Multicolinealidad: definición y consecuencias

Timothy G. Janz and Glenn C. Hamilton

ELECTROCARDIOGRAPHIC HIGHLIGHTS

Anatomic region Coronary artery Descriptive leads

Anterior wall LAD V3and V4

Anteroseptal LAD V1to V4

Anteroseptal–lateral Proximal LAD V1to V6,I and aVL

Septal wall LAD V1and V2

Inferior wall RCA; LCX II, III, and aVF Inferior Proximal RCA II, III, aVF, V1, V2, and

Right ventricle V3Rto V6R

Inferoposterior RCA; LCX II, III, aVF, V1, V2, and V7to V9

Posterior wall RCA; LCX V1, V2, and V7to V9

Lateral wall LAD V5, V6, I, and aVL

Anterolateral LAD; LCX V3to V6, I, and aVL Inferolateral LAD; LCX II, III, aVF, I, aVL, V5,

and V6

Posterolateral LAD; LCX V1, V2, V7to V9, V5, V6, I, and aVL

LAD, left anterior descending coronary artery; LCX, left circumflex coronary artery; RCA, right coronary artery.

174 SECTIONIII: ELECTROCARDIOGRAPHIC MANIFESTATIONS OF DISEASE

FIGURE 33-2• Anteroseptal myocardial infarction. Note the Q waves in leads V1to V4and mild ST segment elevation in leads V1to V3.

FIGURE 33-3• Anteroseptal myocardial infarction (MI). The acute ST segment elevation in leads V1to V4of this 75-year-old man represents an anteroseptal MI. These ST segment changes resolved completely with the administration of a thrombolytic agent.

FIGURE 33-1 • Acute anterior myocardial infarction. This ECG from a 67-year-old man with chest pain demonstrates ST segment elevation with symmetrical T wave inversion in precordial leads V2through V4.

from the involved region. Because no leads of the standard 12-lead ECG are located 180 degrees from the anterior or anteroseptal areas of the LV, acute MI (AMI) in these areas is not associated with reciprocal changes. Additional leads V7

through V9(see section on Posterior Wall), however, would demonstrate reciprocal changes with these anteroseptal infarctions.

STE in lead aVR that is at least as great as STE in lead V1 identifies left main coronary artery occlusion with 81%

sensitivity, 80% specificity, and 81% accuracy (Fig. 33-5).

The degree of STE in lead aVR is a quantitative measure of mortality in septal or anteroseptal MIs. STE in lead aVR of 1.5 mm has been found to predict death with 75% sensitivity, 75% specificity, and 75% accuracy.⁶

Lateral Wall. The lateral wall of the LV is commonly served by the LAD distal to the first septal perforator artery, but can also be supplied by the left circumflex artery (LCX).

The lateral wall is represented by leads V5and V6in the pre-cordial and leads I and aVL in the limb leads. Leads I and aVL represent the high lateral wall of the LV (Fig. 33-6).

Isolated lateral wall ischemia or infarction can occur. More commonly, however, the lateral wall is involved with other regions, such as inferolateral, anterolateral (Fig. 33-7), or anteroseptal with lateral extension. Acute coronary events of the lateral wall can also occur with involvement of the posterior wall (i.e., posterolateral). Anteroseptal ischemia or infarction with lateral extension is represented by involvement in leads V1

through V6, with or without leads I and aVL (Fig. 33-8). This is extensive ischemia or infarction and encompasses a large per-centage of the LV. Reciprocal changes can be seen with lateral wall infarctions but only if the high lateral wall (leads I and aVL) is involved. In this setting, the reciprocal changes appear in leads II, III, and aVF (see Figs. 33-7 and 33-8).

Inferior Wall. Acute coronary events involving the inferior wall of the LV are represented by changes in leads II, III, and aVF. These limb leads represent the electrical activity of the heart in the frontal plane and are oriented downward and infe-riorly. Reciprocal changes of an inferior wall MI are repre-sented by ST segment depression in leads I and aVL.

Myocardial ischemia in this region is typically caused by CHAPTER33: Acute Coronary Syndromes: Regional Issues 175

FIGURE 33-4• Acute anteroseptal myocardial infarction (MI). The ST segment elevation (STE) in leads V1to V4of this 50-year-old man with chest pain is compatible with an acute anteroseptal MI. The STE in lead V1is greater than 2.5 mm, which is a strong prediction of a left anterior descending coronary artery occlusion that is proximal to the first septal perforator coronary artery.

