- Email: [email protected]
Comparison of Angiographic Findings in Patients With Acute Anteroseptal Versus Anterior Wall ST-Elevation Myocardial Infarction
Comparison of Angiographic Findings in Patients With Acute Anteroseptal Versus Anterior Wall ST-Elevation Myocardial Infarction Henry D. Huang, MDa, Viet Tran, MDb, Hani Jneid, MDa, James M. Wilson, MDa,c, and Yochai Birnbaum, MDa,c,* Anteroseptal ST elevation myocardial infarction (AS-STEMI), in which ST elevation is limited to leads V1 to V3, is considered confined to the basal and mid anterior and septal segments, sparing the apex. In contrast, extensive anterior STEMI (EA-STEMI), in which ST elevation extends to leads V4 to V6, is considered to involve more apical segments. However, it has been reported that AS-STEMI affects mainly the apex. Others have suggested that AS-STEMI may occur in patients with extensive anterior involvement if proximal occlusion of a wrapping left anterior descending coronary artery (LAD) results in cancelation of the basal-anterior and apical injury vectors. Therefore, the aim of this study was to identify, in 97 consecutive patients with STEMI, distinct coronary angiographic characteristics that could differentiate between cases of AS-STEMI (n ⴝ 39) and EASTEMI (n ⴝ 58). Angiography was used to determine the length of the LAD, its site of occlusion, and whether there was an alternative blood supply to the apex. Patients with AS-STEMI were more likely than those with EA-STEMI to have >1 branches that reached the apex (p ⴝ 0.0015) and to have proximal LAD occlusion combined with either a short LAD or >1 large side branch (35.9% vs 12.1%, p ⴝ 0.011). However, patients with AS-STEMI were also more likely to have proximal occlusion before the first septal branch of a long LAD (35.9% vs 10.3%, p ⴝ 0.005). In conclusion, AS-STEMI can occur when only the basal and mid portions of the anterior wall are infarcted, but it can also arise when the infarction extensively involves the basal anterior and the distal inferior and apical segments. © 2011 Elsevier Inc. All rights reserved. (Am J Cardiol 2011;107:827– 832) Electrocardiography can be used to assess the size of the ischemic myocardium and the location of the infarct-related artery in acute ST elevation (STE) myocardial infarction (STEMI).1–3 In anterior STEMI (A-STEMI), electrocardiography is useful in determining the site of occlusion relative to the major side branches.4 –7 A-STEMI has been classified as anteroseptal STEMI (AS-STEMI) when STE is limited to leads V1 to V3 and as extensive A-STEMI (EASTEMI) when STE extends to leads V4 to V6 (Figure 1). However, these anatomically based terms are probably misnomers, because neither angiographic nor echocardiographic data have correlated either injury pattern with the expected location of injury.7–10 Two opposing hypotheses11,12 have been offered to explain the occurrence of these 2 distinct electrocardiographic patterns of A-STEMI: (1) AS-STEMI represents A-STEMI in which the area of infarction is relatively small because there is an alternative blood supply to the distal segments (because of the presence of either a short left anterior descending coronary artery [LAD] and/or large diagonal or obtuse marginal branches), or (2) the AS-STEMI pattern occurs in patients with large a Section of Cardiology, bDepartment of Medicine, Baylor College of Medicine; and cTexas Heart Institute at St. Luke’s Episcopal Hospital, Houston, Texas. Manuscript received August 24, 2010; revised manuscript received and accepted October 28, 2010. *Corresponding author: Tel: 713-798-2735; fax: 713-798-0270. E-mail address: [email protected] (Y. Birnbaum).
0002-9149/11/$ – see front matter © 2011 Elsevier Inc. All rights reserved. doi:10.1016/j.amjcard.2010.10.070
areas of infarction because of the proximal occlusion of a long, wrapping LAD, resulting in deceptive attenuation of the expected STE in the lateral precordial leads. In this study, we analyzed data from patients with acute A-STEMI and compared electrocardiographic patterns with coronary angiographic findings to evaluate the influence of the site of occlusion, the morphology of the LAD, and the presence of large side coronary branches on the presenting electrocardiographic pattern. Methods We studied consecutive patients who were admitted with the diagnosis of first-time, acute A-STEMI as indicated by STE at the J point in ⱖ2 adjacent precordial leads (ⱖ0.2 mV in leads V2 and V3 or ⱖ0.1 mV in the other precordial leads, V1 or V4 to V6) and by other signs of myocardial ischemia, such as chest pain and elevated cardiac markers. All patients underwent urgent coronary angiography followed by either primary percutaneous coronary intervention or emergent coronary artery bypass grafting surgery at either the Michael E. DeBakey Veterans Affairs Medical Center or St. Luke’s Episcopal Hospital in Houston, Texas. The data from the Veterans Affairs hospital were obtained from a preexisting database of 172 consecutive patients who underwent primary percutaneous coronary intervention for STEMI from 2004 to 2008. The data from St. Luke’s Episcopal Hospital came from a preexisting database that lists all patients for whom the STEMI pager had been activated www.ajconline.org
828
The American Journal of Cardiology (www.ajconline.org)
Figure 1. (A) AS-STEMI pattern. STE is limited to leads V1 to V3. (B) EA-STEMI pattern. STE occurs in leads V1 to V6, as well as in leads I and aVL.
