Thrombolysis-related early patency reduces ECG late potentials after acute myocardial infarction

American Heart Journal Founded in 1925

September 1992 Volume 124, Number 3

CLINICAL INVESTIGATIONS

Thrombolysis-related early patency reduces ECG late potentials after acute myocardial infarction

To assess the effects of thrombolysis and reperfusion on late potentials after myocardial infarction, 101 patients (79 men, age 63.2 f 10.5 years) underwent signal-averaged ECG studies at 10.7 + 9.2 days, with the use of a 40 to 250 Hz band-pass filter. Patients were divided into four groups: (1) 54 patients treated with thrombolytic agents at 2.6 f 1.1 hours, with 81% “early” patency/reperfusion (TIMI grades 2 and 3); (2) 47 patients treated conventionally with 45% “late” patencyfreperfusion; (3) 56 patients with patency (TIM grades 2 and 3); and (4) 26 patients without patency (TIMI grades 0 and 1). A late potential was present when 12 of 3 defined criteria were present. There was a significant difference in the incidence of late potentials between groups 1 and 2 (22% vs 43%, respectively; p = 0.048) and between groups 3 and 4 (18% vs 50%, respectively; p = 0.006). Late potentials also tended to occur less often after “early” than after “late” patency/reperfusion (12.5% vs 25%). The odds ratio for developing a late potential was 0.39 for thrombolysis versus no thrombolysis (p < 0.05) and 0.22 for patency/reperfusion (TIMI grades 2 and 3) versus no patency/reperfusion (TIMI grades 0 and 1) (p < 0.05). By analysis of covariance the effects of thrombolysis on late potentials were entirely explained by reperfusion. Thus the risk of late potentials after myocardial infarction is high but is reduced by thrombolysis and reperfusion. In addition, the effectiveness of “early” reperfusion appears to be greater than that of “late” but requires further clarification. (AM HEART J 1992;124:557.)

Fidela LL. Moreno, MD, Labros Karagounis, MD, Hiram Marshall, MD,

Ronald L. Menlove, PhD, Steven Ipsen, RN, and Jeffrey L. Anderson, MD

Salt Lake City, Utah

Treatment with a thrombolytic agent has been shown to improve survival and preserve myocardial function after an acute myocardial infarction.1-7 Patients undergoing successful reperfusion have demonstrated a lower incidence of early and late mortality when treated within 6 to 12 hours, as well as a higher left ventricular ejection fraction when treated within 3 to 4 hours, compared with conventionally treated patients. The effects of reperfusion therapy on electrical function are of interest, in addition to the effects on mechanical function. Late potentials on

From LDS Hospital and the University of Utah School of Medicine, Salt Lake City.

Received for publication Feb. 7, 1992; accepted March 25, 1992.

Reprint requests: Jeffrey L. Anderson, MD, Cardiology Division, LDS Hos- pital, 8th Ave. and C St., Salt Lake City, UT 84143.

4lll39282

signal-averaged ECGs are risk markers for arrhythmias and sudden death in the period of 2 to 24 months after an acute myocardial infarction.8b13 Late potentials refer to low-amplitude, high-frequency signals in the terminal portion of the QRS complex. Indis- tinguishable on the surface ECG, late potentials are actually continuous with the QRS complex and exist for a variable period of time on the ST segment. They correspond to fragmented activation of ventricular tissue and are thought to originate from areas of slow and inhomogeneous conduction within diseased myocardial regions. 14-17 Signal averaging and high-gain amplification of the QRS complex have been used in recent years to detect these signals noninvasively by means of appropriate recording and filtering tech- niques.15* l8

Because the presence of late potentials on signal- averaged ECGs after acute myocardial infarction has

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American HearI Journal

Fig. 1. Signal-averaged EGG from 73-year-old man who was treated conservatively after acute inferior wall myocardial infarction. He had a late potential.

