Monday, January 13, 2014

ECG Interpretation Review #82 (Acute STEMI – RCA – LAD – Circumflex – Acute Occlusion – Culprit Artery – Infarction – Evolution)

     Interpret the ECG shown in Figure-1 — obtained from a patient with new-onset chest pain. There is an obvious acute STEMI (ST Elevation Myocardial Infarction). Follow-up ECGs on this patient are shown in Figure-2 (obtained a short while later) — and finally in Figure-3 (obtained post-cath/reperfusion).
  • Is there evolution of the MI on these serial ECGs? What are the specific changes you see as you compare these sequential tracings?
  • Which coronary artery is likely to be acutely occluded?
  • Was acute reperfusion successful (Figure-3)?
Figure-1: This is ECG #1 (blue border) — from this patient with new-onset chest pain. There is sinus bradycardia with marked precordial ST elevation. Q waves have not yet formed in the anterior leads on this initial ECG #1. Note the hyperacute appearance of ST-T waves in leads V2,V3,V4. Surprisingly — reciprocal changes are minimal (no more than slight ST-T wave flattening/depression in the inferior leads). Despite this — there can be little doubt that this ECG #1 represents a large acute STEMI in evolution. (Figure reproduced from ECG-2014-ePub). NOTE — Enlarge by clicking on Figures — Right-Click to open in a separate window.
What is the Culprit” Artery?: We suspect acute proximal LAD occlusion as the “culprit” artery for the acute STEMI seen in Figure‑1. This is suggested by the ECG finding of diffuse precordial ST elevation that is especially marked in leads V2-to-V4.
  • Acute occlusion of the LMain (Left Main) Coronary Artery is rarely seen in practice — because it usually leads to rapid demise of the patient. In addition to its uncommon occurrence — another clue that the ECG in Figure-1 does not represent LMain occlusion is that ST elevation is clearly more marked in lead V1 than in lead aVR. In contrast, with LMain disease or occlusion — ST elevation is generally more marked in aVR compared to V1.
  • This patient is an ideal candidate for acute reperfusion — because there is marked ST elevation in Figure-1, but no anterior Q waves have yet formed. The cath lab should be immediately activated.
Two follow-up ECGs to Figure‑1 are shown below. For clarity — We use a different color border for each tracing:
  • Figure-1ECG #1 (blue border) = the initial ECG obtained at presentation.
  • Figure-2ECG #2 (red border) = obtained a short while after ECG #1.
  • Figure-3ECG #3 (green border) = obtained after acute cath and angioplasty/stenting of the acutely occluded LAD.
As you evaluate these serial ECGs — Keep in mind the following Questions:
  • Is there ECG evidence of evolution on these serial ECGs?
  • Was acute reperfusion successful (Figure-3)?
Figure-2: This is ECG #2 (red border) — obtained a short while after ECG #1 from this patient with acute STEMI. Note that since ECG #1 — there has been interim development of RBBB (an rSr’ complex is now seen in V1 with wide terminal S waves in leads I,V6). The appearance of lead V2 is concerning — as the large new Q wave and now T wave inversion in this lead suggest ongoing evolution is in progress. (Figure reproduced from ECG-2014-ePub).
Figure-3: This is ECG #3 (green border) — obtained after acute catheterization and angioplasty/stenting of the acutely occluded LAD. The “good news” — is that this post-cath ECG #3 is encouraging! Note that the QRS complex has narrowed and RBBB is no longer present. The Q wave seen earlier in lead V2 of ECG #2 has resolved — and ST-T waves have essentially returned to baseline. R wave progression is essentially normal (with transition between V3-to-V4). It appears that acute reperfusion has salvaged significant myocardium! (Figure reproduced from ECG-2014-ePub).
BOTTOM Line: Use of serial ECGs may be extremely valuable in following the course of acute MI. Lead-to-lead comparison of QRS morphology and ST‑T wave changes facilitates determining which changes are new — as well as providing insight to the likely benefit obtained from acute intervention.
The LAD: Taking A Closer Look
The normal (expected) coronary anatomy of the LCA (Left-Coronary Artery) is depicted in schematic Figure-4:
  • The LCA arises from the left aortic sinus. This vessel begins as the LMain (Left Main Coronary Artery), which is typically a short vessel (<10mm) that then bifurcates into the LAD (Left Anterior Descending Artery) and the LCx (Left Circumflex Coronary Artery).
Major Branches of the LAD: The LAD (Left-Anterior-Descending) Artery runs along the anterior epicardial surface of the heart in the interventricular groove on its path toward the cardiac apex. The LAD generally supplies the anterior wall of the heart, the cardiac apex and a major portion of the conduction system.
  • The major branches of the LAD are i) the Septal perforator vessels; and ii) Diagonal branches.
  • Septal branch anatomy is highly variable. We show 2 septal branches in Figure-4 (S-1; S-2) — but instead there may be only one septal branch or many septal branches, depending on individual anatomy. The 1st septal branch is typically the largest; its takeoff is generally just after the takeoff of the 1st diagonal branch.
  • The interventricular septum is the most densely vascularized area of the heart. This is as it should be given the integral role of the septum in providing blood supply to the heart’s conduction system. Septal perforators normally run a vertical path downward following their takeoff from the proximal LAD.
