left ventricular; A, anterior; AL, anterolateral; PI, posteroinferior; PB, posterobasal; u, normal.

QRS Potential Changes During PTCA

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Preda et al.

313

Fig. 1. Body surface potential map format and lead system. To depict the body surface potential distributions, the torso is represented in a rectangular format with the two vertical sides corresponding to the

right midaxil]ary line, the left half to the anterior torso, and the right half to the posterior torso. The dots represent the 63 leads, and the symbols indi-

cate the locations of the standard ECG and vectorcardiographic leads that were extracted from the 63 leads: RA, LA, and LL for the standard frontal leads, numerals 1-6 for the precordial leads, and the lower case letters (a,c,~,f,h,i,m) for the Frank lead system.

h •

RA

•

•

•

•

-

. 1 . 2 .

•

LA

•

•

•

•

•

•

°

•

•

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•

•

"5

"6

•

3 i

•

•

•

•

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6

•

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e

f simultaneously recorded on paper. Body surface potential maps were obtained with a previously reported technique. 2~ Briefly, the recordings were performed with 63 unipolar leads referenced to the Wilson central terminal (Fig. 1). The electrodes were plastic disks coated with Ag-AgCI. These were relatively radiotranslucent and did not interfere with the evaluation of the PTCA procedure. Electrodes were m o u n t e d on 12 vertical adhesive strips with an interelectrode distance of 6 cm. The first strip was applied over the sternum with the top electrode overlying the suprasternal notch, the other strips were then equally spaced around the torso with the top electrode applied at the same level. Multiple segments of body surface recordings of 10 seconds' duration were obtained during normal sinus r h y t h m before angioplasty and at the end of each balloon inflation episode (typically 3 per patient). The m e a n inflation times are indicated in Table 1. The final measurements were taken in the resting state and 15 minutes after finishing PTCA. Body surface potential mapping recordings during angioplasty were performed at least 2 minutes after the injection of radiopaque dye so as to prevent ECG alterations induced by the contrast material. 22 Using an integrated mapping system, 23 the ECGs were amplified, filtered with a bandwidth of 0 . 0 5 - 2 0 0 Hz, sampled at 500 Hz, averaged

4

c

m

a

~

•

•

6

6

•

•

Q

•

6

•

LL over a 10-second segment to reduce the effects of noise and respiration, and finally recorded on floppy disks. Data processing was carried out on a PDP 11/34 computer (Digital Equipment, Maynard, MA). The onset and offset of the QRS complex were determined by a special algorithm using the spatial magnitude and spatial velocity of each of the unipolar recordings and, w h e n necessary, were corrected by two independent observers w h o took into account the continuous buildup of maxima and minima at the border of the depolarization and repolarization. Two isoelectric points during the TP intervals preceding and following the averaged beat were manually determined by the operator so as to correct baseline shift by subtracting from each signal a straight line joining these isoelectric points. After visual inspection, signals from missing or noisy leads were interpolated from neighboring leads. Isopotential maps were then d r a w n for each sampling instant using the rectangular format presented in Figure 1. In these maps, isopotential lines joining points with the s a m e potential values were obtained by cubic spline interpolation. The zero potential line was identified by a thicker line, and plus and minus signs indicated the locations of the m a x i m u m and m i n i m u m potential values.

