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Effect of coronary angioplasty on late potentials one to two weeks after acute myocardial infarction
The
CORONARY ARTERY DISEASE
American Journal of Cardiology
DECEMBER 15,
1992,VOL. 70, NO. 20
Effect of Coronary Angioplasty on Late Potentials One to Two Weeks After Acute Myocardial Infarction James D. Boehrer, MD, D. Brent Glamann, MD, Richard A. Lange, MD, John E. Willard, MD, Walter C. Brogan, Ill, MD, PhD, Eric J. Eichhorn, MD, Paul A. Grayburn, MD, Azam Anwar, MD, and L. David Hillis, MD
In survivors of acute myocardial infarction (AMI), the restoration of anterograde flow in the infarct artery, even if accomplished beyond the time for myocardial salvage, may reduce the frequency of subsequent arrhythmic events and sudden death. Twelve subjects (8 men and 4 women, aged 39 to 69 years) with a first AMI, signal-averaged electrocardiographic late potentials, and an occluded infarct artery were prospectively identified. Seven (group I) had successful coronary angioplasty 6 to 15 days after AMI, and 5 (group II) were managed conservatively. Follow-up signal-averaged electrocardiography was performed 3 to 7 months later. From baseline to follow-up, the 7 group I subjects had a significant change in QRS duration (117 f 13 [mean + SD] to 102 f 10 ms), root-meansquare voltage (10.4 f 4.7 to 31.0 f 7.6 pV), and low-amplitude signal duration (47.5 f 8.5 to 32.4 f 5.2 ms) (p 50.05 for all 3 variables). No group I patient had a late potential at follow-up. In contrast, the 5 group II patients showed no change in QRS duration or low-amplitude signal duration from baseline to follow-up, and all 5 had a late potential at follow-up. At follow-up, the root-meansquare voltage was significantly greater and the low-amplitude signal and QRS durations significantly less in group I than in group II (p
I
n survivors of a first acute myocardial infarction (AMI), long-term survival is better in those with anterograde flow in the infarct artery than in those whose artery is occluded.1-3Patients with an occluded infarct artery are more likely than those with a patent artery to have late potentials by signal-averagedelectrocardiography.4,5In survivors of AMI, these late potentials identify those at risk of subsequent arrhythmic eventsand suddendeath.6,7Other reports8,9have shown that survivors of AM1 whose infarct artery has anterograde flow are unlikely to have inducible ventricular tachyarrhythmias, whereas the absenceof anterograde flow is frequently accompaniedby provocableventricular tachycardia and fibrillation. It is possible,therefore, that the restoration of anterograde flow in the infarct artery, even if accomplished days or weeks after the acute event, may improve survival by dishing electrical instability. This study was performed to test the hypothesis that the mechanical restoration of anterograde flow in an occluded infarct artery 1 to 2 weeks after AM1 causesa resolution of signal-averagedelectrocardiographic late potentials. METHODS Patient population: From November 1990 to Febru-
ary 1992 we identified 127 patients admitted to Parkland Memorial Hospital (n = 58), the Veterans Administration Medical Center (n = 37), or Baylor University Medical Center (n = 32), Dallas, Texas, with evidence of a first AMI. Subjectswith bundle branch block, previous AMI, ventricular preexcitation, intraventricular conduction delay, ventricular-paced rhythm, and those receiving amiodarone or type IC antiarrhythmic agents were excluded. Patients were enrolled if they had (1) a late potential on signal-averaged electrocardiography (performed 3 to 15 days after AMI) and (2) an occludFrom the Department of Internal Medicine (Cardiovascular Division), ed infarct artery on coronary angiography (performed 1 the University of Texas SouthwesternMedical Center, and the Cardiac Catheterization Laboratories of Parkland Memorial Hospital, Veterans to 13 days after AMI). Coronary angiography was perAdministration Medical Center, and Baylor University Medical Cen- formed before signal-averagedelectrocardiography in 5 ter, Dallas, Texas. Manuscript received June 18, 1992; revised manu- patients and afterward in the other 7 (Table I). No rigscript receivedand acceptedJuly 22,1992. Addressfor reprints: L. David Hillii, MD, Room CS 7.102,Univer- id chronologic relation between angiographic and signal-averaged electrocardiographic studies was required sity of Texas SouthwesternMedical Center, 5323 Harry Hines Boule vard, Dallas, Texas 75235. provided that signal-averagedelectrocardiography was ANGIOPIASTY FOR LATE POTENTIALS
1515
51 2 7
Mean + SD
-
Right Right LAD LC LC
-
Right Right Right Right LAD LAD LC
Infarct Artery
0.46 0.51 0.48 0.61 0.43 0.53 NA
0.52 f 0.11
0.39 0.42 0.53 0.62 0.63 7?4
10 8 5 2 12
724
2 11 7 6 1 7 13
LVEF
0.50 t 0.06
Time from AMI to cc (days)
Electrocardiographic
-
-
11 -t3
6 12 9 15 8 14 13
Time from AMI to PTCA (days) Baseline
Root-Mean-Square Follow-Up
114 f 22
127 102 88 149 94 128 111 10.4 T!z4.7
8.4 3.0 12.1 7.7 16.8 15.1 10.0
Voltage
51.5 65.0 45.5 43.5 45.0 40.0 42.0 47.5 ? 8.5
31.0 2 7.6t$
7k3
8 8 5 4 12
LC = left circumflex;
127 + 49
214 107 112 103 99
LVEF = left ventricular
8.5 A 6.1
8.5 2.8 15.5 2.1 13.7
Baseline
Low-Amplitude
22.1 24.9 26.1 37.1 27.5 38.1 41.1
NA = not available;
coronaly
angiaplasty;
128 -+ 16
47.9 f 4.5
translumlnal
108 129 128 153 123
117 k 13
32.4 t 5.2tt
44.4 47.5 43.0 54.0 50.5
121 137 116 127 105 101 109
Baseline
SAECG = signal-
121 + 5
127 117 117 117 126
102 +- lOT$
110 90 100 113 112 93 94
Follow-Up
Filtered QRS Duration (ms)
28.5 39.0 37.0 25.5 34.5 34.5 27.5
Follow-Up
Signal Duration
PTCA = percutaneous
59.0 zk 18.2
15.4 + 5.07
ejection fraction;
47.5 60.5 48.5 90.0 48.5
10.0 11.4 22.7 16.1 16.7
Group II: Patients Who Did Not Undergo Angioplasty
925
3 10 7 15 3 13 12
Time from AMI to Final SAECG (days)
Group I: Patients Who Underwent Angioplasty
Time from AMI to Baseline SAECG (days)
Data for the 12 Patients
*Denotes those with postinfarction angina. tp so.05 compared with baseline: $p x0.05 compared with group II. AMI = acute myocardial infarction; CC = cardiac catheterization; LAD = left anterior descending; averaged electrocardiogram.