been shown to correlate significantly with ventricular tachycardia and sudden cardiac death, investigators have been interested in the effects of reperfusion therapy on their occurrence. In fact, some recent findings have suggested that patients who have received thrombolytic therapy (and are therefore presumed to be at lower risk for mortality and to

Table I. Patient characteristics

Characteristics Group 1 Group 2 p Value

No. of’ patients Age (yr) Male: N ( % ) AWMI: N (%) History of MI: N (5%) Infarct artery

RCA: N (9; ) LAD/LMCA: N (%) LCX: N ((rh)

LVEF (Cr: ) Patency: N (‘5 )

53 60.2 t 10.7

45 (83) 23 (43)

9 (17)

47 66.6 It 9.2

34 (72) 15 (32) 14 (30)

0.002 0.27 0.37 0.18

23 (44) 10 (33) 22 (42) 14 (47) 7 (14) 5 (17)

57.2 k 13.1 53.8 + 16.9 43 (81) 13 (45)

0.65

0.29 0.003

AWMI, Anterior wall myocardial infarction; LAD, left anterior descending coronary artery; LCX, left circumflex coronary artery; LMCA, left main coronary artery; LVEF, left ventricular ejection fraction; MI, myocardial infarction; N, number of patients; RCA, right coronary artery.

show better myocardial preservation and improved diastolic function) are also at lower risk for developing late potentials. 1g-27 However, to date patient series supporting these findings are still relatively few and the data are not entirely consistent. Turitto et al 28 for example, showed no significant difference in thi incidence of late potentials between patients treated with thrombolysis and conventionally treated patients. The purpose of this study, therefore, was to evaluate the effects of thrombolytic treatment on the incidence of late potentials during the first 30 days after acute myocardial infarction in a series of consecutive patients from our center. In addition, we examined the relationship between late potentials and patency of the infarct-related artery and the time to patency.

METHODS Patient selection. We retrospectively studied 101 con-

secutive patients who were admitted to our hospital for an acute myocardial infarction. Diagnostic criteria included characteristic chest pain, ST segment elevation zz 0.1 mV in at least one limb lead or two adjacent precordial leads, and an increase in the total creatine kinase (>1.5 times the upper limit of normal) and/or creatine kinase MB isoen- zyme (>5 % ) concentration. Patients with atria1 fibrillation and a QRS complex >llO msec on the admission 12-lead ECG and those dependent on a permanent pacemaker were excluded from the study. There were 79 men and 22 women, with a mean age of 63.2 & 10.5 years (range 35 to 81). These patients were classified into four groups. Group 1 consisted of 54 patients who received thrombolytic therapy. Group 2 included 47 patients who did not receive thrombolytic therapy and were treated conventionally. Reasons for withholding thrombolytic therapy were varied and included prolonged chest pain (>4 to 6 hours’ duration), physician preference, or known contraindications to thrombolysis. Patients who underwent coronary angiography and

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Number 3 Thrombolysis and SAECG late potentials 559

had technically adequate results (N = 82) were further classified into two other groups on the basis of patency status irrespective of therapy. 2g Group 3 consisted of 56 patients who demonstrated patency (TIM1 grades 2 and 3), and group 4 included 26 patients who did not achieve patency (TIM1 grades 0 and 1).

Thrombolysis. Thrombolytic therapy was given at a mean of 166 f 63 minutes (range 45 to 325), after the onset of symptoms. Group 1 included 40 patients (74%) who were enrolled in ongoing studies on the use of various thrombolytic agents after acute myocardial infarction30-34 and 14 patients (26%) who received individualized thrombolytic treatment per their attending physician’s preference. Patients received one of the following thrombolytic agents: anistreplase or anisoylated lys-plasminogen streptokinase activator complex (APSAC, N = 16), alteplase or tissue plasminogen activator (TPA, N = 18), streptokinase (N = 15), urokinase (N = 3), or a combination of TPA and urokinase (N = 2). APSAC was given in a dose of 30 U intravenously over 2 to 5 minutes.30-32 TPA was generally given at a dose of 100 mg intravenously over 3 hours (most commonly, 60 mg in the first hour and 20 mg in each of the second and third hours). TPA was weight adjusted for patients less than 60 kg. 33, 34 Streptokinase was given at a dose of 1.5 million units intravenously over 60 minutes.30,32 Urokinase was given intravenously at a dose of 1.5 million units over 2 minutes, then 1.5 million units over 90 minutes.34 Two patients received a combination of 50 mg of TPA and 1.5 million units of urokinase intravenously over 2 hours.34