  • Downward penetrating septal branches from the LAD typically connect with upward penetrating septal branches from the PDA branch of the RCA. In this way — there is usually a network of collaterals from both LCA and RCA systems in the event of disease in one system. How adequately collaterals from one system compensate for disease in the other is subject to individual variation (as well as to how rapidly occlusive disease develops).
  • Clinical Note: Very proximal LAD lesions have been known as “widow-makers”. Especially if proximal to the 1st septal perforator (and the 1st diagonal branch) these lesions are virtual “left-main-equivalents” because of the extent of injury and conduction system damage they cause.
  • Diagonal branch anatomy is also highly variable. We show 2 diagonal branches in Figure-4 (D-1; D-2) — but there may be 1, 2, or 3 diagonal branches supplying the anterolateral wall of the heart. Occasionally — there is no diagonal branch per se, but rather a discrete ramus intermedius arising from between the LAD and LCx to supply the anterolateral surface (not shown on Figure-4). Typically — it is the 1st diagonal branch that is the largest.
  • Clinical Note: Considerable variation in number and course of diagonal branch anatomy (and the angulated path that these vessels follow) may require multiple views on cath to determine if occlusion is present.
  • NOTE-2: Additional variations in anatomy are not uncommon. One to be aware of is a “wraparound” LAD — in which the LAD is a larger and longer vessel, to the point of extending beyond the cardiac apex and “wrapping around” to supply the undersurface (= inferior wall) of the heart. Awareness of this anatomic variant provides one explanation for the ECG pattern of simultaneous ST elevation in inferior and anterior lead areas that may sometimes be seen due to acute occlusion of a single vessel.
Figure-4: Normal coronary anatomy of the left coronary artery and its major branches. The LCA (Left Coronary Artery) begins as a short LMain (Left Main Coronary Artery) branch — which then bifurcates into the LAD (Left Anterior Descending Arteryand the LCx (Left Circumflex Artery). Panel A — anterior view. Panel B — RAO (Right-Anterior Oblique) view. Abbreviations: S‑1,S‑2 (Septal Perforator branches); D‑1,D‑2 (Diagonal branches); M‑1,M‑2 (Obtuse Marginal branches from the LCx). (Figure reproduced from ECG-2014-ePub).
Acute LAD Occlusion:
ECG findings arising from acute LAD occlusion may vary depending on: i) The relative site of occlusion within the LAD (ie, proximal to septal perforators and the 1st diagonal or more distal occlusion); ii) Any prior infarctions that may have occurred; iii) Presence of any anatomic variants (such as a “wrap-around” LAD circulation); and iv) The status of the collateral circulation. For simplicity — our comments below relate to expected ECG findings assuming no prior infarctions; no alteration in collateral circulation; and no anatomic variants.
  • Acute LAD occlusion leads to acute anterior MI. This may be extensive and also involve the lateral wall.
  • The most typical ECG manifestation of acute LAD occlusion is ST elevation in anterior leads (usually in ≥2 leads between V1-to-V4).
PEARL: ST elevation in lead aVL — may provide an invaluable clue to the location of the acutely occluded coronary artery. According to a study by Birnbaum et al (Am Heart J 131:38, 1996):
  • Suspect acute LAD occlusion proximal to the 1st Diagonal IF in addition to ST elevation in aVL — there is also ST elevation in leads V2-through-V5. This is the most common situation when there is ST elevation in lead aVL.
  • Suspect 1st Diagonal branch occlusion IF in addition to ST elevation in aVL — there is ST elevation in lead V2 (but not in V3,V4,V5).
  • Suspect LCx occlusion (especially of the 1st obtuse marginal branch) — IF there is ST elevation in aVL but not in lead V2 (and not in other anterior leads).
NOTE: Anterior ST elevation without ST elevation in lead aVL — usually suggests more distal LAD occlusion after takeoff of the 1st Diagonal.
  • PEARL: In addition to recognizing ST elevation in lead aVL with marked anterior ST elevation — there are 2 additional ways to identify patients at high risk of impending proximal LAD occlusion. These are: i) Recognition of Wellens’ Syndrome (Click here for more on Wellens' Syndrome); and ii) Recognition of DeWinter T Waves (See ECG Blog #53).
RETURN to Figure-1: Is this Proximal LAD Occlusion?
Application of the above concepts to the ECG shown in Figure-1 (reproduced below in Figure-5) — supports our presumption of a proximal LAD occlusion. Although this patient “failed to read the textbook”, in that there is no ST elevation in lead aVL — proximal LAD occlusion is still strongly suggested because: i) There is marked ST elevation in all anterior leads, including significant ST elevation in lead V1; ii) ST elevation in lead V1 is clearly more than in lead aVR (virtually no ST elevation in aVR); and iii) The patient developed septal Q waves (in lead V2) as well as RBBB on the follow-up tracing (Figure-2). RBBB and the septal Q wave fortunately resolved following the good result obtained from acute reperfusion.
Figure-5: This is ECG #1 (reproduced from Figure-1) — obtained from this patient with new-onset chest pain. Despite lack of ST elevation in lead aVL — we strongly suspect proximal LAD occlusion (See text).
Link to Section 10.0 for pdf download on the ECG Diagnosis of Acute MI (from our ECG-2014-ePub).
  • ECG Changes of Acute MI — begins in Section 10.1 - 
  • Discussion of the Coronary Circulation (and determining the "culprit" artery) — begins in Section 10.16 - 
  • See ECG BLOG #80 for a case involving differentiation between acute RCA vs LCx occlusion.


