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Location of Q-wave myocardial infarction in the era of cardiac magnetic resonance imaging techniques: An update
Journal of Electrocardiology 40 (2007) 69 – 71 www.elsevier.com/locate/jelectrocard
Location of Q-wave myocardial infarction in the era of cardiac magnetic resonance imaging techniques: An updateB A. Baye´s de Luna Institut Catala` Cie`ncies Cardiovasculars–Hosp. Sant Pau, Barcelona, Spain Received 10 May 2006; accepted 9 October 2006
Cardiac magnetic resonance (CMR) imaging with delayed contrast enhancement (CE) has emerged as a new anatomical gold standard technique that provides precise identification of infarcted myocardium in vivo.1-3 It is therefore appropriate to use CE-CMR verification of the accuracy of electrocardiographic (ECG) localization of infarction. The correlation between abnormal Q waves in various ECG leads and the affected left ventricular (LV) walls has been documented in the literature.4,5 Therefore, it is necessary to develop a new terminology by considering the relationships between changes in particular leads and infarct location as documented by CE-CMR. In 2005, a consensus group sponsored by the International Society of Noninvasive Cardiology met in Barcelona to develop a document containing this new terminology, which had been published in Circulation.6 The left ventricle is generally divided into approximately equal halves: the anteroseptal zone perfused by the left anterior descending (LAD) coronary artery as well as its branches and the inferolateral zone perfused by either the right or the circumflex coronary arteries. Fig. 1 shows the correspondence between the 17 segments of the left ventricle and their supplying coronary arteries.7 Variation among individuals in coronary anatomy affects the relationship between coronary arteries and myocardial segments. Pathologic Q waves have been defined by classic criteria8-14 and by criteria (Selvester criteria) documented by computer application.15 Infarcts identified using both of these criteria sets have now been studied using the CE-CMR as a gold standard.2,3 Recently, Q-wave myocardial infarction (MI) patterns, using the classic criteria that match better with the infarcted areas, have been defined,4 and the correlation of these ECG criteria with their corresponding infarction areas detected by CE-CMR has been reported to be high (86% overall concordance).5 Preliminary studies on the Selvester criteria of the infarcts in the anteroseptal half of the left ventricle have also documented a high correlation with CMR assessment.16,17 B This is an update to the summary of the consensus document [J Electrocardiol 2006;39:S79].
0022-0736/$ – see front matter D 2007 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2006.10.009
My colleagues and I decided to classify the different infarct locations by using the name of the wall or the name of the more affected segment of the wall. The 7 most commonly occurring patterns of abnormal Q waves and Q-wave equivalents are shown in Fig. 2. 1.
2.
Septal MI (Fig. 2, A1): The ECG shows Q waves in leads V1 through V2. The CE-CMR reveals involvement of the septal wall and often a small part of the adjacent anterior wall. The infarct is caused by the occlusion either of septal branches or of the LAD artery distal to the diagonal branches. Apical anterior MI (Fig. 2, A2): Compared with septal infarction, the abnormal Q waves extend into the more leftward precordial leads (typically V3 through V4 and sometimes V5 and V6). There are no abnormal Q waves in leads aVL and I. The CE-CMR documents MI in the LV apex, often with extension
Fig. 1. The 17 segments of the left ventricle (A) and the supplying coronary arteries: (B) LAD artery; (C) right coronary artery; and (D) LCX artery. Panel A shows in gray the areas of shared perfusion between the LAD artery and the right coronary artery or that between the LAD artery and the LCX artery.
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A. Baye´s de Luna / Journal of Electrocardiology 40 (2007) 69 – 71
Fig. 2. The 7 ECG patterns of Q-wave MI or Q-wave equivalent MI on the 17-segment model of the left ventricle, with the names given to the infarcted LV regions documented by CE-CMR. The 4 MI regions in the anteroseptal zone are designated as A1, A2, A3, and A4; the 3 MI regions in the inferolateral zone are designated as B1, B2, and B3. Note that only the example of septal branch occlusion is shown for septal MI.