by the hospital’s emergency department or by hospital staff members from January 2007 to August 2009. The database contained data regarding 542 consecutive patients, of whom 305 underwent cardiac catheterization and 172 underwent acute reperfusion therapy. Index electrocardiograms from these hospitalizations were selected if they showed STE with positive T waves in ⱖ2 anterior leads (V1 to V6), typical evolution consistent with acute A-STEMI on follow-up electrocardiography (i.e., a decrease in STE magnitude with T-wave inversions after primary percutaneous coronary intervention), and elevated cardiac markers that confirmed myocardial necrosis. Patients were excluded if their index electrocardiograms showed intraventricular conduction delay (left or right bundle branch block or nonspecific intraventricular conduction block), ventricular rhythms (including electronic ventricular pacing), or Wolff-Parkinson-White syndrome. Patients were also excluded if their electrocardiographic findings were consistent with partial reperfusion or an advanced stage of infarction (Q waves with negative T-waves), or if they had previously undergone coronary artery bypass grafting surgery. Patients with A-STEMI were divided into 2 groups according to their electrocardiographic characteristics. An index electrocardiogram (obtained before revascularization) that showed STEs limited to leads V1 to V3 (STE ⱖ0.1 mV in lead V1 and ⱖ0.2 mV in leads V2 and V3) was considered to indicate AS-STEMI, whereas an electrocardiogram with precordial STEs (ⱖ0.1 mV) extending to lead V4, V5, or V6 was considered to indicate EA-STEMI. Of the 289 patients with acute STEMI from the 2 hospitals, 114 patients met the inclusion criteria and were
selected for subsequent review of their coronary angiographic films. Films were primarily interpreted by 2 experienced angiographers who were blinded to each patient’s identity and group assignment (i.e., AS-STEMI or EASTEMI). A third investigator adjudicated the review of the coronary angiographic films when needed. Angiographic characteristics of interest included the location of culprit occlusion within the LAD relative to the major diagonal and septal branches, the size of the LAD (short of the apex, reaches the apex, or wraps the apex), the presence or absence of ⱖ1 large side branch (ⱖ2 mm in diameter; i.e., a large ramus intermedius, large obtuse marginal branch, or large diagonal branch proximal to site of culprit occlusion that reached the apical region of the left ventricle), initial and post–primary percutaneous coronary intervention Thrombolysis In Myocardial Infarction (TIMI) flow grade, the presence or absence of collaterals, and the number of diseased vessels (1, 2, or 3). Discrete data are presented as absolute numbers and percentages. Continuous data are presented as mean ⫾ SD. The chi-square test was used to analyze differences between discrete variables, and Student’s t test was used for continuous variables. A p value ⬍0.05 was considered statistically significant. Results Of the 114 patients initially selected according to their electrocardiographic findings, 17 were excluded for various reasons: 8 patients underwent primary percutaneous coronary intervention on a vessel other than the LAD (5 right
Coronary Artery Disease/Anteroseptal vs Anterior Wall STEMI Table 1 Demographic and clinical data
829
Table 2 Angiographic data
Variable
AS-STEMI (n ⫽ 39)
EA-STEMI (n ⫽ 58)
p Value
Men Age (years) Race White Black Hispanic Other Coronary artery disease*,† Myocardial infarction* Percutaneous coronary intervention* Diabetes mellitus*,‡ Hypertension* Hyperlipidemia*,§ Heart failure* Peak creatine kinase (U/L) Peak creatine kinaseMB (ng/ml) Peak troponin I (ng/ml) ⬍10 10–50 ⬎50
35 (90%) 63.4 ⫾ 12.0
50 (86%) 58.3 ⫾ 12.4
0.838 0.050 0.453
22 (56%) 11 (28%) 2 (5%) 4 (10%) 16 (41%)
35 (60%) 15 (26%) 6 (10%) 2 (3%) 23 (40%)
0.939
5 (13%) 12 (31%)
11 (19%) 11 (19%)
0.603 0.273
11 (28%) 24 (62%) 22 (56%) 3 (8%) 1,223 ⫾ 1816
13 (22%) 38 (66%) 30 (52%) 3 (5%) 1,794 ⫾ 2114
0.683 0.854 0.806 0.940 0.168
103 ⫾ 163
155 ⫾ 226
0.193
19 (49%) 10 (26%) 10 (26%)
13 (22%) 22 (38%) 23 (40%)
0.026
Data are expressed as mean ⫾ SD or as number (percentage). * Established diagnosis in chart or receiving medications for this condition. † History of myocardial infarction, effort-induced chest pain, or coronary angiography with documentation of coronary artery disease. ‡ Established diagnosis in chart, receiving medications for diabetes, or glycosylated hemoglobin ⱖ 6.5%. § Established diagnosis in chart, receiving lipid-modifying medications, or abnormal lipid panel ⬍24 hours after admission.
coronary artery, 1 left circumflex coronary artery, 1 with culprit lesions in the right and left circumflex coronary arteries, and 1 left main coronary artery), 4 patients did not have clear culprit lesions or significant coronary artery disease on coronary angiography, and 5 patients had missing angiographic data. Thus, 97 patients (12 women, 85 men; mean age 60.2 ⫾ 12.1 years, range 29 to 90) met all criteria and were included in the study. Baseline and demographic data are listed in Table 1. Patients with AS-STEMI tended to have lower peak creatine kinase levels and peak creatine kinase-MB levels than patients with EA-STEMI, but these differences did not reach statistical significance. The percentage of patients with peak cardiac troponin I levels ⬍10 ng/ml was greater in the AS-STEMI group than in the EA-STEMI group. Figure 1 depicts sample electrocardiograms from patients with AS-STEMI and EA-STEMI. With regard to angiographic findings (Table 2), patients with AS-STEMI were more likely to have proximal LAD occlusion than patients with EA-STEMI, but this difference was not statistically significant. There was no difference between the 2 groups in the size of the LAD (short, reaches the apex, or wraps around the apex) or in the number of vessels with ⬎50% luminal diameter narrowing. Additionally, the prevalence of collaterals did not differ between the
Variable Site of LAD occlusion Preseptal 1 Prediagonal 1 Prediagonal 1 and preseptal 1 LAD size Short Reaches apex Wraps the apex Side branches that supply the apex Large diagonal Large ramus intermedius Large obtuse marginal Number branches that supply the apex 0 1 2 3 Number of narrowed coronary arteries 1 ⱖ2 Collaterals TIMI flow before primary percutaneous coronary intervention 0 1 2 3 TIMI flow after primary percutaneous coronary intervention 0 1 2 3
AS-STEMI (n ⫽ 39)
EA-STEMI (n ⫽ 58)
p Value
16 (41%) 18 (46%) 14 (36%)
15 (26%) 19 (33%) 12 (21%)
3 (8%) 9 (23%) 27 (69%)
4 (7%) 14 (24%) 40 (69%)
0.178 0.263 0.154 0.984 — — —
11 (28%) 6 (15%) 33 (85%)
8 (14%) 6 (10%) 28 (48%)
0.136 0.671 0.0006 0.0015
5 (13%) 21 (54%) 12 (31%) 1 (3%)
27 (47%) 24 (41%) 5 (9%) 2 (3%)
— — — — 0.351
10 (26%) 29 (74%) 24 (62%)
20 (35%) 38 (66%) 42 (72%)
— — 0.366 0.904
27 (69%) 4 (10%) 6 (15%) 2 (5%)
37 (64%) 7 (12%) 9 (16%) 5 (9%) 0.084
2 (5%) 1 (3%) 7 (18%) 29 (74%)
5 (9%) 4 (7%) 2 (3%) 47 (81%)
groups, and TIMI flow grades recorded before and after primary percutaneous coronary intervention were comparable between the groups. Patients with AS-STEMI more often had large obtuse marginal branches that reached the apex, but the prevalence of large diagonal branches or a large ramus intermedius did not significantly differ between the AS-STEMI and EASTEMI groups. Overall, significantly more patients with AS-STEMI had ⱖ1 branch that supplied the apex (Table 2). When we examined potential predictors of ischemia extent (Table 3), we found that proximal occlusion of a short LAD before the first septal branch was relatively rare in our cohort. Compared with the patients with EA-STEMI, more of the patients with AS-STEMI had coronary anatomy that favored ischemia that was limited to the basal and mid segments of the left ventricle and that spared the apex. Patients in the AS-STEMI group were 3 times as likely as patients in the EA-STEMI group to have a proximal occlusion of the LAD before the first septal branch combined
830
The American Journal of Cardiology (www.ajconline.org)
Table 3 Angiographic predictors of the extent of ischemia in patients with proximal left anterior descending artery lesions Variable Anatomy favoring basal ischemia with sparing of the apex Preseptal 1 occlusion ⫹ short LAD Preseptal 1 ⫹ ⱖ1 large branch Preseptal 1 ⫹ either ⱖ1 large branch or a short LAD Anatomy favoring extensive basal ischemia that masks ischemia of the apex Preseptal 1 of a wrapping LAD
AS-STEMI (n ⫽ 16)
EA-STEMI (n ⫽ 15)
p Value
1 (6%)
2 (13%)
0.953
Among the 42 patients with occlusion of a wrapping LAD distal to the first diagonal branch, 10 of 11 patients (90.9%) with AS-STEMI had ⱖ1 large branch supplying the apex, compared with only 19 of 31 patients (61.3%) with EA-STEMI (p ⫽ 0.148). Among the 47 patients with occlusion of a wrapping LAD distal to the first septal branch, 12 of 13 patients (92.3%) with AS-STEMI had ⱖ1 large branch supplying the apex, compared with 20 of 34 patients (58.8%) with EA-STEMI (p ⫽ 0.064).
