Schweitzer P, Keller S, Misra D, Fox J. Úloha 12-zvodového EKG pri určovaní artérie postihnutej infarktom. Cardiol 2003;12(4):192–202
EKG je prvým diagnostickým testom pacientov s bolesťou na hrudi. Tento jednoduchý a ľahko prístupný diagnostický nástroj pomáha potvrdiť a rozlišovať rôzne typy akútnych koronárnych syndrómov, odhadovať riziko myokardu, ako aj hodnotiť účinok reperfúzie koronárnej artérie. EKG ďalej pomáha identifikovať artériu postihnutú infarktom, čo je predmetom tohto článku.
Pri akútnom infarkte myokardu prednej steny IRA je ľavá predná zostupujúca koronárna artéria. Miesto LAD oklúzie je alebo proximálne (pred prvou diagonálnou alebo septálnou vetvou), alebo distálne. Diagnostické kritéria pre proximálnu LAD oklúziu sú ST elevácia v zvode aVL a spodná ST depresia. U pacientov s distálnou LAD oklúziou je ST segment elevácia obmedzená len na prekordiálne zvody. Pri AIM dolnej steny je IRA alebo pravá koronárna artéria, alebo ľavá cirkumflexná (zatočená) koronárna artéria. U pacientov s AIM dolnej steny kvôli RCA oklúzii je dôležité diferencovať medzi proximálnou a distálnou oklúziou. Nálezy EKG konzistentné s proximálnou RCA oklúziou sú ST elevácia vo zvode V3R, V4R, V1 a V2. U týchto pacientov môže EKG navyše pomôcť pri identifikácii vysoko rizikových pacientov a mnohocievného ochorenia. U vysokorizikových pacientov je ST segment depresia v pravých prekordiálnych zvodoch a pri mnohocievnych ochoreniach je viac vyčnievajúca ST segment depresia vo zvodoch V4 – 6.
Oklúzia LCF spôsobuje AIM spodnej a zadnej steny. Diagnostická presnosť 12-zvodového EKG pri LCF oklúzii nie je taká dobrá ako u pacientov s LAD a RCA oklúziou. Možno ju zlepšiť zaznamenávaním zvodu V7 – 9. Dôležité sú aj obmedzenia diagnózy IRA pomocou EKG najmä u pacientov s mnohocievnym koronárnym ochorením a predchádzajúcim infarktom myokardu.
Kľúčové slová: ST elevácie akútneho infarktu myokardu – 12-zvodové EKG – Diagnóza artérie postihnutej infarktom

Ten years ago, we reviewed the role of the 12 lead ECG in the management of acute myocardial infarction (AMI) in the thrombolytic era (1). Since that time, new improved criteria for identification of the IRA have been reported, particularly how to differentiate between the right coronary artery (RCA) and the left circumflex coronary artery (LCF) obstruction (2 – 5), to localize the site of the left anterior descending coronary artery (LAD) occlusion (6 – 10), to diagnose isolated first diagonal branch disease (11, 12) and left main coronary artery obstruction (13). In addition, the diagnosis of proximal RCA occlusion and posterior wall AMI can be improved by recording leads V3R, V4R and V7-9 respectively. The purpose of this article is to review the role of the ECG in the identification of the IRA in patients with AMI.

Localization of LAD occlusion. According to Blanke et al (14), the ECG cannot differentiate between proximal and distal LAD occlusion (14, 15), a view not shared by others (6 – 10, 16). In 1984 Lew et al (16) suggested that inferior ST segment depression is consistent with proximal LAD occlusion, which was confirmed by Birnbaum et al and others (6 – 10). Another ECG abnormality consistent with proximal LAD occlusion is ST elevation in aVL (6 – 10). According to Arbane and Goyl (10) and others (7 – 10), in proximal LAD occlusion, the incidence of ST elevation in lead aVL > 1.0 mm and ST segment depression in the inferior leads varies between 66 to 81%, and 58 – 90% respectively (7 – 10). ST segment elevation in lead aVL and I with ST depression in the inferior leads is seen in patients with proximal LAD occlusion (Figure 1). More recently, Engelen et al (9) also evaluated the ECG changes of LAD occlusion before the first septal branch. According to these authors (9), in addition to inferior lead ST segment depression, occlusion of the LAD before the first septal artery causes ST segment elevation in lead aVR, and in V1 (> 2.5 mm) or a right bundle branch block.