314

Journal of Electrocardiology Vol. 27 No. 4 October 1994

So as to r e l a t e b o d y surface p o t e n t i a l m a p s to t h e s t a n d a r d 1 2 - l e a d ECG, t h e l a t t e r w e r e o b t a i n e d directly f r o m s o m e o f t h e 63 t h o r a c i c l e a d s (eg, l e a d s V5, V6) o r b y t h e i n t e r p o l a t i o n b e t w e e n t w o n e i g h b o r i n g l e a d s (eg, l e a d Vl RA). To assess t h e ECG a l t e r a t i o n s p r o d u c e d b y o c c l u sion of a given coronary artery, average isopotential m a p s w e r e c o m p u t e d at e a c h 4 m s o f t h e h e a r t cycle for t h e f o l l o w i n g p a t i e n t g r o u p s : LAD, LCX, a n d RCA. T i m e integrals o v e r t h e QRS c o m p l e x ( d i v i d e d i n t o 3 e q u a l parts) w e r e d i s p l a y e d b y i s o i n t e g r a l lines to a l l o w for a m o r e d e t a i l e d d e s c r i p t i o n of t h e c a r d i a c electrical d e p o l a r i z a t i o n . F r o m t h e s e i n t e g r a l m a p s , w h i c h w e r e c o n s t r u c t e d for t i m e i n s t a n t s b e f o r e a n d d u r i n g (3 c o n s e c u t i v e sessions i n e a c h case) d i l a t i o n , m e a n i s o i n t e g r a l m a p s w e r e c o m p u t e d for t h e LAD, RCA, a n d LCX g r o u p s , w h i l e b e f o r e d i l a t i o n integrals were subtracted from the integral values obtained d u r i n g dilation. The m e a n difference m a p s for d u r ing-minus-before dilation were computed by summ a t i o n of t h e m a t r i c e s , w i t h difference v a l u e s div i d e d b y t h e n u m b e r o f subjects for t h e LAD, RCA, a n d LCX g r o u p s .

Statistical Analysis Results a r e e x p r e s s e d as m e a n _+ SD. C o m p a r i s o n s w e r e p e r f o r m e d u s i n g p a i r e d S t u d e n t ' s t-test. A P v a l u e < .05 w a s c o n s i d e r e d significant.

Results T h e resting h e a r t rate v a r i e d b e t w e e n 39 a n d 80 b e a t s / r a i n . D u r i n g PTCA, n o m a j o r a r r h y t h m i c epis o d e w a s o b s e r v e d , a n d a l t e r a t i o n s o f t h e h e a r t rate w e r e less t h e n 2 0 % o f t h e r e s t i n g v a l u e for all p a tients. The m e a n b a l l o o n i n f l a t i o n t i m e s for t h e t h r e e c o n s e c u t i v e p e r i o d s d u r i n g w h i c h b o d y surface p o t e n t i a l m a p s w e r e t a k e n l a s t e d 33 _+ 14, 40 _+ 13, a n d 39 -+ 14 s e c o n d s , r e s p e c t i v e l y . A l l p a t i e n t s h a d clinically u n c o m p l i c a t e d PTCAs; n o n e h a d a p r o c e d u r e - r e l a t e d m y o c a r d i a l i n f a r c t i o n o r r e q u i r e d card i a c surgery. F o r t w o p a t i e n t s (cases 7 a n d 18), dilat i o n g a v e n o significant i n c r e a s e in c o r o n a r y flow. Table 2 s h o w s t h e QRS d u r a t i o n s as m e a s u r e d b y

T a b l e 3. Greatest Variation in QRS and QTc Time Intervals (ms) Before QRS

During QTc

LAD (n = 10) 85.4 + 13 407 + 37 RCA (n = 6) 85.0 -4- 10 416 _+ 2 LCX (n = 4) 80.5 + 7 405 ± 26

QRS

73.6 -+ 9 401 _+ 26 77.3 _+ 9 401 _+ 9 81.0 -+ 6 427 + 69

Abbreviations the same as in Table 1.