3.
into both the anterior and septal walls but not into the lateral wall. The infarct is caused usually by midLAD artery occlusion. Extensive anterior MI (Fig. 2, A3): The extensive anterior infarction is essentially a combination of types A, B, and D. Consequently, the ECG shows abnormal Q waves in the precordial leads and in leads aVL and sometimes I. The CE-CMR documents that the infarct extensively involves the anterior, septal, and mid-low lateral walls. The infarct is caused by the occlusion of the LAD artery proximal to both the initial septal and diagonal branches.
4.
5.
Midanterior MI (Fig. 2, A4): Characteristically, this infarction presents abnormal Q waves in leads aVL and sometimes I but not in leads V5 through V6. A Q wave in leads V2 through V3 may be present. Contrast enhancement CMR shows that the infarction encompasses especially the mid-low segments (7 and 13) of the anterior wall. The infarct is usually caused by the occlusion of the first diagonal branch of the LAD artery. Lateral MI (Fig. 2, B1): This infarct may produce the Q-wave equivalents of abnormally prominent R waves in leads V1 and V2. There may also be
A. Baye´s de Luna / Journal of Electrocardiology 40 (2007) 69 – 71
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coronary artery in approximately 90% and the LCX artery in approximately 10% of human beings. 7. Inferolateral MI (Fig. 2, B3): When the right coronary artery or LCX artery are very dominant and the occlusion is proximal, the infarction encompasses both the inferior and lateral walls, and thus the ECG pattern is the combination of criteria for inferior and lateral MI. References
Fig. 3. Short-axis CE-CMR view from the bottom part of a chronic lateral infarct appearing above its representation by increased R waves in ECG leads V1, V2, and V3. The interstitial space created by the infarcted myocardium has been filled by gadolinium to reveal a patchy scar between the mitral papillary muscles. The ECG is recorded at the standard 10-mm/mVamplitude as documented by the calibration signal but at 50-mm/s paper speed.
6.
abnormal Q waves in leads I, aVL, and/or V3 through V6. The CE-CMR documents this infarction in the middle of the LV lateral wall (Fig. 3). The infarct is caused by the occlusion of a nondominant left circumflex (LCX) artery or of its marginal branch. Inferior MI (Fig. 2, B2): This infarct produces Q waves in leads II, III, and aVF, but without increased R waves in leads V1 and V2. The CE-CMR shows involvement of the inferior wall, including very often the basal segment. It should be noted that there may be involvement of the inferior part of the septal wall because the posterior descending artery has perforating branches that supply part of the inferior portion of the septum. The infarct is caused by the occlusion of the dominant coronary artery that supplies the posterior descending branch. This is the right
1. Judd RM, Kim RJ. Imaging time after Gd-DTPA injection is critical in using delayed enhancement to determine infarct size accurately with magnetic resonance imaging. Circulation 2002;106:36. 2. Moon JC, De Arenaza DP, Elkington AG, et al. The pathologic basis of Q-wave and non–Q-wave myocardial infarction: a cardiovascular magnetic resonance study. J Am Coll Cardiol 2004;44:554. 3. Kaandorp TA, Bas JJ, Lamb HJ, et al. Which parameters on magnetic resonance imaging determine Q waves on the electrocardiogram? Am J Cardiol 2005;95:925. 4. Cino JM, Pujadas S, Carreras F, et al. Baye´s de Luna, Utility of contrast-enhanced cardiovascular magnetic resonance (CE-CMR) to assess how likely is an infarct to produce a typical ECG pattern. Journal of Cardiovascular Magnetic Resonance 2006;8:335. 5. Baye´s de Luna A, Cino JM, Pujadas S, et al. Concordance of electrocardiographic patterns and healed myocardial infarction location detected by cardiovascular magnetic resonance. Am J Cardiol 2006;97:443. 6. Baye´s de Luna A, Wagner G, Birnbaum Y, et al. A new terminology for left ventricular walls and location of myocardial infarcts that present Q wave based on the standard of cardiac magnetic resonance imaging: a statement for healthcare professionals from a committee appointed by the International Society for Holter and Noninvasive Electrocardiography. Circulation 2006;114:1755. 