It should be stressed that ST elevation in lead aVL or inferior ST segment depression does not exclude distal LAD occlusion. For example, 1 mm ST segment elevation in lead aVL and the same degree of inferior depression can be seen in 1/3 of patients with distal LAD occlusion. However, ST segment depression of 2 mm or more was present only in 7 – 11% of patients’ with distal occlusion (10). In addition, according to Engelen et al (9) ST segment elevation in lead aVL is not helpful for localization of proximal LAD occlusion. The main criteria for mid and distal LAD occlusion are ST segment elevation in the precordial leads, depression in lead aVL and isoelectric ST segment in the inferior leads.

Patients with anterior wall AMI frequently have three-vessel coronary artery disease, collateral circulation and previous myocardial infarction, all of which can influence inferior ST segment changes (16, 17). According to some older studies, in a smaller number of patients, the ECG is helpful in the differential diagnosis between inferior wall ischemia and reciprocal changes (16 – 19). However, as mentioned, newer studies suggest that inferior ST segment depression is more likely due to proximal LAD occlusion than inferior wall ischemia (6 – 10, 18, 19). Finally the type of ST segment deviation in the inferior lead depends on the length of the LAD. Recently Sasaki et al (20) divided 159 patients with LAD occlusion into three groups according to inferior ST segment changes. In the first were 40 patients with ST segment depression, 25 with ST elevation and 94 patients with isoelectric ST segment in the inferior leads. These authors confirmed previous studies according to which wrapped around LAD significantly influences the inferior ST segments i.e. in patients with proximal occlusion and wrapped LAD, the ST segment is isoelectric and in those with mid occlusion of the LAD there is ST segment elevation in the inferior leads. This is illustrated in Figure 2 of a patient with wrapped around apex LAD and its occlusion after the first septal artery.

Tombstoning of the ST segment. Recently Guo et al (21) suggested that “tombstoning” of the ST segment, originally described by Wimalaratna (22), is seen mostly in patients with anterior wall AMI due to proximal LAD occlusion in the presence of three-vessel disease. According Guo et al (21) 83.3% and 92% of patients with tombstoning of the ST segment had anterior wall AMI and proximal LAD occlusion respectively. The diagnostic criteria of “tombstoning” of the ST segment are: absent or short duration of the R wave (< 0.04”), convex and merging ST segment with the T wave and with the descending limb of the R wave or ascending limb of the QS/QR wave. However this ECG pattern is not pathognomic for anterior wall AMI and can also be seen in patients with proximal RCA occlusion. In addition, tombstoning of the ST segment resembles distortion of the terminal QRS complex described by Birnbaum et al (23).

In summary, the following ECG findings are helpful to localize the site of LAD occlusion (Table 1). First, prominent (> 1 mm) ST segment elevation in lead aVL and inferior ST segment depression is consistent with proximal LAD occlusion (10). Second, ST segment depression in lead aVL particularly if combined with isoelectric ST segments in the inferior leads suggests distal LAD occlusion (8 – 10). Third, there is some controversy about the cause of the ST segment depression in the inferior leads. Some older studies (16, 17) particularly those in which coronary angiography was supplemented with wall-motion abnormalities and perfusion studies suggested that inferior myocardial ischemia and or previous myocardial infarction can influence the degree of inferior ST segment changes. Fourth, in patients with proximal LAD occlusion and wrapped around LAD, inferior ST segment depression is less prominent and the T waves are positive in lead III (24) or the ST segment is isoelectric (20). Fifth, collateral blood flow from the LCF wall could attenuate ST segment elevation in lead aVL, masking proximal LAD obstruction. Sixth, in the majority of patients with tombstoning of the ST segment (92%) had proximal LAD occlusion.

Combined ST segment elevation in anterior and inferior leads. In some patients with anterior wall AMI there is also ST segment elevation in the inferior leads. The most common cause of combined ST segment elevation is mid LAD occlusion “wrapped” around the apex (Figure 2). In general, these type of occlusion causes smaller myocardial infarcts and better prognosis (20, 25, 26). Another possible cause of combined ST segment elevation is proximal RCA occlusion with right ventricular involvement. Ilia et al (27) reported a rare case of combined chronic LAD and recent RCA occlusion suggesting that the anterior wall became ischemic due to loss of collateral circulation from the RCA.

