Birnbaum, Yochai

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543www.foliacardiologica.euEDITORIALFolia Cardiol.2006, Vol. 13, No. 7, pp. 543–546Copyright © 2006 Via MedicaISSN 1507–4145Address for correspondence: Yochai Birnbaum, MDDivision of Cardiology University of Texas Medical Branch5.106 John Sealy Annex, 301 University Blvd.Galveston, Texas 77555-0553, USATel: 409 772 2794, fax: 409 772 4982e-mail: yobirnba@utmb.eduReceived: 16.09.2006 Accepted: 2.10.2006Can we use the electrocardiogram to refine theestimation of the size and location of ischemiain anterior ST elevation myocardial infarction?Yochai BirnbaumDivision of Cardiology, University of Texas Medical Branch, Galveston, Texas, USAArticle p. 570IntroductionBased on the results of several clinical rand-omized trials the current guidelines recommendthat every patient with suggestive symptoms andST elevation (> 0.2 mV ST elevation at the J-pointin leads V1–V3 and > 0.1 mV in all other leads)should be immediately subjected to reperfusiontherapy, preferentially by primary percutaneousintervention (PCI) [1, 2]. Many cardiologists deve-loped an approach that since every patient with STelevation is triaged for immediate heart catheteri-zation; there is no need to obtain any other informa-tion from the electrocardiogram (ECG). However,in systems with more limited resources there is anincreased need for improving our ability for earlydiagnosis and risk stratification in order to decidewhether the patient will receive thrombolytic ther-apy or be referred for PCI. When this decision ismade, the clinician can rely only on the clinical data(history and physical examination) and the present-ing ECG.Many studies have been published trying tocorrelate different parameters in the presentingECG with coronary anatomy, ischemic area at risk,final infarct size, left ventricular function and/orprognosis in patients with ST elevation myocardialinfarction (STEMI). For a recent review the read-ers are referred to [3].Correlations with coronary anatomyThe left anterior descending coronary artery(LAD) is located above the anterior interventricu-lar septum, supplying septal branches to the sep-tum and diagonal branches to the anterolateralzones of the heart. However, there are considerablevariations in the anatomy of the coronary arteries.The left anterior descending coronary artery can beshort, not reaching the apex; intermediate size; orlong, wrapping the cardiac apex and supplying var-ious portions of the apical, distal lateral and distalinferoposterior segments. In addition, various por-tions of the anterior free wall of the right ventriclealso get blood supply from LAD branches. The ba-sal, mid and distal anterolateral and inferolateralsegments may get blood supply from the diagonalbranches of the LAD, marginal branches of the leftcircumflex artery or from a ramus intermediusbranch. In patients with multivessel disease, thevariations in regional blood supply can be evengreater due to the presence of collaterals. Thus, theECG findings in a patient with an acute occludedshort LAD and proximal chronic occlusion of a rightcoronary artery with collaterals from the LAD to theright posterior descending artery actually should besimilar to those of a patient with occlusion of a longwrapping LAD. It has to be remembered that thesurface 12-lead ECG shows the summation of theelectrical activity of the heart rather than reflect-ing the actual coronary anatomy.We have also a problem with the “goal standard”of the coronary angiogram, especially in studiesusing angiograms of patients after thrombolytictherapy or predischarge angiograms, as most of the544Folia Cardiol. 