7. Cerqueira M. Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart. A statement for healthcare professionals from the Cardiac Imaging Committee of the Council on Clinical Cardiology of the American Heart Association. Circulation 2002;105:539. 8. Surawicz B, Uhley B, Borun T. Task force I: standardization of terminology and interpretation. Am J Cardiol 1978;41:130. 9. Friedman HH. Diagnostic electrocardiography and vectorcardiography. New York7 McGraw-Hill; 1985. 10. Chou T. Electrocardiography in clinical practice. 1st ed. New York7 Grune & Stratton; 1979. 11. McFarlane P, Veitch L. Comprehensive electrocardiology. New York7 Pergamon Press; 1989. 12. Baye´s de Luna A. Textbook of clinical electrocardiography. 2nd ed. New Jersey, NY7 Futura Publishing; 1999. 13. Wagner GS. Marriot’s electrocardiography. 10th ed. Philadelphia, PA7 Lippincot Williams and Wilkins; 2001. 14. Fisch Ch. Electrocardiography in Braunwald’s textbook on heart diseases. 5th ed. Philadelphia7 Saunders; 1997. 15. 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. 16. Engblom H, White R, Selvester RH, et al. Development and validation of techniques for comparative quantitative clinical assessment of chronic anterior myocardial infarction by delayed enhancement magnetic resonance imaging and ECG. Am Heart J 2003; 146:359. 17. Engblom H, Hedstrfm E, Heiberg E, Wagner GS, Pahlm O, Arheden H. Size and transmural extent of first-time reperfused myocardial infarction assessed by cardiac magnetic resonance can be estimated by 12-lead ECG. Am Heart J 2006;150:290.e1.
Location of Q-wave myocardial infarction in the era of cardiac magnetic resonance imaging techniques: An updateB A. Baye´s de Luna Institut Catala` Cie`ncies Cardiovasculars–Hosp. Sant Pau, Barcelona, Spain Received 10 May 2006; accepted 9 October 2006
Cardiac magnetic resonance (CMR) imaging with delayed contrast enhancement (CE) has emerged as a new anatomical gold standard technique that provides precise identification of infarcted myocardium in vivo.1-3 It is therefore appropriate to use CE-CMR verification of the accuracy of electrocardiographic (ECG) localization of infarction. The correlation between abnormal Q waves in various ECG leads and the affected left ventricular (LV) walls has been documented in the literature.4,5 Therefore, it is necessary to develop a new terminology by considering the relationships between changes in particular leads and infarct location as documented by CE-CMR. In 2005, a consensus group sponsored by the International Society of Noninvasive Cardiology met in Barcelona to develop a document containing this new terminology, which had been published in Circulation.6 The left ventricle is generally divided into approximately equal halves: the anteroseptal zone perfused by the left anterior descending (LAD) coronary artery as well as its branches and the inferolateral zone perfused by either the right or the circumflex coronary arteries. Fig. 1 shows the correspondence between the 17 segments of the left ventricle and their supplying coronary arteries.7 Variation among individuals in coronary anatomy affects the relationship between coronary arteries and myocardial segments. Pathologic Q waves have been defined by classic criteria8-14 and by criteria (Selvester criteria) documented by computer application.15 Infarcts identified using both of these criteria sets have now been studied using the CE-CMR as a gold standard.2,3 Recently, Q-wave myocardial infarction (MI) patterns, using the classic criteria that match better with the infarcted areas, have been defined,4 and the correlation of these ECG criteria with their corresponding infarction areas detected by CE-CMR has been reported to be high (86% overall concordance).5 Preliminary studies on the Selvester criteria of the infarcts in the anteroseptal half of the left ventricle have also documented a high correlation with CMR assessment.16,17 B This is an update to the summary of the consensus document [J Electrocardiol 2006;39:S79].