14 (88%) 14 (88%)
6 (40%) 7 (47%)
0.017 0.041
Discussion
14 (88%)
6 (40%)
0.017
Table 4 Angiographic findings in patients with mid to distal left anterior descending artery occlusion Variable Site of LAD occlusion Distal to diagonal 1 Between diagonal 1 and diagonal 2 Distal to diagonal 2 Distal to diagonal 1⫹ Short LAD Midsize LAD Wrapping LAD Distal to septal 1 Distal to septal 1⫹ Short LAD Midsize LAD Wrapping LAD
AS-STEMI
EA-STEMI
p Value
20 (51%) 13 (33%)
39 (67%) 23 (40%)
0.171 0.676
7 (18%)
16 (28%)
0.395 0.143
2 (10%) 7 (35%) 11 (55%) 23 (59%)
2 (5%) 6 (15%) 31 (80%) 43 (74%)
2 (9%) 8 (35%) 13 (75%)
2 (5%) 7 (16%) 34 (79%)
0.178 0.155
with either a short LAD that did not reach the apex or ⱖ1 large side branch that supplied the apex (p ⫽ 0.011). In contrast, more patients in the AS-STEMI group than the EA-STEMI group had proximal pre–first septal branch occlusion of a long LAD that wrapped the apex (Table 3), supporting the theory that the AS-STEMI pattern represents a large area of infarction caused by proximal occlusion of a long, wrapping LAD. Interestingly, among the 67 patients with infarction due to an occlusion of a wrapping LAD, the occlusion was more commonly proximal to the first septal branch in the AS-STEMI group (14 of 27 patients [51.9%]) than in the EA-STEMI group (6 of 40 patients [15.0%]) (p ⫽ 0.0031). Anatomy favoring more distal ischemia, sparing the basal portion of the left ventricle, tended to be more prevalent in the EA-STEMI group (Table 4). There was no difference between the groups in the percentage of patients with LAD occlusion between the first and second diagonal branches or distal to the second diagonal branches; however, in patients with LAD occlusion distal to the first diagonal branch, wrapping LAD tended to be more common in the EA-STEMI group than in the AS-STEMI group (p ⫽ 0.096).
The classic electrocardiographic paradigm suggests that the voltage changes detected at each lead are affected mainly by local events in the myocardial zone closest to the electrode.13 Because of the positions of leads V1 to V3 on the chest wall, STE limited to these leads during A-STEMI was ascribed by early observers to injury from transmural ischemia limited to the basal portion of the interventricular septum and the anterior wall; therefore, this pattern was named AS-STEMI (Figure 1). STE that extends to leads V5 and V6 was termed EA-STEMI because this pattern was thought to represent the extension of ischemia to the distal and apical segments of the anterolateral wall of the left ventricle. Shalev et al10 suggested that AS-STEMI actually involves the apical segments of the anterior wall of the left ventricle. In 85% of their patients, the culprit lesion occurred in the mid to distal LAD. However, the angiographic data were obtained several days after infarction, not during primary percutaneous coronary intervention. In our study, 59% of the patients with AS-STEMI had lesions distal to the first septal branch, and 54% had lesions distal to the first diagonal branch. Porter et al,9 using transthoracic echocardiography, showed that whereas STE in lead V1 is associated with regional dysfunction of the basal anterior, anteroseptal, and inferoseptal segments, STE in lead V2 is correlated with dysfunction of the apical inferior region. There are 2 reasonable but opposing explanations for the presence of these 2 patterns in A-STEMI (Figure 2). Investigators11,14 have shown that in acute A-STEMI, the number of precordial leads with STE correlated well with the final electrocardiographic Selvester QRS score, an estimate of final infarct size in patients who have not undergone reperfusion therapy, suggesting that the number of leads with STE correlates with the size of the ischemic zone. If so, patients with AS-STEMI should have smaller ischemic zones than patients with EA-STEMI. This could occur if the distal and apical segments of the septum and anterior wall have an alternative blood supply. The second hypothesis is that AS-STEMI actually represents more severe injury than EA-STEMI. Because of severe ischemia of the basal portion of the anterior wall and septum, the injury vector is directed anterosuperiorly. Lead V1 and leads V5 and V6 are positioned almost 180° from each other, so an injury vector that causes STE in leads V1 and V2 should cause ST depression, or at least attenuation of STE, in leads V5 and V6, even if the more distal and apical segments are involved.12 STE in lead V1 and ST depression in lead V5 may indicate LAD occlusion proximal to the first septal branch.6 Zhong-Qun et al12 suggested that the AS-
Coronary Artery Disease/Anteroseptal vs Anterior Wall STEMI
831
Figure 2. Schematic presentation of 2 possible explanations for the AS-STEMI pattern. (A) Ischemia limited to the basal and mid anterior and anteroseptal regions (gray zone). The LAD is short, and there is a large obtuse marginal branch of the left circumflex coronary artery supplying the apex. (B) There is a large ischemic zone involving the basal anterior and anteroseptal regions as well as the distal and apical segments (gray zone). The LAD is long and supplies the apex, and there are no large branches supplying the apical zones. The injury vectors (arrows) of the basal and the distal segments are oriented in opposite directions, attenuating STE in leads V4 to V6 on the surface electrocardiogram.
