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J Am Coll Cardiol, 2000; 35:127-135 © 2000 by the American College of Cardiology Foundation |
* Fondazione Maugeri, Istituto Di Ricovero E Cura A Carattere Scientifico, Veruno, Italy
Ospedale Bassini, Cinisello Balsamo, Italy
Centro Studi Associazione Nazionale Medici Cardiologi Ospedalieri, Firenze, Italy
Ospedale S. Matteo, Pavia, Italy
|| Ospedale Civile, Udine, Italy
¶ Ospedale Civile, Pordenone, Italy
# Ospedale Civile, S.Vito al Tagliamento, Italy
** Ospedale Civile, Rho, Italy
Ospedale Civile, Vasto, Italy
Ospedale Cervello, Palermo, Italy
Manuscript received March 15, 1999; revised manuscript received July 8, 1999, accepted September 10, 1999.
Reprint requests and correspondence: Dr. Enzo Bosimini, "Salvatore Maugeri" Foundation, IRCCS; Division of Cardiology, Via Revislate, 13; 28010 Veruno (NO), Italy
ebosimini{at}fsm.it
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Abstract |
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The aim of this study was to describe the electrocardiographic (ECG) evolutionary changes after an acute myocardial infarction (AMI) and to evaluate their correlation with left ventricular function and remodeling.
BACKGROUND
The QRS complex changes after AMI have been correlated with infarct size and left ventricular function. By contrast, the significance of T wave changes is controversial.
METHODS
We studied 536 patients enrolled in the GISSI-3-Echo substudy who underwent ECG and echocardiographic studies at 24 to 48 h (S1), at hospital discharge (S2), at six weeks (S3) and six months (S4) after AMI.
RESULTS
The number of Q waves (nQ) and QRS quantitative score (QRSs) did not change over time. From S2 to S4, the number of negative T waves (nT NEG) decreased (p < 0.0001), wall motion abnormalities (%WMA) improved (p < 0.001), ventricular volumes increased (p < 0.0001) while ejection fraction remained stable. According to the T wave changes after hospital discharge, patients were divided into four groups: stable positive T waves (group 1, n = 35), patients who showed a decrease 
1 in nT NEG (group 2, n = 361), patients with no change in nT NEG (group 3, n = 64) and those with an increase 1 in nT NEG (group 4, n = 76). The QRSs and nQ remained stable in all groups. Groups 3 and 4 showed less recovery in %WMA, more pronounced ventricular enlargement and progressive decline in ejection fraction than groups 1 and 2 (interaction time x groups p < 0.0001).
CONCLUSIONS
The analysis of serial ECG can predict postinfarct left ventricular remodeling. Normalization of negative T waves during the follow-up appears more strictly related to recovery of regional dysfunction than QRS changes. Lack of resolution and late appearance of new negative T predict unfavorable remodeling with progressive deterioration of ventricular function.
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Evolutionary T wave changes after AMI are attributed to abnormal prolongation of ventricular action potential in the regions adjacent to the necrotic area, so that the degree of prolonged repolarization may influence T wave voltage and polarity (8). In the setting of unstable angina, persistently negative T waves may identify the presence of viable but abnormally functioning myocardium (9). During the acute phase of myocardial infarction, the degree of T wave inversion may be indicative of the presence of a large amount of stunned myocardium (10,11). However, the clinical significance of evolutionary T wave changes after AMI is poorly understood. Actually, myocardial infarction results in complex alterations in ventricular architecture involving both the infarcted and noninfarcted zones, often referred to as "ventricular remodeling" (12). The interrelation between infarct size, scar formation and dysfunctioning but viable and normal adjacent myocardium generates different local electrical fields that may be responsible for the evolutionary surface ECG changes over time. However, the relationship between ECG changes and ventricular remodeling after AMI has been poorly investigated.
Accordingly, the purposes of our study were: 1) to describe the evolutionary changes in QRS and T waves between the acute phase of myocardial infarction and the following six months and 2) to investigate the correlation between ECG changes and left ventricular function and remodeling in a subset of patients enrolled in the GISSI-3 Echo substudy.