Signal-averaged ECG. Signal-averaged ECG studies were performed as ordered by the physicians at an overall mean of 10.7 t- 9.2 days (range 1 to 30 days). Testing was done near the time of discharge in 79 (78%) patients and within 48 hours after admission in the other 22 (22%). A commercially available ECG analyzer (1200 EPX, Arrhyth- mia Research Technology, Inc., Austin, Texas) was used. This system records three bipolar orthogonal leads, filtered bidirectionally between 40 and 250 Hz, and combined into a vector of magnitude quantified as the square root of the sum of (X” + Y2 + Z2). We used a computer program algo- rithm to determine the onset and offset of the QRS complex and calculated the high-frequency QRS characteristics. We attempted to average 600 cycles or reach a noise level 5 1.0 pV. All signal-averaged ECGs were analyzed by consensus of t,wo of us (F. LL. M. and J. L. A.) without knowledge of clinical data. A late potential was present when r2 of the following criteria were met: (1) root mean square voltage of the last 40 msec of the filtered QRS complex (RMS40) <20 pV; (2) duration of the total filtered QRS complex (TFQRSD) >120 msec; and (3) duration of low-amplitude signals less than 40 rV in the terminal portion of the QRS complex (LAS40) >42 msec. These criteria were defined prospectively and based on those recom- mended by Kuchar et allo and Gomes et a1.35

Coronary angiography. Selective coronary angiography was performed by the Judkins technique, obtained in mul- tiple orthogonal views, and recorded at standardized angles on cineangiographic film. After catheterization the cinean-

Fig. 2. Signal-averaged ECG from 45-year-old man who was treated with streptokinase after acute anterior wall myocardial infarction. He did not have a late potential.

giograms were reviewed independently and without knowledge of the signal-averaged ECG to identify the artery involved in the infarction, Additional information from the ECG and the pattern of regional left ventricular dysfunc- tion was used whenever necessary. Anterograde perfusion of the infarct-related artery was graded according to the classification system of the Thrombolysis in Myocardial Infarction (TIMI) tria12g as follows: grade 0 = no antero-

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Table II. Average quantitative values of the signal-averaged ECG parameters

Parameter Group I Group 2 p Value Group 3 Group 4 p Value

. RMS40 (fiV) 26.9 + 22.2 23.9 t 19.7 0.47 29.6 + 21.7 23.3 t 23.3 0.24 TFQRSD (msec) 102.5 k 15.2 109.8 s 18.3 0.03 101.1 t 14 111 + 21.9 0.02 LAS40 (msec) 37.1 * 10.3 39.7 I 15.3 0.31 34.9 i 8.6 43.3 rt 17.3 0.004

See text for abbreviations.

grade perfusion; grade 1 = minimal perfusion: penetration of the obstructed lumen with negligible distal flow; grade 2 = partial perfusion: coronary bed perfusion distal to the obstruction but at a delayed rate of filling and clearing; and grade 3 = complete perfusion: coronary bed perfusion distal to the obstruction with a normal rate of filling and clearance. The number of coronary vessels with significant (>60%) diameter obstruction was also noted. All angio- grams were assessed visually by one of us (H. M.) without knowledge of clinical data. Angiography was performed during the hospital stay in 84 of 101 patients (83%) at a mean of 2.7 + 2.6 days (range 1 to lo), as determined by the clinical trial protocol or the patient’s physician. In 37 of these patients (45 % ) angiography was performed within 24 hours of admission. In the remaining 46 patients (55 % ) angiography was performed at 4.4 t 2.2 days after admission.