STEMI pattern may be seen in patients with proximal occlusion of a wrapping LAD. In our study, we compared coronary angiographic data concerning the site of occlusion, the length of the LAD, and the presence of side branches that supply the apex between patients with AS-STEMI and those with EA-STEMI. This study produced several new findings regarding the influence of the anatomy of the vascular bed and the location of the LAD occlusion site on the pattern of injury in A-STEMI. To the best of our knowledge, this is the first study to examine the influence of major side branches on the pattern of STE in the precordial leads. Our study supports the idea that the precordial leads are affected by the activation vector of the whole heart, rather than by local events. The lack of STE in leads V4 to V6 in AS-STEMI may occur when the distal segments are protected by an alternative blood supply (usually large obtuse marginal branches), so that ischemia is limited to the basal and mid portions of the anterior wall and septum. However, an AS-STEMI pattern may also be caused by a cancelation effect of vectors during ischemic injury: the anterosuperior (leads V1 and V2) and the inferolateral (leads V5 and V6) injury vectors mask each other.12 More than 1/3 of our patients with AS-STEMI had proximal occlusion of a wrapping LAD, which could create this type of cancelation effect by causing ischemia on both sides of the heart. Although ST depression in the inferior leads is a specific sign of LAD occlusion proximal to the first diagonal branch, the sensitivity of this sign is low.5 Our findings agree with those of Sasaki et al,15 who found that when proximal occlusion occurs in a long, wrapping LAD, there is no ST depression in the inferior leads. This finding was explained by concomitant ischemia of the opposing anterosuperior and inferior zones, which led to attenuation of the inferior injury vector. Ben-Gal et al16,17 observed that STE in lead V1 is associated with a small conal branch of the right coronary artery, because a larger conal branch could provide an alternative blood supply to the basal septum during occlusion of the LAD. In the present study, we found a similar effect of blood supply on electrocardiographic injury patterns: the presence of an alternative blood supply to the
cardiac apex by large side branches prevented STE in leads V4 to V6. Our findings suggest that there is no simple linear correlation between the number of leads with STE and the extent of the ischemic zone, as suggested by Aldrich et al.11 A total of 36% of our patients with the AS-STEMI pattern had proximal occlusion of a wrapping LAD before the first septal branch, suggesting a large ischemic area at risk. Limitations: This was a retrospective study that included a relatively small number of patients in relation to the number of variables that were found to affect the magnitude and extent of STE in the various leads. In current practice, coronary injections during primary percutaneous coronary intervention are short and do not allow full demonstration of the collateral circulation. Moreover, coronary angiography is not considered a sensitive method for the detection of small collateral vessels. In the present study, we did not use radionuclide data to assess regional perfusion or echocardiography to assess regional function in the acute setting, as this is not part of standard practice. Our findings suggest the validity of 2 opposing explanations for AS-STEMI. These results illustrate the disconnect that is sometimes present between simplified traditional linear electrocardiographic analysis and the actual physiologic complexity of ischemia. ST deviation in each lead is probably the result of a complex culmination of multiple injury vectors caused by local ischemia close to the electrocardiographic electrode and remote ischemia from other sources. It should be emphasized that our findings do not contradict the general American Heart Association and American College of Cardiology recommendation that all patients who present with A-STEMI undergo prompt reperfusion. Acknowledgment: Stephen N. Palmer, PhD, ELS, contributed to the editing of this report. 1. Blanke H, Cohen M, Schlueter GU, Karsch KR, Rentrop KP. Electrocardiographic and coronary arteriographic correlations during acute myocardial infarction. Am J Cardiol 1984;54:249 –255.
832
The American Journal of Cardiology (www.ajconline.org)
2. Christian TF, Gibbons RJ, Clements IP, Berger PB, Selvester RH, Wagner GS. Estimates of myocardium at risk and collateral flow in acute myocardial infarction using electrocardiographic indexes with comparison to radionuclide and angiographic measures. J Am Coll Cardiol 1995;26:388 –393. 3. Sullivan W, Vlodaver Z, Tuna N, Long L, Edwards JE. Correlation of electrocardiographic and pathologic findings in healed myocardial infarction. Am J Cardiol 1978;42:724 –732. 4. Birnbaum Y, Sclarovsky S, Solodky A, Tschori J, Herz I, Sulkes J, Mager A, Rechavia E. Prediction of the level of left anterior descending coronary artery obstruction during anterior wall acute myocardial infarction by the admission electrocardiogram. Am J Cardiol 1993;72: 823– 826. 5. Birnbaum Y, Solodky A, Herz I, Kusniec J, Rechavia E, Sulkes J, Sclarovsky S. Implications of inferior ST-segment depression in anterior acute myocardial infarction: electrocardiographic and angiographic correlation. Am Heart J 1994;127:1467–1473. 6. Engelen DJ, Gorgels AP, Cheriex EC, De Muinck ED, Ophuis AJ, Dassen WR, Vainer J, van Ommen VG, Wellens HJ. Value of the electrocardiogram in localizing the occlusion site in the left anterior descending coronary artery in acute anterior myocardial infarction. J Am Coll Cardiol 1999;34:389 –395. 7. Roberts WC, Gardin JM. Location of myocardial infarcts: a confusion of terms and definitions. Am J Cardiol 1978;42:868 – 872. 8. Bogaty P, Boyer L, Rousseau L, Arsenault M. Is anteroseptal myocardial infarction an appropriate term? Am J Med 2002;113:37– 41. 9. Porter A, Wyshelesky A, Strasberg B, Vaturi M, Solodky A, Imbar S, Sagie A, Battler A, Birnbaum Y. Correlation between the admission electrocardiogram and regional wall motion abnormalities as detected by echocardiography in anterior acute myocardial infarction. Cardiology 2000;94:118 –126.