2006, Vol. 13, No. 7www.foliacardiologica.euolder studies did. The site of the most severe cor-onary narrowing does not necessarily reflect thesize and location of the ischemic bed. In many cas-es the plaque ruptures at bifurcation site. The oc-clusive thrombus may progress proximally and dis-tally in the vessel, so during acute ischemia sidebranches could have been occluded and later on,after (partial) dissolution of the clot, the side branch-es appear patent. Moreover, coronary angiographyis not sensitive for depicting small collateral vesselsthat may (at least partially) nourish the segmentsassumed to be supplied by the infarct related artery.Even visible collaterals may disappear shortly afterrecanalization of the infarct-related artery.Nevertheless, studies have repeatedly shownseveral patterns. Ischemia of the lateral zones caus-es ST elevation in leads I and aVL [4, 5] andST depression in the inferior leads [6]. This patternis detected whether the first acute marginal branchof the left circumflex is involved (usually accompa-nied by ST depression in leads V2–V3); or when thefirst diagonal branch is involved (usually with con-comitant ST elevation in the anterior precordialleads) [4]. However, when there is concomitantischemia of the inferior segments (as may occurwith proximal occlusion of a long wrapping LAD ora proximal occlusion of a dominant left circumflexartery), the injury vector of the inferior zone andthat of the lateral zone cancel each other and noST elevation is detected. Sasaki et al. [7] has shownthat indeed, proximal occlusion of a short LAD caus-es ST elevation in leads I and aVL. However, prox-imal occlusion of a wrapping LAD is not associatedwith ST elevation in leads I and aVL or reciprocalST depression in the inferior leads [7]. Thus,ST elevation in leads I and aVL or ST depressionin the inferior leads is a specific, but insensitive signfor proximal occlusion of the LAD. The findings ofCzechowska et al. [8], presented in the present is-sue, reflect these facts. Because lack of ST eleva-tion in leads I and aVL in a patient with anteriorSTEMI may reflect either LAD occlusion distal tothe first diagonal branch, or proximal occlusion ofa long wrapping LAD, it is not expected thatST elevation in these leads would be associated withlower left ventricular ejection fraction or more seg-ments with regional dysfunction.Czechowska et al. [8] have confirmed our pre-vious observation that ST elevation in lead V1 doesnot reflect LAD occlusion before the first septalbranch, or lower ejection fraction [9], althoughEngelen et al suggested that ST elevation > 2.5 mmin lead V1 can predict LAD occlusion proximal tothe first septal branch [10].Correlations with regional and globalleft ventricular systolic functionFinal infarct size is determined by the size ofthe ischemia area at risk, the severity of ischemia(ischemic preconditioning, various drugs, residualflow by collaterals or partial or intermittent occlu-sion of the infarct related artery), the duration ofischemia and by events occurring during reper-fusion (reperfusion injury) [3, 11]. The presentingECG may reflect the size of the ischemic area atrisk and/or the severity of ischemia and may showsigns that irreversible damage has already occurred(presence of Q waves); however, it cannot predictthe total time of ischemia (especially the time peri-od between the ECG and the actual recanalizationof the artery) and the severity of “reperfusion inju-ry”. Therefore, the expected correlation betweenthe presenting ECG and final infarct size can be onlyfair, especially in patients undergoing reperfusiontherapy.Currently we have difficulties in demonstrat-ing the size of the ischemic area at risk. Echocardio-grams obtained before reperfusion may show theextent of ischemia. However, in most cases thequality of such echocardiogram is low due to the factthat in the acute stages of STEMI the patient maybe dyspneic, cannot lay on his left side, and duringoff hours the examinations are done by less experi-enced technicians. Furthermore, complete studymay be long and delay transfer to the catheteriza-tion laboratory, although echocardiogram can bedone in patients receiving intravenous thrombolytictherapy. The echocardiograms in many of the stud-ies were obtained the next day [12–14]. Although,due to the effect of stunning (delayed recovery ofregional function after reperfusion), regional func-tion at the time of the examination may still reflectthe pattern during acute ischemia, it is less thanideal. Pretreatment technetium 99m-sestamibiperfusion defect size has been used by some inves-tigators [15, 16]; however, they are technically dif-ficult to obtain and there is no evidence that thecorrelation between the perfusion