Article, Cardiology

Lead aVL on electrocardiogram: emerging as important lead in early diagnosis of myocardial infarction?

a b s t r a c t

Although a diagnosis of acute myocardial infarction (AMI) that mandates emergency reperfusion therapy requires ST-segment elevation greater than 1 mm in at least 2 contiguous leads, some of the early electrocardiogram changes of AMI can be subtle. Any ST-segment depression or T-wave inversion in lead aVL may be implicated in left anterior descending artery lesion or early reciprocal changes of inferior wall myocardial infarction, particularly when the Clinical context suggests ischemia. Early recognition of reciprocal changes and serial ECG help initiate early appropriate intervention. Heightened awareness of ST segment and T-wave changes in lead aVL is of paramount importance to quickly identifying life- threatening condition.

(C) 2014

This short communication was compiled based on ongoing stud- ies from our group and cases that we have encountered with regards to T-wave inversion (TWI) as well as ST-segment depression in lead aVL (Fig.) We wish to highlight the Diagnostic significance of these electrocardiogram changes in the setting of Acute Coronary Syndrome (ACS).

ST segment elevation is the hallmark of acute myocardial infarction (AMI) and is identified on the ECG which can specify the Culprit coronary artery [1-3]. Reciprocal ST Segment and T wave changes accompanying anterior wall myocardial infarction (AWMI) are well known [4]; However the role of reciprocal ST segment and T wave changes in lead aVL reflecting early acute changes in inferior wall myocardial infarction (IWMI) have not been well studied or emphasized [5-18]. AVL changes are thought to be an early sign and sensitive marker of AMI before ST segment elevations occur [5]. Early diagnosis and initiation of appropriate intervention is of paramount importance for improved outcome of patients with ACS [19].

Much attention has been given to ST and T wave changes and their role in ACS and AMI in recent years [5,9,10,12-14,20-24]. Changes in ST segments and T waves in general represent abnormalities in ventricular repolarization. Causes of ST segment or T wave changes

* Corresponding author. Metropolitan Hospital Center, New York, NY 10029, USA. Tel.: +1 2124236464.

E-mail address: [email protected] (G.W. Hassen).

unrelated to QRS abnormalities, also known as primary Repolarization abnormalities, include ischemia, electrolyte abnormalities especially potassium, pericarditis, myocarditis and medications such as digoxin [13]. Abnormalities in ST segment and T wave can also result from non ACS causes such as subarachnoid hemorrhage and pulmonary embolism [13,25-28]. ST segment depression and TWI may represent reciprocal changes of AMI in areas opposite the site of the myocardial injury due to electric field effect or may be due to ischemia secondary to vasospasm in a non-occluded coronary vessel [4,12,14,15,30-36]. Factors such as the size and location of the infarct as well as the presence of a left anterior descending (LAD) lesion influence the presence and magnitude of reciprocal changes [7]. Reciprocal changes in lead aVL are less influenced by the infarct size [13]. There is no standard limb lead representing -60o. Lead aVL (-30o) is the closest to -60o and positioned over the superior and /or high lateral aspect of the inferior wall directly opposing lead III. Therefore aVL can truly be considered reciprocal to the inferior wall. Lead aVL shows changes earlier than ST segments elevation in the inferior leads in the setting of IWMI. Moreover, ST segment depression may represent an area of ischemia of the anterior wall or it could be the sign of acute posterior wall MI (PWMI) when it is present in leads V1 and V2. It may represent reciprocal changes of acute AWMI when present in inferior leads (II, III and aVF). In addition, ST segment depression in lead aVL may represent early reciprocal changes of IWMI when present in lead aVL [4,5,21,31-33,37]. ST-segment depression in lead aVL has been considered to predict poor outcome after AMI [9,37-39]. Some studies have shown the significance of ST-segment depression in lead aVL as

http://dx.doi.org/10.1016/j.ajem.2014.02.038

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786 G.W. Hassen et al. / American Journal of Emergency Medicine 32 (2014) 785-788

