Effects on the signal-averaged electrocardiogram of opening the coronary artery by thrombolytic therapy or percutaneous transluminal coronary angioplasty during acute myocardial infarction

Effects on the Signal-Averaged Electrocardiogram of Opening the Coronary

Artery by Thrombolytic Therapy or Percutaneous Transluminal Coronary

Angioplasty During Acute Myocardial Infarction Christian de Chillou, MD, Luz-Maria Rodriguez, MD, Pieter Doevendans, MD,

Kostas Loutsidis, MD, Adri van den Dool, BS, Jacques Metzger, MD, Frits W. H. M. B&-, MD, Joep L. R. M. Smeets, MD, and Hein J. J. Wellens, MD

One hundred twenty-nine patients were retrospec- tively analyzed and divided into 3 groups accord ing to (1) the presence of a patent artery obtained either spontaneously or after thrombolytic thera py but without percutaneous transluminal core nary angioplasty (PEA) (group I, n = 63), (2) the presence of a patent artery after opening by PTCA (group II, n q 29), or (3) absence of reperfusion despite thrombolytic therapy or P7CA (group Ill, n = 17). Thrombolytic therapy was given within 4 hours after onset of symptoms (mean 2.5 f 1.0 hours) and P7CA was performed within 24 hours after the onset of symptoms (mean 6 + 6 hours). Signal averaging was performed within 24 hours after cardiac catheterization. An abnormal signaC averaged electrocardiogram was present in 10 of 63 (12%) group I, 9 of 29 (31%) group II and 7 of 17 (41%) @oup Ill patients (p CO.05 group I vs II, p co.01 group I vs Ill, no statistical difference group II vs Ill). Therefore, in contrast to reperfusion by thrombolytic therapy the incidence of abnonnali- ties on the signal-averaged electrocardiogram early after myocardial infarction is not reduced by an early opening of the culprit vessel by P7CA

(Am J Cardiol1993;7lSO!S609)

From the Department of Cardiology, University of Limburg Academic Hospital, Maastricht, the Netherlands. Dr. de Chillou is supported by a grant from the Federation Franqaise de Cardiologie, Paris, France. Manuscript received July 6, 1992; revised manuscript received and accepted October 14, 1992.

Address for reprints: Christian de Chillou, MD, Department of Car- diology, University of Limburg Academic Hospital, 6202 AZ Maas- tricht, the Netherlands.

P revious studies’” have shown that the presence of an abnormal signal-averaged electrocardiogram after a myocardial infarction is highly correlated with an

occluded infarct-related coronary artery. When given in the acute phase of myocardial infarction, thrombolytic therapy increases the patency rate of the infarct-related arteryloJ 1 but does not reduce the incidence of an abnormal signal-averaged electrocardiogram to the same de- gree.1-4,8 Percutaneous transluminal coronary angioplasty (PTCA) is another technique that is able to open the infarct-related coronary artery during acute myocardial infarction.12J3 This study evaluates the role of a successful reperfusion obtained by PTCA on the incidence of abnormalities on the signal-averaged electrocardiogram as registered during the first acute myocardial infarction.

METHODS Patients: One hundred twenty-nine of 450 patients

with acute myocardial infarction admitted to our coronary care unit between April 1990 and November 1991 fulfilled the following criteria: (1) development of a first acute myocardial infarction conlirmed by both serial electrocardiograms and serum enzyme changes; (2) age ~75 years; (3) absence of bundle branch block, intra- ventricular conduction delay (QRS 220 ms), atrial fibrillation or ventricular pacing; (4) cardiac catheterization within 24 hours after admission; (5) registration of a signal-averaged electrocardiogram within 2 to 24 hours after the coronary angiography; and (6) absence of reinfarction or recurrence of chest pain in the time interval between coronary angiography and the signal-averaged electrocardiogram.

Ninety-three patients (72%) admitted within 4 hours after the onset of symptoms were treated intravenously by thrombolytic therapy either by prourokinase (n = 75) anistreplase (n = 14), streptokinase (n = 3) or recombi- nant tissue-type plasminogen activator (n = 1). The remaining 36 patients did not receive thrombolytic therapy because of a long delay (24 hours) between onset of symptoms and admission (n = 23), primary ventricular fibrillation requiring resuscitation (n = 4), history of gastric ulcer (n = 3) or cerebral stroke (n = 2), cardio- genie shock on admission (n = 2) recent surgery (n = l), or head trauma (n = 1).

SIGNAL-AVERAGED ELECTROCARDIOGRAM AND MYOCARDIAL INFARCTION 805

Cardiac catheterization was performed mainly under 2 circumstances, either when the patient was included in a specific thrombolytic agent protocol or when no sign of reperfkion (spontaneous or after thrombolytic therapy) was observed within the first hour after throm- bolytk therapy, or when patients not treated with thrombolytic therapy continued to complain.

