Author + information
- Received October 21, 1998
- Revision received March 4, 1999
- Accepted April 9, 1999
- Published online August 1, 1999.
- Domien J Engelen, MDa,* (, )
- Anton P Gorgels, MDa,
- Emile C Cheriex, MDa,
- Ebo D De Muinck, MDa,
- Anton J Oude Ophuis, MD∗,
- Willem R Dassen, PhDa,
- Jindra Vainer, MDa,
- Vincent G van Ommen, MDa and
- Hein J Wellens, MD, FACCa
- ↵*Reprint requests and correspondence: Domien J.M. Engelen, Department of Cardiology, University Hospital Maastricht, Box 5800, 6202 AZ, Maastricht, The Netherlands
The study assessed the value of the electrocardiogram (ECG) as predictor of the left anterior descending coronary artery (LAD) occlusion site in relation to the first septal perforator (S1) and/or the first diagonal branch (D1) in patients with acute anterior myocardial infarction (AMI).
In anterior AMI, determination of the exact site of LAD occlusion is important because the more proximal the occlusion the less favorable the prognosis.
One hundred patients with a first anterior AMI were included. The ECG showing the most pronounced ST-segment deviation before initiation of reperfusion therapy was evaluated and correlated with the exact LAD occlusion site as determined by coronary angiography.
ST-elevation in lead aVR (ST↑aVR), complete right bundle branch block, ST-depression in lead V5 (ST↓V5) and ST↑V1>2.5 mm strongly predicted LAD occlusion proximal to S1, whereas abnormal Q-waves in V4–6 were associated with occlusion distal to S1 (p = 0.000, p = 0.004, p = 0.009, p = 0.011 and p = 0.031 to 0.005, respectively). Abnormal Q-wave in lead aVL was associated with occlusion proximal to D1, whereas ST↓aVLwas suggestive of occlusion distal to D1 (p = 0.002 and p = 0.022, respectively). For both the S1 and D1, inferior ST↓ ≥1.0 mm strongly predicted proximal LAD occlusion, whereas absence of inferior ST↓ predicted distal occlusion (p ≤ 0.002 and p ≤ 0.020, respectively).
In anterior AMI, the ECG is useful to predict the LAD occlusion site in relation to its major side branches.
In acute anterior myocardial infarction (AMI), the site of occlusion in the left anterior descending (LAD) coronary artery is related to the extent of the myocardial necrosis and prognosis (1–5). Electrocardiographically, anterior myocardial infarction is classified as anteroseptal, anterolateral and apical (6). With a few exceptions, such as the study of Ideker et al. (7), most studies show poor correlation between the electrocardiogram (ECG) and the exact extent of myocardial involvement as determined by autopsy (8,9). In the present descriptive study, we assessed the value of the ECG to predict the occlusion site of the LAD in relation to the first septal perforator (S1) and/or the first diagonal branch (D1).
One hundred consecutive patients admitted to the coronary care unit of the University Hospital Maastricht with the diagnosis of anterior AMI, defined as chest pain lasting more than 30 min accompanied by ST-segment elevation (ST↑) ≥ 2.0 mm in V2 and V3 (ST↑v2–3), were studied. In 98 patients AMI was confirmed enzymatically. The remaining two patients were treated for AMI but did not show an enzyme rise because of early reperfusion (one after thrombolysis and the other after primary percutaneous transluminal coronary angioplasty). Patients with complete left bundle branch block, left ventricular hypertrophy (Sokolow index), ECG signs of an old MI or previous cardiac surgery were excluded.
This study was approved by the institutional ethics committee, and informed consent was obtained in all patients.
All patients underwent coronary angiography: 89 patients during the acute phase (70 of 89 after thrombolytic therapy) and eleven patients 3 to 14 days after the acute episode (10 of 11 after thrombolytic therapy). In the latter 11 patients, immediate angiography was planned but logistically not possible. The severity of the stenosis was graded by using the CAAS II (Coronary Angiogram Analyzing System II, Pie Medical, Maastricht, The Netherlands ). The culprit lesion in the LAD was defined as the most severe and/or that lesion with local dissection or thrombus and was related to the take-off of S1 and D1. Flow over the culprit lesion was graded using Thrombolysis in Myocardial Infarction Trial (TIMI) criteria (11)and collateral circulation was classified according to Rentrop et al. (12). The presence of a wrap-around LAD (partially supplying the left ventricular inferior wall) was also assessed.