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Fig 1. electrocardiogram changes in lead aVL [TWI (red arrow) and ST segment depression (green arrow)].

an early and sensitive marker for acute IWMI [5]. Kracoff et al [7,8] have shown from coronary angiographic studies in humans that occlusion of the LAD demonstrated peaked T wave and ST-segment elevation in leads I, aVL, and precordial leads as primary site of ischemia and reciprocal ST-segment depression or TWI in leads II, III, and aVF. Likewise, they showed that occlusion of right coronary artery revealed primary ST-segment elevations and TWI in leads II, III, and aVF with reciprocal changes such as ST-segment depression and TWI in leads I and aVL. These reciprocal changes manifested earlier than the primary ST-segment elevation in the primary areas. Contrary to other reports and theories that reciprocal changes represent electric field changes, Kracoff et al [7,8] found that these changes are indicative of distant ischemia in multivessel coronary artery disease (CAD).

It is important to recognize that the magnitude of ST-segment elevation and reciprocal ST-segment depression is affected by the distance of the leads recording these changes from the ischemic region and their angle of deviation from the ischemic region [29]. This particularly explains why the reciprocal ST-segment depres- sion is more prominent when the overall amplitude of the QRS complex is low, and the magnitude of ST-segment elevation is small.

In fact, in the absence of left ventricular hypertrophy or Left bundle branch block, the reciprocal ST-segment depression should be sought. It is of great utility in patients with ACS and elevation of ST segments in 2 contiguous leads, as it strongly suggests the diagnosis of STEMI rather than other causes of mild ST-segment elevation (1-1.5 mm) [11].

In addition, Shah et al [37] have shown that these reciprocal changes have prognostic significance. Their data indicate that patients with inferior wall infarction who have associated pre- cordial ST-segment depression have greater global and regional left ventricular dysfunction, presumably due to associated ischemia or infarction in areas remote from the inferior wall and also have relatively high in-hospital mortality and morbidity rates. Early noninvasive detection of this high-risk subset may permit the testing of aggressive modes of therapy designed to limit the extent of myocardial ischemic damage with resultant decrease in mortality and morbidity. Akhras et al [9] also showed that reciprocal ST- segment depression occurring at the time of acute myocardial infarction may identify patients with severe coronary disease. It appeared that the presence of this reciprocal change was as reliable as an early postinfarction exercise test in predicting the underlying

G.W. Hassen et al. / American Journal of Emergency Medicine 32 (2014) 785-788 787

coronary anatomy. In the absence of reciprocal ST change at the time of acute myocardial infarction, however, it remains important to perform early exercise testing to exclude additional CAD. Their conclusion was that reciprocal ST depression should be considered indicative of severe multivessel coronary arterial disease and a risk factor for subsequent cardiac events. Angiography is advised for these patients. When there is no reciprocal change, early exercise testing provides valuable additional information about underlying CAD and is recommended routinely.

Hyperacute T wave is a well recognized early sign of AMI [40-42], but the importance of TWI as a reciprocal change in identifying AMI without accompanying ST-segment elevation in the setting of ACS has been the subject of controversy and many studies [5,9- 11,13,16,20,25,43-48]. T-wave inversion in lead aVL has been associated with LAD artery lesion [24,49]. Changes in this specific ECG lead may represent significant CAD in the LAD segment or represent an early reciprocal change for IWMI in the appropriate clinical presentation [5,7,8]. Farhan et al [49] and our group [24] demonstrated that presence of TWIs in lead aVL may signify a mid- LAD lesion. As reported by Farhan et al [49], the corresponding TWI in lead aVL of the patients with mid-LAD lesions was read as normal by the referring physicians. Given the significance of TWI in lead aVL, it is instrumental that serial ECG be performed to differentiate the 2 conditions (the presence of a significant LAD lesion vs early reciprocal change of acute IWMI). Serial ECG helps detect the dynamic changes of myocardial infarction. A TWI in lead aVL as a result of chronic LAD lesion should not change on serial ECGs, whereas TWI as a result of reciprocal change of acute IWMI should evolve from TWI to ST- segment depression in the reciprocal leads and later to ST elevation the primary leads (leads II, III, and aVF).