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Methods |
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The protocol was approved by the local Ethics Committee. Patients were clearly informed, and a consent statement was requested about their participation in the trial after they had recovered from the acute phase.
ECG data..
Standard 12-lead electrocardiograms were recorded at 25-mm/s paper speed and calibrated at 1.0 mV/10 mm in the same settings for the echocardiographic study. Analysis of electrocardiograms was performed at the core laboratory using a computerized off-line system that at each lead (excluding avR) calculated the duration and voltage of the P,Q,R,S waves and the voltage of T waves from baseline to apex. The isoelectric line was obtained for each lead from three points identified in the PQ or PR segment. All measurements were obtained by the same operator (E.B.), and the following variables were derived: the number of Q waves at 12-lead electrocardiogram (nQ) 30 ms, the QRS score (QRSs) as elaborated by Selvester et al. (14) and later modified by Wagner and Palmeri (15,16) and the number of negative T waves (nT NEG) excluding aVr and V1 leads. T waves (either symmetric or byphasic) were considered negative when the negative amplitude was at least 0.1 mV.
Echocardiographic study.
Echocardiographic data were obtained using commercially available instruments. Images were recorded in real time on VHS 0.5-in. videotapes to permit real-time and slow-motion playback review and quantitative analysis. In each patient, multiple views were recorded in the parasternal long and short axis, apical four-chamber, apical two-chamber, apical long- and short-axis planes and subcostal long- and short-axis planes (17). Short-axis views were recorded at basal (mitral valve level), middle (papillary muscle level) and apical position. All two-dimensional echocardiograms were submitted to the core laboratory at the Research Centre of the National Association of Hospital Cardiologist (Associazione Nazionale Medici Cardiologi Ospedalieri [ANMCO]) in Florence for a centralized assessment of technical quality and suitability for quantitative analysis. The definition of a technically acceptable echocardiogram was one that allowed visualization of all myocardial segments from at least two complementary or orthogonal views and the assessment of both endocardial motion and thickening of the myocardium. For wall motion analysis, a 16-segment model was used, and each myocardial segment was scored using the semiquantitative visual grading system proposed by the American Society of Echocardiography (1 = normal, 2 = hypokinetic, 3 = akinetic, 4 = dyskinetic, 5 = aneurismal) (18). Videotape analysis was performed centrally by three expert investigators (G.LN., F.G., P.L.T.) unaware of patients’ clinical, ECG or angiographic data, who assigned the wall motion score at echocardiographic study by consensus. A percentage of wall motion abnormalities (%WMA), as an index of the extent of left ventricular ischemic damage, was obtained by dividing the number of akinetic, dyskinetic and aneurysmal segments by the total number of segments evaluated. The myocardial infarction was arbitrarily defined as "large" when the asynergy extent included five or more segments in a 16-segment model of left ventricle (%WMA 31.25%). Inter- and intraobserver reproducibility in assessing the wall motion score has been previously reported (19) and was 89% and 93%, respectively.
Echocardiographic images were then transferred to the hard disk of an imaging off-line computer analysis system (Tomtec-Freeland Medical, Louisville, Colorado) and digitized to obtain endocardial contours and left ventricular cavity areas at end diastole and end systole from two apical orthogonal views (the four-chamber and either the apical long-axis or apical two-chamber view). The modified Simpson rule was used to obtain left ventricular volumes, and ejection fraction was derived from the standard equation. All measurements were obtained in blinded fashion by a single experienced operator (P.L.T.) from three cardiac cycles, and the mean value was considered for analysis and corrected for body surface area to obtain volume index. Intraobserver variability in the evaluation of end-diastolic and end-systolic volumes by quantitative analysis was 2.6 ± 2% and 3.7 ± 3%, respectively.
Statistical analysis. Changes in both ECG and echocardiographic measurements over time were assessed using two-way repeated measures analysis of variance, with time being the "within-subjects" variable. Different trends over time between groups were assessed by evaluating the interaction term in the model. Correlation between parameters were evaluated using Pearson’s linear regression analysis. Results are reported as the mean value ± SD. In all the tests used, the significance level was defined as p < 0.05.