Data analysis. All values are expressed as mean I+_ one standard deviation. Differences in normally distributed continuous variables were compared by means of analysis of variance. Statistical analysis of discrete variables was performed with the chi-square test, as well as Fisher’s ex- act test when appropriate. The value of p < 0.05 was con- sidered significant.

RESULTS Thrombolysis versus conventional treatment. Char-

acteristics are described for patients treated with thrombolysis (group I) and conventionally treated patients (group 2) in Table I. Patients in group 1 were significantly younger than those in group 2 (60.2 + 11 vs 66.6 k 9; p = 0.002). Signal-averaged ECGs were recorded earlier after myocardial infarction in group 1 than in group 2 (7.5 k 7.8 vs 14.3 k 9.3 days; p < 0.05). There were no other significant differences between the two groups including sex, site of infarct, previous history of myocardial infarction, infarct-related artery, number of coronary vessels ~60% oc- cluded, left ventricular ejection fraction, and time after myocardial infarction for the performance of coronary angiography. As expected, significantly more patients in group 1 achieved patent coronary artery status than in group 2 (81% vs 45 % of those undergoing angiography, p = 0.003).

Figs. 1 and 2 are examples of signal-averaged ECGs in patients with and without late potentials, respectively. Fig. 3 compares the incidence of late potentials

between the two treatment groups, regardless of patency outcome. Of the 54 patients in group 1 who received thrombolytic therapy, late potentials were recorded in 12 (22%). In contrast, of 47 patients treated conventionally, 20 (43 % ) had late potentials (p = 0.048). The same results were observed when the analysis included only patients who had signal- averaged ECGs recorded 12 days after myocardial infarction (N = 79). Late potentials were demonstrated in 7 (19%) versus 17 (41%) patients treated with thrombolysis (N = 37) versus conventional therapy (N = 42), respectively (p = 0.037). Of the three individual criteria for a late potential, only the average quantititive value of TFQRSD was significantly different between groups 1 and 2, whereas the average quantitative values of both TFQRSD and LAS40 were significantly different between groups 3 and 4 (Table II).

Reperfusion versus nonreperfusion. Of 84 patients who underwent coronary angiography, 82 had technically adequate results. Infarct segments were iden- tified and assigned a TIM1 flow grade. Comparison of patients in group 3 (TIM1 grades 2 and 3, N = 56) and group 4 (TIM1 grades 0 and 1, N = 26) showed a significantly higher incidence of late potentials in group 4 (18 % vs 50%) p = 0.006; Fig. 4). The result was not improved if TIM1 grade 3 only was compared with TIM1 grades 0 to 2 (12.5% vs 43%) respectively; p = 0.03).

Further comparison of patients with TIM1 grade 3 who were treated with thrombolytic agents (“early” reperfusion) and those treated conventionally (“late” reperfusion) showed that 4 of 32 (12.5 % ) and 3 of 12 (25% ) patients demonstrated late potentials, respectively, an insignificant trend in favor of “early” reperfusion (Fig. 5). By stepwise logistic regression analysis, all of the beneficial effects of thrombolysis on prevention of late potentials were explained by reperfusion or patency. After accounting for the effects of reperfusion/patency, no significant residual effect of thrombolysis was observed (p = 0.77).

Odds ratio for late potentials with thrombolysislreper- fusion. The odds ratio for developing a late potential was 0.39 for thrombolysis (group 1) versus no thrombolysis (group 2) (p = 0.048) and 0.22 for reperfusion

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0 THROMBOLYTIC CONVENTIONAL

(N&) (N=47)

TYPE OF TREATMENT F.ig. 3. Comparison of incidence of late potentials between patient groups treated with and without thrombolysis.

