ECG Cases 24 Reciprocal Change and Occlusion MI

In this ECG Cases blog we look at how reciprocal changes can help diagnose occlusion MI

Written by Jesse McLaren; Peer Reviewed and edited by Anton Helman. August 2021

10 patients presented with potentially ischemic symptoms. Which had occlusion MI?

Case 1: 50yo with throat pain. Normal vitals.

Case 2: 50yo with three hours of chest pain and diaphoresis. Normal vitals. Triage ECG and then repeat ECG:

Case 3: 40yo with 6 hours of constant retrosternal chest pain. Normal vitals. Old then new ECG:

Case 4: 70yo with 6 hours of chest tightness radiating to the arms, now constant. Normal vitals. Old then new ECG:

Case 5: 50yo with a few days of on/off bilateral shoulder pain and nausea, now constant. Normal vitals

Case 6: 65yo with 30min exertional chest pain radiating to the arm. Normal vitals. Old then new ECG:

Case 7: 50yo with 1 hour of chest pain and diaphoresis. Normal vitals. Old ECG then new ECG, and then ECG with posterior leads:

Case 8. 20 year old with one week positional and pleuritic chest pain following viral prodrome. Normal vitals.

Case 9: 70 year old collapse, VSA then ROSC with hyperdynamic LV on POCUS, GCS 3 with fixed dilated pupils

Case 10: 65yo diabetic with epigastric pain. Normal vitals. Old then new ECG:

Reciprocal change and occlusion MI

The STEMI paradigm dichotomizes MI into ST elevation vs non-ST elevation. But as a couple of cardiologists explained a decade ago, “any deflection will produce a reciprocal image 180 degrees removed, on the opposite aspect of the field. (Contemplation of V₁ and V₆ in the setting of bundle branch block or of ventricular hypertrophy should make this concept abundantly clear.)” [1] In other words, ST elevation can produce reciprocal ST depression and vice versa, just like tall T waves can produce reciprocal T wave inversion and versa—and posterior Q waves can produce tall anterior R waves. So the important question is not whether there is ST elevation, but are the ST/T changes secondary repolarization abnormalities or primary changes (or both), which is the main deflection and which is the reciprocal change, and what is the cause.

Reciprocal change can be the first sign of acute coronary occlusion, leading to serial ECGs. It can also remain the dominant sign, pointing to subtle ST elevation and hyperacute T-waves. As two recent studies found, minor ST elevation and reciprocal ST depression or T-wave inversion were the most helpful signs in identifying occlusion MI that do not meet STEMI criteria, or STEMI(-)OMI [2,3]. But the standard 12-lead does not represent the entire electrocardiographic field, so ST/T changes and reciprocal change do not always coexist on the 12 lead: some occlusion MIs do not reveal any reciprocal change, while others only have reciprocal change. So how can we use reciprocal change to identify occlusion MI?

Step 1 – understand which leads are reciprocal to each other:

• Limb leads: frontal plane
  • III (inferior) reciprocal to aVL (high lateral)
  • aVR (basal septum) reciprocal to II (LV apex)
• Precordial leads: horizontal plane
  • V1 (septal) reciprocal to V6 (lateral)
  • V2-3 (anterior) reciprocal to V8-9 (posterior)

Step 2 – integrate this with coronary anatomy. Leads III and aVL are reciprocal to each other, so inferior reciprocal change can help identify lateral Occlusion MI (from circumflex or diagonal occlusion) and reciprocal change in aVL can help identify inferior Occlusion MI (from RCA or circumflex occlusion). New primary ST depression in aVL (not from an old MI or secondary to LBBB/LVH) can be the first sign of inferior MI [4], is more sensitive than STEMI criteria and excludes pericarditis [5]. The anterior leads V2-3 are reciprocal to posterior leads, so posterior ST elevation and Q waves produce anterior ST depression and tall R waves. Like inferior MI the reciprocal change in posterior OMI can be the dominant sign, and posterior leads can be falsely negative.