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Results |
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ECG changes and left ventricular remodeling. Evolutionary ECG and echocardiographic changes during the six-month period of the study are reported in Table 1. At S1, mean QRSs and nQ were 5 ± 3 and 2 ± 1, respectively, and they did not show any significant variation over time. The number of negative T waves increased at S2 (from 3.2 ± 2 to 3.5 ± 2), and thereafter it decreased to 1.9 ± 1 at six months (time effect p < 0.001) (Table 1). The percentage of the extent of wall motion abnormalities progressively decreased from 26 ± 14 at S1 to 20 ± 15 at S4 (time effect: p < 0.001). Despite this significant reduction of regional dysfunction, left ventricular end-diastolic volume index and left ventricular end-systolic volume index progressively increased from 80 ± 20 and 43 ± 16 at S1 to 87 ± 26 and 48 ± 21 ml/m2 at S4, respectively (time effect: p < 0.0001), while ejection fraction did not change over time (from 47 ± 8% to 46 ± 9%, NS) (Table 1).
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31.25% (arbitrarily defined as large AMI) compared with patients with %WMA <31.25% (arbitrarily defined as small AMI) (interaction time x groups: p < 0.00001; Table 2). The decrease in %WMA over time was more evident in patients with large AMI (interaction time x groups: p < 0.00001), while ejection fraction, which was significantly lower in large than in small AMIs, did not change over time in either group (interaction time x groups: NS; Table 2). As expected, patients with 31.25 %WMA showed greater values of nQ, QRSs and nT NEG than patients with <31.25 %WMA (Table 3 ), but the correlation between left ventricular volumes, %WMA, ejection fraction and ECG changes were weak, although statistically significant (p < 0.001) at each time of the study (the coefficient of correlation ranging from 0.01 to 0.46, with the higher values at six months). In both groups with large and small AMI, QRSs and nQ remained stable during the follow-up (time effect, NS), while nT NEG, after an initial increase from S1 to S2, progressively decreased to S4 (interaction time x groups: p = 0.003109, Table 3).
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1 decrease in nT NEG in 144 (27%), persistently negative T waves with no change in nT NEG in 113 (21%) and a 1 increase in nT NEG in 246 (46%). These groups with different patterns of in-hospital evolutionary T wave changes showed similar trends in ventricular dilation and recovery of regional dysfunction with no change in ejection fraction over time.
We then analyzed the T wave changes after hospital discharge. From S2 to S4, 35 (7%) patients showed persistently positive T waves (group 1), 361 (67%) patients had a 1 decrease in nT NEG (group 2), 64 (12%) showed no change in nT NEG (group 3) and 76 (14%) demonstrated a 1 increase in nT NEG (group 4). At hospital discharge, patients in group 4 had slightly higher values of nQ and QRSs than patients in the other groups (Fig. 1 ), associated with larger end-diastolic volume index and end-systolic volume index, more extensive %WMA and lower ejection fraction (Fig. 2). The nQ and QRSs did not change over time in any group (Fig. 1). During the follow-up, patients in groups 1 and 2 had more evident %WMA recovery and less pronounced left ventricular dilation, with no substantial changes in ejection fraction. Conversely, group 3 and especially group 4 showed less recovery in %WMA, more pronounced ventricular enlargement and a progressive decrease in ejection fraction (interaction time x groups: p = 0.000026 for end-diastolic volume index, p < 0.00001 for end-systolic volume index, p = 0.024582 for %WMA and p = 0.000582 for ejection fraction)(Fig. 2).
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Discussion |
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ECG changes and asynergy correlation. Numerous studies comparing 12-lead ECG and pathologic findings or %WMA have shown the reliability of QRS abnormalities in diagnosing myocardial infarction, though some limitations of the electrocardiogram in recognizing the exact location and extent of necrosis have been highlighted (23–25). With the QRS scoring system proposed by Selvester et al. (14) and later modified by Wagner and Palmeri (15,16), a good correlation has also been reported between ECG findings and ventricular function as expressed by ejection fraction (7,26,27). However, these initial results have not been confirmed by other studies, which found only modest correlation between QRS score, asynergy and ejection fraction in the postacute phase of AMI (28,29). In addition, no clear evidence of correlation between negative T waves and the extent of the infarcted area has been reported. In the present study, patients with more extensive %WMA (larger AMI) also had more relevant electrocardiogram changes in terms of greater values of nQ, QRS score and nT NEG; however, the correlation between ECG variables and left ventricular volumes, %WMA and ejection fraction during the first six months after infarction, though better in the late follow-up than during the hospital phase, were poor.