ST segment elevation in leads V1. The two main causes of prominent ST segment elevation in lead V1 are anteroseptal AMI and proximal occlusion of the RCA with right ventricular involvement. The significance of ST segment elevation in lead V1 in anterior wall AMI is not completely clear. According to Engelen et al (9), ST segments elevation of > 2.5 mm in lead V1 is one of the criteria of LAD occlusion before the first septal branch (9). In comparison, Ben-Gal et al (28, 29) showed that, ST segment elevation in lead V1and its degree depends on the blood supply to the intraventricular septum i.e. ST segment elevation is most prominent in patients in whom the right paraseptal area is only supplied by the first septal branch. In patients with additional blood supply from the conus artery, the degree of ST segment in lead V1 depends on its size. If the conus artery is large, the ST segment remains isoelectric, if small, the ST segment is more elevated in lead V1 than V2 (29).

According to Stadius et al (15), the 12-lead ECG can diagnose an inferior wall AMI in 70 – 90% of cases. The incidence of proximal and mid RCA occlusion seems to be similar in 30% each. In the remaining patients, the obstruction is in the distal, posterior descending artery or the posterolateral branch of the RCA (30).

Proximal RCA occlusion. Occlusion of the RCA before the right ventricular branches causes right ventricular and inferior wall AMI. The involvement of proximal RCA occlusion frequently causes hypotension mimicking true cardiogenic shock and sinus bradycardia or second and third degree AV block (31). In addition, patients with proximal RCA occlusion have higher mortality and morbidity than those with mid or distal RCA occlusion.

The best criterion for proximal RCA occlusion is ST segment elevation in V4R or V3R (Figure 3), which in 50% of patients is transient, and normalizes within 10 hours (32) (Figure 3). Less frequently, right ventricular involvement causes ST segment depression in lead V3R and V4R (33). The second ECG abnormality in proximal RCA occlusion is ST segment elevation in the right precordial leads. In the majority of cases, maximal ST elevation is in lead V1 and is usually limited to lead V1-3. Occasionally, however, ST segment elevation extends to leads V4, 5 followed by the development of Q waves. In these patients, the differential diagnosis between right ventricular and anteroseptal myocardial infarction could be difficult (34). The third finding of proximal RCA disease is second and third degree AV block, which is also associated with worse prognosis (31) (Table 2).

Precordial ST segment depression. An important ECG finding in inferior wall AMI is precordial ST segment depression, the incidence of which varies between 60 to 73 % (30, 35 – 37). According to Peterson et al (35), ST segment depression is most common in lead V1-3 (57.9%), followed by V1-6 of 33.4% and 8.7% in V4-6. This topic was the subject of multiple studies and reviews, some of which are quoted in this article (1, 30, 35 – 39). The possible causes of precordial ST segment depression are: a. reciprocal ST depression being an electrophysiological phenomenon, b. anterior wall ischemia, c. extension of myocardial necrosis to the posterolateral wall and posterior third of the intraventricular septum. The last mechanism is the most common and was originally suggested by Shah et al (36) in 1980. These authors further showed that patients with precordial ST segment depression have a higher incidence of complications and worse prognosis. These findings were recently confirmed in a large multicenter study in patients undergoing coronary artery thrombolysis (35).

Different mechanisms of right and left precordial ST segment depression. Some newer studies suggested different mechanisms of right and left precordial ST segment depression (37, 40, 41). Strassberg et al (40) found significant LAD disease in 86% and 11% of patients with ST segment depression in V1-6 and V1-4 respectively. Hasdai et al (41) showed higher in-hospital mortality in patients with more prominent ST segment depression in V4-6 than V1-3. According to Birnbaum et al (37), patients with more marked ST segment depression in leads V4-6 than V1-3 have higher incidence of multivessel disease, lower ejection fraction and increased long term mortality. In comparison, Peterson et al (35) who analyzed 16.522 patients with inferior wall AMI, did not find differences in the clinical outcome in patients with right and left precordial ST segment depression. However, as expected, regardless of site of ST segment depression, these patients had higher incidence of postinfarction complications, in-hospital and one-year mortality.

The effect of proximal RCA occlusion on the ST segment shift in the precordial leads. The next question is the effect of proximal RCA occlusion in patients with inferoposterior extension on the right precordial ST segment. According to Lew et al (38) and others (42), proximal RCA occlusion causes right precordial ST segment elevation masking ST segment depression which is usually seen in patients with more extensive inferior wall AMI. This finding was not confirmed by Wong and Freedman (43) and others (44) who showed that, despite occlusion of the proximal RCA, involvement of the posterolateral wall causes ST segment depression in the right precordial leads. In other words, the absence of ST elevation in V4r and V1, 2 on the admission ECG (< 10 hours after the onset) does not rule out proximal RCA occlusion. Occasionally, in patients with proximal RCA occlusion there is ST segment elevation in lead V1 and depression in V2 (45).

The differential diagnosis between RCA and LCF occlusion will be discussed below.