Cardiac catheterization: After informed consent, coronary angiography was performed. The following parameters were recorded: (1) the number of diseased arteries (number of coronary arteries with a stenosis diameter ~50%); (2) the infarct-related coronary artery determined from the entry electrocardiogram, ventricu- lographic contraction abnormality and coronary angiographic findings; (3) perfusion status using the grading of the Thrombolysis in Myocardial Infarction trial;14 and (4) presence or absence of collateral vessels as detined in the Rentrop et al classification15 (grade 0 and 1 indi- cating absence of and grade 2 and 3 presence of collateral vessels toward the occluded infarct coronary artery). In case of an occluded infarct-related artery, the physi- cian performing the catheterization decided whether a PTCA should be performed. Factors involved in this decision included accessibility of the lesion, size of the lesion, and delay from chest pain to PTCA. When a PTCA was performed, perfusion status of the artery was reevaluated at the end of the procedure by using the thrombolysis in myocardial infarction trial classification.

Left ventricular ejection fraction: Left ventricular ejection fraction was measured in all patients either by angiography during cardiac catheterization (90%) or by echocardiography (10%) performed within 48 hours after admission. As previously reported from our insti- tution, there is a good correlation between the echocar-

PATENTS

ADMISSION 129

THR-YSIS “’

/’

ARTERY PATENT Y N

BEFORE PTCA

PTCA

I 67

I 26

A i i

20 6

A ARTERY PATENT

AFTER PTCA i i

I ‘i i I SAE+ a 5 2 2

(12%) (30%) (66%) (33%) (12%) (33%) (37%)

RGURE 1. Flow chart of the treatment received, evolution a the coronary patency and presence of an abnormal signal- averaged electrocardiogram. N q no; PTCA q percutaneous transluminal coronary engioplasty; SAE+ q abnormal sighal- avereged electrocardiogram; Y 7 yes.

diographic and angiographic determination of left ventricular ejection fraction.16

Signalaveraged recording Time-domain signal- averaged recordings were performed with the MAC- 12/15 electrocardiogram Marquette system recorder using previously reported techniques. l7 Briefly, signal- averaging was performed with the subjects supine. After the skin was prepared with a mildly abrasive pad and washed with ether, 7 self-adhesive silver-silver chloride electrodes were attached: the horizontal (X) electrodes in the right and left midaxillary lines at the fourth inter- costal spaces, the vertical (Y) electrodes on the suprastemal notch and Vs position, and the sag&al (Z) electrodes in the Vz position anteriorly and at the cor- responding position posteriorly. The seventh indifferent electrode was placed on the eighth rib in the right midaxillary line. Positive electrodes were left, superior and anterior. Two hundred QRS complexes were amplified, averaged, filtered with a high-pass filter of 40 Hz and combined into a vector magnitude dXA + YL + ZL according to the method described by Simson. The noise level was ~0.7 p\! A computer program algorithm determined the onset and offset of the QRS complex and calculated 3 parameters: the total QRS duration, the root-mean-square voltage of the last 40 ms and the duration of the low-amplitude signals ~40 p,V The signal- averaged electrocardiogram was graded as abnormal if 2 of the following criteria were present: QRS duration >114 ms, root-mean-square voltage of the last 40 ms ~25 p,V, and the duration of the low-amplitude signals >39 ms.

Statistical analysis: Continuous variables are expressed as mean k SD and were compared by use of the unpaired Student’s t test. Noncontinuous variables were compared by use of the &i-square test. A p value <0.05 was considered statistically significant.

RESULTS Results of thrombolytic therzqy and percutaneous

tranduminal -@oplastymcoronaryaHery patency (Figure 1): Ninety-three patients received thrombolytic therapy within 4 hours after onset of chest pain (mean 2.5 + 1.0 hours). Sixty-seven of the 93 patients (72%) treated with thrombolytic therapy were found to have a patent infarct-related artery versus 16 of 36 (44%) in the group of patients not receiving thrombolytic treatment (p <O.OOl).

In 32 of 46 patients (70%) with an occluded artery (20 patients from the thrombolytic and 12 patients from the other group), PTCA was performed during the acute phase of the myocardial infarction in an attempt to reopen the artery. The delay between onset of symptoms and PTCA was 6.2 + 6.6 hours (range 1 to 24). In 23 of 32 patients (72%), the procedure was performed within 6 hours after the onset of chest pain. The PTCA reopened the artery in 29 of 32 patients (91%).

In 17 patients the infarct-related artery was occluded at the end of cardiac catheterization (including 14 patients in whom no PTCA was attempted).