Left anterior descending (LAD) artery occlusion is more complicated because of its branches, which can produce different ST changes depending on the site of occlusion.[6,7]

• Proximal to septal branch: ST elevation aVR/V1, reciprocal in V5-6
• Proximal to diagonal branch: ST elevation anterior (V2-4) + high lateral (I/aVL) with reciprocal inferior (II, III, aVF)
• Mid-distal (beyond diagonal branch): ST elevation anterior (V2-4), with inferior leads isoelectric or ST elevation (from distal or wraparound occlusion) with reciprocal in aVL

In other words, like inferior MI the presence of reciprocal change can help identify subtle proximal LAD occlusion. But unlike inferior MI, which nearly always has reciprocal change in aVL, distal LAD occlusion often lacks reciprocal change on the 12 lead (because the diagonal branch is not involved so there is no inferior reciprocal change, and posterior reciprocal changes are not seen on the 12 lead).

When it comes to ST change in lead aVR, it can be part of the main deflection (from LAD occlusion proximal to the septal branch) or it can be reciprocal to diffuse changes in the other leads. Pericarditis produces diffuse concave ST elevation greatest in II, with reciprocal ST depression in aVR only. Diffuse subendocardial ischemia produces diffuse ST depression with reciprocal ST elevation in aVR—a high-risk but non-specific pattern that can be seen with any emergency that disrupts oxygen supply/demand (including sepsis, GI bleed, PE, dissection, return of spontaneous circulation after an arrest, triple vessel disease, or Occlusion MI).

Lastly, occlusive and non-occlusive patterns can co-exist. Dr. Aslanger has described a new pattern representing a combination of inferior OMI (inferior ST elevation with reciprocal ST depression in aVL) and concomitant critical stenosis in another vessel (diffuse ST depression with reciprocal ST elevation in aVR): “The ST-vector of inferior MI localizes the area of infarction and is directed inferiorly and frequently rightwards, whereas the ST-vector of subendocardial ischemia does not localize the area of ischemia and is directed to the lead aVR irrespective of involved coronary territory. The summation of these two vectors results in an average ST-vector directed rightwards at right angles to aVF, projects to the negative pole of lead II, but still points to the positive pole of lead III. In this situation, standard 12-lead ECG only shows STE in lead III and aVR, which accompanies STD in lead I and II, and a nearly isoelectric ST-segment in aVF. Also, lateral chest leads show some STD due to the ST-vector pointing away from them.” This is a high-risk pattern, which is usually treated as NSTEMI because it does not meet STEMI criteria, but has similar mortality rates to STEMI patients because it shares the underlying pathology of occlusion MI.

Back to the cases

Case 1: LVH with secondary ST depression/T wave inversion and reciprocal change

• Heart rate/rhythm: sinus arrhythmia
• Electrical conduction: normal conduction
• Axis: normal axis
• R-wave: normal R wave progression
• Tall/small voltage: tall voltage from LVH
• ST/T: lateral ST depression and asymmetric T wave inversion secondary to LVH, with reciprocal septal STE and tall T waves

Impression: LVH with repolarization abnormalities. This can mimic STEMI but patient had negative workup.

Case 2: proximal LAD occlusion starting with inferior reciprocal change

• H: normal sinus rhythm
• E: normal conduction
• A: normal axis
• R: normal progression, but small q develops in V2
• T: normal voltage
• S: first ECG has inferior down-up T waves reciprocal to biphasic T wave in aVL. Repeat ECG has ST elevation in aVR/V1-2 (septal) with reciprocal ST depression in V5-6, and ST elevation in aVL with reciprocal inferior ST depression

Impression: septal STEMI(-) OMI. Delayed repeat ECG, with ECG-to-Activation (ETA) time of 60 minutes. 95% proximal LAD occlusion, trop I rise from 13ng/L to 12,000. Discharge ECG revealed QS wave in V2 and reperfusion T wave inversion in V1-3, and resolution of reciprocal changes:

Case 3: proximal LAD occlusion with more obvious inferior reciprocal change

• H: normal sinus
• E: normal conduction
• A: new left axis from LAFB
• R: new late R wave progression with new QS wave in V2
• T: normal voltage
• S: Q + STE in aVL (with inferior reciprocal change) and V2, and hyperacute T wave across precordial leads

Impression: anterolateral STEMI(-)OMI, diagnosed early with ETA time of 14 minutes. 90% proximal LAD occlusion (some spontaneous reperfusion) but Trop I rose from 35 to 138,000. Discharge ECG had ongoing loss of precordial R waves and anterolateral reperfusion T wave inversion:

Case 4: mid LAD occlusion without any reciprocal change on 12 lead

• H: normal sinus rhythm
• E: normal conduction
• A: normal axis
• R: normal R wave progression but new small q in V2
• T: normal voltage
• S: V2-3 have new ST elevation with straightening of ST segment and hyperacute T waves, but no reciprocal change

Impression: anterior STEMI(-)OMI not initially recognized. Had 15 lead ECG demonstrating mild reciprocal posterior ST depression.

First trop 600 and then cath lab activated, with ETA time 78 minutes. 100% distal LAD occlusion, peak trop 50,000. Discharge ECG had anterior Q waves with reperfusion T wave inversion.

Case 5: wraparound LAD occlusion with anterior ST elevation and inferior ST elevation (with reciprocal change)

• H: normal sinus rhythm
• E: normal conduction
• A: normal axis
• R: poor R wave progression with QS wave in V3
• T: normal voltage
• S: convex STE and T wave inversion in V2-3, and concave ST elevation inferiorly with reciprocal ST depression in aVL

Impression: antero-inferior OMI, delayed diagnosis with ETA time of 111 minutes. 100% mid LAD occlusion, trop I rise from 10,000 to 20,000. Discharge ECG had anterior T wave inversion and inferior Q waves:

Case 6: inferior OMI with reciprocal change in aVL the more dominant sign

• H: normal sinus rhythm
• E: normal conduction
• A: normal axis
• R: normal R wave
• T: normal voltage
• S: clear ST depression and discordant T wave inversion in aVL, which is new and reciprocal to subtle inferior ST elevation and hyperacute T waves

Impression: inferior STEMI(-)OMI diagnosed despite ‘normal’ ECG. ETA time of 22 minutes. 100% RCA occlusion, trop I rise from 25 to 50,000. Discharge ECG had inferior Q wave and reperfusion T wave inversion with reciprocal tall T wave in aVL, and anterior tall R waves and tall T waves (reciprocal to posterior Q waves and T wave inversion):

Case 7: posterolateral OMI with reciprocal changes the first and more dominant sign

• H: normal sinus
• E: normal conduction
• A: physiologic left axis
• R: new tall R wave in V2
• T: normal voltage
• S: clear inferior ST depression reciprocal to subtle ST straightening in aVL, and clear anterior ST depression with Q wave and minimal ST elevation in V9

Impression: posterolateral STEMI(-)OMI. Delayed diagnosis with ETA time of 102 minutes, cath lab activated after ongoing chest pain and repeat ECG showed ST elevation in aVL:

100% circumflex occlusion, trop I rise from 8 to 43,000. Discharge ECG had ongoing Q wave inferiorly and posteriorly (tall R wave in V2):

Case 8. myocarditis with reciprocal change

• H: normal sinus
• E: normal conduction
• A: right axis
• R: poor R wave progression
• T: normal voltage
• S: inferolateral concave STE and PR depression, but also reciprocal ST depression in aVL and ST depression with T wave inversion in V2

Impression: history classic for pericarditis but ECG has the appearance of inferoposterior OMI, which myocarditis can mimic. First trop 7,000 and peak 13,000. Cardiac MRI confirmed myocarditis, with RV dilation and reduced function and edema to basolateral (posterior) and inferior walls corresponding with ECG changes. Discharge ECG had normalization of ST/T and reciprocal changes:

Case 9: post-ROSC (from subarachnoid hemorrhage) with diffuse ST depression and reciprocal STE in aVR

• H: normal sinus
• E: normal conduction
• A: right axis
• R: normal R wave
• T: normal voltage
• S: diffuse ST depression with reciprocal STE in aVR

Impression: ROSC with diffuse ST depression and reciprocal STE in aVR, nonspecific pattern. Had normal coronaries on cath and then CT diagnosed subarachnoid hemorrhage.