58M 56F 49M 51F 40M
53211
41M 51M 65M 39M 50M 69F 54F
8 9 10 11 12
Mean 2 SD
1 2* 3 4* 5 6* 7
Pt.
Age (yr) & sex
TABLE I Clinical and Signal-Averaged
performed within 3 to 15 days of AMI. Patients with continuing angina were offered angioplasty of the occluded artery for symptom relief. The remaining subjects were assigned randomly to angioplasty (group I) versus no angioplasty (group II). For each group I subject, the benefits and risks of angioplasty were explained and each gave written informed consent. Each patient was seen regularly over the ensuing months. A signalaveragedelectrocardiogram was repeated 3 to 7 months after AMI and compared with baseline. Signal-averaged electrocardiography: Signal-averaged electrocardiography was performed with the Predictor Signal Averaging Electrocardiogram System (Corazonix Corp, Oklahoma City, Oklahoma), according to methods described previously.4 A late potential was prospectively defined as 12 of the following: (1) a root-mean-squarevoltage <20 PV in the terminal 40 ms of the QRS, (2) a low-amplitude signal duration >38 ms, and (3) a QRS duration > 114 rns.‘OThe signalaveragedelectrocardiogramswere not overread, and the computer-derived tracings were not adjusted manually. No patient received medications known to alter the signal-averaged electrocardiogram. Coronary angiography: Anterograde flow in the infarct artery was graded in accordancewith the criteria of the Thrombolysis in Myocardial Infarction investigators.” To be eligible for enrollment, all patients had Thrombolysis in Myocardial Infarction trial grade 0 perfusion on the baseline angiogram. Collateral flow to the distal infarct artery wasjudged as presentor absent. Left ventricular ejection fraction was determined by standard techniques from single plane ventriculography. Statistical analysis: All data are reported as mean f 1 standard deviation (SD). For each group, the rootmean-square voltage, low-amplitude signal duration, and QRS duration before and 3 to 7 months after angiography/angioplasty were compared with a paired t test. At baseline and follow-up, those undergoing angioplasty (group I) and those treated without angioplasty (group II) were compared with Student’s t test. For all analyses,a p value 50.05 was considered significant. RESULTS
and QRS duration decreased(Figure 3) (p 10.05 for all 3 variables) (Table I). In contrast, in the 5 group II patients, follow-up signal-averagedelectrocardiography showedno significant change in low-amplitude signal duration (Figure 2) or QRS duration (Figure 3) when comparedwith baseline. Although the root-mean-squarevoltage increased from baseline to follow-up, the average value at follow-up was below the lower limit of normal (Figure 1). Of the 5 group II patients, all retained a late potential at follow-up. At follow-up, the root-mean-squarevoltage was greater and the low-amplitude signal and QRS durations lessin group I than in group II (Table I; Figures 1, 2 and 3). Coronary angiography: At baseline, collateral flow to the distal infarct artery was present in 6 of 7 group I patients and in all 5 group II subjects (p = not significant [NS]). Coronary artery disease(170% luminal diameter narrowing) in vesselsother than the infarct artery was present in 3 group I patients and in 2 group II subjects(p = NS). Two patients in each group received intravenous thrombolytic therapy (p = NS). DISCUSSION
The mechanical restoration of anterograde flow in an occluded infarct artery 6 to 15 days after AM1 causes a resolution of signal-averaged electrocardiographic late potentials, whereaslate potentials persist in 40 -
30-
20 -
lo-
Twelve patients (8 men and 4 women, aged 39 to 69 years) fulfilled the entrance criteria (Table I). Three were offered angioplasty because of postinfarction angina. Of the other 9, 4 were 0 follow-up baseline baseline follow-up assignedrandomly to angioplasty versus 5 to no angioplasty. The 7 subjectshad successfulangioplasty (residPTCA Control (Group I) (Group II) ual stenosis<50% luminal diameter narrowing) 11 f 3 (range 6 to 15) days after AMI and formed group I; the 5 who were managed without angioplasty formed group FIGURE 1. Root-mean-square voltage, in microvolts, at baseII. The 2 groups were similar in age, sex, infarct artery, RneandfoRowy,forthe7PatkntswhohadangioPlasty and left ventricular ejection fraction (Table I). mpmentsdatafromlpatlent,andmeani Signal-averaged ekctrecardiography: Signal-aver- lSDis~wnaneithersideafeaehsetoflineb.Doffedlines aged electrocardiography was performed 8 f 4 (range 3 denote lower limit of normal (20 pV). In group I, the rootto 15) days after AMI. In the patients who underwent mean-square voWage inueased sigllificantly; ai followup, it angioplasty (group I), follow-up signal-averaged elec- wasinthenonnalrangeinaU7Pat&ts.IngroupII,itinslgniticantly from baseiii to foRow-ql bul renlalnt?d trocardiography showed resolution of late potentials in creased -20 pV in 4 of 5 Patients. *p 10.05 compared with baseline all 7: root-mean-square voltage increased (Figure I), and ths other group al foRow-up. PTCA = percutaneous translow-amplitude signal duration decreased (Figure 2), luminal -w ae3W-W Patient characteristics:
ANGl0PLASl-Y FOR LATE POTENTIALS
1517
survivors of AM1 in whom anterograde flow is not restored. Signal-averaged electrocardiographic late potentials arise from areas where normal myocytes interdigitate with fibrotic or ischemic cells, or both.12J3When such areasare surgically excised,the signal-averagedelectrocardiogram reverts to normaLl In survivors of AMI, late potentials are predictive of inducible and spontaneous ventricular tachycardia, an arrhythmic event within the first year, and sudden cardiac death.i5-l7 After AMI, late potentials are usually found in subjectswhose infarct artery is occluded.4~5 Although several studies have examined the natural history of late potentials in survivors of AMI?J8J9 the data are difficult to interpret becauseof differences in patient populations, definitions of late potentials, and elapsedtime from AM1 to signal-averagedelectrocardiography. In a few survivors of AMI, a late potential that is present 1 to 2 weeksafter the event resolvesover the ensuing months. In our 5 group II subjects,followup signal-averaged electrocardiography was performed 127 f 49 days after AMI. Compared with baseline,the root-mean-square voltage remained abnormal in 4 of the 5 patients (Figure l), and the low-amplitude signal duration (Figure 2) and QRS duration (Figure 3) remained prolonged in all 5. In contrast, these variables were in the normal range on the follow-up study in 6 or 7 of the group I subjects (Table I; Figures 1, 2 and 3). The mechanism(s) by which the restoration of anterograde flow in the infarct artery causesa resolution of late potentials are unclear. In survivors of AMI, a pat100
160-
1
60 60 I% 40-
oJ
T 140-
A -& I ..