Comparison of patients with or without an abnor mal signal-averaged el- (Wale I): The overall incidence of an abnormal signal-averaged elec-

806 THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 71 APRIL 1, 1993

TABLE I Clinical and Angiographic Characteristics of Patients Studied in Relation to the

Presence of an Abnormal Signal-Averaged Electrocardiogram

QRS duration Low-amplitude signal duration Root-mean-square duration Men (%) Age (year + SD) Anterior MI (%I LVEF (mean + SD) Thrombolytic therapy (%)

Delay onset of symptoms to TT (hours t SD)

PTCA (%I Delay onset of symptoms to

PTCA (hours + SD) Peak OT (IUiliter) Peak CK (IU/lrter) No. of diseased coronary arteries

narrowed > 50% in diameter 1 2 3

Infarct-related patency artery

Before PTCA (%) *Presence of collaterals (%)

SAE+ (26)

118 i 11 (108-144) 47 i- 9 (37-69) 16 k 5 (6-25)

22 (85%) 60 zt 9

9 (35%) 47 + 10

17 (65%) 2.7 t 1.0

SAE- (103)

103 + 7 (86-121) 28 zk 7 (11-48) 47 + 20 (19-99)

58 (66%) 592 11

41 (40%) 50 + 10

76 (74%) 2.3 2 1.0

16 (62%) 16 (16%) 5.7 2 6.2 6.5 i- 6.8

308 t 179 304 + 217 2,581 k 1,918 2,896 2 2,359

13 (50%) 56 (54%) 7 (27%) 28 (27%) 6 (23%) 19 (19%)

10 (38%) 73 (71%)

8116 (50%) 14130 (47%)

p Value

<0.0001 < 0.0001 <0.0001

NS NS NS NS NS

NS

<0.0001 NS

NS NS

NS NS NS

0.004

NS

*In patients with an occluded infarct-related coronary artery at the beglnning of catheterization. CK = creatine kinase; LVEF = left ventricular ejection fraction; MI = myocardial infarction; OT = ox&t transaminase:

PTCA = percutaneous transluminal coronary angioplasty; SAEt = abnormal signal-averaged electrocardiogram; SAE- = normal signal-averaged electrocardiogram; T T = thrombolytic therapy.

TABLE II Incidence of an Abnormal Signal-Averaged Electrocardiogram in Relation to the

Evolution of the Infarct-Related Artery Reperfusion Status

Delay to CC Incidence (%I (hours) of Abnormal SAE QRSd LAS RMS

Group I(83 pts.) Artery patent without PTCA 5.2 k 4.6 10183 (12%) 104 + 8 31 k 9 42 f 19

I (86-139) (1 l-56) (7-99) NS p <0.05

Group II (29 pts.) I Artery patent with PTCA 6.4 2 6.9 9/29 (31%) 107 t 9 33 + 10 40 + 24

I ~ 1 (88-129) (17-60) (6-99) NS NS p <O.Ol

Group Ill (17 pts.) I Artery occluded at end of CC 7.3 5 5.6 7117 (41%) J 111214 35+17 39228

(91-144) (11-69) (6-99)

CC = cardiac catheteruation; LAS = low-amplitude signals; QRSd = PRS duration: RMS = root-mean-square; PTCA = percutaneous translumlnal coronary angiaplasty: SAE = signal-averaged electrocardiogram.

trocardiogram was 20% (26 of 129). Patients with late farct-related artery at the beginning of coronary angiog- potentials were not significantly different from patients raphy, 30 patients (23%) (group II) had an infarct artery without late potentials with regard to gender, age, throm- that was reopened by PTCA, and the remaining 16 bolytic treatment, delay from onset of symptoms to patients (13%) (group III) did not have reperfusion at thrombolytic therapy or to PTCA, infarct location, the end of catheterization. In group I patients the inci- enzyme level, number of diseased coronary arteries, left dence of an abnormal signal-averaged electrocardiogram ventricular ejection fraction, or presence of collaterals in (10 of 83, 12%) was significantly lower than in group II patients with an occluded infarct-related artery. (9 of 29, 31%) and group IU (7 of 17, 41%) patients (p

In patients showing an abnormal signal-averaged co.05 and p ~0.01, respectively). No statistical difference electrocardiogram the incidence of spontaneous or was found between groups II and III. Left ventricular thrombolysis-induced artery patency was lower than in ejection fraction was not different between the 3 groups patients without an abnormal signal-averaged electro- (group I, 50 f 10; group II, 49 + 9; group III, 48 f 10) cardiogram (10 of 26 (38%) vs 73 of 103 (71%), (Table II). p = 0.004). If we classify the patients with successful PTCA into

I- of an abnormal signal-averaged de&o- 2 groups according to the delay between the onset of cardiiin&ationtovesselpatencyandpercuta symptoms and the moment of unblocking the artery no neous trzmsluminal COCOllSYY amH=tY mu= statistical difference in incidence of an abnormal signal- Eighty-three patients (64%) (group I) had a patent in- averaged electrocardiogram was present (6 of 21 [29%]


having FICA within 6 hours vs 3 of 8 [37%] after 6 hours, p = 0.9).