Of further note, 25% to 53% of patients with IWMI have right

ventricular involvement [50]. These cases carry higher morbidity and mortality than an IWMI without right ventricular involvement, which has a favorable outcome in general. The value of ST-segment depression in lead aVL in identifying involvement of the right ventricle has been studied. Turhan et al [50] have shown that the presence of more than 1 mm ST-segment depression in lead aVL has a sensitivity of 87% and a positive predictive value of 90% in diagnosing right ventricular involvement in acute IWMI.

In summary, TWI alone in lead aVL with no pathologic QS and/or ST-T changes in other leads is usually described as normal ECG by the referring physicians and computer-assisted ECG interpretation. The aforementioned cases and studies highlight the importance of the ECG changes in lead aVL and their prognostic significance. Health care providers should be alert of TWI in aVL especially in presence of major risk factors for CAD and in absence of secondary causes that might alter the polarity of T wave. New or presumed new TWI as well as ST-segment depression in lead aVL in the setting of ACS should alarm the physician of impending IWMI or the presence of LAD lesion. Serial ECG and follow-up of dynamic ST-T changes in inferior leads help differentiate these 2 diagnoses. Emergency physicians in particular should pay close attention to these subtle findings as it is vital to identify patients with increased risk for cardiac events and initiate appropriate treatment and further intervention.

1. Conclusion

There is accumulating evidence that ST segment and T-wave changes in lead aVL may have diagnostic and prognostic signifi- cance. These ECG changes may represent early reciprocal change of acute IWMI or indicate the presence of a significant LAD lesion. Serial ECG may help differentiate these 2 conditions and initiate appropriate therapy to avoid significant morbidity and mortality. The presence of these specific ECG findings should not be considered nonspecific, and the diagnosis should not be missed or

delayed as it can affect the outcome of patients with ACS. Physician training should emphasize the importance and significance of these changes in lead aVL.

Acknowledgment

We thank Dr Shaw and Laura Gabbe for reviewing and editing the manuscript.

References

  1. Brady WJ, Perron AD, Chan T. Electrocardiographic ST-segment elevation: correct identification of acute myocardial infarction (AMI) and non-AMI syndromes by emergency physicians. Acad Emerg Med 2001;8:349-60.
  2. Brady WJ, et al. Electrocardiographic ST-segment elevation: the diagnosis of acute myocardial infarction by morphologic analysis of the ST segment. Acad Emerg Med 2001;8:961-7.
  3. Jayroe JB, et al. Differentiating ST elevation myocardial infarction and nonischemic causes of ST elevation by analyzing the presenting electrocardiogram. Am J Cardiol 2009;103:301-6.
  4. Myers GB, Klein HA, Stofer BE. Correlation of electrocardiographic and pathologic

    findings in anteroseptal infarction. Am Heart J 1948;36:535-75.

    Birnbaum Y, Sclarovsky S, Mager A, Strasberg B, Rechavia E. ST segment depression in a VL: a sensitive marker for acute Inferior myocardial infarction. Eur Heart J 1993;14:4-7.