The MAC VU electrocardiograph (Marquette Medical Systems, Milwaukee, Wisconsin) with a frequency range of 0.01 to 150 Hz was used. In the acute phase, every 10 min a 12-lead ECG was recorded and also whenever the clinical condition changed. The one showing the most pronounced ST-segment deviation before start of reperfusion therapy was evaluated. The TP-segment was used as the iso-electric line; the PR-segment was used when the T-wave and the P-wave merged. The J-point was determined for each lead independently. Using electronic vernier calipers (Mitutoyo, Kawasaki-Shi, Japan), both ST↑ and ST-segment depression (ST↓) were measured at the J-point in all leads (1 mm = 0.1 mV). The accuracy of these calipers is ±0.02 mm, and in practice we measured with an accuracy of 0.1 mm. Although this system is semi-automatic, the accuracy of our measurements was clearly higher than usual in clinical practice.
Besides ST-segment deviation, the incidence of complete right bundle branch block (cRBBB) and abnormal Q-waves on the acute ECG was assessed (13).
The data were analyzed using SPSS 7.0 for Windows (SPSS Inc., Chicago, Illinois). Data were expressed as median plus minimum and maximum for continuous variables and as rates (%) for categorical variables. For comparison of continuous variables, the Mann-Whitney Utest was used. For comparison of categorical variables, the chi-square test or the Fisher exact test was used. A probability value <0.05 was considered statistically significant.
The S1 may have its take-off from the LAD proximal to the D1 and in other patients distal to the D1. The culprit lesion was proximal to both S1 and D1 in 31 patients, proximal to S1 and distal to D1 in 11 patients, distal to S1 but proximal to D1 in 10 patients and distal to both S1 and D1 in 48 patients. For correlation with the ECG, patients were divided into those with LAD occlusion proximal (31 + 11 = 42) or distal to S1 (10 + 48 = 58), respectively. The analysis was thereafter repeated in the same group of patients, but this time the patients were allocated to subgroups based on the site of occlusion in relation to D1: patients with LAD occlusion proximal (31 + 10 = 41) or distal to D1 (48 + 11 = 59), respectively.
Demography and clinical data
The baseline characteristics of the patients are listed in Table 1. Subgroups were comparable with regard to gender, mean age and the time delay between onset of chest pain and recording of the ECG. When the culprit lesion was proximal to either S1 or D1, the peak serum creatine kinase was significantly higher.
Between proximal and distal lesions, there were no differences regarding the presence of single-, two- and three-vessel disease or a wrap-around LAD (Table 1). One patient had left main stenosis. No significant differences regarding TIMI or Rentrop flow grade were found. Angiographic signs of thrombus were present in 47 patients.
ECG predictors of LAD occlusion proximal to S1
ST↑aVRwas present in 43% of the occlusions proximal to S1 and in only 5% of the occlusions distal to S1 (p = 0.000). The amount of ST↑ was small, the median being 0.4 (0.2 to 1.8) mm (Table 2, Figs. 1 and 2). ⇓⇓
ST-segment depression in leads II, III and aVF was present in 74%, 86% and 91% of the occlusions proximal to S1, and in 33%, 66% and 55% of the occlusions distal to S1, respectively. In proximal occlusions, the amount of ST↓ was significantly higher: 0.9 (0.2 to 4.5) versus 0.4 (0.2 to 0.9) mm, 1.9 (0.2 to 7.7) versus 0.9 (0.2 to 4.0) mm and 1.3 (0.2 to 6.2) versus 0.6 (0.2 to 2.5) mm, for leads II, III and aVF, respectively (p = 0.000, p = 0.002 and p = 0.008). Inferior ST↓ ≥ 1.0 mm was highly predictive of LAD occlusion proximal to S1 (p ≤ 0.002).
cRBBB was registered in six patients. In all of them, the culprit lesion was situated proximal to S1.