.._......
I
. .. .
.
‘ii 0 E c .g 2
120-
2 :: Q
*
loo-
?
baseline
follow-up PTCA (Group I)
baseline
follow-up
60 ’ baseline
Control (Group II)
FIGURE 2. Low-amplitude signal duation, in mikeconds, at baseWeantlfollow-upforthe7patkntswhohadangioptasty (group I, /et%) and tbs 5 not having angioplasty (gruup II, dabflWll1pdkllt,d~f right). Each line repmae& lsDisshownoneithersideofeachSaotlines.~ffedlined denote upper limit of normal (38 ms). In group I, the low-ampl&$eenal dvation &creased sim at follows, it nermal range in 6 patkmtq in gray, II, it was similardba~neamlfolowup,andremained>38msinaU5. *p <0.0!5 comparsd with basehs and gray, II at fahw-up. PTCA = percutaneour transhaninal csrona~ angkpkW. isi8
ent infarct artery appearsto diminish the extent of infarct expansion and left ventricular remodeling after AMI.20,21The processof remodeling begins with thinning and lengthening of the infarcted segment in the hours to days after the event (infarct expansion), after which lengthening of the noninfarcted segmentsoccurs in the ensuing weeks to months.22,23 When these processesare extensive, a left ventricular aneurysm may result, often providing a substrate for ventricular tachyarrhythmias9 In survivors of AMI, aneurysm formation is seenmore often in subjectswith an occluded infarct artery.24-26The mechanical restoration of anterograde perfusion may alter the anatomic substrate for ventricular arrhythmias by limiting the magnitude of left ventricular remodeling. Alternatively, the restoration of anterogradeflow in the infarct artery may favorably alter the electrophysiologic characteristics of the border zone.21Since several studies failed to demonstrate changesin the signal-averagedelectrocardiogram during myocardial ischemia,27-29 we included our 3 patients with postinfarction angina in group I. Study Imitations: First, although it was conducted at 3 large hospitals over 16 months, only 12 subjects met the stringent enrollment criteria: survivors of a first AM1 with a late potential 3 to 15 days afterwards and angiographic evidence of an occluded infarct artery. Currently, many patients with AM1 receivethrombolytic therapy, so that anterograde perfusion of the infarct artery is quickly restored pharmacologically. Ideally, our data should be confirmed in a larger patient cohort. Second,becausewe do not have angiographic informa-
THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 70
follow-up PTCA (Group I,
follow-up
baseline
Conlrol (Group II)
FIGURE 3. QRS durattan, in millisecsmls, at baseline and fdlow-up fur ths 7 subjeh who had angioplasty (group I, left) and the 5 net bavlng angbplasty (group II, right). Each line
representrrdataframlpatknt,andmeanflSDisshownon sither side of each set of lines. Dotted lines ¬e upper limit of normal (114 ms). In group I, ths QRS duration decreased . . gnmcantly; at fsllow-up, it was in the -aI range in all 7 Z~bjftcts. In group II, it was unchanged from baseline to fdlow-up, and it remahd >114 ms in all 5 subjects. *p <0.0!5 cempared with baseline and group II at follow-up. PTCA = per+utaneoucl transluminal -w =siM. DECEMBER 15, 1992
tion at the time of follow-up signal-averagedelectrocardiography, we cannot correlate the electrocardiographic and angiographic results at this point in time. Similarly, we did not reassessleft ventricular performance or geometry. Third, although the restoration of anterograde perfusion in the infarct artery causesresolution of late potentials, it is unknown if this will result in improved long-term survival. This possibility awaits the results of a prospective, randomized trial in which survival is the end point. At the same time, our study has strengths. First, it was performed prospectively. Second,only 3 of the 12 patients were offered angioplasty because of postinfarction angina; the other 9 were assigned randomly to angioplasty or no angioplasty. Our findings may have profound implications regarding the manner in which survivors of AMI are managedafter the acute event. The restoration of anterograde flow in the infarct artery - accomplisheddays or even weeks after AM1 - may improve survival by reducing the propensity for an arrhythmic event. If this is true, coronary angiography should be performed routinely in survivors of AM1 within 1 to 2 weeks,so that those with an occluded infarct artery are identified and encouragedto undergo mechanical restoration of anterograde perfusion. This possibility awaits confirmation in a large, properly-designed prospective trial. REFERENCES 1. Cigarroa RG, Lange RA, Hillis LD. Prognosis after acute myocardial infarction in patients with and without residual anterograde coronary blood flow. Am J Cardiol 1989;64:155-160. 2. Lange RA, Cigarroa RG, Hillis LD. Influence of residual antegrade coronary blood flow on survival after myocardial infarction in patients with multivessel coronary artery disease. Coronary Artery Disease 1990;1:59-63. 3. Trappe HJ, Lichtlen PR, Klein H, Wenzlaff P, Hartwig CA. Natural history of single vessel disease. Risk of sudden coronary death in relation to coronary anatomy and arrhythmia profile. Eur Heart J 1989;10:514-524. 4. Lange RA, Cigarroa RG, Wells PJ, Kremers MS, Hillis LD. Influence of anterograde flow in the infarct artery on the incidence of late potentials after acute mywardial infarction. Am J Cardiol 1990;65:554-558. 5. Gang ES, Lew AS, Hong M, Wang FZ, Siebert CA, Peter T. Decreased incidence of ventricular late potentials after successful thrombolytic therapy for acute myocardial infarction. N Engl J Med 1989;321:712-716. 6. Games JA, Mehra R, Barreca P, El-Sherif N, Hariman R, Holtzman R. Quantitative analysis of the high-frequency components of the signal-averaged QRS complex in patients with acute myocardial infarction: A prospective study. Circularion 1985;72:105-111. 