t h e s e q u e n c e of b o d y surface p o t e n t i a l m a p s . QRS d u r a t i o n d e c r e a s e d in 14 cases (9 in t h e LAD, 4 in t h e RCA, a n d 1 in t h e LCX g r o u p s ) , a n d e i t h e r inc r e a s e d o r r e m a i n e d t h e s a m e i n 6 cases. W h e n QRS d u r a t i o n d e c r e a s e d , it w a s m o r e p r o n o u n c e d d u r i n g t h e s e c o n d o r t h i r d d i l a t i o n t h a n d u r i n g t h e first one. T h e m e a n QRS d u r a t i o n o f t h e f o u r LCX p a t i e n t s s h o w e d a n o n s i g n i f i c a n t increase. F o r t h e LAD cases, t h e d e c r e a s e i n QRS w i d t h d u r i n g t h e s e c o n d a n d t h i r d b a l l o o n d i l a t i o n s is statistically significant (P < .05). By c o n s i d e r i n g t h a t d u r i n g t h e t h r e e dilations, different QRS d u r a t i o n s w e r e m e a s u r e d , t h e greatest s h o r t e n i n g in e a c h Ease w a s a n a l y z e d (Table 3). I n t h a t w a y , t h e total QRS s h o r t e n e d f r o m 85 __+ 13 to 74 + 9 m s ( P < .01) for t h e LAD p a t i e n t s a n d f r o m 85 _+ 10 to 77 --_ 9 m s (P < .05) for t h e R C A patients, b u t d i d n o t c h a n g e significantly for t h e LCX g r o u p . Right ventricular epicardial breakthrough, thought to b e o n e of t h e m o s t c h a r a c t e r i s t i c e v e n t s a p p e a r i n g o n b o d y surface p o t e n t i a l m a p s , 24 o c c u r r e d 3 - 6 m s e a r l i e r d u r i n g d i l a t i o n in 13 cases, a n d in 6 cases (4 LAD, 1 RCA, a n d 1 LCX p a t i e n t ) , it o c c u r r e d at least 6 m s s o o n e r (22 _+ 6 vs 32 -+ 6 ms; P < .001) t h a n b e f o r e c o r o n a r y o c c l u s i o n (Table 4). T e r m i n a l slowi n g o f t h e QRS w a s o b s e r v e d in 17 p a t i e n t s (9 f r o m t h e LAD, 5 f r o m t h e RCA, a n d 3 f r o m t h e LCX g r o u p s ) a n d w a s m a n i f e s t e d as a n excess p o s i t i v e p o t e n t i a l l o c a t e d in a c e r t a i n a r e a o v e r t h e chest d u r i n g the terminal third of the depolarization complex. This l o c a t i o n c o r r e s p o n d e d to t h e s p a t i a l p r o j e c t i o n of t h e o c c l u d e d vessel; i n d i v i d u a l v a r i a t i o n s will be shown. A l l six cases of c o n d u c t i o n c h a n g e s b e l o n g e d to t h e LAD g r o u p . T w o o f t h e m w e r e a c c o m p a n i e d b y a c l e a r s h o r t e n i n g o f t h e right e p i c a r d i a l b r e a k t h r o u g h t i m e (cases 1 a n d 3). I n t h e s e t w o cases, a n initial

T a b l e 2. QRS Duration T i m e s Before, D u r i n g (3 Sessions), and After Balloon Inflation (ms)

LAD (n = 10) RCA (n = 6)

LCX (n = 4)

Before

First

During Second

Third

After

85 -+ 13 85 -+ 10 77 + 6

80 _+ 12 82 + 11 86 + 8

77 -+ 9 80 ± 10 83 ± 7

77 -+ 9 81 -+ 10 81 -+ 8

89 _+ 14 85 + 10 84 -4- 8

Abbreviations the same as in Table 1.

QTc

QRS Potential Changes During PTCA

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Pr@daet al.

315

T a b l e 4. R e l a t i o n of Q R S D u r a t i o n a n d Arrival o f R i g h t E p i c a r d i a l P o t e n t i a l B r e a k t h r o u g h to the Different F o r m s o f Intraventricular Focal B l o c k s a n d T e r m i n a l Q R S S l o w i n g O b s e r v e d D u r i n g P T C A

Patient No.