Isolated RVMI is rare and mostly known from case reports (46 – 49). RVMI can be seen in: a. occlusion of a non-dominant RCA, b. occlusion of the right ventricular branches with poor collateral circulation or during percutaneous coronary intervention, c. proximal RCA disease with good collateral circulation to the posterior descending artery preventing infero-posterior wall myocardial infarction and in right ventricular hypertrophy (46 – 49). A RVMI post percutaneous coronary intervention is seen in Figure 4. A few hours after a stent placement into the proximal and mid RCA, the patient developed chest pain associated with prominent ST elevation and positive T wave in lead V1-3. The coronary angiogram confirmed an occlusion of the first right ventricular branch.

The diagnosis of isolated RVMI is important because it could mimic anterior wall myocardial infarction, or can cause atrial or ventricular fibrillation and syncope (46 – 49).

The LCF supplies the posterior, posterolateral and, in a left dominant system, also the inferior wall of the left ventricle. The infarct size depends on the area of myocardium, which is supplied by the LCF. At one end of the spectrum are small AMI with normal or non-specific ECG changes and at the other end, extensive necrosis (50) or hemodynamic impairment and mitral regurgitation (51). The incidence of LCF at the IRA is variable, depending on the diagnostic criteria. In patients presenting with chest pain (15) or positive CK enzyme levels (52), the LCF is the culprit coronary artery in 17% of patients. In patients presenting with ST elevation, the incidence of LCF occlusion is only 8% (16).

In LCF occlusion, the following questions are of clinical significance: a. the diagnostic accuracy of the 12 lead ECG, b. the differential diagnosis between RCA and LCF occlusion, c. the ECG changes in posterior and posterolateral AMI.

The diagnostic accuracy of the ECG in LCF occlusion. The ECG is less helpful in LCF than in LAD or RCA disease. According to Blanke et al (15), ST elevation in lead V6, and ST segment depression in lead V2 was seen in 36% and 48% respectively. Huey et al (52) found acute ST segment elevation and tall R wave in leads V1, 2 in 48% and 50% of patients with LCF occlusion respectively. Movahed and Becker (53) evaluated the ECG abnormalities in 31 patients with perfusion defects in the LCF distribution. Inferior ST segment elevation was present in 10 cases (32%) and ST segment elevation in leads aVL V5, 6 and I in five patients (23%). All patients with perfusion defect of the anterolateral wall had ST segment elevation in I aVL or V5, 6, six of whom also had ST segment depression in the inferior leads. Finally O’Keefe et al (50) studied 42 patients with LCF occlusion. ST segment elevation was absent in 10 cases (23%). However, myocardium at risk, measured by Technetium-99m- sestamibi imaging, was similar, regardless of the presence or absence of ST segment elevation.

The differential diagnosis between RCA and LCF occlusion. The most helpful ECG criteria to differentiate between RCA and LCF occlusion are the following (Table 3). First, in RCA occlusion there is more ST segment elevation in lead III than II and the opposite is true for LCF disease (2, 5). The explanation for these findings is the relationship between the inferior leads and the blood supply. In other words, lead III faces more the right side and lead II the left side of the inferior wall, which are supplied by the RCA and LCF respectively. Second, because lead aVL is reciprocal to lead III, occlusion of RCA causes more ST depression in lead aVL than in lead I. According to Chia et al (5) isoelectric ST segment in lead I is consistent with LCF occlusion. Third, LCF occlusion causes more pronounced ST depression in lead V3 and less ST elevation in lead III in comparison to the obstruction of the RCA, and therefore a ratio of ST depression in lead V3 to ST elevation lead III is less than 1 in RCA and more than 2.5 in LCF occlusion (3). Finally, Asali et al (4) suggested a S/R ratio of < 1/3 and ST segment depression less than < 1 mm in lead aVL as criteria for LCF occlusion, because lateral wall ischemia increases the R and decreases the S wave. In summary, the differentiation between RCA and LCF occlusion can be difficult because of large overlap between the ECG pattern of RCA and LCF occlusion (54).

Figure 5 illustrates the difficulties in the differential diagnosis between RCA and LCF occlusion. The 12-lead ECG shows prominent R wave, ST segment depression and positive T wave in lead V2 and ST segment elevation in lead V4-6 suggestive of LCF occlusion. However, the more prominent ST segments elevation in lead III than in II, together with ST segment depression in aVL is consistent with RCA occlusion. Coronary angiography showed 70% obstruction of the dominant RCA, 60% LMCA obstruction, nonobstructive LAD and moderate to severe diffuse disease of the LCF.

