LETTER TO THE EDITOR
Manifestation of left main coronary artery stenosis is diffuse st depression in inferior and precordial leads on ECG
Samuel Sclarovsky, MDa,
Nikus Kjell, MDa and
Yochai Birnbaum, MDa
a Cardiac Intensive Care Unit,Division of Cardiology,The University of Texas Medical Branch,5,106 John Sealy Annex,301 University Boulevard,Galveston, Texas 77555-0553,USA
yobirnba{at}utmb.edu
In the November 1, 2001, issue of the Journal of the American College of Cardiology, Yamaji et al. (1) reported on a novel electrocardiographic (ECG) sign for prediction of acute ischemia caused by left main coronary artery obstruction. They found that ST elevation in lead aVR with less ST elevation in lead V1 is a predictor of left main obstruction. Searching the English-language literature they found only 42 previous reported patients with acute left main stenosis. The ECG description in these studies included right bundle branch block, anterior ST elevation or precordial ST depression. However, our experience, supported by several studies that were not quoted by Yamaji et al., (1) is that the predominant ECG manifestation of left main stenosis is diffuse ST depression in both the inferior and precordial leads (2–4).
It was shown in both the experimental laboratory and in clinical studies that a sudden obstruction of a left main coronary artery induces an increase of the end diastolic pressure without increasing the end diastolic volume, thus shifting the pressure/volume curve upright (5,6). The sudden increase of the end diastolic pressure reduces the subendocardial coronary flow, resulting in a circumferential subendocardial ischemia (6). The electrical vector is shifted from the epicardium toward the subendocardium, causing diffuse ST depression with inverted T waves in the precordial leads on the surface ECG (2,3,7). Lead aVR faces the cavity of the left ventricle from a right superior axis and thus records a mirror image of the apical leads V5 and V6. Hence, if there is ST depression in leads V5 and V6, lead aVR will usually show ST elevation. This phenomenon is seen on the ECG in various clinical situations associated with an increase of the left ventricular end diastolic pressure, such as tachycardia-induced ischemia and in chronic infarction with restrictive remodeling (8).
In their study, Yamaji et al. (1) reported on the incidence of ST elevation in each lead, but not on the incidence of ST depression. In two of the three cases reported by Frierson et al. (4) there was ST elevation in lead aVR in addition to marked ST depression in leads V3 through V6. In the third case with acute ischemia due to left main stenosis, only mild ST depression was seen in leads V3 through V6 and no ST elevation in lead aVR, supporting the concept of lead aVR representing the mirror image of leads V5 and V6. Figure 1a of Yamaji et al. (1) shows ST elevation in leads aVR, aVL and V2, with marked ST depression in the inferior leads. We have previously reported this pattern to represent mid-anterior myocardial infarction (MI) caused by first diagonal branch occlusion (9). In the classic presentation, there is ST elevation in leads I, aVL and V2, reciprocal ST depression with negative T waves in the inferior leads, and ST depression with tall positive T waves in leads V4 and V5 (representing anterior subendocardial ischemia). Four of the eight patients reported in that study had ST elevation in lead aVR in the acute phase and six had ST elevation in lead aVR in the predischarge ECG. All these patients had an occlusion of the first diagonal branch without stenosis of the left main coronary artery. Thus, it might be that the ECG in Figure 1a presented by Yamaji and colleagues (1) represents ischemia induced by embolization of a thrombus from the left main coronary artery to the first diagonal branch.
It might be that there are cases in which the "reciprocal" ST elevation in lead aVR is more prominent than the ST depression in the leads facing the apex. Previously we reported that "reciprocal" ST depression in lead aVL is seen more often than ST elevation in leads II, III and aVF in the early stages of inferior acute MI (10).
In conclusion, ST elevation in lead aVR is probably a "reciprocal" change to ST depression in leads oriented toward the cardiac apex. Although ST elevation in lead aVR may occur with left main coronary artery occlusion, it may also be detected in other situations with ST depression, such as infarction caused by a first diagonal branch occlusion.
 |
References
|
|---|
1. 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;38:1348–1354[Abstract/Free Full Text]
2. Sclarovsky S, Davidson E, Strasberg B, et al. Unstable angina: the significance of ST segment elevation or depression in patients without evidence of increased myocardial oxygen demand. Am Heart J. 1986;112:463–467[CrossRef][Medline]
3. Sclarovsky S, Rehavia E, Strasberg B, et al. Unstable angina: ST segment depression with positive versus negative T wave deflection—clinical course, ECG evolution, and angiographic correlation. Am Heart J. 1988;116:933–941[CrossRef][Medline]
4. Frierson JH, Dimas AP, Metzdorff MT, Page US. Critical left main stenosis presenting as diffuse ST segment depression. Am Heart J. 1993;125:1773–1777[CrossRef][Medline]
5. Palacios I, Morvell SB, Powel WJ. Left ventricle end diastolic pressure volume relationship with experimental global ischemia. Circulation. 1976;39:744–755
6. Visner M, Aventzen CE, Parresh DG, et al. Effect of global ischemia on the diastolic properties of the left ventricle in conscious dogs. Circulation. 1985;71:610–619[Abstract/Free Full Text]
7. Guyton R, McClenenthan JH, Newman G, et al. Significance of subendocardial ST segment elevation caused by coronary stenosis in dogs: Epicardial ST depression, local ischemia and subsequent necrosis. Am J Cardiol. 1977;40:373–380[CrossRef][Medline]
8. Assali A, Sclarovsky S, Hertz I, et al. Persistent ST-segment depression in precordial leads V5–V6 after Q-wave anterior wall myocardial infarction is associated with restrictive physiology of the left ventricle. J Am Coll Cardiol. 2000;35:352–357[Abstract/Free Full Text]
9. Sclarovsky S, Birnbaum Y, Solodky A, et al. Isolated mid-anterior myocardial infarction: a special electrocardiographic subtype of acute myocardial infarction with ST elevation in nonconsecutive leads and two different morphological types of ST depressione. Int J Cardiol. 1994;46:37–47[CrossRef][Medline]
10. Birnbaum Y, Sclarovsky S, Mager A, Strasberg B, Rechavia E. ST segment depression in aVL: a sensitive marker for acute inferior myocardial infarction. Eur Heart J. 1993;14:4–7[Abstract/Free Full Text]
|
Top
References