7. Kuchar DL, Thorburn CW, Sammel NL. Late potentials detected after myocardial infarction: Natural history and prognostic significance. Circulation 1986;74:1280-1289. 8. Kersschot IE, Brugada P, Ramentol M, Zehender M, Waldecker B, Stevenson WG, Geibel A, DeZwaan C, Wellens HJJ. Effects of early reperfusion in acute myocardial infarction on arrhythmias induced by programmed stimulation: a prospective, randomized study. J Am CON Cardiof 1986;7:1234-1242. 9. Sager PT, Perlmutter RA, Rosenfeld LE, McPherson CA, Wackers FJT, Batsford WP. Electrophysiologic effects of thrombolytic therapy in patients with a transmural anterior myocardial infarction complicated by left ventricular aneurysm formation. J Am Co11 Cardiol 1988;12:19-24. 10. Breithardt G, Cain ME, El-Sherif N, Flowers NC, Hombach V, .Janse M, Simson MB, Steinbeck G. Standards for analysis of ventricular late potentials using high-resolution or signal-averaged electrocardiography: a statement by a task force committee of the European Society of Cardiology, the American Heart
Association, and the American College of Cardiology. J Am Co11 Cardiol 1991;17:999-1006. 11. Chesebro JH, Knatterud G, Roberts R, Borer J, Cohen LS, Dale” J, Dodge HT, Francis CK, Hillis D, Ludbrcok P, Markis JE, Mueller H, Passamani ER, Powers ER, Rao AK, Robertson T, Ross A, Ryan TJ, Sobe1 BE, Willerson J, Williams DO, Zaret BL, Braunwald E. Thrombolysis in Myocardial Infarction (TIMI) trial, phase I: a comparison between intravenous tissue plasminogen activator and intravenous streptokinase. Clinical findings through hospital discharge. Circulation 1987;76:142-154. 12. Simson MB, Untereker WJ, Spielman SR, Horowitz LN, Marcus NH, Falcone RA, Harken AH, Josephson ME. Relation between late potentials on the body surface and directly recorded fragmented electrograms in patients with ventricular tachycardia. Am J Cardiol 1983;51:105-112. 13. Gardner PI, Ursell PC, Fenoglio JJ, Wit AL. Electrophysiologic and anatomic basis for fractionated electrograms recorded from healed myocardial infarcts. Circulation 1985;72:596-611. 14. Denniss AR, Johnson DC, Richards DA, Ross DL, Uther JB. Effect of excision of ventricular myocardium on delayed potentials detected by the signalaveraged electrocardiogram in patients with ventricular tachycardia. Am J Cardial 1987;59:591-595. 15. Games JA, Winters SL, Martinson M, Machac J, Stewart D, Targonski A. The prognostic significance of quantitative signal-averaged variables relative to clinical variables, site of myocardial infarction, ejection fraction and ventricular premature beats: A prospective study. J Am CON Cardiol 1989;13:377-384. 16. Denniss AR, Richards DA, Cody DV, Russell PA, Young AA, Cooper MJ, Ross DL, Uther JB. Prognostic significance of ventricular tachycardia and fibrillation induced at programmed stimulation and delayed potentials detected on signal-averaged electrocardiograms of survivors of acute myocardial infarction. Circulation 1986;74:731-745. 17. Kuchar DL, Thorburn CW, Sammel NL. Prediction of-serious arrhythmic events after myocardial infarction: signal-averaged electrocardiogram, Halter monitoring and radionuclide ventriculography. J Am Coil Cardiol 1987;9:
531-538. 18. Rodriguez LM, Krijne R, van den Dool A, Brugada P, Smeets J, Wellens HJJ. Time course and prognostic significance of serial signal-averaged electrwardiagrams after a first acute myocardial infarction. Am J Cardiol 1990;66: 1199-1202. 19. Verzoni A, Romano S, Pozzoni L, Tarricone D, Sangiorgio S, Crow L. Prognostic significance and evolution of late ventricular potentials in the first year after myocardial infarction: a prospective study. PACE 1989;12:41-50. 20. Force T, Kemper A, Leavitt M, Parisi AF. Acute reduction in functional infarct expansion with late coronary reperfusion: assessment with quantitative two-dimensional echocardiography. J Am Coil Cardiol 1988;ll: 192-200. 21. Hochman JS, Choo H. Limitation of myocardial infarct expansion by reperfusion independent of myocardial salvage. Circulation 1987;75:299-306. 22. Erlebacher JA, Weiss JL, Weisfeldt ML, Bulkley BH. Early dilation of the infarcted segment in acute transmural myocardial infarction: Role of infarct expansion in acute left ventricular enlargement. J Am CON Card&l 1984;4: 201-208. 23. McKay RG, Pfeffer MA, Pasternak RC, Markis JE, Come PC, Nakao S, Alderman JD, Ferguson JJ, Safian R, Grossman W. Left ventricular remodeling following myocardial infarction: A corollary in infarct expansion. Circulation 1986;74:693-702. 24. Hirai T, Fujita M, Nakajima H, Asanoi H, Yamanishi K, Ohno A, Sasayama S. Importance of collateral circulation for prevention of left ventricular aneurysm formation in acute myocardial infarction. Circulation 1989;79:791-796. 25. Forman MB, Collins HW, Kopelman HA, Vaughn WK, Perry JM, Virmani R, Friesinger GC. Determinants of left ventricular aneurysm formation after anterior myocardial infarction: a clinical and angiographic study. J Am Coil Cardiol 1986;8:1256-1262. 26. Meizlish JL, Berger HJ, Plankey M, Enrico D, Levy W, Zaret BL. Functional left ventricular aneurysm formation after acute anterior myocardial infarction: incidence, natural history, and prognostic implications. N Engl J Med 1984;311: 1001-1006. 27. Turitto G, Zanchi E, Risa AL, Maddaluna A, Saltarocchi ML, Vajola SF, Prati PL. Lack of correlation between transient myocardial ischemia and late potentials on the signal averaged electrocardiogram. Am J Cardiol 1990;65:
290-296. 28. Caref EB, Goldberg N, Mendelson L, Hanley G, Okereke R, Stein RA, ElSherif N. Effects of exercise on the signal averaged electrocardiogram in coronary artery disease. Am J Cardiol 1990;66:54-58. 29. Turitto G. Caref E. Zanchi E. Menahini F. Kelen G. El-Sherif N. Soontaneous myocardial ischemia and the signal averaged electrocardiogram. Am J Cardial 1991;67:676-680.