10. Shalev Y, Fogelman R, Oettinger M, Caspi A. Does the electrocardiographic pattern of “anteroseptal” myocardial infarction correlate with the anatomic location of myocardial injury? Am J Cardiol 1995; 75:763–766. 11. Aldrich HR, Wagner NB, Boswick J, Corsa AT, Jones MG, Grande P, Lee KL, Wagner GS. Use of initial ST-segment deviation for prediction of final electrocardiographic size of acute myocardial infarcts. Am J Cardiol 1988;61:749 –753. 12. Zhong-Qun Z, Wei W, Jun-Feng W. Does left anterior descending coronary artery acute occlusion proximal to the first septal perforator counteract ST elevation in leads V5 and V6? J Electrocardiol 2009; 42:52–57. 13. Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice: Adult and Pediatric. Philadelphia: Saunders, 2001. 14. Richardson K, Engel G, Yamazaki T, Chun S, Froelicher VF. Electrocardiographic damage scores and cardiovascular mortality. Am Heart J 2005;149:458 – 463. 15. Sasaki K, Yotsukura M, Sakata K, Yoshino H, Ishikawa K. Relation of ST-segment changes in inferior leads during anterior wall acute myocardial infarction to length and occlusion site of the left anterior descending coronary artery. Am J Cardiol 2001;87:1340 –1345. 16. Ben-Gal T, Herz I, Solodky A, Birnbaum Y, Sclarovsky S, Sagie A. Acute anterior wall myocardial infarction entailing ST-segment elevation in lead V1: electrocardiographic and angiographic correlations. Clin Cardiol 1998;21:399 – 404. 17. Ben-Gal T, Sclarovsky S, Herz I, Strasberg B, Zlotikamien B, Sulkes J, Birnbaum Y, Wagner GS, Sagie A. Importance of the conal branch of the right coronary artery in patients with acute anterior wall myocardial infarction: electrocardiographic and angiographic correlation. J Am Coll Cardiol 1997;29:506 –511.
0002-9149/11/$ – see front matter © 2011 Elsevier Inc. All rights reserved. doi:10.1016/j.amjcard.2010.10.070
areas of infarction because of the proximal occlusion of a long, wrapping LAD, resulting in deceptive attenuation of the expected STE in the lateral precordial leads. In this study, we analyzed data from patients with acute A-STEMI and compared electrocardiographic patterns with coronary angiographic findings to evaluate the influence of the site of occlusion, the morphology of the LAD, and the presence of large side coronary branches on the presenting electrocardiographic pattern. Methods We studied consecutive patients who were admitted with the diagnosis of first-time, acute A-STEMI as indicated by STE at the J point in ⱖ2 adjacent precordial leads (ⱖ0.2 mV in leads V2 and V3 or ⱖ0.1 mV in the other precordial leads, V1 or V4 to V6) and by other signs of myocardial ischemia, such as chest pain and elevated cardiac markers. All patients underwent urgent coronary angiography followed by either primary percutaneous coronary intervention or emergent coronary artery bypass grafting surgery at either the Michael E. DeBakey Veterans Affairs Medical Center or St. Luke’s Episcopal Hospital in Houston, Texas. The data from the Veterans Affairs hospital were obtained from a preexisting database of 172 consecutive patients who underwent primary percutaneous coronary intervention for STEMI from 2004 to 2008. The data from St. Luke’s Episcopal Hospital came from a preexisting database that lists all patients for whom the STEMI pager had been activated www.ajconline.org
828
The American Journal of Cardiology (www.ajconline.org)
Figure 1. (A) AS-STEMI pattern. STE is limited to leads V1 to V3. (B) EA-STEMI pattern. STE occurs in leads V1 to V6, as well as in leads I and aVL.
by the hospital’s emergency department or by hospital staff members from January 2007 to August 2009. The database contained data regarding 542 consecutive patients, of whom 305 underwent cardiac catheterization and 172 underwent acute reperfusion therapy. Index electrocardiograms from these hospitalizations were selected if they showed STE with positive T waves in ⱖ2 anterior leads (V1 to V6), typical evolution consistent with acute A-STEMI on follow-up electrocardiography (i.e., a decrease in STE magnitude with T-wave inversions after primary percutaneous coronary intervention), and elevated cardiac markers that confirmed myocardial necrosis. Patients were excluded if their index electrocardiograms showed intraventricular conduction delay (left or right bundle branch block or nonspecific intraventricular conduction block), ventricular rhythms (including electronic ventricular pacing), or Wolff-Parkinson-White syndrome. Patients were also excluded if their electrocardiographic findings were consistent with partial reperfusion or an advanced stage of infarction (Q waves with negative T-waves), or if they had previously undergone coronary artery bypass grafting surgery. Patients with A-STEMI were divided into 2 groups according to their electrocardiographic characteristics. An index electrocardiogram (obtained before revascularization) that showed STEs limited to leads V1 to V3 (STE ⱖ0.1 mV in lead V1 and ⱖ0.2 mV in leads V2 and V3) was considered to indicate AS-STEMI, whereas an electrocardiogram with precordial STEs (ⱖ0.1 mV) extending to lead V4, V5, or V6 was considered to indicate EA-STEMI. Of the 289 patients with acute STEMI from the 2 hospitals, 114 patients met the inclusion criteria and were
selected for subsequent review of their coronary angiographic films. Films were primarily interpreted by 2 experienced angiographers who were blinded to each patient’s identity and group assignment (i.e., AS-STEMI or EASTEMI). A third investigator adjudicated the review of the coronary angiographic films when needed. Angiographic characteristics of interest included the location of culprit occlusion within the LAD relative to the major diagonal and septal branches, the size of the LAD (short of the apex, reaches the apex, or wraps the apex), the presence or absence of ⱖ1 large side branch (ⱖ2 mm in diameter; i.e., a large ramus intermedius, large obtuse marginal branch, or large diagonal branch proximal to site of culprit occlusion that reached the apical region of the left ventricle), initial and post–primary percutaneous coronary intervention Thrombolysis In Myocardial Infarction (TIMI) flow grade, the presence or absence of collaterals, and the number of diseased vessels (1, 2, or 3). Discrete data are presented as absolute numbers and percentages. Continuous data are presented as mean ⫾ SD. The chi-square test was used to analyze differences between discrete variables, and Student’s t test was used for continuous variables. A p value ⬍0.05 was considered statistically significant. Results Of the 114 patients initially selected according to their electrocardiographic findings, 17 were excluded for various reasons: 8 patients underwent primary percutaneous coronary intervention on a vessel other than the LAD (5 right
Coronary Artery Disease/Anteroseptal vs Anterior Wall STEMI Table 1 Demographic and clinical data
829
Table 2 Angiographic data
Variable
AS-STEMI (n ⫽ 39)
EA-STEMI (n ⫽ 58)
p Value
Men Age (years) Race White Black Hispanic Other Coronary artery disease*,† Myocardial infarction* Percutaneous coronary intervention* Diabetes mellitus*,‡ Hypertension* Hyperlipidemia*,§ Heart failure* Peak creatine kinase (U/L) Peak creatine kinaseMB (ng/ml) Peak troponin I (ng/ml) ⬍10 10–50 ⬎50
35 (90%) 63.4 ⫾ 12.0
50 (86%) 58.3 ⫾ 12.4
0.838 0.050 0.453
22 (56%) 11 (28%) 2 (5%) 4 (10%) 16 (41%)
35 (60%) 15 (26%) 6 (10%) 2 (3%) 23 (40%)
0.939
5 (13%) 12 (31%)
11 (19%) 11 (19%)
0.603 0.273
11 (28%) 24 (62%) 22 (56%) 3 (8%) 1,223 ⫾ 1816
13 (22%) 38 (66%) 30 (52%) 3 (5%) 1,794 ⫾ 2114
0.683 0.854 0.806 0.940 0.168
103 ⫾ 163
155 ⫾ 226
0.193
19 (49%) 10 (26%) 10 (26%)
13 (22%) 22 (38%) 23 (40%)
0.026
Data are expressed as mean ⫾ SD or as number (percentage). * Established diagnosis in chart or receiving medications for this condition. † History of myocardial infarction, effort-induced chest pain, or coronary angiography with documentation of coronary artery disease. ‡ Established diagnosis in chart, receiving medications for diabetes, or glycosylated hemoglobin ⱖ 6.5%. § Established diagnosis in chart, receiving lipid-modifying medications, or abnormal lipid panel ⬍24 hours after admission.