Vessel

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20

LAD LAD LAD LAD LAD LAD LAD LAD LAD LAD RCA RCA RCA RCA RCA RCA LCX LCX LCX LCX

Collateral Circulation

R-L+ R-L+ R-L +

L-R + L- R + L-R+ +

Arrival of Breakthrough Beforeduring Dilation (ms)

QRS Width (ms) 98-88 76-64 70-60 90-76 76-64 100-80 106-74 70-68 86-82 80-80 70-72 84-82 84-72 98-76 80-68 94- 94 72-72 90-82 76-82 84- 88

Focal Block

36-28 28-28 24-16 28-16 26-30 22-20 34-36 34-30 20-22 38-28 24-18 32-34 34-30 22-18 24-36 40 -40 34-26 26-24 26-24 42-42

Left septal Right anterior Left septal Right posterior Left posterior Left posterior

ST-T Time Beforeduring Dilation (ms)

Terminal Slowing + + + + + + + -+ + + + + + + + + +

392-356 322-314 406-250 372- 364 340-296 346-278 298-304 418-360 322-314 270-270 400-392 316-278 360-372 426-446 326- 326 404- 360 342-322 416-354 354-344 300- 316

Abbreviations the same as in Table 1.

a c t i v a t i o n loss s e e m e d to be c h a r a c t e r i s t i c , w h e r e a s

d e f i n e d d e c r e a s e i n Q R S d u r a t i o n ( 7 2 ± 10 v s 8 6 +

in the other four, a rather diffuse terminal slowing

13 m s ; P < . 0 2 ) , a n d all h a d a t e r m i n a l Q R S d e l a y .

of intraventricular conduction

Figure 2 shows

could be considered.

six selected chest leads before and

All o f t h e s i x c a s e s i n w h i c h i n t r a v e n t r i c u l a r c o n d u c -

d u r i n g P T C A f r o m a r e p r e s e n t a t i v e p a t i e n t ( c a s e 3).

tion abnormalities were found also showed

D u r i n g P T C A , t h e r e is a d e f i n i t e l o s s o f a s m a l l r w a v e

a well-

f

54

t, I v'-ll {

Before PTCA

.

.

.

.

.

.

.

During PTCA

Fig. 2. R e p r e s e n t a t i o n of t h e m o s t characteristic c h e s t leads before a n d d u r i n g p e r c u t a n e o u s t r a n s l u m i n a l c o r o n a r y a n g i o plasty of a p a t i e n t (case 3) w i t h left septal c o n d u c t i o n block. D u r i n g b a l l o o n inflation, t h e initial QRS v e c t o r of t h e r i g h t w a r d a n d a n t e r i o r direction is m i s s i n g .

316

Journal

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of Electrocardiology

Vol.

27 No. 4 October

1994

(CSt-CBi)

Before

PTCA

During

0.0 Msec

PTCA

BurinQ

0.0 Msec 0 . 0 2 0 Mv Max:

0.140

Min:-O.090

O.O05Mv

Max:

0.032

Min:-O.044

0.020

~20 0.050

Mv

MSeE Max:

0.327

Min:-0.146

1 2 . 0 Msec 0 . 0 5 0 Mv Max:

0.230

Nin:-0.110

24.0 0.200

Msec My Max:

0.957

Min:-0.833

24. O Nsec 0 . 1 0 0 Nv Max:

0.804

46.0 0.050

Mv Max:

0.176

Min:-0.467

36.0 0.200

Msec Mv Max:

56.0 Msec O.020Mv Max:

0.064

Min:-0.185

46.0 0.050

7 0 . 0 Msec 0 . 0 2 0 Mv Mex:

0.079

Min:-O.~44

60.0 0.010

Msec

Mv

-

Before

Max:

0.083

Min:-O.151

O.020Mv

Max:

0.139

Min:-0.118

Min:-0.716

0.050

Max:

0.222

Min:-0.204

1.038

Min:-O.955

0.200Mv

Max:

1.266

Min:-0.675

Msec Mv Max:

0.419

Min:-0.269

0.050

Max:

0.594

Min:-0.202

Nsec My Max:

0.050

Min:-O,034

O.020Mv

Max:

0.141

Min:-O.045

Mv

Mv

Fig. 3. Series of time-normalized body surface potential maps during the QRS complex and before (left column) and during (middle column) percutaneous transluminal coronary angioplasty of the same patient in Figure 2. Difference maps (duringminus-before dilation) are depicted on the right.