A similar number of patients with either an occlusion proximal or distal to S1 had ST↑V1(88% vs. 86%), although the amount of ST↑ was significantly higher in patients with the LAD occluded proximal to S1: 1.2 (0.2 to 5.1) versus 0.6 (0.2 to 2.5 mm; p = 0.004). ST↑V1> 2.5 mm was only present in LAD occlusion proximal to S1, but the sensitivity of this criterion was very low. In occlusions proximal to S1, the amount of ST↑V2was significantly higher: 4.9 (0.9 to 12.2) versus 3.2 (0.3 to 13.5 mm; p = 0.001). However, no cut-off points were found to discriminate between proximal and distal LAD lesion. No relation was found between the sum of ST↑ in the precordial leads (ΣST↑V1–V4or ΣST↑V1–V6) and the occlusion site.
ST↓V5was very specific for LAD occlusion proximal to S1: it was present in 17% of the proximal lesions and only in 2% of the distal lesions (p = 0.009). The median ST↓ in the former group was 0.5 (0.2 to 2.9) mm.
ECG predictors of LAD occlusion proximal to D1
Considering the location of the culprit lesion in relation to D1, ST↓ in leads II, III and aVF was present in 73%, 95% and 90% of the proximal and in 34%, 59% and 56% of the distal lesions, respectively. In proximal LAD disease, inferior ST↓ was significantly more: 0.9 (0.2 to 4.5) versus 0.5 (0.2 to 1.6) mm, 1.7 (0.2 to 7.7) versus 0.9 (0.2 to 4.6) mm, 1.3 (0.2 to 6.2) versus 0.4 (0.2 to 2.2) mm for leads II, III and aVF, respectively (p = 0.001, p = 0.005 and p = 0.001). Inferior ST↓ ≥ 1.0 mm was also highly predictive of LAD occlusion proximal to D1 (p = 0.000). (See Table 2, Figs. 1 and 3.) ⇓
An abnormal Q-wave in lead AVL (QaVL; width ≥30 ms) was more frequent in LAD occlusion proximal to D1 in comparison with distal occlusion (44% vs. 15%; p = 0.002).
The ST↑ in leads I and aVL was present in 83% of the LAD lesions proximal to D1 but also in 61% of the distal lesions (p = NS). The amount of ST↑aVLwas significantly higher in proximal occlusion: 1.2 (0.3 to 5.2) versus 0.5 (0.2 to 4.6 mm; p = 0.006). However, no cut-off point was found to discriminate between proximal and distal disease.
ECG predictors of LAD occlusion distal to S1
Absence of inferior ST↓, particularly in leads II and aVF, was strongly related to LAD disease distal to S1. Except for one, all patients without inferior ST↓ had a wrap-around LAD. (Table 3, Figs. 3 and 4.) ⇓
Q-waves in V4 (width ≥ 20 ms), V5 (width ≥ 30 ms) and V6 (width ≥ 30 ms) were rather specific for LAD occlusion distal to S1 and were found in 55%, 24% and 17% of the occlusions distal to S1 and in only 31%, 7% and 0% of the proximal occlusions (p = 0.015, p = 0.031 and p = 0.005).
ECG predictors of LAD occlusion distal to D1
Absence of inferior ST↓, particularly in lead III, was also strongly related to LAD disease distal to D1. (See Table 3, Figs. 2 and 4). Also, ST↓aVLwas rather specific for occlusion distal to D1. The amount of ST↓ was 0.3 (0.2 to 1.1) mm.
This article describes several new findings regarding the electrocardiographic prediction of the LAD occlusion site in anterior AMI (Table 4). Lead aVR was found to be very useful to identify LAD occlusion proximal to S1. Besides ST↑aVR, both cRBBB, ST↓V5and ST↑V1> 2.5 mm were strongly predictive of LAD occlusion proximal to S1, whereas abnormal Q-waves in V4 through V6 were indicative of occlusion distal to S1. Considering the LAD occlusion site in relation to D1, an abnormal Q-wave in lead aVL was suggestive of proximal occlusion, while ST↓ in the same lead was associated with distal occlusion. For both S1 and D1, marked ST↓ in the inferior leads predicted proximal occlusion, whereas absence of inferior ST↓ predicted distal occlusion.