(group 3, TIM1 grades 2 and 3) versus no reperfusion (group 4, TIM1 grades 0 and 1) (p = 0.006).

DISCUSSION Study summary and perspective. The use of throm-

bolytic agents reduces the mortality rate after infarction,‘-5 but the mechanisms of this benefit con- tinue to be debated, potentially including improve- ments in both mechanical (systolic and diastolic effects) and electrical function. In this study of postinfarction patients, we have shown that thrombolysis reduces the incidence of late potentials, con- firming some recently published results 20-27 and contradicting others. 28 Furthermore, we have shown that this favorable effect relates to patency of the infarct-related artery. Thus, by establishing patency, thrombolytic therapy may also prevent the development of an abnormal electrophysiologic milieu after myocardial infarction. The mechanism by which thrombolysis decreases late potentials is not specif- ically known. However, it appears likely that reperfusion itself might be the key factor, mediated by various mechanisms that could affect the electrical properties of the heart, 36-38 which in turn suppress the appearance of ventricular late potentials. These effects appear to occur rapidly. Results of a prelim- inary study suggest that the signal-averaged ECG may be helpful in the prompt recognition of myocardial reperfusion in patients with acute myocardial infarction after treatment with thrombolytic agents.20 In our study the correlation of a decreased incidence of late potentials with thrombolytic therapy was good. When the incidence of late potentials

60 1

GRADE O-l GRADE 2-3 (N=26) (N=56)

TIMI GRADE CLASSIFICATION Fig. 4. Comparison of incidence of late potentials between patients groups with patent (TIM1 grades 2 and 3) and nonpatent (TIM1 grades 0 and 1) infarct-related coronary arteries.

EARLY LATE (N=32) (N=12)

TIME OF REPERFUSION Fig. 5. Incidence of late potentials by presumed timing of reperfusion. Late potentials tended to occur less often after “early reperfusion” (defined as patency achieved after thrombolysis in thrombolysis-treated patients) than “late reperfusion” (defined as patency achieved spontaneously in conventionally treated patients).

was correlated with patency of the infarct vessel, a more significant association was observed between decreased incidence and patent vessels. Stepwise logistic regression analysis further demonstrated that all of the beneficial effect of thrombolysis on prevention of late potentials was explained by reperfusion or patency. Our results tilt the balance toward a pos-

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American Hean Journal

itive association between decreased incidence of late potentials and thrombolysis and patencylreperfu- sion. They further underscore the need for studies (preferably larger, better controlled, cooperative efforts) that would recommend standardized defini- tions, equipment, methodology, and criteria for late potentials.

Incidence and definition of late potentials. The incidence of late potentials in our study, both in patients treated with thrombolysis and conventionally treated patients (22 % and 43 % , respectively), is greater than that of Gang et a1.20 (5 96 and 23%) respectively) or Zimmerman et a1.27 (10 % and 24 9; , respectively), in spite of the stricter quantitative criteria for the presence of late potentials that we used. This may be due in part to the inclusion of patients who have had a previous infarction in our study, whereas those patients were excluded in the other two studies. The criteria for detecting late potentials, as well as the difference in filter settings used, could also be factors. Overall, however, the conclusions of our study are quite similar to those of others. Another study28 failed to show a significant correlation between the decreased incidence of late potentials and patency of the infarct artery. That study did show a trend toward a decreased incidence of late potentials in patients treated with thrombolysis, however, and a larger series may have shown significant results.