ANGIOPIASTY FOR LATE POTENTIALS
1519
CORONARY ARTERY DISEASE
American Journal of Cardiology
DECEMBER 15,
1992,VOL. 70, NO. 20
Effect of Coronary Angioplasty on Late Potentials One to Two Weeks After Acute Myocardial Infarction James D. Boehrer, MD, D. Brent Glamann, MD, Richard A. Lange, MD, John E. Willard, MD, Walter C. Brogan, Ill, MD, PhD, Eric J. Eichhorn, MD, Paul A. Grayburn, MD, Azam Anwar, MD, and L. David Hillis, MD
In survivors of acute myocardial infarction (AMI), the restoration of anterograde flow in the infarct artery, even if accomplished beyond the time for myocardial salvage, may reduce the frequency of subsequent arrhythmic events and sudden death. Twelve subjects (8 men and 4 women, aged 39 to 69 years) with a first AMI, signal-averaged electrocardiographic late potentials, and an occluded infarct artery were prospectively identified. Seven (group I) had successful coronary angioplasty 6 to 15 days after AMI, and 5 (group II) were managed conservatively. Follow-up signal-averaged electrocardiography was performed 3 to 7 months later. From baseline to follow-up, the 7 group I subjects had a significant change in QRS duration (117 f 13 [mean + SD] to 102 f 10 ms), root-meansquare voltage (10.4 f 4.7 to 31.0 f 7.6 pV), and low-amplitude signal duration (47.5 f 8.5 to 32.4 f 5.2 ms) (p 50.05 for all 3 variables). No group I patient had a late potential at follow-up. In contrast, the 5 group II patients showed no change in QRS duration or low-amplitude signal duration from baseline to follow-up, and all 5 had a late potential at follow-up. At follow-up, the root-meansquare voltage was significantly greater and the low-amplitude signal and QRS durations significantly less in group I than in group II (p
I
n survivors of a first acute myocardial infarction (AMI), long-term survival is better in those with anterograde flow in the infarct artery than in those whose artery is occluded.1-3Patients with an occluded infarct artery are more likely than those with a patent artery to have late potentials by signal-averagedelectrocardiography.4,5In survivors of AMI, these late potentials identify those at risk of subsequent arrhythmic eventsand suddendeath.6,7Other reports8,9have shown that survivors of AM1 whose infarct artery has anterograde flow are unlikely to have inducible ventricular tachyarrhythmias, whereas the absenceof anterograde flow is frequently accompaniedby provocableventricular tachycardia and fibrillation. It is possible,therefore, that the restoration of anterograde flow in the infarct artery, even if accomplished days or weeks after the acute event, may improve survival by dishing electrical instability. This study was performed to test the hypothesis that the mechanical restoration of anterograde flow in an occluded infarct artery 1 to 2 weeks after AM1 causesa resolution of signal-averagedelectrocardiographic late potentials. METHODS Patient population: From November 1990 to Febru-
ary 1992 we identified 127 patients admitted to Parkland Memorial Hospital (n = 58), the Veterans Administration Medical Center (n = 37), or Baylor University Medical Center (n = 32), Dallas, Texas, with evidence of a first AMI. Subjectswith bundle branch block, previous AMI, ventricular preexcitation, intraventricular conduction delay, ventricular-paced rhythm, and those receiving amiodarone or type IC antiarrhythmic agents were excluded. Patients were enrolled if they had (1) a late potential on signal-averaged electrocardiography (performed 3 to 15 days after AMI) and (2) an occludFrom the Department of Internal Medicine (Cardiovascular Division), ed infarct artery on coronary angiography (performed 1 the University of Texas SouthwesternMedical Center, and the Cardiac Catheterization Laboratories of Parkland Memorial Hospital, Veterans to 13 days after AMI). Coronary angiography was perAdministration Medical Center, and Baylor University Medical Cen- formed before signal-averagedelectrocardiography in 5 ter, Dallas, Texas. Manuscript received June 18, 1992; revised manu- patients and afterward in the other 7 (Table I). No rigscript receivedand acceptedJuly 22,1992. Addressfor reprints: L. David Hillii, MD, Room CS 7.102,Univer- id chronologic relation between angiographic and signal-averaged electrocardiographic studies was required sity of Texas SouthwesternMedical Center, 5323 Harry Hines Boule vard, Dallas, Texas 75235. provided that signal-averagedelectrocardiography was ANGIOPIASTY FOR LATE POTENTIALS
1515
51 2 7
Mean + SD
-
Right Right LAD LC LC
-
Right Right Right Right LAD LAD LC
Infarct Artery
0.46 0.51 0.48 0.61 0.43 0.53 NA
0.52 f 0.11
0.39 0.42 0.53 0.62 0.63 7?4
10 8 5 2 12
724
2 11 7 6 1 7 13
LVEF
0.50 t 0.06
Time from AMI to cc (days)
Electrocardiographic
-
-
11 -t3
6 12 9 15 8 14 13
Time from AMI to PTCA (days) Baseline
Root-Mean-Square Follow-Up
114 f 22
127 102 88 149 94 128 111 10.4 T!z4.7
8.4 3.0 12.1 7.7 16.8 15.1 10.0
Voltage
51.5 65.0 45.5 43.5 45.0 40.0 42.0 47.5 ? 8.5
31.0 2 7.6t$
7k3
8 8 5 4 12
LC = left circumflex;
127 + 49
214 107 112 103 99
LVEF = left ventricular
8.5 A 6.1
8.5 2.8 15.5 2.1 13.7
Baseline
Low-Amplitude
22.1 24.9 26.1 37.1 27.5 38.1 41.1
NA = not available;
coronaly
angiaplasty;
128 -+ 16
47.9 f 4.5
translumlnal
108 129 128 153 123
117 k 13
32.4 t 5.2tt
44.4 47.5 43.0 54.0 50.5
121 137 116 127 105 101 109
Baseline
SAECG = signal-
121 + 5
127 117 117 117 126
102 +- lOT$
110 90 100 113 112 93 94
Follow-Up
Filtered QRS Duration (ms)
28.5 39.0 37.0 25.5 34.5 34.5 27.5
Follow-Up
Signal Duration
PTCA = percutaneous
59.0 zk 18.2
15.4 + 5.07
ejection fraction;
47.5 60.5 48.5 90.0 48.5
10.0 11.4 22.7 16.1 16.7
Group II: Patients Who Did Not Undergo Angioplasty
925
3 10 7 15 3 13 12
Time from AMI to Final SAECG (days)
Group I: Patients Who Underwent Angioplasty
Time from AMI to Baseline SAECG (days)
Data for the 12 Patients
*Denotes those with postinfarction angina. tp so.05 compared with baseline: $p x0.05 compared with group II. AMI = acute myocardial infarction; CC = cardiac catheterization; LAD = left anterior descending; averaged electrocardiogram.
