In this ECG Cases blog we look at 9 patients with possible transient STEMI and discuss pitfalls and pearls in ECG interpretation and management.

Written by Jesse McLaren; Peer Reviewed and edited by Anton Helman, January 2023

9 patients presented with possible transient STEMI. How would you interpret the ECGs and manage these patients?

Case 1: 75 year old with 4 days on/off chest pain, brought by EMS as code STEMI, pain resolved after aspirin. ECG after resolution of symptoms.

Case 2: 60 year old with exertional dizziness and epigastric pain, brought by EMS as possible STEMI. Serial ECG with improving but ongoing pain.

Case 3: 55 year old with intermittent chest pain to jaw. First ECG with pain and repeat 5 minutes later pain free.

Case 4: 80 year old with 3 days intermittent CP now constant; serial ECG 10min apart.

Case 5: 75 year old with acute and ongoing chest pain, serial ECG.

Case 6: 55 year old with acute exertional chest pain. Old ECG and new ‘normal’ ECG.

Case 7: 70 year old with two weeks intermittent chest pain, worse today but resolved on arrival.

Case 8: 60 year old with 3 days on/off chest pain and sob, resolved symptoms on arrival.

Case 9: 55 year old with one day intermittent chest pain, 12 lead and 15 lead 4 minutes later.

Transient STEMI

In the current paradigm, the treatment for ACS is dichotomized into immediate angiography for STEMI, and delayed angiography for Non-STEMI. This poses a dilemma for the 6% of ACS patients with “transient STEMI”, defined as patients who present with STEMI but whose ischemic symptoms and ST elevation completely resolve before reperfusion therapy.[1]

Not surprisingly, patients with transient STEMI have better outcomes than persisting STEMI, because the artery has apparently spontaneously reperfused.[2,3] This has led to recommendations that patients with transient STEMI do not need immediate angiography and can be treated as high-risk NSTEMIs. This is based on studies, including the TRANSIENT trial, suggesting there is no difference to immediate vs delayed angiography.[4,5]

But as an analysis explained, “there are concerning signals in this under-powered trial. There were trends toward larger infarct size with delayed angiography, both by cMR and integral high-sensitivity troponin concentration, as well as toward higher rate of major adverse cardiovascular events (MACE) (8.5 vs. 2.9%; P = 0.28) in the delayed group. This latter figure includes the four patients randomized to delayed angiography who underwent urgent revascularization for recurrent ischaemia, and mirrors a trend observed in the ELISA-3 post hoc analysis of transient STEMI patients. As recurrent ischaemia is the principle event reduced by early intervention in NSTE-ACS, these are important endpoint events occurring with delayed angiography and there is a consistent signal for harm now from two data sources”[6]

3 pitfalls and pearls for transient STEMI

  1. Incomplete resolution of symptoms or ST elevation = persisting STEMI

Studies on transient STEMI exclude patients with refractory ischemia and electrical or hemodynamic instability, because current NSTEMI guidelines recommend urgent angiography for these patients even without ECG changes. But this is rarely followed [7], and transient STEMI should not become another reason to delay angiography for refractory ischemia. If there are persisting ischemic symptoms, it does not matter if ST elevation was transient – the patient needs immediate angiography. On the other hand, symptom resolution does not guarantee the artery has reperfused. If there is still ischemic ST elevation it doesn’t matter if symptoms have resolved – the patient needs immediate angiography.

  1. Transient STEMI but ongoing occlusion: STEMI(-)OMI

A quarter of NSTEMIs have a totally occluded artery which is associated with higher mortality, and these can be identified by signs of Occlusion MI that do not meet STEMI criteria, i.e. STEMI(-)OMI. [8] As the new ACC expert consensus on the evaluation of chest pain in the ED states, applying STEMI criteria will “miss a significant minority of patients who have acute coronary occlusion.” [9] But studies on transient STEMI have not looked at the subgroup of STEMI(-)OMI. So if the ECG no longer meets STEMI criteria but is still diagnostic of Occlusion MI, then the artery is still occluded and requires reperfusion.

  1. Transient works both ways: from reperfusion to reocclusion

If there is complete resolution of ischemic symptoms and ECG signs of STEMI and OMI, then the patient has transient spontaneous reperfusion. The ECG might also show reperfusion T wave inversion. But reperfusion can be transient, and reocclusion could occur at any time. If angiography is delayed, the patient needs to be closely monitored for recurring ischemic symptoms and recurring ECG signs of reocclusion. These include not only STEMI criteria but subtle ST elevation, reciprocal change, pseudo-normalization of inverted T waves, and hyperacute T waves. Transient STEMI/OMI can also work in reverse: patients can arrive with resolved chest pain with an ECG showing signs of transient reperfusion (eg Wellens’ syndrome), which are at high risk of reocclusion.