QRS Potential Changes During PTCA

in five of the six leads, which reflects a left septal conduction abnormality. The corresponding b o d y surface potential m a p s are s h o w n in Figure 3. F r o m left to right, the columns correspond to the m a p s recorded during the QRS complex before dilation, during dilation, and to the difference b e t w e e n them. Since the duration of the QRS complex was shortened during dilation, the m a p s are presented at different time intervals. Before PTCA, the initial maxim u m is over the right anterior thorax. During dilation, this m a x i m u m is attenuated (value of the initial m a x i m u m is 0.032 vs 0.14 mY). This is w h y the m a x i m u m of the first during-minus-before dila-

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tion difference m a p is over the lower posterior torso. The late activation phase of the during dilation m a p shows considerable terminal activation delay, which is m o r e evident o n the during-minus-before dilation difference map. The m a p s displayed in Figure 4 represent the isointegral values for three equidistant time intervals during the QRS complex for the same patient before and during coronary angioplasty. The difference m a p obtained by subtracting the before dilation potentials f r o m the during dilation potentials shows the characteristic initial activation loss caused by left septal focal block, 2~ and also a terminal depolarization delay that

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Fig. 4. Isointegral values for the first third (left side), last third (middle), and entire QRS complex (right side) before and during percutaneous transluminal coronary angioplasty (upper and middle rows) of the same patient in Figure 2. The lower row of isointegral maps stand for the potential differences between the during and before dilations, and they characterize both the initial anterior activation loss and terminal depolarization delay.

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Fig. 5. Averaged isointegral difference maps (during-minus-before dilation) for the first third of the QRS complex (left side), last third of the QRS complex (middle), and the whole QRS complex (right side).

occurs in spite of the considerably decreased QRS duration. Figure 5 displays average isointegral difference maps for the LAD, RCA, and LCX patients, that is, the time-integral maps for the first third of the QRS complex, the last third, and the whole QRS complex were averaged for the three groups of patients before dilation and then subtracted from the corresponding maps obtained during dilation. We will first consider the first third of the QRS complex. For the LAD patients, a m i n i m u m appeared on the averaged difference map close to the anterior wall of the left ventricle on the left side of the sternal line. This characteristic m i n i m u m also appeared on the difference maps of individual patients. There were only

two exceptions where the individual difference maps revealed either an early m i n i m u m on the right side of the back (case 6) or o n the upper side of the right anterior thoracic wall (case 3). In the cases of RCA dilations, the m e a n isointegral difference map revealed an initial m i n i m u m on the upper part of the back. Three of the individual difference maps coincided with this very location (cases 11, 15, and 16), whereas in the other three patients, the initial negativity was located either in the middle (case 13) or on the left part (cases 12 and 14) of the anterior thoracic wall. In the LCX cases, the m e a n difference map is not helpful since the four individual difference maps showed considerable variability, and only one case (case 17) coincided with the m e a n difference