  5. Rashduni DL, Tannenbaum AK. Utility of ST segment depression in lead AVL in the diagnosis of Right ventricular infarction. N J Med 2003;100:35-7.
  6. Kracoff OH, et al. Twelve-lead electrocardiogram recording during percutaneous transluminal coronary angioplasty. Analysis of reciprocal changes. J Electrocardiol 1990;23:191-8.
  7. Kracoff OH, et al. Reciprocal changes as the presenting electrocardiographic manifestation of acute myocardial ischemia. Am J Cardiol 1993;71:1359-62.
  8. Akhras F, Upward J, Jackson G. Reciprocal change in ST segment in acute myocardial infarction: correlation with findings on exercise electrocardiography and coronary angiography. Br Med J (Clin Res Ed) 1985;290:1931-4.
  9. Bischof, JE. New strategy distinguishes inferior STEMI from pericarditis.
  10. Brady WJ, et al. Reciprocal ST segment depression: impact on the electrocardio- graphic diagnosis of ST segment elevation acute myocardial infarction. Am J Emerg Med 2002;20:35-8.
  11. Goldberger AL, Erickson R. Subtle ECG sign of acute infarction: prominent reciprocal ST depression with minimal primary ST elevation. Pacing Clin Electrophysiol 1981;4:709-12.
  12. Hanna EB, Glancy DL. ST-segment depression and T-wave inversion: classification, differential diagnosis, and caveats. Cleve Clin J Med 78, 404-414.
  13. Haraphongse M, Tanomsup S, Kappagoda CT, Rossall RE. Significance of ST- segment depression in inferior leads in patients with acute anterior infarction. Clin Invest Med 1984;7:143-8.
  14. Jennings K, Reid DS, Julian DG. “Reciprocal” depression of the ST segment in acute myocardial infarction. Br Med J (Clin Res Ed) 1983;287:634-7.
  15. Menown IB, Allen J, Anderson JM, Adgey AA. ST depression only on the initial 12-lead ECG: early diagnosis of acute myocardial infarction. Eur Heart J 2001;22:218-27.
  16. Odemuyiwa O, Peart I, Albers C, Hall R. Reciprocal ST depression in acute myocardial infarction. Br Heart J 1985;54:479-83.
  17. Pollehn T, Brady WJ, Perron AD. Electrocardiographic ST segment depression. Am J

    Emerg Med 2001;19:303-9.

    Akhras F, Upward J, Keates J, Jackson G. Early exercise testing and elective coronary artery bypass surgery after uncomplicated myocardial infarction. Effect on morbidity and mortality. Br Heart J 1984;52:413-7.

  18. Ando H, Yotsukura M, Sakata K, Yoshino H, Ishikawa K. Prognosis following acute myocardial infarction in patients with ST-T abnormalities on electrocardiograms obtained before myocardial infarction. Clin Cardiol 2001;24:107-13.
  19. Becker RC, Alpert JS. Electrocardiographic ST segment depression in coronary heart disease. Am Heart J 1988;115:862-8.
  20. Croft CH, et al. Clinical implications of anterior S-T segment depression in patients with acute inferior myocardial infarction. Am J Cardiol 1982;50:428-36.
  21. Hayden GE, Brady WJ, Perron AD, Somers MP, Mattu A. Electrocardiographic T-wave inversion: differential diagnosis in the chest pain patient. Am J Emerg Med 2002;20:252-62.
  22. Hassen GW, et al. The neglected lead on electrocardiogram: T wave inversion in lead aVL, nonspecific finding or a sign for left anterior descending artery lesion? J Emerg Med 2013. http://dx.doi.org/10.1016/j.jemermed.2013.08.079.
  23. Brady W.J. ST segment and T wave abnormalities not caused by acute coronary syndromes. Emerg Med Clin North Am 2006;24:91-111, [vi].
  24. Rosenbaum MB, Blanco HH, Elizari MV, Lazzari JO, Davidenko JM. Electrotonic modulation of the T wave and cardiac memory. Am J Cardiol 1982;50:213-22.
  25. Surawicz B. The pathogenesis and clinical significance of primary T wave abnormalities. Advances in electrophysiology. New York: Grune & Stratton; 1972.

    p. 377.

    Walder LA, Spodick DH. Global T wave inversion. J Am Coll Cardiol 1991;17:1479-85.

  26. Wagner GS, et al. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part VI: acute ischemia/infarction: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee; Council on Clinical Cardiology; the American College of

    788 G.W. Hassen et al. / American Journal of Emergency Medicine 32 (2014) 785-788

    Cardiology Foundation; and the Heart Rhythm Society. Endorsed by the International Society for Computerized Electrocardiology. J Am Coll Cardiol 2009;53:1003-11.

