ECG Blog #141 (Anatomy - Lat - Post - Inf - MI)

The ECG in Figure-1 was obtained from a man in his 50s, who presented with new severe chest pain.

• How would you interpret this­­ tracing?
• What area(s) of the heart are involved?
• What is the likely “culprit” artery?

Figure-1: 12-lead ECG obtained from a man in his 50s with chest pain. What is the likely “culprit” artery? 

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Interpretation: The underlying rhythm is sinus at a rate of 75-80/minute. Intervals and axis are normal. There is no chamber enlargement. Regarding Q-R-S-T Changes:

• Narrow but fairly deep Q waves are seen in leads III and aVF. There is also a small and narrow q wave in lead II, and a tiny q wave in lead V6.
• Overall R wave progression across the chest leads is appropriate — although R wave amplitude in lead V2 is a bit taller-than-expected. Small s waves persist through to leads V5, V6.
• There is dramatic ST elevation in each of the inferior leads (leads II,III,aVF) with a “check-mark” appearance that strongly suggests acute injury. As a subtle finding, there appears to be slight ST segment elevation in lead V1. The ST segment in this lead is coved and clearly more prominent than is usually the case.
• There is marked reciprocal ST depression in leads I and aVL. Note how the shape of this ST depression in lead aVL is a precise “mirror-image” picture of the ST elevation in lead III.
• There is at least 4mm of “shelf-like” ST depression in lead V2 — which surprisingly largely resolves by lead V3. There is a hint of J-point depression in leads V3-thru-V6.

Impression: In a patient with new-onset chest pain — the ECG appearance in Figure-1 is virtually diagnostic of a large acute infero-postero STEMI (ST Elevation Myocardial Infarction). In addition, there is almost certainly acute RV (Right Ventricular) involvement. This strongly suggests acute RCA (Right Coronary Artery) occlusion. In support of this conclusion — we make the following points:

• Statistically, approximately 80-90% of patients have a “right-dominant” circulation (Figure-2). This means that after supplying the RV (right ventricle) — the RCA continues as the PDA (Posterior Descending Artery) along the undersurface of the heart to supply the posterior and inferior walls of the LV (left ventricle). In contrast, about 15% of patients have a left-dominant circulation, in which the RCA is less prominent. To compensate, the LCx (Left Circumflex) artery is a relatively larger vessel, and it (rather than the RCA) provides most (or all) of the blood supply to the PDA. As a result not only the lateral, but also the inferior and posterior walls of the LV are predominantly supplied by LCx artery in patients with a left-dominant circulation. Bottom Line — Statistically then, even before looking at the ECG, we can predict that the “culprit artery” for the vast majority of patients with acute inferior STEMI is likely to be the RCA (See also ECG Blog #80).

Figure-2: Overview of normal coronary anatomy. Panel A — the most common situation (80-90%), in which the RCA is a dominant vessel that supplies the RV as well as the posterior and inferior walls of the LV. The RCA also provides blood supply to the RV. The LAD (Left Anterior Descending) artery normally supplies the anterior wall of the heart (via diagonal branches); part of the cardiac apex; and a major portion of the conduction system (via septal perforators that run vertically down through the septum). The LCx (Left Circumflex) artery supplies the lateral wall of the LV. Panel B — represents a left-dominant circulation, in which the LCx (rather than the RCA) supplies the posterior and inferior walls of the left ventricle.

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ECG features in Figure-1 that further support the likelihood of the RCA as the “culprit artery” are: i) ST elevation in lead III > II; ii) Marked reciprocal ST depression in lead aVL; iii) Relatively less (or no) lateral ST elevation, with the amount of ST elevation in lead III > V6; and, iv) Evidence of acute RV involvement.

• PEARL: The LCx does not supply the right ventricle. Therefore, if there is ECG evidence suggesting acute RV involvement in association with inferior STEMI — this is virtually diagnostic of the RCA being the culprit artery. While ST elevation in right-sided leads (especially in lead V4R) is clearly the best indicator of acute RV MI — lead V1 is a right-sided lead, and on occasion it may provide insight as to whether or not there is likely to be significant associated RV infarction. Normally the ST segment in lead V1 is flat or slightly depressed. With acute inferior STEMI — ST segments in leads V1, V2 and V3 often show ST depression due to accompanying posterior infarction and/or reciprocal changes due to the inferior STEMI. Typically, such ST depression is maximal in lead V2 — but it should also be present in V1. If ever there is ST segment coving (especially if accompanied by some ST elevation) in lead V1 — there is almost certainly acute RV involvement.
• In this case, the marked ST depression in lead V2 (Figure-1) indicates acute posterior involvement. This is supported by the taller-than-expected R wave in lead V2 (positive “mirror test” — See Figure 2 in ECG Blog #80). However, rather than ST depression in lead V1 — there is prominent ST segment coving with suggestion of slight elevation. In the setting of acute inferior STEMI — this is almost certainly the net result of right-sided ST elevation from acute RV infarction attenuating (opposing) the ST depression that should also be seen in lead V1 from acute posterior infarction. And, since the LCx does not provide blood supply to the RV — this finding of ST coving with slight elevation in lead V1, but with marked ST depression by V2 incriminates the RCA as the culprit vessel. It most often indicates proximal RCA occlusion.
• Note that the extent of acute infarction is obviously large in this case — since the amount of ST elevation is profound; ST elevation is accompanied by marked reciprocal ST depression; inferior Q waves have already formed; and inferior, posterior and right ventricular walls are involved.

BOTTOM LINE: Due to the possibility of anatomic variants and/or collateral circulation — definitive identification of the “culprit” artery is only possible with cardiac catheterization. That said, recognition of probable proximal RCA occlusion in this case with associated acute RV involvement is clinically important — because hemodynamics may differ compared to predominant LV infarction (ie, nitroglycerin is not advised because it may excessively lower BP; hypotension in the setting of acute RV involvement responds well to volume infusion).

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Acknowledgment: My thanks to MG for allowing me to use this tracing and clinical case.

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• See also ECG Blog #80.