The quantitative normal values used in our study were similar to those proposed by Kuchar et al.rO and Gomes et a1.35 The criteria for presence of a late potential used in this study were also similar to those of Chew et a1.22 and Vatterott et a1.26 (i.e., r2 of 3 defined quantitative criteria), although the normal cutoff values used were slightly different for TFQRSD and LAS40. Filtering at 40 Hz was used in this study because previous studies in which multivariate analysis was used showed this to be the most reproduc- ible signal-averaged ECG filter.sg Furthermore, greater predictive sensitivity and specificity were achieved at this filter setting.40

Timing of signal-averaged ECGs. In this study the recording of signal-averaged ECGs in 22 % of our patients was early (within 48 hours after myocardial infarction), and there was a difference between groups 1 and 2 in the time after myocardial infarction for the recording of signal-averaged ECGs. The effects of timing on the results of signal-averaged ECGs after myocardial infarction have been reported.12, 21, 41, 42 In one study Eldar et al. 21 found no difference in the incidence of late potentials between conventionally treated and thrombolysis-treated patients in the first 1 to 2 days after myocardial infarction, and later recording of the signal-averaged ECG improved the

chances of detecting a late potential. These findings were confirmed by Strasberg et a1.42 On the other hand, Gang et a1.20 showed that signal-averaged ECGs obtained within 48 hours after myocardial infarction did show significant differences in the incidence of late potentials between conventionally treated and thrombolysis-treated patients. Still other studies suggest a low likelihood that late potentials recorded early during an acute infarction will disap- pear before discharge. 2, 2o These series of patients were small and differed from one another with respect to equipment, lead systems, filter setting, normal value ranges, and late potential criteria. We did not find the time of signal-averaged ECG recording to be problematic in our study, because when the analysis involved only patients who had signal-averaged ECGs >2 days after myocardial infarction, a similar incidence of late potentials was found. Fur- thermore, the optimal time after myocardial infarction for recording the signal-averaged ECG has not yet been agreed on either by various investigators as cited previously or by the Task Force Committee.43

Early versus late reperfusion and late potentials. Spontaneous reperfusion in patients who do not receive thrombolytic therapy may often represent a late phenomenon, that is, occurring outside the necessary time range during which reperfusion may substantially modify infarct size. In our patients with TIMI grade 3 flow, comparison of the incidence of late potentials between conventionally treated patients (“late” patency/reperfusion) and patients treated with thrombolysis within 4 hours (“early” patency/reperfusion) yielded groups of small size and did not show a significant difference. However, a positive trend is observed, associating a decreased incidence of late potentials with thrombolysis (12.5 Cc) in “early” and 2590 in “late” reperfusion). It will be interesting to see whether a significant association is observed when additional patients are studied. If so, these results would support the myocardial salvage concept to explain the relationship between patency and electrical stability, as has also been suggested by others.“O* 44

Limitations. Our study was not a randomized, pla- cebo-controlled trial of thrombolysis. However, thrombolysis is now established therapy for acute myocardial infarction, and to withhold such treatment from a control population may be viewed as unethical. Patients who received thrombolytic therapy in our study were younger than those who received conventional therapy. Most patients in the thrombolysis-treated group (74 % ) were participants in clinical trials that had protocol restrictions on age. However, no age-related association of late potential

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development after acute myocardial infarction has been described. Previous studies have in fact demonstrated by multifactorial analysis that the influ- ence of age on the presence of late potentials is not important.22~45

Conclusions. The risk of late potentials after myocardial infarction is high but is reduced by thrombolysis and by reperfusion or patent coronary artery status. Analysis of covariance showed that the effect of thrombolysis on late potentials could be entirely explained by thrombolysis-related reperfusion. Fur- thermore, the effectiveness of “early” reperfusion appears to be greater than that of “late” reperfusion but will require more study. The reduction by thrombolytic therapy of late potentials may be prognosti- tally important with respect to future arrhythmic events in patients after myocardial infarction and a mechanism of therapeutic benefit. Future studies, preferably large cooperative efforts, which are well controlled and standardized with respect to equipment, methodology, and late potential criteria and assess long-term outcome, will be of interest to con- firm and expand on these observations.

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Thrombolysis-related early patency reduces ECG late potentials after acute myocardial infarction