coronary artery, 1 left circumflex coronary artery, 1 with culprit lesions in the right and left circumflex coronary arteries, and 1 left main coronary artery), 4 patients did not have clear culprit lesions or significant coronary artery disease on coronary angiography, and 5 patients had missing angiographic data. Thus, 97 patients (12 women, 85 men; mean age 60.2 ⫾ 12.1 years, range 29 to 90) met all criteria and were included in the study. Baseline and demographic data are listed in Table 1. Patients with AS-STEMI tended to have lower peak creatine kinase levels and peak creatine kinase-MB levels than patients with EA-STEMI, but these differences did not reach statistical significance. The percentage of patients with peak cardiac troponin I levels ⬍10 ng/ml was greater in the AS-STEMI group than in the EA-STEMI group. Figure 1 depicts sample electrocardiograms from patients with AS-STEMI and EA-STEMI. With regard to angiographic findings (Table 2), patients with AS-STEMI were more likely to have proximal LAD occlusion than patients with EA-STEMI, but this difference was not statistically significant. There was no difference between the 2 groups in the size of the LAD (short, reaches the apex, or wraps around the apex) or in the number of vessels with ⬎50% luminal diameter narrowing. Additionally, the prevalence of collaterals did not differ between the
Variable Site of LAD occlusion Preseptal 1 Prediagonal 1 Prediagonal 1 and preseptal 1 LAD size Short Reaches apex Wraps the apex Side branches that supply the apex Large diagonal Large ramus intermedius Large obtuse marginal Number branches that supply the apex 0 1 2 3 Number of narrowed coronary arteries 1 ⱖ2 Collaterals TIMI flow before primary percutaneous coronary intervention 0 1 2 3 TIMI flow after primary percutaneous coronary intervention 0 1 2 3
AS-STEMI (n ⫽ 39)
EA-STEMI (n ⫽ 58)
p Value
16 (41%) 18 (46%) 14 (36%)
15 (26%) 19 (33%) 12 (21%)
3 (8%) 9 (23%) 27 (69%)
4 (7%) 14 (24%) 40 (69%)
0.178 0.263 0.154 0.984 — — —
11 (28%) 6 (15%) 33 (85%)
8 (14%) 6 (10%) 28 (48%)
0.136 0.671 0.0006 0.0015
5 (13%) 21 (54%) 12 (31%) 1 (3%)
27 (47%) 24 (41%) 5 (9%) 2 (3%)
— — — — 0.351
10 (26%) 29 (74%) 24 (62%)
20 (35%) 38 (66%) 42 (72%)
— — 0.366 0.904
27 (69%) 4 (10%) 6 (15%) 2 (5%)
37 (64%) 7 (12%) 9 (16%) 5 (9%) 0.084
2 (5%) 1 (3%) 7 (18%) 29 (74%)
5 (9%) 4 (7%) 2 (3%) 47 (81%)
groups, and TIMI flow grades recorded before and after primary percutaneous coronary intervention were comparable between the groups. Patients with AS-STEMI more often had large obtuse marginal branches that reached the apex, but the prevalence of large diagonal branches or a large ramus intermedius did not significantly differ between the AS-STEMI and EASTEMI groups. Overall, significantly more patients with AS-STEMI had ⱖ1 branch that supplied the apex (Table 2). When we examined potential predictors of ischemia extent (Table 3), we found that proximal occlusion of a short LAD before the first septal branch was relatively rare in our cohort. Compared with the patients with EA-STEMI, more of the patients with AS-STEMI had coronary anatomy that favored ischemia that was limited to the basal and mid segments of the left ventricle and that spared the apex. Patients in the AS-STEMI group were 3 times as likely as patients in the EA-STEMI group to have a proximal occlusion of the LAD before the first septal branch combined
830
The American Journal of Cardiology (www.ajconline.org)
Table 3 Angiographic predictors of the extent of ischemia in patients with proximal left anterior descending artery lesions Variable Anatomy favoring basal ischemia with sparing of the apex Preseptal 1 occlusion ⫹ short LAD Preseptal 1 ⫹ ⱖ1 large branch Preseptal 1 ⫹ either ⱖ1 large branch or a short LAD Anatomy favoring extensive basal ischemia that masks ischemia of the apex Preseptal 1 of a wrapping LAD
AS-STEMI (n ⫽ 16)
EA-STEMI (n ⫽ 15)
p Value
1 (6%)
2 (13%)
0.953
Among the 42 patients with occlusion of a wrapping LAD distal to the first diagonal branch, 10 of 11 patients (90.9%) with AS-STEMI had ⱖ1 large branch supplying the apex, compared with only 19 of 31 patients (61.3%) with EA-STEMI (p ⫽ 0.148). Among the 47 patients with occlusion of a wrapping LAD distal to the first septal branch, 12 of 13 patients (92.3%) with AS-STEMI had ⱖ1 large branch supplying the apex, compared with 20 of 34 patients (58.8%) with EA-STEMI (p ⫽ 0.064).