The culprit coronary artery in posterior wall AMI is the LCF. The diagnosis of isolated posterior wall AMI is difficult because no conventional precordial leads are facing the posterior wall of the left ventricle. The main criteria for isolated posterior wall AMI are: Tall R waves in leads V1-2 (> 0.04 sec) and ST segment depression in lead V1-4 with positive T waves (52, 53). However, these changes are not pathognomic for posterior wall AMI. Tall R waves can also be seen in normal subjects, in patients with hypertrophic cardiomyopathy, in pre-excitation syndrome and right ventricular hypertrophy. Similarly, ST segment depression in lead V1-3 has to be differentiated from anterior wall myocardial ischemia. It is suggested that in posterior wall AMI there is horizontal ST segment depression followed by positive T waves and in anterior ischemic syndrome, the ST segment depression is convex, downward, with negative T waves. However, in the early phase of posterior wall AMI the T wave may be negative. According to Boden et al, (55) in 40% of patients presenting with chest pain and ST segment depression in leads V1-4, the final diagnosis was posterior wall.

The diagnostic value of leads V7-9. Recording of lead V7-9 can improve the diagnosis of posterior wall AMI (51, 56 – 59). The main component of the QRS complex in leads V7-9 is a R wave with or without a q or s waves. The amplitude of the R is smaller than in lead V4-6, the ST segment is isoelectric and the T waves are positive. In lead V7-9 ST segments elevation of 1 mm is considered abnormal. Recently, Wung and Drew (59), considering on transient ischemia induced during percutaneous coronary intervention, suggested 0.5 mm ST segment elevation as a criterion for posterior wall AMI. There are few recent reports evaluating the role of lead V7-9 in the diagnosis of posterior wall AMI. Based on the analysis of 533 patients, Zalenski et al (57) showed an incidence of isolated ST elevation in lead V7-9 in 1.7% patients with chest pain. Matetzky et al (51) compared the coronary anatomy, echocardiography and clinical outcome in 33 patients with ST elevation in leads V7-9 and found that in all patients the IRA was either the main LCF or its marginal branch. Agarwal et al (58) recorded lead V7-9 in 18 patients with AMI confirmed by increased CPK enzymes and MB fraction with non-diagnostic 12-lead ECG. As expected, the LCF or its marginal branch was the culprit coronary artery. According to Agarwal et al, (58) and others (56, 57), ST elevation in V7-9 is frequently associated with ST segment depression in the right precordial leads (65 – 72%). Based on these studies (51, 57, 58), the main indications for leads V7-9 are ischemic chest pain with normal or non-specific ECG abnormalities and early differentiation between posterior wall AMI and non-ST segment elevation AMI.

ST segment elevation in lead aVL and I is classified as high lateral wall AMI, either due to occlusion of the LCF or its marginal branch or the first diagonal branch of the LAD (12, 14). The differential diagnosis between first diagonal and marginal branch occlusion is the following. In the former, there is ST segment elevation in lead I, aVL and V2 with isoelectric ST segment in the left precordial leads as seen in Figure 6. In patients with marginal branch occlusion there is ST segment elevation in lead I and aVL with or without elevation in lead V6 and ST segment depression in lead V2 (60).

Occlusion of the left main coronary artery (LMCA) is rare and frequently with fatal outcome. Recently, Yamaji and coworkers (13) analyzed the role of the 12-lead ECG in 16 patients with acute LMCA occlusion. According to these authors, the best criterion for LCFA occlusion is more prominent ST segment elevation in lead aVR than in lead V1. The opposite is true for proximal LAD occlusion. The sensitivity and specificity of this ECG abnormality was 81 and 80% respectively. Figure 7 is from a patient with acute LMCA occlusion showing ST elevation in lead aVR > V1. The ST segment is also elevated in lead III and there is marked ST segment depression in the remaining nine leads. Because of the low incidence of LMCA occlusion, we may need additional experiences to confirm the suggestion of Yamaji et al (13).

In patients with suspected acute coronary syndrome, the 12 lead ECG remains the first diagnostic test to confirm the ischemic origin of the chest pain. As discussed, the ECG also helps to localize the IRA, particularly in those with ST segment elevation. A more accurate diagnosis of the IRA and its level can be achieved by quantitative analysis of the ST segment shifts and by comparing the degree of ST segment elevation and depression in various leads. The ECG is most helpful in patients with first AMI and single vessel disease and is less accurate in those with multivessel coronary disease. Some of the ECG changes can be influenced and modified by previous myocardial infarction, collateral circulation and individual variation of the coronary anatomy.

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