  1. Can lead I ,aVL, or V6 has negative QRS complex in anterior MI ? If so what is the mechanism for this ?
    Why in most proximal LAD occlusion we see RBBB rather than LBBB or IVCD?

  2. Lead aVL (at -30 degrees) is negative in this example of a large anterior STEMI — which is consistent with the inferior axis (note predominant positivity in the inferior leads). In contrast, lead I (at 0 degrees) rarely is all negative when the leads are correctly placed — although it is possible that with an extensive infarction of the antero-lateral wall, that loss of all lateral forces might wipe out positivity in lead I and/or V6. But that is uncommon …

    As to your question about which conduction defect is likely to be cause with which injury pattern — the Right Bundle Branch is a fairly thin conduction fascicle that is primarily supplied by septal perforators from the LAD (occasionally with collateral circulation provided by the RCA or LCx) — so it is VERY susceptible to injury from proximal LAD occlusion. The LAH (Left Anterior Hemifascicle) — is also relatively thin and susceptible to injury from proximal LAD occlusion that affects septal perforators — so it is quite common to see both RBBB/LAHB with proximal LAD occlusion. In contrast — the LPH (Left Posterior Hemifascicle) is a much thicker conduction fascicle that enjoys a dual blood supply (from LAD + RCA) — and it is therefore much less susceptible to injury — which is why LBBB is less commonly seen.

  3. Hello Dr Ken
    How can we differentiate betweeen LCx occlusion Vs 1st obtuse marginal branch on ECG leads , as both shows STE aVL?
    as you says "Suspect LCx occlusion (especially of the 1st obtuse marginal branch) — IF there is ST elevation in aVL but not in lead V2 " .
    I think that If there STE in aVL and V5,V6 It goes with LCx occlusion rather than 1st obtuse marginal branch ? and if only STE in aVL without STE V5,V6 it will be 1st obtuse marginal rather than LCx oclussion
    am i correct ?
    please explain

    1. Hi Mostafa. I believe you are asking for more discrimination in determining the IRA (Infarct-Related Artery) than is usually possible from the surface 12-lead ECG. The answer to your question (in my opinion) — depends on many factors. The LCx (Left Circumflex) is a variable size vessel. It is relatively smaller in ~85% of patients who have a right-dominant circulation — and larger in the 15% who have a left-dominant circulation. The Obtuse Marginal IS a part of the LCx. There may be more than 1 Obtuse Marginal branch. So in theory, we might see isolated ST elevation in aVL if there was acute occlusion of the Obtuse Marginal — though depending on specifics of the vessel at hand (size, distribution) and presence of prior infarction/collateral vessels — other lateral leads might be affected. I don’t think hard and fast rules can be stated ...