FIGURE 33-5 • Acute myocardial infarction secondary to left main coronary artery disease. This ECG from a 75-year-old man with acute chest pain demonstrates ST segment elevation (STE) in leads V1and V2as well as leads I and aVL. The precordial leads represent the septal region of the left ventricle and leads I and aVL represent the high lateral wall. Also note the ST segment depression in leads II, III, and aVF. These changes are compatible with recipro-cal changes from the infarction of the high lateral wall of the left ventricle. Figures 33-1 through 33-4 do not show reciprorecipro-cal changes because there are no leads of the standard 12-lead ECG that are anatomically 180 degrees opposite the anterior or septal regions of the left ventricle. This tracing also demonstrates STE in lead aVR that is greater in amplitude than the elevation in lead V1, a relatively sensitive and specific indicator of left main coronary artery disease.

176 SECTIONIII: ELECTROCARDIOGRAPHIC MANIFESTATIONS OF DISEASE

FIGURE 33-6• High lateral wall myocardial infarction (MI). As in other regions of the left ventricle (LV), an isolated lateral wall MI is unusual. This ECG demonstrates ST segment elevation in leads I and aVL. The ST segment depression in leads II, III, and aVF most likely represents reciprocal changes from the high lateral wall MI. On the other hand, the ST segment depression in leads V5and V6corresponds with myocardial ischemia in the remainder of the lateral wall of the LV.

FIGURE 33-7• Acute anterolateral myocardial infarction (MI). This ECG is from a 99-year-old man who presented with chest pain and dyspnea. The tracing shows ST segment elevation in leads V3to V6as well as in leads I and aVL, and corresponds to an acute anterolateral MI. The ST segment depressions in II, III, and aVF are most likely reciprocal changes from the infarction involving the high lateral wall of the left ventricle.

FIGURE 33-8• Extensive acute myocardial infarction (MI). The ECG tracing from this 55-year-old man shows marked ST segment elevation in the septal, anterior, and lateral walls of the left ventricle (LV). The ST segment depression in the inferior leads represents reciprocal changes. The large anatomic region of the LV involved with this MI predicts extensive coronary artery disease.

disease of the RCA and, less commonly, the LCX. The presence of STE in lead III exceeding the elevation in lead II can predict an occlusion in the proximal or mid-portion of the RCA (Fig. 33-9). The presence of STE in lead III, equal to that of lead II, is a strong predictor of LCX occlusion^7,8 (Fig. 33-10). This finding is attributable to the anatomic distribution of the respective coronary arteries; the RCA is

more right-sided, leading to greater changes in the right-sided lead III.

Isolated inferior wall involvement can occur but more commonly extends to the lateral wall, posterior wall, or the RV. The involvement of more than just the inferior wall of the LV is an indication of extensive disease. The presence of STE of 2 mm or more in leads V5and V6(Fig. 33-11), in association CHAPTER33: Acute Coronary Syndromes: Regional Issues 177

FIGURE 33-9 • Acute inferior myocardial infarction, right coronary artery (RCA). This ECG tracing from a 70-year-old man demonstrates marked ST segment elevation (STE) in leads II, III, and aVF. The ST segment depression in leads I and aVL associated with this isolated inferior myocardial infarction represents reciprocal changes in these leads. The STE in lead III that is of greater amplitude than that of lead II suggests an occlusion of the proximal or mid-portion of the RCA.

FIGURE 33-10 • Acute inferior myocardial infarction (MI), left circumflex coronary artery (LCX). The inferior MI of this 80-year-old woman is associated with ST segment elevation of relatively the same magnitude in leads II and III. This is often a predictor of an occlusion in the LCX. The ST segment depression in leads V1to V5may represent ischemia of the posterior region of the left ventricle or, more likely, ischemia of the anteroseptal region.

FIGURE 33-11 • Acute inferior myocardial infarction with extreme coronary artery disease. This ECG is from a 70-year-old man with chest pain of 3 to 4 hours’ duration. The tracing reveals ST segment elevation in leads II, III, and aVF, as well as leads V3to V6, indicating extensive coronary artery disease.

with an inferior wall MI, is a sensitive and specific indicator of extensive coronary artery disease and a large area of involvement.⁹

Right Ventricle. Approximately one fourth to one third of inferior wall AMIs are associated with RV infarction. The criteria for RV infarction are included in Table 33-1.

Approximately 87% of RV infarctions occur in association with inferior wall infarctions and are associated with occlu-sion of the proximal RCA.¹⁰Infarction of the RV allows the vector from the interventricular septum to pass unopposed.

This vector is usually directed anterior, inferior, and to the right. Lead III lies directly in this vector’s path, which causes the STE of an inferior wall MI to be of greater amplitude in lead III than in lead II. Because the unopposed vector from the interventricular septum is directed anterior and to the right, the ST segment in lead V1can be elevated (Fig. 33-12).