    Myers GB, Klein HA, Hiratzka T. Correlation of electrocardiographic and pathologic

    findings in anteroposterior infarction. Am Heart J 1949;37:205-36.

    Myers GB, Klein HA, Hiratzka T. Correlation of electrocardiographic and pathologic

    findings in posterior infarction. Am Heart J 1949;38:547-92.

    Myers GB, Klein HA, Stofer BE. Correlation of electrocardiographic and pathologic

    findings in lateral infarction. Am Heart J 1949;37:374-417.

    Schuster EH, Bulkley BH. Ischemia at a distance after acute myocardial infarction: a cause of early postinfarction angina. Circulation 1980;62:509-15.

  27. Bertrand ME, et al. The provocation of coronary arterial spasm in patients with recent transmural myocardial infarction. Eur Heart J 1983;4:532-5.
  28. Dunn RF, Kelly DT, Sadick N, Uren R. Multivessel coronary artery spasm. Circulation 1979;60:451-5.
  29. Mirvis DM. Physiologic bases for anterior ST segment depression in patients with acute inferior wall myocardial infarction. Am Heart J 1988;116:1308-22.
  30. Shah PK, et al. Noninvasive identification of a high risk subset of patients with acute inferior myocardial infarction. Am J Cardiol 1980;46:915-21.
  31. Platia EV, Grunwald L, Mellits ED, Humphries JO, Griffith LS. Clinical and arteriographic variables predictive of survival in coronary artery disease. Am J Cardiol 1980;46:543-52.
  32. Schuster EH, Griffith LS, Bulkley BH. Preponderance of acute proximal left anterior descending coronary arterial lesions in fatal myocardial infarction: a clinicopath- ologic study. Am J Cardiol 1981;47:1189-96.
  33. Wasserburger RH, Corliss RJ. Prominent precordial T waves as an expression of coronary insufficiency. Am J Cardiol 1965;16:195-205.
  34. Dressler W, Roesler H. High T waves in the earliest stage of myocardial infarction. Am Heart J 1947;34:627-45.
  35. Sagie A, et al. Acute anterior wall myocardial infarction presenting with positive T waves and without ST segment shift. Electrocardiographic features and angio- graphic correlation. Chest 1989;95:1211-5.
  36. Glancy DL, Doghmi W. Use of indicative and reciprocal electrocardiographic changes to help localize the site of coronary occlusion. Proc (Bayl Univ Med Cent) 2001;14:104-5.
  37. Haraphongse M, Tanomsup S, Jugdutt BI. Inferior ST segment depression during acute anterior myocardial infarction: clinical and angiographic correlations. J Am Coll Cardiol 1984;4:467-76.
  38. Norell MS, Lyons JP, Gardener JE, Layton CA, Balcon R. Significance of “reciprocal” ST segment depression: left ventriculographic observations during left anterior descending coronary angioplasty. J Am Coll Cardiol 1989;13:1270-4.
  39. Parale GP, Kulkarni PM, Khade SK, Athawale S, Vora A. Importance of reciprocal leads in acute myocardial infarction. J Assoc Physicians India 2004;52:376-9.
  40. Sorensen JT, et al. Significance of T-wave amplitude and dynamics at the time of reperfusion in patients with acute ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention. J Electrocardiol 2009;42:677-83.
  41. Tamura A, Kataoka H, Mikuriya Y, Nasu M. Inferior ST segment depression as a useful marker for identifying proximal left anterior descending artery occlusion during acute anterior myocardial infarction. Eur Heart J 1995;16:1795-9.
  42. Farhan HL, Hassan KS, Al-Belushi A, Sallam M, Al-Zakwani I. Diagnostic value of electrocardiographic T wave inversion in lead aVL in diagnosing coronary artery disease in patients with chronic stable angina. OMJ 2010;25:124-7.
  43. Turhan H, et al. Diagnostic value of aVL derivation for right ventricular involvement in patients with acute inferior myocardial infarction. Ann Noninva- sive Electrocardiol 2003;8:185-8.

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