defect size andthe actual size of the ischemic area at risk is good.Obviously, in patients with previous myocardial in-farction (and assuming that ~30% of the infarcts aresubclinical) the correlation cannot be good. Cardiacmagnetic resonance imaging is a promising evolv-ing technique that may help in the future depictingthe ischemic area at risk [17]. However, this imag-ing modality is expensive and still timeconsuming, thus may delay the initiation of prima-ry PCI. Czechowska et al. [8] used two parameters545Yochai Birnbaum, Can we use ECG to refine the estimation of the size and location...www.foliacardiologica.eufor estimation of infarct size: echocardiogram andpeak CK-MB. From the methods it is unclearwhether the patients were treated with reperfusiontherapy upon arrival. Although it is stated that allpatients underwent coronary angiography, it is un-clear whether it was part of primary PCI or laterrisk stratification. Accordingly, the timing of theechocardiogram is unclear. Most of them underwentit before angiography, whereas 3 underwent it with-in 12 hours of admission. Peak CK-MB is deter-mined by the size of the ischemic area at risk, theseverity and duration of ischemia and the quality ofreperfusion. Prompt reperfusion causes a high earlypeak of CK-MB due to wash out from the previous-ly ischemic zone with rapid decline in levels overtime. In the past it has been suggested that the areaunder the curve of CK levels over the first 24 hourscorrelates with final infarct size. Although for con-venience reasons many investigators have used thevalue of peak CK or peak CK-MB as a surrogateendpoint of infarct size, this methods has not beenvalidated. Nevertheless, Czechowska et al. [8] havefound correlation between the sum of ST elevationin all leads and peak CK-MB. Interestingly, Aldrichet al. [18] and Clemmensen et al. [19] reported thatin anterior STEMI, the number of leads with STelevation better correlated with the final QRSSylvester score (a measure of final infarct size) inpatients not subjected to reperfusion therapy. How-ever, Christian et al. [16] reported no correlationbetween the sum of ST elevation or the number ofleads with ST elevation and the perfusion defectsize before reperfusion therapy. As previouslymentioned, due to the effect of opposing vectors (forexample inferior and lateral) and the fact that notall myocardial segments are equally represented bythe 12-lead ECG, a simple linear correlation be-tween the number of leads with ST elevation (ordeviation), or the sum of ST elevation (or deviation)and infarct size cannot be expected. The sum of STelevation is affected by both the extent (the size ofthe ischemic area at risk) and the severity ofischemia (in addition to other non-ischemic varia-ble such as myocardial mass, the width of the chestwall and the distance between the electrode and theischemic zone). This explains therefore, the fact thesum of ST elevation correlated with peak CK-MB,but probably not with left ventricular ejection frac-tion, or regional wall motion score (data not report-ed) [8]. The study by Sadanandan et al. [20] illus-trates these non-linear relations. Patients with STelevation in both the anterior and inferior leads haveactually smaller apical infarction caused by a distalocclusion of a wrapping LAD, despite having great-er sum of ST elevation in larger number of leadsthan patients with pure anterior ST elevation [20].Moreover, as stated by Czechowska et al. [8], pa-tients with anterior STEMI and ST depression,rather than elevation in leads V5–V6 had more ex-tensive regional wall motion abnormalities andmore severe regional dysfunction.In conclusion, the correlations between thevarious ECG patterns and the size and localizationof the ischemic area at risk in patients with anteri-or STEMI are complex. The situation with non-an-terior STEMI may be even more complicated [3].Further studies are needed to better understand theinformation that can be obtained from the present-ing ECG of STEMI and how to use it for diagnosis,risk stratification and triage for therapy.References1. Van de Werf F, Ardissino D, Betriu A et al. Manage-ment of acute myocardial infarction in patients pre-senting with