Case 10: Aslanger pattern of inferior OMI + subendocardial ischemia

• H: borderline sinus tach
• E: normal conduction
• A: normal axis
• R: normal R wave
• T: normal voltage
• S: concave STE and Q in III with reciprocal ST depression in aVL, and ST depression in V2-6 with reciprocal STE in aVR

Impression: inferior STEMI(-)OMI + subendocardial ischemia. Symptoms improved with ASA/nitro, and repeat ECG had resolution of subendocardial ischemia, but evidence of inferoposterior OMI with hyperacute T wave in III and reciprocal STD in I/aVL along with anterior ST depression:

First trop 300 (MI cut off = 100), treated with heparin and admitted as NSTEMI. 95% RCA occlusion and 80% LAD stenosis, trop I rise to 2,500. Discharge ECG had inferior Q wave with T wave inversion, anterior tall R with ST depression, and lateral T wave inversion:

Take home points for reciprocal change and occlusion MI

1. ST/T abnormalities and reciprocal change can be secondary to LBBB/LVH, primary changes, or both
2. Reciprocal change can be the first and remain the dominant sign of occlusion, pointing to subtle ST elevation or hyperacute T-waves
3. Reciprocal change can highlight subtle inferior, lateral or proximal LAD occlusions; it can be the only sign of posterior OMI; and it can be absent in mid-distal LAD occlusion
4. ST change isolated to aVR is reciprocal to other leads, including the diffuse ST elevation of pericarditis or the diffuse ST depression of subendocardial ischemia

References for reciprocal changes and occlusion MI

1. Phibbs B, Nelson W. Differential classification of acute myocardial infarction into ST- and non-ST segment elevation is not valid or rational. Ann Noninvasive Electrocardiol 2010 July;15(3):191-199
2. Aslanger E, Yıldırımtürk Ö, Şimşek B, et al. DIagnostic accuracy oF electrocardiogram for acute coronary OCClUsion resulting in myocardial infarction (DIFFOCCULT Study). IJC Heart & Vasc 2020, 30: 100603
3. Meyers HP, Bracy A, Lee D, et al. Accuracy of OMI ECG findings versus STEMI criteria for diagnosis of acute coronary occlusion myocardial infarction. IJC Heart & Vasc 2021;33:100767
4. Birnbaum Y, Sclarovsky S, Mager A, et al. ST segment depression in aVL: a sensitive marker for acute inferior myocardial infarction. Eur Heart J 1993 Jan;14(1):4-7
5. Bischof JE, Worrall C, Thompson P, et al. ST depression in lead aVL differentiates inferior ST-elevation myocardial infarction from pericarditis. Am J Emerg Med 2016 Feb;34(2):149-54
6. Birnbaum Y, Drew BJ. The electrocardiogram in ST elevation acute myocardial infarction: correlation with coronary anatomy and prognosis. Postgrad Med J 2003;79:490-504
7. Fiol M, Cygankiewicz I, Guindo J, et al. Evolving myocardial infarction with ST elevation: ups and downs of ST in different leads identifies the culprit artery and location of the occlusion. Ann Noninvasive Electrocardiol 2004 Apr;9(2):180-6
8. Aslanger E, Yıldırımtürk Ö, Şimşek B, et al. A new electrocardiographic pattern indicating inferior myocardial infarction. J of Electrocardiol 2020, 61:41-46