In this ECG Cases blog we look at 8 patients with T-wave inversions, with a focus on Wellens syndrome, reperfusion and reocclusion MI

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

Eight patients presented with potentially ischemic symptoms and T-wave inversion. Which had occlusion MI, which were reperfused and which were reoccluded?

Case 1: 17yo with syncope, normal vitals

Case 2: 60yo with acute chest pain, normal vitals. ECG on arrival and repeat after nitro when symptoms resolved

Case 3: 65yo with exertional chest pain, now pain-free with normal vitals. Old then new ECG:

Case 4: 45yo with 2 days on/off chest pain. Triage ECG when pain-free, then repeat after chest pain recurrence

Case 5: 55yo with 4 hours of chest pain, now resolved. Normal vitals, old then new ECG

Case 6: 60yo with 5 days on/off chest pain, currently pain-free. Old then new ECG

Case 7: 60yo with 12 hours of ongoing chest pain. Normal vitals.

Case 8: 75yo with 3 days of shortness of breath and ongoing chest pain. HR 110, BP 120/70, R24, O2 90%. Old the new ECG

‘Wellens syndrome’, reperfusion and reocclusion MI

T-wave inversion (TWI) has a wide differential (see this previous post for the INVERSION mnemonic), one of which includes impending coronary artery (re)occlusion. As Dr. Wellens described in 1982, “we can define a subset of people with a proximal LAD lesion, with a 75% chance of losing 35% of their myocardium within 2 weeks, and I believe that they should be distinguished from patients who develop ST segment elevations or depressions during pain. The pattern that I described develops after the pain, and it remains.”[1]. In 1989 he described the same pattern in a larger cohort, which included the following features[2]:

  1. Symptoms: unstable angina which has resolved, either spontaneously or after treatment
  2. ECG:
    1. Preserved R wave progression and no pathologic Q waves, i.e. no major infarct yet
    2. Primary TWI in the anterior leads (i.e. not secondary to bundle branch block or ventricular hypertrophy):
      1. Type A: concave/straight ST segment followed by terminal TWI
      2. Type B: convex ST segment followed by deep and symmetric TWI
  3. Cardiac biomarkers: normal or minimally elevated on initial presentation
  4. Angiogram: severe LAD stenosis, or total occlusion with collateral circulation
  5. Clinical course: high risk for large anterior MI without revascularization
    1. Recurrence of chest pain results in normalization of T waves and elevation of ST segments

Around the same time, this phenomenon was called “staccato LAD occlusion” to explain the underlying pathology: subtotal stenosis that produces repetitive episodes of ischemia as the vessel occludes and spontaneously reperfuses, and which is at risk for prolonged occlusion resulting in a large infarct [3]. This has become known as “Wellens syndrome” and is often labeled a “STEMI equivalent.” But this is another example of the STEMI/NSTEMI false dichotomy: if “STEMI” is supposed to mean an acute coronary occlusion, then Wellens’ syndrome is a “non-STEMI” which is also a “post-STEMI” and a “pre-STEMI”. In other words, this represents “high-risk postischemic T wave inversions…after spontaneous reperfusion of acute thrombotic occlusion, in which there is active thrombus and risk of reocclusion.”[4]

This phenomenon is not specific to the LAD: the year after Wellens’ first study, postischemic inferior TWI was reported in subtotal RCA/circumflex occlusion[5], and reperfused posterior MI results in posterior TWI that appears on the 12 lead ECG as reciprocal tall T waves in V2-3[6] Longer periods of occlusion prior to spontaneous reperfusion can also result in postischemic TWI with acute Q waves, and postischemic TWI is routinely seen after reperfusion therapy (which progress from “type A” to “type B”). So rather than relying on the STEMI acronym or the Wellens eponym, it’s more useful to focus on the underlying pathology of Occlusion MI (OMI). This can be a dynamic/staccato process alternating between occlusion, reperfusion (spontaneous or after treatment) and re-occlusion. Each of these phases have corresponding ECG findings:

  1. Occlusion: hyperacute T waves +/- ST elevation +/- Q waves
  2. Reperfusion: ST segments normalize, hyperacute T waves normalize and then invert (progressing from the terminal TWI to symmetric TWI)
  3. Reocclusion: inverted T waves normalize (pseudonormalization), ST segments elevate again

While resolved symptoms and ECG signs of reperfusion don’t require immediate cath lab activation, post-ischemic TWI require aggressive treatment while awaiting angiography, with close monitoring for symptoms or ECG signs of reocclusion: “in case of spontaneous reperfusion, there is a potential for impending reocclusion, especially if not recognized and treated aggressively…In patients who develop inverted T waves, episodes of re-ischemia often manifest as a change in the T wave vector with positive T waves, with or without STE (“pseudonormalization”), in the ischemic region.” [7] Finally, if the patient has ongoing ischemic symptoms and TWI then these are not postischemic TWI but rather ischemic TWI: including acute occlusion MI (reciprocal to hyperacute T wave and ST elevation), refractory occlusion MI (prolonged symptoms with Q waves and TWI) or PE (anterior-inferior TWI and other signs of right heart strain).

Back to the cases

Case 1:  secondary TWI from hypertrophic cardiomyopathy (pseudo-Wellens, false-STEMI)

  • Heart rate/rhythm: sinus bradycardia
  • Electrical conduction: normal intervals
  • Axis: normal
  • R-wave: delayed transition
  • Tall: tall voltages, with LVH/strain pattern
  • ST/T changes: secondary ST/T wave changes, including anterior STE and terminal T wave inversion secondary to LVH

Impression: LVH with secondary secondary repolarization abnormalities from hypertrophic cardiomyopathy

Case 2: primary postischemic TWI from LAD reperfusion after nitro (from “STEMI” to “Wellens”)

  • H: normal sinus rhythm
  • E: normal conduction
  • A: normal axis
  • R: normal R wave progression
  • T: normal voltage
  • S: first ECG has V2-5 ST elevation (becoming non-concave) and hyperacute T waves, and after nitro the ST segment normalizes in amplitude but becomes convex with TWI

Impression: transiently reperfused LAD occlusion. Treated with heparin/antiplatelets and cath lab activated because of transient STEMI: 90% proximal LAD occlusion, trop I rose from 150 ng/L to 2,500.

Case 3: primary postischemic TWI from spontaneous LAD reperfusion (Wellens syndrome, with progression from “type A” to “type B”)

  • H: sinus bradycardia
  • E: normal conduction
  • A: normal axis
  • R: normal R wave progression
  • T: normal voltage
  • S: second ECG has new terminal T wave inversion in V2-3

Impression: spontaneously reperfused LAD occlusion. First trop 3,000 and admitted as NSTEMI. Angiogram: 99% LAD occlusion. Post-stent progression of post-ischemic TWI, from Wellens A to B patterns:

Case 4: primary postischemic TWI from spontaneous RCA reperfusion (“inferior Wellens”), then reocclusion starting with pseudonormalization

  • H: normal sinus rhythm
  • E: normal conduction
  • A: normal axis
  • R: normal R wave progression
  • T: normal voltage
  • S: first ECG has TWI in III/aVF and posteriorly (tall T in V2), and repeat ECG has normalization of T waves

Impression: inferoposterior TWI when symptoms resolved (reperfusion) and then normalization when symptoms recurred (pseudonormalization). Serial ECGs 10 minutes apart, with ongoing symptoms, revealed inferior reocclusion MI–starting with hyperacute T waves with reciprocal TWI in aVL and then obvious inferoposterior MI:

Treated with heparin and antiplatelets and taken to the cath lab, by which time they had spontaneously reperfused again: 90% RCA occlusion, trop I rose from 70 to 300.