DISCUSSION Our tindings indicate that despite a high rate of

patency induced by PTCA, the procedure does not reduce the appearance of an abnormal signal-averaged electrocardiogram when compared with patients showing a persistently occluded infarct-related artery.

Previous studies1-9 have shown a clear relation between the presence of an abnormal signal-averaged electrocardiogram after myocardial infarction and the occlusion of the infarct-related artery; the incidence of late potentials ranged from 6 to 34% in a patient with a patent artery, and from 25 to 65% in a patient with an occluded artery (p <O.OOOOOl when using a meta-analysis of these studies1-9).

The time interval between onset of symptoms to the moment of reopening of the artery by PTCA can be measured. However in patients with a patent artery at the start of catheterization, it is impossible to know pre- cisely the time of reopening of the artery. Although cardiac catheterization delay is comparable in our 3 groups of patients (Table lI), the reperfusion delay has obvi- ously been shorter for group I patients. Therefore, because PICA did not reduce the incidence of an abnormal signal-averaged electrocardiogram, we may specu- late either that the reperfusion delay was already too long to prevent the appearance of an abnormal signal- averaged electrocardiogram in these patients or that thrombotic material dislodged by angioplasty blocked peripheral arteries, thereby preventing reperfusion.

The optimal time for recording the signal-averaged electrocardiogram to detect abnormalities after a myocardial infarction has yet to be defined.r9 Previous re- ports17,2S24 have shown variations in the incidence of an abnormal signal-averaged electrocardiogram depend- ing on the registration time. Rodriguez et ali7 showed that the incidence of an abnormal signal-averaged electrocardiogram decreases from 19% within the first 3 days after myocardial infarction to 15% at 15 days and 12% after 3 months. Verzoni et a120 performed serial recordings after myocardial infarction and noticed variations from 15 to 28% in the presence of abnormalities between the different recordings, with a decrease of 20% in the incidence of abnormalities (normalization of the registration) between day 15 and 6 months after myocardial infarction.

Data on the signiiicance of the timing of the registration of an abnormal signal-averaging electrocardiogram as a predictor of risk for life-threatening ventricular arrhythmias are not only still controversial24 but also do not include patients in whom the occluded infarct artery has been reopened by FTCA.

Previous studies have shown that reocclusion of the infarct artery occurs within the tirst week after myocardial infarction in 19% of patients receiving thrombolytic therapy25 and in 12% of patients in whom PTCA was performed acutely.26 A major problem in the recognition of reocclusion is the high rate (58%) of silent reocclusion.26 In our study, we decided to perform the signal- averaged recordings within 24 hours after coronary

angiography to minimize a potential bias in the analysis due to changes in the perfusion status of the infarct- related artery.

Recent reports have indicated that PICA after thrombolytic therapy in the acute phase of a myocardial infarction does not reduce the rate of reinfarction nor the mortality during a follow-up period of 6 weeks after admission.27,28 In the subgroup of patients with an occluded artery after thrombolytic therapy, PTCA was associated with an 85 to 90% rate of reperfusion,27,28 but the overall mortality was not reduced, even when the procedure was performed early (~2 hours after thrombolytic therapy).28 Despite the high rate of reperfusion, Baim et al29 recently showed that the l-year mortality of such patients was 4 times higher (9.5 vs 2.9%, p <O.OOl) than it was in patients whose infarct-related artery was patent and treated with FTCA in the acute phase of myocardial infarction. The cause of mortality was not given, but the incidence of a new coronary event (myocardial infarction, coronary artery bypass grafting) as well as the left ventricular ejection fraction were comparable between the 2 groups.

Study limitations: To interpret the results correctly some limitations of our study have to be stressed. Our study was a retrospective one; patients with an occluded infarct coronary artery were not randomized to FTCA or conservative treatment. However, patients treated with PICA were comparable to those treated conventionally with regard to age, gender, delay from onset of symptoms to catheterization, infarct location, number of coronary diseased arteries, presence of collateral vessels and use of thrombolytic therapy. Also the time interval between onset of symptoms and performance of FTCA was not standardized and longer (mean 6 hours) than the time of thrombolytic therapy (mean 2.5 hours). The difference in timing of intervention may play a role in our results. However, in patients whose FTCA was performed within 6 hours after the onset of chest pain (which is a delay often considered acceptable for thrombolytic therapy), the incidence of an abnormal signal- averaged electrocardiogram was still 28%.

Another limitation of this study was that signal-averaged electrocardiograms were not recorded before reperfusion.

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Effects on the signal-averaged electrocardiogram of opening the coronary artery by thrombolytic therapy or percutaneous transluminal coronary angioplasty during acute myocardial infarction