The STE is usually restricted to lead V1but occasionally can extend across the precordial leads.^11–13At times, the STE in lead V1 is accompanied by ST segment depression in lead V2.¹⁴This depression occurs because the vector originating from the interventricular septum is directed toward the right (lead V1) and away from the left (lead V2). Using the right 178 SECTIONIII: ELECTROCARDIOGRAPHIC MANIFESTATIONS OF DISEASE

33-1 • ELECTROCARDIOGRAPHIC CRITERIA FOR RIGHT VENTRICULAR INFARCTION

Presence of an inferior wall myocardial infarction ST segment elevation in lead III > lead II ST segment elevation in lead V1

ST segment depression in lead V2

ST segment elevation >2 mm in lead V4R(leads V3Rto V6R)

A

B

FIGURE 33-12• Inferior wall and right ventricular (RV) infarction. A, The inferior myocardial injury pattern of a 60-year-old woman also demonstrates ST segment elevation (STE) in lead V1. This finding often predicts an associated RV infarction. B, Right-sided precordial leads from this patient demonstrate STE in leads V3Rto V6R, which strongly suggests an RV infarction. Involvement of the RV is usually associated with occlusion of the proximal right coronary artery. This is also suggested by the STE in lead III that is of greater amplitude than that of lead II.

• Reciprocal changes are located anatomically 180 degrees away from the involved region of the left ventricle.

• Septal or anteroseptal myocardial infarctions (MIs) with ST segment elevation in lead aVR that is greater than or equal to the ST segment elevation in lead V₁are often associated with occlusion of the left main coronary artery.

• Anteroseptal MIs associated with lateral wall involvement are associated with extensive coronary artery disease.

• The ST segment elevation of an acute inferior MI that is of greater amplitude in lead III than in lead II is a strong predictor of occlusion of the proximal right coronary artery.

• Acute inferior MI associated with ST segment elevation in lead V₁is suggestive of right ventricular infarction.

• Posterior MI can be differentiated from septal myocardial ischemia by the presence of an R:S wave amplitude ratio of at least 1.

ELECTROCARDIOGRAPHIC PEARLS

precordial leads can often make the ECG diagnosis of RV infarction. The right precordial leads are placed as mirror images of the left precordial leads. Although STE can be seen in leads V3R through V6R, STE in lead V4R is most sensitive and specific for RV infarction^11,15 (Fig. 33-12). STE in the right precordial leads is not specific for RV infarction.

Infarction of the LV (anteroseptal) as well as pericarditis, blunt chest trauma, and pulmonary embolism may also be associated with similar findings in these leads.^16–19

Posterior Wall. The posterior wall of the LV is perfused by the posterior descending coronary artery, which usually orig-inates from the RCA and occasionally from the LCX.

Isolated, or pure, posterior wall ischemia or infarction is uncommon (Fig. 33-13). Infarction of the posterior wall is more commonly associated with AMI of either the inferior (Fig. 33-14) or lateral walls (Fig. 33-15). The standard 12-lead

ECG does not directly image the posterior wall. Therefore, identifying reciprocal changes in leads that are 180 degrees away from the posterior region, namely, leads V1 and V2, establishes the ECG diagnosis of posterior wall MI; in other words, ST segment depression in leads V1, V2, or V3 is strongly suggestive of posterior wall MI. The classic ECG changes in leads V1and V2 associated with a posterior wall MI are tall R waves relative to S waves, ST segment depression, and upright T waves. The R wave in the right precordial leads associated with posterior wall infarction has an R:S amplitude ratio of at least 1. The R waves are wider than normal and usu-ally have a duration of at least 0.03 sec. ST segment depres-sion in the right precordial leads can represent posterior wall infarction or septal ischemia. The ST segment depression of septal ischemia is associated with an R:S amplitude ratio of less than 1 and an R wave width less than 0.03 sec.

CHAPTER33: Acute Coronary Syndromes: Regional Issues 179

FIGURE 33-13 • Acute posterior wall myocardial infarction (MI). This tracing was obtained from a 66-year-old patient who presented with substernal chest pain. It has ST segment depression in primarily leads V2 and V3. Because the R wave in lead V2is of equal or greater amplitude compared with the S wave in the same lead and the duration of the R wave is greater than 0.03 sec, this tracing represents a true or isolated posterior MI and not ischemia of the anterior or septal regions of the left ventricle.