The discrepancy between electrocardiogram and asynergy extent may have several explanations. First of all, the assessment of %WMA tends to overestimate the true infarcted area (30). Indeed, asynergy includes not only transmural and nontransmural necrosis (31), but also stunned or hibernated viable myocardium (32). The significant reduction of %WMA observed in our population underlines the important role of dysfunctioning viable myocardium in the assessment of left ventricular asynergy after AMI. Although recovery of regional dysfunction may continue well after the first six months (4), we can speculate that the observed asynergy late after AMI (when the functional recovery of postischemic viable myocardium has been almost completed) is more expressive of the total necrotic tissue than that occurring during the acute or postacute phases, as indicated by the improvement of correlation between ECG QRS changes and %WMA we observed at six months. Another important factor in determining variability may be the different spatial relations between a fixed recording system (standard 12-lead electrocardiogram) and the heart, a structure with a varying position in the thorax. In addition, left ventricular dilation induced by AMI is not uniform, and represents another important variable that greatly influences the relationship between the electrocardiogram and the heart (25).
ECG changes and left ventricular remodeling. Previous studies have demonstrated a partial or complete recovery of QRS complex during different follow-up periods after AMI (3,4). Six months to six years was indicated as the time required for QRS resolution, with few changes reported to occur before or after this time interval (4). The resolution of QRS complex changes has been attributed to the "healing" process of the infarcted area resulting in retraction of the scar tissue associated with hypertrophy of adjacent myocardium (33), and it has been considered indicative of preserved left ventricular function (34). In fact, in patients not treated with reperfusion therapies, without reinfarction or revascularization procedures, the improvement of the QRS complex changes at four-year follow-up was associated with a parallel resolution of both regional and global left ventricular dysfunction, possibly related to late spontaneous reperfusion (4). Therefore, it has been hypothesized that early reperfusion accelerating the healing process and the recovery of left ventricular dysfunction may also facilitate the resolution of the QRS changes (4). The majority of patients in our study were treated with thrombolytic agents, and yet the QRS complex changes remained stable from 24 to 48 h to six months after AMI, despite the progressive recovery of regional function. This finding indicates that QRS abnormalities (nQ and QRSs) induced by AMI do not predict the functional recovery and ventricular enlargement that occur during the first six months after infarction.
The significance of the evolutionary T wave changes after infarction has still not been clarified. In patients with successful reperfusion, the degree of T wave inversion within three days of AMI was reported to be predictive of a large amount of stunned myocardium in the chronic phase (35). Similarly, persistently inverted T waves in the setting of unstable angina and in the absence of documented myocardial infarction identified patients with viable but abnormally functioning myocardium (9). By contrast, in a recent pathologic study (10) persistent negative T waves in the chronic stage of infarction were indicative of transmural infarction with a thin fibrotic layer, whereas positive T waves were indicative of nontransmural infarct containing viable myocardium.
In our study, two different trends in the evolutionary T waves changes were evident. During the hospital phase, from 24 to 48 h to predischarge, the majority of patients showed an increase (46%) or stability (21%) in the number of negative T waves, while during the late follow-up after discharge, a sizeable number of patients (67%) demonstrated a progressive decrease in the number of negative T waves, a finding that was again more evident in larger infarcts. The in-hospital T wave changes were not associated with different patterns of left ventricular remodeling or functional recovery during the follow-up. On the contrary, persistently positive T waves and the resolution of negative T waves at six-month follow-up were paralleled by a substantial recovery of wall motion abnormalities. The most important finding of our study, however, is that persistently inverted T waves and the appearance of new negative T waves in the late follow-up after discharge are indicative of less recovery of regional dysfunction, which results in a more pronounced ventricular enlargement and progressive decline of global ventricular function over time. Thus, our data would indicate that normalization of previously inverted T waves at serial electrocardiograms in the chronic phase of infarctions identifies functional recovery of viable myocardium; conversely, persistently inverted T waves and, more importantly, an increase in the number of negative T waves after discharge, indicates a greater myocardial damage with more extensive necrotic tissue or less viable myocardium and unfavorable left ventricular remodeling.