58M 56F 49M 51F 40M
53211
41M 51M 65M 39M 50M 69F 54F
8 9 10 11 12
Mean 2 SD
1 2* 3 4* 5 6* 7
Pt.
Age (yr) & sex
TABLE I Clinical and Signal-Averaged
performed within 3 to 15 days of AMI. Patients with continuing angina were offered angioplasty of the occluded artery for symptom relief. The remaining subjects were assigned randomly to angioplasty (group I) versus no angioplasty (group II). For each group I subject, the benefits and risks of angioplasty were explained and each gave written informed consent. Each patient was seen regularly over the ensuing months. A signalaveragedelectrocardiogram was repeated 3 to 7 months after AMI and compared with baseline. Signal-averaged electrocardiography: Signal-averaged electrocardiography was performed with the Predictor Signal Averaging Electrocardiogram System (Corazonix Corp, Oklahoma City, Oklahoma), according to methods described previously.4 A late potential was prospectively defined as 12 of the following: (1) a root-mean-squarevoltage <20 PV in the terminal 40 ms of the QRS, (2) a low-amplitude signal duration >38 ms, and (3) a QRS duration > 114 rns.‘OThe signalaveragedelectrocardiogramswere not overread, and the computer-derived tracings were not adjusted manually. No patient received medications known to alter the signal-averaged electrocardiogram. Coronary angiography: Anterograde flow in the infarct artery was graded in accordancewith the criteria of the Thrombolysis in Myocardial Infarction investigators.” To be eligible for enrollment, all patients had Thrombolysis in Myocardial Infarction trial grade 0 perfusion on the baseline angiogram. Collateral flow to the distal infarct artery wasjudged as presentor absent. Left ventricular ejection fraction was determined by standard techniques from single plane ventriculography. Statistical analysis: All data are reported as mean f 1 standard deviation (SD). For each group, the rootmean-square voltage, low-amplitude signal duration, and QRS duration before and 3 to 7 months after angiography/angioplasty were compared with a paired t test. At baseline and follow-up, those undergoing angioplasty (group I) and those treated without angioplasty (group II) were compared with Student’s t test. For all analyses,a p value 50.05 was considered significant. RESULTS
and QRS duration decreased(Figure 3) (p 10.05 for all 3 variables) (Table I). In contrast, in the 5 group II patients, follow-up signal-averagedelectrocardiography showedno significant change in low-amplitude signal duration (Figure 2) or QRS duration (Figure 3) when comparedwith baseline. Although the root-mean-squarevoltage increased from baseline to follow-up, the average value at follow-up was below the lower limit of normal (Figure 1). Of the 5 group II patients, all retained a late potential at follow-up. At follow-up, the root-mean-squarevoltage was greater and the low-amplitude signal and QRS durations lessin group I than in group II (Table I; Figures 1, 2 and 3). Coronary angiography: At baseline, collateral flow to the distal infarct artery was present in 6 of 7 group I patients and in all 5 group II subjects (p = not significant [NS]). Coronary artery disease(170% luminal diameter narrowing) in vesselsother than the infarct artery was present in 3 group I patients and in 2 group II subjects(p = NS). Two patients in each group received intravenous thrombolytic therapy (p = NS). DISCUSSION
The mechanical restoration of anterograde flow in an occluded infarct artery 6 to 15 days after AM1 causes a resolution of signal-averaged electrocardiographic late potentials, whereaslate potentials persist in 40 -
30-
20 -
lo-
Twelve patients (8 men and 4 women, aged 39 to 69 years) fulfilled the entrance criteria (Table I). Three were offered angioplasty because of postinfarction angina. Of the other 9, 4 were 0 follow-up baseline baseline follow-up assignedrandomly to angioplasty versus 5 to no angioplasty. The 7 subjectshad successfulangioplasty (residPTCA Control (Group I) (Group II) ual stenosis<50% luminal diameter narrowing) 11 f 3 (range 6 to 15) days after AMI and formed group I; the 5 who were managed without angioplasty formed group FIGURE 1. Root-mean-square voltage, in microvolts, at baseII. The 2 groups were similar in age, sex, infarct artery, RneandfoRowy,forthe7PatkntswhohadangioPlasty and left ventricular ejection fraction (Table I). mpmentsdatafromlpatlent,andmeani Signal-averaged ekctrecardiography: Signal-aver- lSDis~wnaneithersideafeaehsetoflineb.Doffedlines aged electrocardiography was performed 8 f 4 (range 3 denote lower limit of normal (20 pV). In group I, the rootto 15) days after AMI. In the patients who underwent mean-square voWage inueased sigllificantly; ai followup, it angioplasty (group I), follow-up signal-averaged elec- wasinthenonnalrangeinaU7Pat&ts.IngroupII,itinslgniticantly from baseiii to foRow-ql bul renlalnt?d trocardiography showed resolution of late potentials in creased -20 pV in 4 of 5 Patients. *p 10.05 compared with baseline all 7: root-mean-square voltage increased (Figure I), and ths other group al foRow-up. PTCA = percutaneous translow-amplitude signal duration decreased (Figure 2), luminal -w ae3W-W Patient characteristics:
ANGl0PLASl-Y FOR LATE POTENTIALS
1517
survivors of AM1 in whom anterograde flow is not restored. Signal-averaged electrocardiographic late potentials arise from areas where normal myocytes interdigitate with fibrotic or ischemic cells, or both.12J3When such areasare surgically excised,the signal-averagedelectrocardiogram reverts to normaLl In survivors of AMI, late potentials are predictive of inducible and spontaneous ventricular tachycardia, an arrhythmic event within the first year, and sudden cardiac death.i5-l7 After AMI, late potentials are usually found in subjectswhose infarct artery is occluded.4~5 Although several studies have examined the natural history of late potentials in survivors of AMI?J8J9 the data are difficult to interpret becauseof differences in patient populations, definitions of late potentials, and elapsedtime from AM1 to signal-averagedelectrocardiography. In a few survivors of AMI, a late potential that is present 1 to 2 weeksafter the event resolvesover the ensuing months. In our 5 group II subjects,followup signal-averaged electrocardiography was performed 127 f 49 days after AMI. Compared with baseline,the root-mean-square voltage remained abnormal in 4 of the 5 patients (Figure l), and the low-amplitude signal duration (Figure 2) and QRS duration (Figure 3) remained prolonged in all 5. In contrast, these variables were in the normal range on the follow-up study in 6 or 7 of the group I subjects (Table I; Figures 1, 2 and 3). The mechanism(s) by which the restoration of anterograde flow in the infarct artery causesa resolution of late potentials are unclear. In survivors of AMI, a pat100
160-
1
60 60 I% 40-
oJ
T 140-
A -& I ..