14 (88%) 14 (88%)
6 (40%) 7 (47%)
0.017 0.041
Discussion
14 (88%)
6 (40%)
0.017
Table 4 Angiographic findings in patients with mid to distal left anterior descending artery occlusion Variable Site of LAD occlusion Distal to diagonal 1 Between diagonal 1 and diagonal 2 Distal to diagonal 2 Distal to diagonal 1⫹ Short LAD Midsize LAD Wrapping LAD Distal to septal 1 Distal to septal 1⫹ Short LAD Midsize LAD Wrapping LAD
AS-STEMI
EA-STEMI
p Value
20 (51%) 13 (33%)
39 (67%) 23 (40%)
0.171 0.676
7 (18%)
16 (28%)
0.395 0.143
2 (10%) 7 (35%) 11 (55%) 23 (59%)
2 (5%) 6 (15%) 31 (80%) 43 (74%)
2 (9%) 8 (35%) 13 (75%)
2 (5%) 7 (16%) 34 (79%)
0.178 0.155
with either a short LAD that did not reach the apex or ⱖ1 large side branch that supplied the apex (p ⫽ 0.011). In contrast, more patients in the AS-STEMI group than the EA-STEMI group had proximal pre–first septal branch occlusion of a long LAD that wrapped the apex (Table 3), supporting the theory that the AS-STEMI pattern represents a large area of infarction caused by proximal occlusion of a long, wrapping LAD. Interestingly, among the 67 patients with infarction due to an occlusion of a wrapping LAD, the occlusion was more commonly proximal to the first septal branch in the AS-STEMI group (14 of 27 patients [51.9%]) than in the EA-STEMI group (6 of 40 patients [15.0%]) (p ⫽ 0.0031). Anatomy favoring more distal ischemia, sparing the basal portion of the left ventricle, tended to be more prevalent in the EA-STEMI group (Table 4). There was no difference between the groups in the percentage of patients with LAD occlusion between the first and second diagonal branches or distal to the second diagonal branches; however, in patients with LAD occlusion distal to the first diagonal branch, wrapping LAD tended to be more common in the EA-STEMI group than in the AS-STEMI group (p ⫽ 0.096).
The classic electrocardiographic paradigm suggests that the voltage changes detected at each lead are affected mainly by local events in the myocardial zone closest to the electrode.13 Because of the positions of leads V1 to V3 on the chest wall, STE limited to these leads during A-STEMI was ascribed by early observers to injury from transmural ischemia limited to the basal portion of the interventricular septum and the anterior wall; therefore, this pattern was named AS-STEMI (Figure 1). STE that extends to leads V5 and V6 was termed EA-STEMI because this pattern was thought to represent the extension of ischemia to the distal and apical segments of the anterolateral wall of the left ventricle. Shalev et al10 suggested that AS-STEMI actually involves the apical segments of the anterior wall of the left ventricle. In 85% of their patients, the culprit lesion occurred in the mid to distal LAD. However, the angiographic data were obtained several days after infarction, not during primary percutaneous coronary intervention. In our study, 59% of the patients with AS-STEMI had lesions distal to the first septal branch, and 54% had lesions distal to the first diagonal branch. Porter et al,9 using transthoracic echocardiography, showed that whereas STE in lead V1 is associated with regional dysfunction of the basal anterior, anteroseptal, and inferoseptal segments, STE in lead V2 is correlated with dysfunction of the apical inferior region. There are 2 reasonable but opposing explanations for the presence of these 2 patterns in A-STEMI (Figure 2). Investigators11,14 have shown that in acute A-STEMI, the number of precordial leads with STE correlated well with the final electrocardiographic Selvester QRS score, an estimate of final infarct size in patients who have not undergone reperfusion therapy, suggesting that the number of leads with STE correlates with the size of the ischemic zone. If so, patients with AS-STEMI should have smaller ischemic zones than patients with EA-STEMI. This could occur if the distal and apical segments of the septum and anterior wall have an alternative blood supply. The second hypothesis is that AS-STEMI actually represents more severe injury than EA-STEMI. Because of severe ischemia of the basal portion of the anterior wall and septum, the injury vector is directed anterosuperiorly. Lead V1 and leads V5 and V6 are positioned almost 180° from each other, so an injury vector that causes STE in leads V1 and V2 should cause ST depression, or at least attenuation of STE, in leads V5 and V6, even if the more distal and apical segments are involved.12 STE in lead V1 and ST depression in lead V5 may indicate LAD occlusion proximal to the first septal branch.6 Zhong-Qun et al12 suggested that the AS-
Coronary Artery Disease/Anteroseptal vs Anterior Wall STEMI
831
Figure 2. Schematic presentation of 2 possible explanations for the AS-STEMI pattern. (A) Ischemia limited to the basal and mid anterior and anteroseptal regions (gray zone). The LAD is short, and there is a large obtuse marginal branch of the left circumflex coronary artery supplying the apex. (B) There is a large ischemic zone involving the basal anterior and anteroseptal regions as well as the distal and apical segments (gray zone). The LAD is long and supplies the apex, and there are no large branches supplying the apical zones. The injury vectors (arrows) of the basal and the distal segments are oriented in opposite directions, attenuating STE in leads V4 to V6 on the surface electrocardiogram.