Back to the cases on transient STEMI

Case 1: resolved chest pain but ongoing STEMI(+)OMI, false cancellation of cath lab

  • Heart rate: normal sinus
  • Electrical conduction: first degree AV block
  • Axis: normal axis
  • R-wave progression: late R wave progression
  • Tall/small voltages: normal voltages
  • ST/T: precordial and inferior convex ST elevation and hyperacute T waves

Impression: resolved symptoms but ongoing ECG evidence of STEMI(+)Occlusion MI, from wraparound or distal LAD occlusion. Cath lab initially cancelled because of resolution of chest pain, then reactivated: 100% distal LAD occlusion. Initial troponin I was 7,000ng/L (normal <16 in females and <26 in males) and peak 15,000, EF 40% with anteroseptal and inferior akinesis. Discharge ECG had further loss of R waves, resolution of ST elevation and development of reperfusion T wave inversion:

Case 2: inferior STEMI(-)OMI with transient resolution of ECG changes but ongoing ischemia, delayed cath lab activation

  • H: normal sinus
  • E: first degree AV block
  • A: normal axis
  • R: normal R wave
  • T: LVH
  • S: inferior STE with reciprocal STD in aVL, which resolved

Impression: inferior Occlusion MI with transient resolution of ECG changes but ongoing ischemic symptoms. Cath lab not activated because of resolution of ST changes. An hour later developed hypotension and ECG was repeated:

Sinus with 2:1 AV block, recurrence of inferior STE with STD-aVL and STD in V2. Cath lab activated: 100% RCA occlusion, peak trop 40,000. Discharge ECG had normal AV conduction, resolution of ST changes, mild reperfusion TWI.

Case 3: recurring transient ST elevation, cath lab activated, and negative troponin because of rapid reperfusion

  • H: normal sinus
  • E: normal conduction
  • A: normal axis
  • R: normal R wave progression
  • T: normal voltages
  • S: first ECG shows inferolateral STE and hyperacute T waves and anterior ST depression, which resolves

Transient STEMI. Cath lab activated. Before procedure had recurrence of chest pain, with another set of serial ECGs:

Had 99% circumflex occlusion but serial troponin negative because of rapid spontaneous reperfusion

Case 4: transient STEMI but persisting OMI, cath lab activated

  • H: normal sinus
  • E: normal conduction
  • A: normal axis
  • R: normal R wave
  • T: normal voltages
  • S: inferior Q wave; inferior ST elevation with reciprocal ST depression in aVL, and ST depression V2. Second ECG “STEMI negative” but still OMI

Impression: infero-posterior transient STEMI but persisting OMI. Cath lab activated after first ECG, admitted as “Non-STEMI” after repeat ECG but still taken immediately to cath lab. On angiogram had 95% RCA occlusion, first troponin 700 and peak 15,000. Discharge diagnosis “NonSTEMI”, with resolution of ST changes, persisting inferior Q and tall R in V2

Case 5: transient STEMI with reperfusing OMI, cath lab activated

  • H: normal sinus
  • E: normal conduction
  • A: normal axis
  • R: normal R wave
  • T: normal voltages
  • S: inferior ST elevation and hyperacute T waves with reciprocal STD/TWI in aVL and precordial ST depression, which improved but did not completely resolve, with ongoing inferior STE but subtle terminal T wave inversion

Impression: from STEMI(+)OMI to STEMI (-)OMI with a hint of reperfusion. Cath lab activated. ECG prior to cath showed further development of inferior reperfusion T wave inversion

Angiogram showed 90% RCA occlusion, wiht small troponin rise from 2000 to 3000 from rapid reperfusion.

Case 6: transient STEMI(-)OMI, missed

  • H: normal sinus
  • E: normal conduction
  • A: normal axis
  • R: normal R wave
  • T: normal voltages
  • S: new inferior STE with reciprocal STD in aVL, and flat ST segment in V2 with smaller T wave

Impression: inferoposterior Occlusion MI. Missed on ED assessment. Pain resolved after aspirin and ECG repeated two hours later when first troponin returned at 500, showing resolution of ST changes.