Case 5: primary postischemic TWI from LAD reperfusion after Q waves (i.e not Wellens)

  • H: normal sinus rhythm
  • E: normal conduction
  • A: normal axis
  • R: new loss of anterior R waves, with new Q wave in V2
  • T: low voltage
  • S: new anterior convex ST segment with TWI

Impression: resolved symptoms with postischemic T-waves and new Q waves. Stat cardiology consult, who took patient to cath lab: 100% mid LAD occlusion (so either reoccluded on the way to cath lab, or was perfused through collaterals), trop I rise from 4,000 to 9,000.

Case 6: primary postischemic TWI from RCA reperfusion after Q waves, then reocclusion with pseudonormalization

  • H: normal sinus rhythm
  • E: normal conduction
  • A: new left axis from inferior Q waves
  • R: new early R wave progression
  • T: normal voltage
  • S: new inferior convex ST segment with TWI and reciprocal change in I/AVL, and anterior STD with large T waves (posterior TWI)

Impression: inferoposterior MI with Q waves, spontaneously reperfused but was not treated until troponin came back at 14,000. Then ECG repeated, showing inferior T wave pseudonormalization and ST elevation, with increased reciprocal changes in I/aVL, increased anterior STD and smaller posterior TWI:

Treated with heparin and antiplatelets, and cath lab activated. ECG after treatment and prior to cath lab showed reperfusion TWI again, and at cath was found to have 95% RCA occlusion. Peak trop 15,000.

Case 7: primary ischemic TWI from refractory OMI

  • H: normal sinus rhythm
  • E: normal conduction
  • A: normal axis
  • R: loss of anterior R waves with Q waves
  • T: low voltage in limb leads
  • S: TWI anterolatreal

Impression: subacute and ongoing ischemic symptoms with Q waves and TWI. Cath lab activated: 99% LAD occlusion, first trop 50,000. Discharge ECG the same.

Case 8: primary ischemic TWI from PE

  • H: sinus tach
  • E: normal conduction
  • A: left axis but also deep S wave in I
  • R: normal R wave progression
  • T: normal voltage
  • S: antero-inferior TWI

Impression: ongoing ischemic symptoms with sinus tachycardia, S wave in I and antero-inferior TWI suggesting right ventricular strain. CT: bilateral PE with RV strain, trop 50.

Take Home Points for Wellens Syndrome, reperfusion and reocclusion MI

  1. TWI can be a secondary repolarization abnormality (eg bundle branch block or ventricular hypertrophy)
  2. Primary postischemic TWI (resolved symptoms) indicates a transiently reperfused occlusion MI, requiring urgent treatment and close observation for reocclusion (pseudonormalization)
  3. Primary ischemic TWI (ongoing ischemic symptoms) includes acute occlusion MI (reciprocal to hyperacute T waves and ST elevation), refractory occlusion MI (prolonged symptoms + Q wave + TWI), and PE (antero-inferior TWI and other signs of right heart strain)

References for ECG Cases 23 -Wellens syndrome, reperfusion and reocclusion MI

  1. De Zwaan C, Bar FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J 1982 Apr;103(4 Pt 2): 730-6
  2. de Zwann C, Bar FW, Janssen JH, et al. Angiographic and clinical characteristics of patients with unstable angina showing an ECG pattern indicating critical narrowing of the proximal LAD coronary artery. Am Heart J 1989;117(3):657-665
  3. Miranda DF, Lobo AS, Walsh B, et al. New insights into the use of the 12 lead electrocardiogram for diagnosing acute myocardial infarction in the emergency department. Can J Cardiol 2018;34:132-145
  4. Neill WA. Staccato left anterior descending artery occlusion: a recognizable subset of unstable angina. J Lab Clin Med 1985 Mra;105(3):390-6
  5. Haines DE, Raabe DS, Gundel WD. Anatomic and prognostic significance of new T-wave inversion in unstable angina. Am J of Cardiol July 1983;51(1):14-18
  6. Driver BE, Shroff G, Smith SW. Posterior reperfusion T waves: Wellens’ syndrome of the posterior wall. Emerg Med J 2017 Feb;34(2):119-123
  7. Nikus et al. Electrocardiographic classification of acute coronary syndromes: a review by a committee of the International Society for Holter and Non-Invasive Electrocardiology.
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