.._......
I
. .. .
.
‘ii 0 E c .g 2
120-
2 :: Q
*
loo-
?
baseline
follow-up PTCA (Group I)
baseline
follow-up
60 ’ baseline
Control (Group II)
FIGURE 2. Low-amplitude signal duation, in mikeconds, at baseWeantlfollow-upforthe7patkntswhohadangioptasty (group I, /et%) and tbs 5 not having angioplasty (gruup II, dabflWll1pdkllt,d~f right). Each line repmae& lsDisshownoneithersideofeachSaotlines.~ffedlined denote upper limit of normal (38 ms). In group I, the low-ampl&$eenal dvation &creased sim at follows, it nermal range in 6 patkmtq in gray, II, it was similardba~neamlfolowup,andremained>38msinaU5. *p <0.0!5 comparsd with basehs and gray, II at fahw-up. PTCA = percutaneour transhaninal csrona~ angkpkW. isi8
ent infarct artery appearsto diminish the extent of infarct expansion and left ventricular remodeling after AMI.20,21The processof remodeling begins with thinning and lengthening of the infarcted segment in the hours to days after the event (infarct expansion), after which lengthening of the noninfarcted segmentsoccurs in the ensuing weeks to months.22,23 When these processesare extensive, a left ventricular aneurysm may result, often providing a substrate for ventricular tachyarrhythmias9 In survivors of AMI, aneurysm formation is seenmore often in subjectswith an occluded infarct artery.24-26The mechanical restoration of anterograde perfusion may alter the anatomic substrate for ventricular arrhythmias by limiting the magnitude of left ventricular remodeling. Alternatively, the restoration of anterogradeflow in the infarct artery may favorably alter the electrophysiologic characteristics of the border zone.21Since several studies failed to demonstrate changesin the signal-averagedelectrocardiogram during myocardial ischemia,27-29 we included our 3 patients with postinfarction angina in group I. Study Imitations: First, although it was conducted at 3 large hospitals over 16 months, only 12 subjects met the stringent enrollment criteria: survivors of a first AM1 with a late potential 3 to 15 days afterwards and angiographic evidence of an occluded infarct artery. Currently, many patients with AM1 receivethrombolytic therapy, so that anterograde perfusion of the infarct artery is quickly restored pharmacologically. Ideally, our data should be confirmed in a larger patient cohort. Second,becausewe do not have angiographic informa-
THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 70
follow-up PTCA (Group I,
follow-up
baseline
Conlrol (Group II)
FIGURE 3. QRS durattan, in millisecsmls, at baseline and fdlow-up fur ths 7 subjeh who had angioplasty (group I, left) and the 5 net bavlng angbplasty (group II, right). Each line
representrrdataframlpatknt,andmeanflSDisshownon sither side of each set of lines. Dotted lines ¬e upper limit of normal (114 ms). In group I, ths QRS duration decreased . . gnmcantly; at fsllow-up, it was in the -aI range in all 7 Z~bjftcts. In group II, it was unchanged from baseline to fdlow-up, and it remahd >114 ms in all 5 subjects. *p <0.0!5 cempared with baseline and group II at follow-up. PTCA = per+utaneoucl transluminal -w =siM. DECEMBER 15, 1992
tion at the time of follow-up signal-averagedelectrocardiography, we cannot correlate the electrocardiographic and angiographic results at this point in time. Similarly, we did not reassessleft ventricular performance or geometry. Third, although the restoration of anterograde perfusion in the infarct artery causesresolution of late potentials, it is unknown if this will result in improved long-term survival. This possibility awaits the results of a prospective, randomized trial in which survival is the end point. At the same time, our study has strengths. First, it was performed prospectively. Second,only 3 of the 12 patients were offered angioplasty because of postinfarction angina; the other 9 were assigned randomly to angioplasty or no angioplasty. Our findings may have profound implications regarding the manner in which survivors of AMI are managedafter the acute event. The restoration of anterograde flow in the infarct artery - accomplisheddays or even weeks after AM1 - may improve survival by reducing the propensity for an arrhythmic event. If this is true, coronary angiography should be performed routinely in survivors of AM1 within 1 to 2 weeks,so that those with an occluded infarct artery are identified and encouragedto undergo mechanical restoration of anterograde perfusion. This possibility awaits confirmation in a large, properly-designed prospective trial. REFERENCES 1. Cigarroa RG, Lange RA, Hillis LD. Prognosis after acute myocardial infarction in patients with and without residual anterograde coronary blood flow. Am J Cardiol 1989;64:155-160. 2. Lange RA, Cigarroa RG, Hillis LD. Influence of residual antegrade coronary blood flow on survival after myocardial infarction in patients with multivessel coronary artery disease. Coronary Artery Disease 1990;1:59-63. 3. Trappe HJ, Lichtlen PR, Klein H, Wenzlaff P, Hartwig CA. Natural history of single vessel disease. Risk of sudden coronary death in relation to coronary anatomy and arrhythmia profile. Eur Heart J 1989;10:514-524. 4. Lange RA, Cigarroa RG, Wells PJ, Kremers MS, Hillis LD. Influence of anterograde flow in the infarct artery on the incidence of late potentials after acute mywardial infarction. Am J Cardiol 1990;65:554-558. 5. Gang ES, Lew AS, Hong M, Wang FZ, Siebert CA, Peter T. Decreased incidence of ventricular late potentials after successful thrombolytic therapy for acute myocardial infarction. N Engl J Med 1989;321:712-716. 6. Games JA, Mehra R, Barreca P, El-Sherif N, Hariman R, Holtzman R. Quantitative analysis of the high-frequency components of the signal-averaged QRS complex in patients with acute myocardial infarction: A prospective study. Circularion 1985;72:105-111. 