Admitted as Non-STEMI. Next day angiogram showed 90% RCA occlusion, peak troponin 12,000 and on discharge had infero-posterior reperfusion T wave inversion:

Case 7: Wellens’ syndrome = transient STEMI/LAD OMI with reperfusion

  • H: normal sinus
  • E: normal conduction
  • A: normal axis
  • R: normal R wave
  • T: normal voltages
  • S: anterior convex mild ST elevation and terminal T wave inversion

Impression: resolved ischemic symptoms with preserved R waves and anterior T wave inversion = Wellens’ syndrome = critical LAD stenosis. Had cath lab activated: 90% LAD lesions, with very small troponin elevation from 60 to 200. Discharge diagnosis “STEMI.” Discharge ECG had evolution of anterior reperfusion T wave inversion:

Case 8: from reperfusion to STEMI(+)OMI reocclusion

  • H: normal sinus
  • E: normal conduction
  • A: new left axis from inferior Q waves
  • R: new early R waves
  • T: normal voltages
  • S: inferior convex ST and T wave inversion, with reciprocal down/upT wave in aVL, and STD V2-4 with taller T waves

Impression: infero-posterior Occlusion MI with transient reperfusion. Initial troponin was 14,000, making this a “non-STEMI.” But patient developed recurrence of chest pain. Repeat 12 lead, and then 15 lead 10 minutes later:

12 lead showed inferior STE/hyperacute T wave with reciprocal STD-aVL and STD-V2-3 from infero-posterior re-occlusion, then 15 lead showed reperfusion again. On angiogram 95% RCA occlusion, and peak trop 15,000.

Case 9: from reperfusion to STEMI(-)OMI reocclusion

  • H: normal sinus
  • E: normal conduction
  • A: normal axis
  • R: normal R wave progression
  • T: normal voltages
  • S: initial ECG had T wave inversion III/aVF with down-up T wave in aVL (reperfused inferior OMI) and repeat had mild ST elevation in III with pseudonormal T waves, and reciprocal STD in aVL (inferior OMI). Both also had precordial ST depression max V4-5 (posterior OMI vs subendocardial ischemia),

Impression: inferior +/- posterior Occlusion MI, from reperfusion to re-occlusion. Cath lab activated: 99% circumflex occlusion. First troponin 2000 and peak 85,000, EF 50% with inferior hypokinesis. Discharge diagnosis “STEMI”, ECG had inferior Q waves with reperfusion T wave inversion inferior and posterior

Take home points for transient STEMI

  1. “Transient STEMI” = complete resolution of both ischemic symptoms and ST elevation. If not it’s persisting STEMI, and requires immediate angiogram
  2. Resolved STEMI but ongoing Occlusion MI = STEMI(-)OMI = coronary artery is still occluded and requires reperfusion
  3. If both symptoms and ECG signs of STEMI/OMI have completely resolved and angiography is delayed, the patient needs close monitoring for recurrence of symptoms or ECG signs of reocclusion – including subtle ST elevation, reciprocal change, pseudo-normalized T waves, and hyperacute T waves
  4. If patients arrive with resolved symptoms and reperfusion T wave inversion, they are at high risk for reocclusion

References for ECG Cases 39 – transient STEMI pitfalls and pearls

  1. Meisel S, Dagan Y, Blondheim D, et al. Transient ST-elevation myocardial infarction: clinical course with intense medical therapy and early invasive approach, and comparison with persistent ST-elevation myocardial infarction. Am Heart J 2008; 155(5): 848-854
  2. Blondheim DS, Kleiner-Shochat M, Asis A, et al. Characteristics, management, and outcome of transient ST-elevation versus persistent ST-elevation and non-ST-elevation myocardial infarction. Am J Cardiol 2018;121:1449-1455
  3. Janssens GN, Lemkes JS, van der Hoeven NW, et al. Transient ST-elevation myocardial infarction versus persistent ST-elevation myocardial infarction. An appraisal of patient characteristics and functional outcome. Int J Cardiol 2021; 336:22-28
  4. Badings EA, Remkes RS, The SHK, et al. Early or late intervention in patients with transient ST-segment elevation acute coronary syndrome: subgroup analysis of the ELISA-3 trial. Cath Cardiovasc Interven 2016;88:755-764
  5. Lemkes JS, Janssens GN, van der Hoeven NW, et al Timing of revascularization in patients with transient ST-segment elevation myocardial infarction: a randomized clinical trial. Eur Heart J 2019 Jan;40(3):283-291
  6. Bergmark BA, Faxxon DP. Transient ST-segment myocardial infarction: a new category of high risk acute coronary syndrome? Eur Heart J 2019;40:292-294
  7. Lupu L, Taha L, Banai A, et al. Immediate and early percutaneous coronary intervention in very high and high risk non-ST segment elevation myocardial infarction patients. Clin Cardiol 2022 Apr;45(4):359-369
  8. Meyers HP, Bracey A, Lee D, et al. Accuracy of OMI ECG findings versus STEMI criteria for diagnosis of acute coronary occlusion myocardial infarction. Int J Cardiol Heart Vasc 2021 Apr 12;33:100767
  9. Kontos MC, de Melos JA, Deitelzweig SB, et al. 2022 ACC expert consensus decision pathway on the evaluation and disposition of acute chest pain in the emergency department: a report of the American College of Cardiology solution set oversight committee. J Am Coll Cardiol 2022 Nov,80(20):1925-1960