0022-0736/$ – see front matter D 2007 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2006.10.009
My colleagues and I decided to classify the different infarct locations by using the name of the wall or the name of the more affected segment of the wall. The 7 most commonly occurring patterns of abnormal Q waves and Q-wave equivalents are shown in Fig. 2. 1.
2.
Septal MI (Fig. 2, A1): The ECG shows Q waves in leads V1 through V2. The CE-CMR reveals involvement of the septal wall and often a small part of the adjacent anterior wall. The infarct is caused by the occlusion either of septal branches or of the LAD artery distal to the diagonal branches. Apical anterior MI (Fig. 2, A2): Compared with septal infarction, the abnormal Q waves extend into the more leftward precordial leads (typically V3 through V4 and sometimes V5 and V6). There are no abnormal Q waves in leads aVL and I. The CE-CMR documents MI in the LV apex, often with extension
Fig. 1. The 17 segments of the left ventricle (A) and the supplying coronary arteries: (B) LAD artery; (C) right coronary artery; and (D) LCX artery. Panel A shows in gray the areas of shared perfusion between the LAD artery and the right coronary artery or that between the LAD artery and the LCX artery.
70
A. Baye´s de Luna / Journal of Electrocardiology 40 (2007) 69 – 71
Fig. 2. The 7 ECG patterns of Q-wave MI or Q-wave equivalent MI on the 17-segment model of the left ventricle, with the names given to the infarcted LV regions documented by CE-CMR. The 4 MI regions in the anteroseptal zone are designated as A1, A2, A3, and A4; the 3 MI regions in the inferolateral zone are designated as B1, B2, and B3. Note that only the example of septal branch occlusion is shown for septal MI.
3.
into both the anterior and septal walls but not into the lateral wall. The infarct is caused usually by midLAD artery occlusion. Extensive anterior MI (Fig. 2, A3): The extensive anterior infarction is essentially a combination of types A, B, and D. Consequently, the ECG shows abnormal Q waves in the precordial leads and in leads aVL and sometimes I. The CE-CMR documents that the infarct extensively involves the anterior, septal, and mid-low lateral walls. The infarct is caused by the occlusion of the LAD artery proximal to both the initial septal and diagonal branches.
4.
5.
Midanterior MI (Fig. 2, A4): Characteristically, this infarction presents abnormal Q waves in leads aVL and sometimes I but not in leads V5 through V6. A Q wave in leads V2 through V3 may be present. Contrast enhancement CMR shows that the infarction encompasses especially the mid-low segments (7 and 13) of the anterior wall. The infarct is usually caused by the occlusion of the first diagonal branch of the LAD artery. Lateral MI (Fig. 2, B1): This infarct may produce the Q-wave equivalents of abnormally prominent R waves in leads V1 and V2. There may also be
A. Baye´s de Luna / Journal of Electrocardiology 40 (2007) 69 – 71
71
coronary artery in approximately 90% and the LCX artery in approximately 10% of human beings. 7. Inferolateral MI (Fig. 2, B3): When the right coronary artery or LCX artery are very dominant and the occlusion is proximal, the infarction encompasses both the inferior and lateral walls, and thus the ECG pattern is the combination of criteria for inferior and lateral MI. References
Fig. 3. Short-axis CE-CMR view from the bottom part of a chronic lateral infarct appearing above its representation by increased R waves in ECG leads V1, V2, and V3. The interstitial space created by the infarcted myocardium has been filled by gadolinium to reveal a patchy scar between the mitral papillary muscles. The ECG is recorded at the standard 10-mm/mVamplitude as documented by the calibration signal but at 50-mm/s paper speed.
