By Magnus Nossen
This ECG is from a young man with no risk factors for CAD, he presented with chest pain. How would you assess this ECG? How confident are you in your assessment? What is your next step? Note: lead format is Cabrera
I was sent this ECG in real time. The patient is a young adult male with chest pain. The chest pain was described as pressure like and radiation to both arms and the jaw. Symptoms were on and off. The pain was worse in the night and better when moving. The patient sought medical attention when the pain recurred for a second straight night accompanied by arm numbness as well as radiating pain. The above ECG was recorded.
It is easy to say pericarditis in such a case. (young male no risk factors and ST-elevation in several leads) As Dr. Smith has emphasized many times you diagnose pericarditis at your patient's and your own peril. The ST segment depression in V1 had me worried, the (inappropriately) almost isoelectric ST segment in V2 worried me even more. In conjunction with the inferior and lateral minimal ST elevation I felt I had to rule out inferoposterolateral OMI as the consequences can be catastrophic.
I sent this out to our "EKG Nerdz" group and in spite of his usual warning, Dr. Smith texted back: "I am going to go out on a limb and say it is a fake."
Dr. Smith's top 2 most important features for differentiating OMI from Pericarditis are 1) absence of reciprocal ST depression in any lead except aVR and 2) "flat" ST segments, meaning without large T-waves, perhaps more specifically stated as a low T/ST ratio.
I accepted the patient for transfer to our PCI center. On arrival patient was slightly tachycardic. HR about 90-100/min. Other vital signs normal. No fever. Hand held echo showed overall ejection fraction being normal. With normal EF the tachycardia is not compensatory. ACS then becomes less likely. Before the lab values returned this patient had an emergent coronary CT angiogram done that ruled out CAD. Final diagnosis was myocarditis. Initial Troponin T returned at 1233ng/L. Myocarditis can be very difficult if not impossible to differentiate from OMI based on ECG changes. The ECG can show ST-elevation with reciprocal changes and myocarditis can have regional WMA on echo, just as OMI. Invasive or non-invasive angiogram should strongly be considered for this group of patients. A false positive cath lab activation is also off course acceptable for this diagnosis if you cannot get an emergent coronary CT angiogram.
Retrospectively one can say that the ST depression in V1 and relative ST depression in V2 is likely reciprocal to diffuse ST elevation. (The same reciprocal relationship is seen in severe subendocardial ischemia, just with opposite vector direction where V1 can show ST elevation)
Below you can find the 3D model of the heart and coronary vessels. Each main coronary artery (LAD, RCA and LCx) are shown in separate images. There are no coronary stenoses.
The Queen of Hearts PM Cardio App is now available in the European Union (CE approved) the App Store and on Google Play. For Americans, you need to wait for the FDA. But in the meantime:
MY Comment, by KEN GRAUER, MD (4/11/2024):
- For clarity in Figure-1 — I've reproduced today's ECG. I highlighted in RED the 3rd lead on the left to remind readers that this is lead -aVR (which corresponds to a frontal axis angle = +30 degrees) — in this ECG that displays the Cabrera Format (See My Comment at the bottom of the page in the October 26, 2020 post of Dr. Smith's ECG Blog for review of the Cabrera format).
- This case is challenging because of the young age of this patient, who presented with severe chest pain — and because of the fairly subtle abnormalities on ECG. In addition to the V1,V2 leads that concerned Dr. Nossen — I would add that there is straightening of the ST segment takeoff in sequential leads -aVR through to lead III, each of which are associated with subtle-but-real J-point ST elevation. (There is a Q wave in lead III of uncertain significance).
- Support that these ST-T wave findings in the limb leads are real, is forthcoming by the utterly flat ST segment in lead aVL. While not the "mirror-image opposite" picture featured by the "magical" reciprocal lead III-to-lead aVL relationship typically seen when there is acute inferior OMI — I interpreted this uncharacteristic ST-T wave flattening in lead aVL as a reciprocal ST-T wave change.
- Similar straightening of the ST segment takeoff, with slight ST elevation is also seen in leads V5,V6.
- And the patient has sinus tachycardia ... (at ~100/minute).
- As emphasized many times in Dr. Smith's ECG Blog — it may sometimes not be possible to distinguish between acute myocarditis vs acute OMI on the basis of ECG findings and clinical history (See My Comments in the April 25, 2023 — July 21, 2019 — December 10, 2019 — and January 10, 2020 posts).
- P.S.: A diagnosis of acute myocarditis (rather than acute OMI ) — is a much better "fit" for this case because: i) The patient is younger than the usual OMI patient — and description of his chest pain is somewhat atypical; and, ii) The ECG is not quite as we'd expect for an acute infero-postero OMI (ie, there is abnormal ST flattening in lead aVL, but not the expected mirror-image opposite picture of ST-T wave changes as seen in lead III — there is no reciprocal ST-T wave change at all in lead I — and lead V1 rather than V2,V3,V4 shows the clearly abnormal ST segment straightening).
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| Figure-1: The initial ECG in today's case. The insert that I've added in the lower right shows the rationale for limb lead sequencing used in the Cabrera format. (NOTE: To improve visualization — I've digitized the original ECG using PMcardio). |
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