STEMI pattern may be seen in patients with proximal occlusion of a wrapping LAD. In our study, we compared coronary angiographic data concerning the site of occlusion, the length of the LAD, and the presence of side branches that supply the apex between patients with AS-STEMI and those with EA-STEMI. This study produced several new findings regarding the influence of the anatomy of the vascular bed and the location of the LAD occlusion site on the pattern of injury in A-STEMI. To the best of our knowledge, this is the first study to examine the influence of major side branches on the pattern of STE in the precordial leads. Our study supports the idea that the precordial leads are affected by the activation vector of the whole heart, rather than by local events. The lack of STE in leads V4 to V6 in AS-STEMI may occur when the distal segments are protected by an alternative blood supply (usually large obtuse marginal branches), so that ischemia is limited to the basal and mid portions of the anterior wall and septum. However, an AS-STEMI pattern may also be caused by a cancelation effect of vectors during ischemic injury: the anterosuperior (leads V1 and V2) and the inferolateral (leads V5 and V6) injury vectors mask each other.12 More than 1/3 of our patients with AS-STEMI had proximal occlusion of a wrapping LAD, which could create this type of cancelation effect by causing ischemia on both sides of the heart. Although ST depression in the inferior leads is a specific sign of LAD occlusion proximal to the first diagonal branch, the sensitivity of this sign is low.5 Our findings agree with those of Sasaki et al,15 who found that when proximal occlusion occurs in a long, wrapping LAD, there is no ST depression in the inferior leads. This finding was explained by concomitant ischemia of the opposing anterosuperior and inferior zones, which led to attenuation of the inferior injury vector. Ben-Gal et al16,17 observed that STE in lead V1 is associated with a small conal branch of the right coronary artery, because a larger conal branch could provide an alternative blood supply to the basal septum during occlusion of the LAD. In the present study, we found a similar effect of blood supply on electrocardiographic injury patterns: the presence of an alternative blood supply to the
cardiac apex by large side branches prevented STE in leads V4 to V6. Our findings suggest that there is no simple linear correlation between the number of leads with STE and the extent of the ischemic zone, as suggested by Aldrich et al.11 A total of 36% of our patients with the AS-STEMI pattern had proximal occlusion of a wrapping LAD before the first septal branch, suggesting a large ischemic area at risk. Limitations: This was a retrospective study that included a relatively small number of patients in relation to the number of variables that were found to affect the magnitude and extent of STE in the various leads. In current practice, coronary injections during primary percutaneous coronary intervention are short and do not allow full demonstration of the collateral circulation. Moreover, coronary angiography is not considered a sensitive method for the detection of small collateral vessels. In the present study, we did not use radionuclide data to assess regional perfusion or echocardiography to assess regional function in the acute setting, as this is not part of standard practice. Our findings suggest the validity of 2 opposing explanations for AS-STEMI. These results illustrate the disconnect that is sometimes present between simplified traditional linear electrocardiographic analysis and the actual physiologic complexity of ischemia. ST deviation in each lead is probably the result of a complex culmination of multiple injury vectors caused by local ischemia close to the electrocardiographic electrode and remote ischemia from other sources. It should be emphasized that our findings do not contradict the general American Heart Association and American College of Cardiology recommendation that all patients who present with A-STEMI undergo prompt reperfusion. Acknowledgment: Stephen N. Palmer, PhD, ELS, contributed to the editing of this report. 1. Blanke H, Cohen M, Schlueter GU, Karsch KR, Rentrop KP. Electrocardiographic and coronary arteriographic correlations during acute myocardial infarction. Am J Cardiol 1984;54:249 –255.
832
The American Journal of Cardiology (www.ajconline.org)
2. Christian TF, Gibbons RJ, Clements IP, Berger PB, Selvester RH, Wagner GS. Estimates of myocardium at risk and collateral flow in acute myocardial infarction using electrocardiographic indexes with comparison to radionuclide and angiographic measures. J Am Coll Cardiol 1995;26:388 –393. 3. Sullivan W, Vlodaver Z, Tuna N, Long L, Edwards JE. Correlation of electrocardiographic and pathologic findings in healed myocardial infarction. Am J Cardiol 1978;42:724 –732. 4. Birnbaum Y, Sclarovsky S, Solodky A, Tschori J, Herz I, Sulkes J, Mager A, Rechavia E. Prediction of the level of left anterior descending coronary artery obstruction during anterior wall acute myocardial infarction by the admission electrocardiogram. Am J Cardiol 1993;72: 823– 826. 5. Birnbaum Y, Solodky A, Herz I, Kusniec J, Rechavia E, Sulkes J, Sclarovsky S. Implications of inferior ST-segment depression in anterior acute myocardial infarction: electrocardiographic and angiographic correlation. Am Heart J 1994;127:1467–1473. 6. Engelen DJ, Gorgels AP, Cheriex EC, De Muinck ED, Ophuis AJ, Dassen WR, Vainer J, van Ommen VG, Wellens HJ. Value of the electrocardiogram in localizing the occlusion site in the left anterior descending coronary artery in acute anterior myocardial infarction. J Am Coll Cardiol 1999;34:389 –395. 7. Roberts WC, Gardin JM. Location of myocardial infarcts: a confusion of terms and definitions. Am J Cardiol 1978;42:868 – 872. 8. Bogaty P, Boyer L, Rousseau L, Arsenault M. Is anteroseptal myocardial infarction an appropriate term? Am J Med 2002;113:37– 41. 9. Porter A, Wyshelesky A, Strasberg B, Vaturi M, Solodky A, Imbar S, Sagie A, Battler A, Birnbaum Y. Correlation between the admission electrocardiogram and regional wall motion abnormalities as detected by echocardiography in anterior acute myocardial infarction. Cardiology 2000;94:118 –126.
10. Shalev Y, Fogelman R, Oettinger M, Caspi A. Does the electrocardiographic pattern of “anteroseptal” myocardial infarction correlate with the anatomic location of myocardial injury? Am J Cardiol 1995; 75:763–766. 11. Aldrich HR, Wagner NB, Boswick J, Corsa AT, Jones MG, Grande P, Lee KL, Wagner GS. Use of initial ST-segment deviation for prediction of final electrocardiographic size of acute myocardial infarcts. Am J Cardiol 1988;61:749 –753. 12. Zhong-Qun Z, Wei W, Jun-Feng W. Does left anterior descending coronary artery acute occlusion proximal to the first septal perforator counteract ST elevation in leads V5 and V6? J Electrocardiol 2009; 42:52–57. 13. Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice: Adult and Pediatric. Philadelphia: Saunders, 2001. 14. Richardson K, Engel G, Yamazaki T, Chun S, Froelicher VF. Electrocardiographic damage scores and cardiovascular mortality. Am Heart J 2005;149:458 – 463. 15. Sasaki K, Yotsukura M, Sakata K, Yoshino H, Ishikawa K. Relation of ST-segment changes in inferior leads during anterior wall acute myocardial infarction to length and occlusion site of the left anterior descending coronary artery. Am J Cardiol 2001;87:1340 –1345. 16. Ben-Gal T, Herz I, Solodky A, Birnbaum Y, Sclarovsky S, Sagie A. Acute anterior wall myocardial infarction entailing ST-segment elevation in lead V1: electrocardiographic and angiographic correlations. Clin Cardiol 1998;21:399 – 404. 17. Ben-Gal T, Sclarovsky S, Herz I, Strasberg B, Zlotikamien B, Sulkes J, Birnbaum Y, Wagner GS, Sagie A. Importance of the conal branch of the right coronary artery in patients with acute anterior wall myocardial infarction: electrocardiographic and angiographic correlation. J Am Coll Cardiol 1997;29:506 –511.