6.
abnormal Q waves in leads I, aVL, and/or V3 through V6. The CE-CMR documents this infarction in the middle of the LV lateral wall (Fig. 3). The infarct is caused by the occlusion of a nondominant left circumflex (LCX) artery or of its marginal branch. Inferior MI (Fig. 2, B2): This infarct produces Q waves in leads II, III, and aVF, but without increased R waves in leads V1 and V2. The CE-CMR shows involvement of the inferior wall, including very often the basal segment. It should be noted that there may be involvement of the inferior part of the septal wall because the posterior descending artery has perforating branches that supply part of the inferior portion of the septum. The infarct is caused by the occlusion of the dominant coronary artery that supplies the posterior descending branch. This is the right
1. Judd RM, Kim RJ. Imaging time after Gd-DTPA injection is critical in using delayed enhancement to determine infarct size accurately with magnetic resonance imaging. Circulation 2002;106:36. 2. Moon JC, De Arenaza DP, Elkington AG, et al. The pathologic basis of Q-wave and non–Q-wave myocardial infarction: a cardiovascular magnetic resonance study. J Am Coll Cardiol 2004;44:554. 3. Kaandorp TA, Bas JJ, Lamb HJ, et al. Which parameters on magnetic resonance imaging determine Q waves on the electrocardiogram? Am J Cardiol 2005;95:925. 4. Cino JM, Pujadas S, Carreras F, et al. Baye´s de Luna, Utility of contrast-enhanced cardiovascular magnetic resonance (CE-CMR) to assess how likely is an infarct to produce a typical ECG pattern. Journal of Cardiovascular Magnetic Resonance 2006;8:335. 5. Baye´s de Luna A, Cino JM, Pujadas S, et al. Concordance of electrocardiographic patterns and healed myocardial infarction location detected by cardiovascular magnetic resonance. Am J Cardiol 2006;97:443. 6. Baye´s de Luna A, Wagner G, Birnbaum Y, et al. A new terminology for left ventricular walls and location of myocardial infarcts that present Q wave based on the standard of cardiac magnetic resonance imaging: a statement for healthcare professionals from a committee appointed by the International Society for Holter and Noninvasive Electrocardiography. Circulation 2006;114:1755. 7. Cerqueira M. Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart. A statement for healthcare professionals from the Cardiac Imaging Committee of the Council on Clinical Cardiology of the American Heart Association. Circulation 2002;105:539. 8. Surawicz B, Uhley B, Borun T. Task force I: standardization of terminology and interpretation. Am J Cardiol 1978;41:130. 9. Friedman HH. Diagnostic electrocardiography and vectorcardiography. New York7 McGraw-Hill; 1985. 10. Chou T. Electrocardiography in clinical practice. 1st ed. New York7 Grune & Stratton; 1979. 11. McFarlane P, Veitch L. Comprehensive electrocardiology. New York7 Pergamon Press; 1989. 12. Baye´s de Luna A. Textbook of clinical electrocardiography. 2nd ed. New Jersey, NY7 Futura Publishing; 1999. 13. Wagner GS. Marriot’s electrocardiography. 10th ed. Philadelphia, PA7 Lippincot Williams and Wilkins; 2001. 14. Fisch Ch. Electrocardiography in Braunwald’s textbook on heart diseases. 5th ed. Philadelphia7 Saunders; 1997. 15. 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. 16. Engblom H, White R, Selvester RH, et al. Development and validation of techniques for comparative quantitative clinical assessment of chronic anterior myocardial infarction by delayed enhancement magnetic resonance imaging and ECG. Am Heart J 2003; 146:359. 17. Engblom H, Hedstrfm E, Heiberg E, Wagner GS, Pahlm O, Arheden H. Size and transmural extent of first-time reperfused myocardial infarction assessed by cardiac magnetic resonance can be estimated by 12-lead ECG. Am Heart J 2006;150:290.e1.