7. Kuchar DL, Thorburn CW, Sammel NL. Late potentials detected after myocardial infarction: Natural history and prognostic significance. Circulation 1986;74:1280-1289. 8. Kersschot IE, Brugada P, Ramentol M, Zehender M, Waldecker B, Stevenson WG, Geibel A, DeZwaan C, Wellens HJJ. Effects of early reperfusion in acute myocardial infarction on arrhythmias induced by programmed stimulation: a prospective, randomized study. J Am CON Cardiof 1986;7:1234-1242. 9. Sager PT, Perlmutter RA, Rosenfeld LE, McPherson CA, Wackers FJT, Batsford WP. Electrophysiologic effects of thrombolytic therapy in patients with a transmural anterior myocardial infarction complicated by left ventricular aneurysm formation. J Am Co11 Cardiol 1988;12:19-24. 10. Breithardt G, Cain ME, El-Sherif N, Flowers NC, Hombach V, .Janse M, Simson MB, Steinbeck G. Standards for analysis of ventricular late potentials using high-resolution or signal-averaged electrocardiography: a statement by a task force committee of the European Society of Cardiology, the American Heart
Association, and the American College of Cardiology. J Am Co11 Cardiol 1991;17:999-1006. 11. Chesebro JH, Knatterud G, Roberts R, Borer J, Cohen LS, Dale” J, Dodge HT, Francis CK, Hillis D, Ludbrcok P, Markis JE, Mueller H, Passamani ER, Powers ER, Rao AK, Robertson T, Ross A, Ryan TJ, Sobe1 BE, Willerson J, Williams DO, Zaret BL, Braunwald E. Thrombolysis in Myocardial Infarction (TIMI) trial, phase I: a comparison between intravenous tissue plasminogen activator and intravenous streptokinase. Clinical findings through hospital discharge. Circulation 1987;76:142-154. 12. Simson MB, Untereker WJ, Spielman SR, Horowitz LN, Marcus NH, Falcone RA, Harken AH, Josephson ME. Relation between late potentials on the body surface and directly recorded fragmented electrograms in patients with ventricular tachycardia. Am J Cardiol 1983;51:105-112. 13. Gardner PI, Ursell PC, Fenoglio JJ, Wit AL. Electrophysiologic and anatomic basis for fractionated electrograms recorded from healed myocardial infarcts. Circulation 1985;72:596-611. 14. Denniss AR, Johnson DC, Richards DA, Ross DL, Uther JB. Effect of excision of ventricular myocardium on delayed potentials detected by the signalaveraged electrocardiogram in patients with ventricular tachycardia. Am J Cardial 1987;59:591-595. 15. Games JA, Winters SL, Martinson M, Machac J, Stewart D, Targonski A. The prognostic significance of quantitative signal-averaged variables relative to clinical variables, site of myocardial infarction, ejection fraction and ventricular premature beats: A prospective study. J Am CON Cardiol 1989;13:377-384. 16. Denniss AR, Richards DA, Cody DV, Russell PA, Young AA, Cooper MJ, Ross DL, Uther JB. Prognostic significance of ventricular tachycardia and fibrillation induced at programmed stimulation and delayed potentials detected on signal-averaged electrocardiograms of survivors of acute myocardial infarction. Circulation 1986;74:731-745. 17. Kuchar DL, Thorburn CW, Sammel NL. Prediction of-serious arrhythmic events after myocardial infarction: signal-averaged electrocardiogram, Halter monitoring and radionuclide ventriculography. J Am Coil Cardiol 1987;9:
531-538. 18. Rodriguez LM, Krijne R, van den Dool A, Brugada P, Smeets J, Wellens HJJ. Time course and prognostic significance of serial signal-averaged electrwardiagrams after a first acute myocardial infarction. Am J Cardiol 1990;66: 1199-1202. 19. Verzoni A, Romano S, Pozzoni L, Tarricone D, Sangiorgio S, Crow L. Prognostic significance and evolution of late ventricular potentials in the first year after myocardial infarction: a prospective study. PACE 1989;12:41-50. 20. Force T, Kemper A, Leavitt M, Parisi AF. Acute reduction in functional infarct expansion with late coronary reperfusion: assessment with quantitative two-dimensional echocardiography. J Am Coil Cardiol 1988;ll: 192-200. 21. Hochman JS, Choo H. Limitation of myocardial infarct expansion by reperfusion independent of myocardial salvage. Circulation 1987;75:299-306. 22. Erlebacher JA, Weiss JL, Weisfeldt ML, Bulkley BH. Early dilation of the infarcted segment in acute transmural myocardial infarction: Role of infarct expansion in acute left ventricular enlargement. J Am CON Card&l 1984;4: 201-208. 23. McKay RG, Pfeffer MA, Pasternak RC, Markis JE, Come PC, Nakao S, Alderman JD, Ferguson JJ, Safian R, Grossman W. Left ventricular remodeling following myocardial infarction: A corollary in infarct expansion. Circulation 1986;74:693-702. 24. Hirai T, Fujita M, Nakajima H, Asanoi H, Yamanishi K, Ohno A, Sasayama S. Importance of collateral circulation for prevention of left ventricular aneurysm formation in acute myocardial infarction. Circulation 1989;79:791-796. 25. Forman MB, Collins HW, Kopelman HA, Vaughn WK, Perry JM, Virmani R, Friesinger GC. Determinants of left ventricular aneurysm formation after anterior myocardial infarction: a clinical and angiographic study. J Am Coil Cardiol 1986;8:1256-1262. 26. Meizlish JL, Berger HJ, Plankey M, Enrico D, Levy W, Zaret BL. Functional left ventricular aneurysm formation after acute anterior myocardial infarction: incidence, natural history, and prognostic implications. N Engl J Med 1984;311: 1001-1006. 27. Turitto G, Zanchi E, Risa AL, Maddaluna A, Saltarocchi ML, Vajola SF, Prati PL. Lack of correlation between transient myocardial ischemia and late potentials on the signal averaged electrocardiogram. Am J Cardiol 1990;65:
290-296. 28. Caref EB, Goldberg N, Mendelson L, Hanley G, Okereke R, Stein RA, ElSherif N. Effects of exercise on the signal averaged electrocardiogram in coronary artery disease. Am J Cardiol 1990;66:54-58. 29. Turitto G. Caref E. Zanchi E. Menahini F. Kelen G. El-Sherif N. Soontaneous myocardial ischemia and the signal averaged electrocardiogram. Am J Cardial 1991;67:676-680.
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