ST-segment elevation. The Task Forceon the Management of Acute Myocardial Infarctionof the European Society of Cardiology. Eur Heart J,2003; 24: 28–66.2. Antman EM, Anbe DT, Armstrong PW et al. ACC//AHA guidelines for the management of patients withST-elevation myocardial infarction. A report of theAmerican College of Cardiology/American HeartAssociation Task Force on Practice Guidelines(Committee to Revise the 1999 Guidelines for theManagement of patients with acute myocardialinfarction). J Am Coll Cardiol, 2004; 44: E1–E211.3. Atar S, Barbagelata A, Birnbaum Y. Electrocardio-graphic diagnosis of ST-elevation myocardial infarc-tion. Cardiol Clin, 2006; 24: 343–65.4. Birnbaum Y, Hasdai D, Sclarovsky S, Herz I, Stras-berg B, Rechavia E. Acute myocardial infarction en-tailing ST segment elevation in lead aVL: Electro-cardiographic differentiation among occlusion of theleft anterior descending, first diagonal, and first ob-tuse marginal coronary arteries. Am Heart J, 1996;131: 38–42.5. Birnbaum Y, Sclarovsky S, Solodky A et al. Predic-tion of the level of left anterior coronary artery ob-struction during acute anterior wall myocardial inf-arction by the admission electrocardiogram. Am JCardiol, 1993; 72: 823–826.6. Birnbaum Y, Solodky A, Herz I et al. Implication ofinferior ST segment depression in anterior acute myo-cardial infarction: electrocardiographic and angiograph-ic correlation. Am Heart J, 1994; 127: 1467–1473.7. Sasaki K, Yotsukura M, Sakata K, Yoshino H,Ishikawa K. Relation of ST-segment changes in infe-546Folia Cardiol. 2006, Vol. 13, No. 7www.foliacardiologica.eurior leads during anterior wall acute myocardialinfarction to length and occlusion site of the leftanterior descending coronary artery. Am J Cardiol,2001; 87: 1340–1345.8. Czechowska M, Kornacewicz-Jach Z, Gorący J et al.The value of the initial electrocardiogram in the eva-luation of acute ischaemic area in anterior myocar-dial infarction. Folia Cardiol, 2006; 13: 570–577.9. Birnbaum Y, Herz I, Solodky A et al. Can we differ-entiate by the admission ECG between anterior wallacute myocardial infarction due to a left anterior de-scending artery occlusion proximal to the origin ofthe first septal branch and a postseptal occlusion?Am J Noninvasive Cardiol, 1994; 8: 115–119.10. Engelen DJ, Gorgels AP, Cheriex EC et al. Value ofthe electrocardiogram in localizing the occlusion sitein the left anterior descending coronary artery inacute anterior myocardial infarction. 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Determi-nants of infarct size in reperfusion therapy foracute myocardial infarction. Circulation, 1992; 86:81–90.16. Christian T, Gibbons R, Clements I, Berger P,Selvester R, Wagner G. Estimates of myocardium atrisk and collateral flow in acute myocardial infarctionusing electrocardiographic indexes with comparisonto radionuclide and angiographic measures. J Am CollCardiol, 1995; 26: 388–393.17. Baks T, van Geuns RJ, Biagini E et al. Effects ofprimary angioplasty for acute myocardial infarctionon early and late infarct size and left ventricular wallcharacteristics. J Am Coll Cardiol, 2006; 47: 40–44.18. Aldrich H, Wagner N, Boswick J et al. Use of initialST-segment deviation for prediction of final electro-cardiographic size of acute myocardial infarcts. Am JCardiol, 1988; 61: 749–753.19. Clemmensen P, Grande P, Aldrich H, Wagner G.Evaluation of formulas for estimating the final size ofacute myocardial infarcts from quantitative ST-seg-ment elevation on the initial standard 12-lead ECG. J Electrocardiol, 1991; 24: 77–83.20. Sadanandan S, Hochman JS, Kolodziej A et al. Clinicaland angiographic characteristics of patients with com-bined anterior and inferior ST-segment elevation onthe initial electrocardiogram during acute myocardialinfarction. Am Heart J, 2003; 146: 653–661.

Can we use the electrocardiogram to refine the estimation of the size and location of ischemia in anterior ST elevation myocardial infarction?

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Can we use the electrocardiogram to refine the estimation of the size and location of ischemia in anterior ST elevation myocardial infarction?

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