QRS Potential Changes During PTCA

map, whereas in the other three cases (cases 1 8 - 2 0 ) , the initial m i n i m u m was located on the u p p e r back. For the last third of the QRS, positive changes generally appeared on the difference m a p s w h e r e negative changes had appeared during the first third of the QRS. For the LAD group, an excess of positive potentials was located on the left precordial region. On the individual difference maps, a similar maxim u m was located on the left lateral thoracic surface in eight cases, whereas in two other cases, a maxim u m was found either higher on the anterior chest surface (case 3) or lower on the anteroinferior thoracic wall (case 8). In RCA dilation, positive changes appeared on the average difference m a p on the lower right back, and negative changes occurred in the precordial region. On the individual difference maps, the maps of two patients coincided with the average m a p (cases 12 and 14); for the other patients, positive changes occurred on either the high anterior thoracic region (cases 15 and 16 with left-to-right collateral circulation), left inferior locations (case 11), or left lateral locations (case 13). On the average difference m a p for LCX occlusion, positive changes appeared all over the inferior torso with a m a x i m u m over the lower left midaxillary line, and negative changes occurred in the precordial region. On the individual difference maps, positive changes were similarly located on the left lateral torso (cases 17 and 19) or in the midanterior thoracic areas (case 18 with strong left-to-right collaterals and case 20). The thoracic patterns of the differences measured during the middle third of the QRS complex (not shown) were b e t w e e n those observed during the first and last thirds of the QRS complex, with varying degrees. The differences observed in the integral maps for the last third of the QRS complex were larger t h a n those observed during the first third. Thus, differences in the integral m a p s for the whole QRS complex showed patterns that were similar to the differences observed in the integral m a p s for the last third of the QRS complex.

Discussion Recently, several ECG studies h a v e used PTCA as a model for acute myocardial ischemia and coronary occlusion. 1-6,8-10,13,25--30 Repolarization, as well as depolarization, changes have b e e n described. ~,3-5,7,9, 25,26,29,31 The sequence of changes in intraventricular conduction observed by W a g n e r et al. 7 was related to periischemic i n j u r y 0 f different endocardial areas. Selvester et al. 4 suggested that these conduction changes were linked to ischemia of the m a j o r inser-

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tion sites of the proximal Purkinje fibers, but to our knowledge, no significant changes in total depolarization duration h a v e b e e n documented. Fourteen of our 20 patients revealed a significant decrease in QRS duration, w h i c h was completely reversible after coronary angioplasty. Two different explanations are possible for this observation: ( 1 ) coronary artery occlusion delayed the activation of the portion of the septal region that is normally activated early during the QRS, or (2) coronary artery occlusion increased the p r o p a g a t i o n speed in the ventricles. Concerning the first m e c h a n i s m , the septal region w h o s e activation is responsible for the beginning of the QRS complex w o u l d be activated later during ischemia, thus "chipping off" the onset of the QRS complex. Ischemia w o u l d affect only the insertion sites of the Purkinje fibers within the left middle section of the septum, 32 and not the insertion sites within the right ventricle. This can explain w h y the right ventricular b r e a k t h r o u g h time, which was detected on the isopotential maps, occurred earlier during coronary artery occlusion, rather t h a n before occlusion. A similar p h e n o m e n o n can be observed in patients with left bundle branch block where the right ventricular b r e a k t h r o u g h time also arrives earlier. ~ Also, this focal conduction disturbance can alter the cancelation effects and explain the changes in QRS amplitude that were observed in these patients. ~1 In further support for this hypothesis, we noted that such focal conduction disturbances of the initial portion of the QRS complex were observed only during occlusion of the LAD coronary artery, which irrigates most of septum, and never during occlusion of the right and circumflex coronary arteries. Concerning the second m e c h a n i s m , changes in propagation speed produced by ischemia have been investigated in n u m e r o u s animal experiments with intracardiac recordings. In canine preparations, conduction time m e a s u r e m e n t s s h o w e d that the peak increase in QRS amplitude correlated highly with a fall in conduction velocity. 34-37 However, Holland and Brooks 35 were the first to show, in porcine hearts, that acute myocardial ischemia causes more complex, biphasic changes with an early conduction acceleration and a decrease in QRS magnitude, followed by a slowing of conduction and an increase in QRS magnitude. Similar results have b e e n found by David et al. 37 in dogs: during the first 30 seconds of acute myocardial ischemia, the QRS m a g n i t u d e decreased and intraventricular conduction velocity increased. This was followed by a second phase with gradual slowing of conduction velocity and deterioration of left ventricular function. In the isolated por-