FIGURE 33-14• Acute infero-posterolateral myocardial infarction. This tracing from a 75-year-old man with chest pain, dyspnea, and diaphoresis demon-strates ST segment elevation in the inferior (leads II, III, and aVF) and lateral (leads V5and V6) regions of the left ventricle. The ST segment depression in leads I and aVL are reciprocal changes from the involvement of the inferior wall. The ST segment depression in leads V1to V3represents infarction of the posterior wall.

Using additional ECG leads, namely leads V7through V9,

can make the differentiation between posterior infarction and septal ischemia. Leads V7through V9are located on the same horizontal plane as leads V4through V6. Lead V7 lies along the posterior axillary line, lead V8lies along the inferior angle of the scapula, and lead V9is located at the left paraspinal bor-der. Because these leads lie directly over the posterior wall of the LV, they demonstrate the classic STE, abnormal Q wave, and inverted T wave of an AMI. The tall R wave relative to S wave in the right precordial leads is a more reliable indi-cator of posterior wall infarction than the ST segment or T wave changes in these same leads.^20,21A tall R wave relative to S wave in lead V1is not specific for posterior wall MI and can be seen in other conditions.

References

1. Goldberger AL: Myocardial Infarction: Electrocardiographic Differential Diagnosis, 4th ed. St. Louis, Mosby-Year Book, 1991.

2. Blanke H, Cohen M, Schlueter GU, et al: Electrocardiographic and coronary arteriographic correlations during acute myocardial infarction.

Am J Cardiol 1984;54:249.

3. Roberts WC, Gardin JM: Location of myocardial infarcts: A confusion of terms and definitions. Am J Cardiol 1978;42:868.

4. Hindman NB, Schocken DD, Widmann M, et al: Evaluation of a QRS scoring system for estimating myocardial infarct size: V. Specificity and method of application of the complete system. Am J Cardiol 1985;55:1485.

5. Engelsen DJ, Gorgels AP, Cheriex EC, et al: Value of the electrocardio-gram in localizing the occlusion site in the left anterior descending coronary artery in acute anterior myocardial infarction. J Am Coll Cardiol 1999;34:389.

6. Yamaji H, Iwasaki K, Kusachi S, et al: Prediction of acute left main coronary artery obstruction by 12-lead electrocardiography: ST segment elevation in lead aVR with less ST segment elevation in lead V1. J Am Coll Cardiol 2001;38:1348.

7. Zimetbaum PJ, Krishnan S, Gold A, et al: Usefulness of ST-segment elevation in lead III exceeding that of lead II for identifying the location of the totally occluded coronary artery in inferior wall myocardial infarc-tion. Am J Cardiol 1998;81:918.

8. Chia BL, Yip JW, Tan HC, Lim YT: Usefulness of ST segment II/III ratio and ST deviation in lead I for identifying the culprit artery in inferior wall acute myocardial infarction. Am J Cardiol 2000;

86:341.

9. Assali AR, Sclarovsky S, Herz I, et al: Comparison of patients with inferior wall acute myocardial infarction with versus without ST-segment elevation in leads V5and V6. Am J Cardiol 1998;81:81.

10. Kinch JW, Ryan TJ: Right ventricular infarction. N Engl J Med 1994;330:1211.

11. Lopez-Sendon J, Coma-Canella I, Alcasena S, et al: Electrocardiographic findings in acute right ventricular infarction: Sensitivity and specificity of electrocardiographic alterations in right precordial leads V4R, V3R, V1, V2and V3. J Am Coll Cardiol 1985;6:1273.

12. Andersen HR, Nielsen D, Falk E: Right ventricular infarction: Diagnostic value of ST elevation in lead III exceeding that of lead II during inferior/

posterior infarction and comparison with right-chest leads. Am Heart J 1989;117:82.

13. Saw J, Davies C, Fung A, et al: Value of ST elevation in lead III greater than lead II in inferior wall acute myocardial infarction for predicting in-hospital mortality and diagnosing right ventricular infarction. Am J Cardiol 2001;87:448.

14. Lew AS, Laramee P, Shah PK, et al: Ratio of ST-segment depression in lead V2to ST-segment elevation in lead aVF in evolving inferior acute myocardial infarction: An aid to the early recognition of right ventricular ischemia. Am J Cardiol 1986;57:1047.

180 SECTIONIII: ELECTROCARDIOGRAPHIC MANIFESTATIONS OF DISEASE

FIGURE 33-15• Acute high lateral myocardial infarction with posterior involvement. This ECG demonstrates ST segment elevations in the high lateral leads (I and aVL) with reciprocal changes in the inferior leads. The ST segment depression in leads V1to V4is representative of a posterior wall infarction as well. This is confirmed by the large R wave relative to S wave in the same leads.