ST-elevation in lead aVR
ST↑aVRin unstable angina in three-vessel or left main stem disease has previously been reported (14). However, we did not find literature on ST↑aVRas an indicator to localize ischemia of the left ventricular anterior wall. In the only two articles on ST↑aVRin the setting of ischemia in the perfusion area of the LAD, ST↑aVRwas not used to define the exact LAD occlusion site in relation to the major side branches (15,16). Kataoka et al. (17)found that in anterior AMI, ST↑ in the right precordial leads was associated with LAD occlusion proximal to S1, but the ST-segment in lead aVR was not mentioned. When present, the amount of ST↑aVRis usually small (<1 mm), particularly when measured at the J-point and not 40 to 80 ms thereafter. Therefore, in this selected population with anterior AMI, any ST↑aVRis associated with LAD occlusion proximal to S1 and is probably the result of transmural ischemia of the basal part of the septum (injury current directed toward the right shoulder). This theory is supported by our finding that none of the 10 patients with LAD occlusion proximal to D1 but distal to S1 showed ST↑aVR. ST↑aVRwas absent in 57% of the occlusions proximal to S1. The reason for the rather low sensitivity of this ECG criterion may be due to the rare dominance of the basal septum, being needed for this criterion to become positive, because of the counter balance of the septal ischemia current by ischemia in other large areas of the left ventricle perfused by the LAD such as the lateral and apical inferior wall.
ST-deviation in leads II, III and/or aVF
The amount of inferior ST↓ was significantly higher in proximal LAD disease, and particularly ST↓ ≥ 1.0 mm was highly predictive of a proximal LAD lesion. This finding is consistent with previous studies on inferior ST↓ in anterior AMI (18,19). Inferior ST↓ was not associated with disease of the right coronary artery. This supports the theory that inferior ST↓ in anterior AMI represents reciprocal changes associated with transmural ischemia in the high anterobasal region (20,21). Despite the presence of a wrap-around LAD and thereby transmural ischemia in a part of the inferior left ventricular wall, almost all occlusions proximal to D1 still showed inferior ST↓. The most likely explanation for this finding is the magnitude of the ischemia current produced by the transmural ischemia of the anterobasal wall exceeding the current of the inferior wall. Consequently, besides a wrap-around LAD, a more distally occluded LAD is thought to be a prerequisite of an iso-electric or even elevated ST-segment inferiorly. Indeed, in 90% of the patients without inferior ST↓ (defined as absence of ST↓ in ≥2 inferior leads) the culprit lesion was situated distally to D1, and in all but one (97%) of the patients without inferior ST↓ the coronary angiogram revealed a wrap-around LAD. Similar findings were recently published by other investigators (22–24). In addition, a recent study by Porter et al. (25)showed that the presence of lead III ST↓ with a positive T-wave associated with ST↑aVLcould serve as an early ECG marker of pre-diagonal occlusion of a wrap-around LAD.
ST-deviation in leads I and/or aVL
In the individual patient, ST↑ in the lateral leads did not discriminate between occlusions proximal and distal to D1: ST↑aVLwas not only present in 83% of the LAD occlusions proximal to D1, but also in 66% and 47% of the occlusions distal to D1 and D2, respectively. In contrast, ST↓aVLwas rather specific for LAD occlusion distal to D1 and probably represents reciprocal changes associated with transmural ischemia in the inferoapical region: 6% of the patients with and 43% of the patients without inferior ST↓ showed ST↓aVL, respectively (p = 0.000). The ST-segment shift in aVL could not be explained by the presence or absence of an anterolateral branch.
ST-deviation in leads V1–V6
In 57% and 23% of the patients showing an ECG pattern traditionally termed “anteroseptal infarction” (ST↑V1–V3), the LAD occlusion was located distal to the first and second septal perforator, respectively. This is in agreement with the study by Shalev et al. (26). Analyzing the ST-deviations in leads V1 thru V4, ST↑V1>2.5 mm was the only ECG parameter that could be defined to discriminate between proximal and distal LAD occlusion in the individual patient. Furthermore, ST↓V5appeared to be very specific for LAD occlusion proximal to S1. The occurrence of ST↓V5was interpreted as reciprocal changes associated with transmural ischemia high in the anteroseptal area. Although ST↓V6was seen more often in proximal LAD disease, this difference was not significant.