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cine heart, Kleber et al. 34 s h o w e d both longitudinal and transverse increases of myocardial conduction velocity in the first minute of acute myocardial ischemia. Interestingly, these accelerations in conduction velocity were only achieved during the second interruption of coronary flow, just as we discovered that the second balloon inflation generally revealed the greatest decrease in intraventricular conduction time. Regarding the initial increase in conduction velocity, it has b e e n suggested 35,38'39 that a m o d e r a t e increase of extracellular potassium can partially depolarize the myocardial cell, thus reducing the voltage necessary to reach the rapid sodium current threshold and increasing propagation speed. However, the possible initial increase in myocardial propagation speed during the initial phase of h u m a n coronary dilation remains to be p r o v e n by direct electrophysiologic measurements. The subsequent decrease in intramyocardial conduction velocity can be explained by the reduced slope of the action potential upstroke. A decrease in intramyocardial conduction velocity can also be experimentally produced by an increased extracellular potassium concentration.35"39 Our patients exhibited either terminal slowing of intraventricular conduction ( 17 of 20 patients) or intraventricular periischemic block (8 of the latter 17 patients). This t e m p o r a r y conduction block could be related to h y p o x e m i c injury of one of the m a i n portions of the proximal Purkinje network. It is important to emphasize that the different PTCA sessions were of limited duration, and that is probably w h y an overall delay of intraventricular conduction, w h i c h is characteristic for coronary occlusion of longer duration, 36"37 could not be observed. The relationship b e t w e e n short-term angioplasty sessions and t e m p o r a r y QRS duration shortening is m o r e meaningful if one chooses the greatest shortening observed for each case. The introduction of the guide wire and uninflated balloons of different size for the first occlusion gives the greatest individual variations. 1.] 3,34 Recently, b o t h focal conduction disturbances related to the initial portion of the QRS complex 4"7 and regional conduction delay related to the second half of ventricular depolarization I have been described during coronary angioplasty, but variations found in the total QRS duration were negligible. Spekhorst et al., ~ using comparable body surface potential m a p ping methods, have also s h o w n the typical terminal conduction delay that we observed in 17 of our 20 patients, and they describe 20% of their patients studied before and during dilation with variations in QRS width of up to 8 ms, but w i t h o u t specifying the direction of change. The duration of inflation that

they used ( 4 0 - 6 0 seconds) was slightly longer than our average inflation time (37.3 _+ 12 seconds). In s u m m a r y , QRS duration shortening and focal blocks are observed during LAD dilation, which suggest that ischemic injury m o s t probably affects the proximal insertion sites of the left middle septal portion of the proximal part of the specialized conducting tissue. Consequently, there is chipping off of initial left septal activation, manifesting as various forms of left septal fascicular blocks (grossly measured as an early acceleration of the QRS complex) (Fig. 6a), but this QRS shortening is counterbal-

, control ! J

i i

It

~:- .......... :-............. "'~{

ischemia Fig. 6. Schematic representation of the possible mechanism of QRS complex shortening during left anterior descending coronary artery occlusion, a, initial activation delay of the septal region; b, terminal depolarization slowing.

QRS Potential Changes During PTCA a n c e d , at least partly, by a t e r m i n a l a c t i v a t i o n s l o w ing also c a u s e d by i s c h e m i c i n j u r y (Fig. 6b). H o w ever, t h e h y p o t h e t i c p r e s e n c e o f early a c c e l e r a t i o n of v e n t r i c u l a r a c t i v a t i o n d u r i n g s h o r t - t e r m i s c h e m i a , as described in t h e literature, in e x p e r i m e n t a l p r e p a r a tions c a n n o t b e e x c l u d e d .

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