In conclusion, although this study focuses on patients with low-risk profiles that do not represent the whole postinfarct population, the results provide evidence that a simple analysis of serial 12-lead electrocardiograms after AMI may help identify potentially reversible damaged myocardium and subsequent left ventricular remodeling. Although the extent of regional dysfunction is poorly predictable from ECG changes, normalization of negative T waves after discharge is more strictly related to functional recovery of viable myocardium than QRS changes. Conversely, lack of resolution or an increasing number of negative T waves at late follow-up after discharge predicts more pronounced ventricular enlargement and progressive deterioration of global left ventricular function.
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Appendix |
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TopAbstractMethodsResultsDiscussionAppendixReferences |
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G. L. Nicolosi
Core ECHO Laboratories
F. Gentile, P. Giannuzzi, G. L. Nicolosi, P. L. Temporelli
Core ECG Laboratories
E. Bosimini
Scientific and organising secretariat and data management
A. P. Maggioni, D. Lucci
Participating clinical centres
Barga (M. Lunardi, A. Azzarelli); Borgosesia (P. Devecchi, F. Forni); Cagliari Brotzu (M. Putzu, A. Pani); Cagliari SS Trinità (L. Tocco, W. Boi, S. Piras); Camposampiero (P. Piovesana, F. De Conti); Casarano (F. De Santis, A. Muscella); Castellammare di Stabia (F. Russo, N. Di Martino); Catania Cannizzaro (G. Centamore, A. Milazzotto); Cava dei Tirreni (M. Agrusta); Chieti SS Annunziata (A. Di Pasquale); Cinisello Balsamo (F. Gentile, M. Ornaghi, E. Mangiarotti); Cittadella (A. Carrozza); Città di Castello (S. Misuri, G. Gambarati); Correggio (S. Bendinelli, L. Lusetti); Cosenza Civile (G. Bisignani, O. Serafini); Cuneo (F. Margaria, G. Ugliengo, F. Meinardi); Domodossola (M. Modica, M. Tessitori, F. Barba); Firenze Careggi (A. Santini); Firenze Torregalli (L. Berti, P. Stroder, G. Casolo); Galatina (G. Manca); Garbagnate Milanese (E. Cazzani, P. Di Lavore, M. Civelli); Genova (F. Chiarella, S. Domenicucci); Ivrea (G. Ronzani); Leno (S. Perotti, M. Bonaglia); Lugo (R. Mantovani); Messina Policlinico (S. Carerj, P. Grimaldi, F. Scapellato); Napoli Monaldi (P. Caso); Oristano (S. Marchi, E. Sanna); Penne (D. Di Gregorio, A. Vacri, L. Mantini); Pisa S. Chiara (E. Cabani, U. Conti); Pistoia (A. Giomi, A. Alfieri, E. Balli); Pontedera (A. Paci, G. Squarcini, M. Masini); Pordenone (P. Visentin); Ragusa (R. Licitra, C. Cintolo); Rho (J. Heyman); Roma S. Eugenio (A. Lax); Roma Fatebenefratelli (C. Peraldo Neja); Rossano (S. Salituri); Sarzana (D. Bertoli, F. Vivaldi); Scandiano (G. Gambarati); Tradate (S. Lombroso, S. Giani, D. Barbieri); Vasto (G. Di Marco, G. Levantesi, G. De Vito, E. Bottari); Venezia (L. Facchin, G. Ramuscello); Viterbo (A. Capezzuto); Voghera (P. Gandolfi, G. Bergognoni).
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Footnotes |
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1 The Investigators and Institutions participating in the GISSI-3 Echo Substudy are listed in the Appendix. 
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