Complete right bundle branch block
The development of cRBBB in anterior AMI is an independent marker of poor prognosis (27). This is primarily considered to be due to extensive myocardial damage rather than the conduction disorder itself. Only if cRBBB comes together with left anterior hemiblock is there an increased risk for progression into complete AV-block (28). In our study, cRBBB was registered exclusively in LAD occlusions proximal to S1. As S1 is the main blood supply to the distal part of the bundle of His and the proximal bundle branches, the cRBBB is most likely acquired in the setting of anterior AMI.
Abnormal Q waves
In leads V4, V5 and V6, Q waves were rather specific for LAD disease distal to S1. In distal LAD disease, normal activation of the ventricles starting in the interventricular septum and spreading transversely from left to right through the septum usually remains intact. In case of myocardial necrosis beneath the anterolateral leads, the septal vector in (V5)V6 will facilitate Q-wave formation in those electrodes. In contrast, in proximal to S1 occlusion the septal vector will decrease or even disappear and thereby hinder Q-wave formation. The Q-waves occurred already early after onset of AMI and may indicate local conduction delay rather than necrosis.
The ECG signs described in this study may prove useful in defining the site of LAD occlusion in relation to S1 and D1 in the setting of anterior AMI. In particular, ST↑aVRand ST-deviation in the inferior leads were found to be very helpful. We consider our findings useful in identifying patients with proximal LAD occlusion who need a more aggressive approach to revascularization to prevent extensive myocardial damage resulting in pump failure, the possible development of sub-AV-nodal conduction disturbances and the occurrence of life-threatening ventricular arrhythmias in the second and third week after AMI (29).
The number of patients studied is limited. Therefore, we are now evaluating our findings prospectively in a larger study population. Several ECGs were recorded in the acute stage, and the one showing the most pronounced abnormalities was selected for our study. Therefore, our findings may not be reproducible in a setting where fewer ECGs are recorded. Most of the study population had onset of chest pain within 4 h before the recording of the ECG, and coronary angiography allowing identification of the culprit lesion was performed in the majority of our cases shortly after admission. Thus, we cannot be certain whether our findings are applicable when patients come in later.
- acute myocardial infarction
- complete right bundle branch block
- first diagonal branch
- left anterior descending coronary artery
- abnormal Q-wave in lead x
- ST-segment elevation
- ST-segment depression
- ST-segment elevation in lead x
- ST-segment depression in lead x
- first septal perforator
- Received October 21, 1998.
- Revision received March 4, 1999.
- Accepted April 9, 1999.
- American College of Cardiology
- Gaudron P,
- Eilles C,
- Kugler I,
- Ertl G
- Jeremy R.W,
- Allman K.C,
- Bautovitch G,
- Harris P.J
- Pirolo J.S,
- Hutchins G.M,
- Moore G.W
- ISAM Study Group,
- Voth E,
- Tebbe U,
- Schicha H,
- et al.
- White H.D,
- Norris R.M,
- Brown M.A,
- et al.
- Savage R.M,
- Wagner G.S,
- Ideker R.E,
- et al.
- Rentrop K.P,
- Cohen M,
- Blanke H,
- Phillips R.A
- Karakawa M,
- Iwasaka T,
- Kamihata H,
- et al.
- Tamura A,
- Kataoka H,
- Mikuriya Y,
- Nasu M
- Quyyumi A.A,
- Crake T,
- Rubens M.B,
- et al.
- Sapin P.M,
- Musselman D.R,
- Dehmer G.J,
- Cascio W.E
- Tamura A,
- Kataoka H,
- Nagase K,
- et al.
- Lew A.S,
- Hod H,
- Cercek B,
- et al.
- Ricou F,
- Nicod P,
- Gilpin E,
- et al.
- Lie K.I,
- Wellens H.J.J,
- Schuilenburg R.M,
- et al.