In this ECG Cases blog we look at 10 patients who presented with tall T-waves. Which were hyperacute T-waves from Occlusion MI?

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

10 patients presented with potentially ischemic symptoms and tall T-waves. Which were hyperacute T-waves from Occlusion MI?

Case 1: 30yo previously well with lightheadedness. Normal vitals.

Case 2: 80yo COPD/HTN with shortness of breath and wheezing, HR 105 BP 200/120, R30, sat 80%

Case 3: 50yo HTN with acute epigastric pain. Normal vitals; Old then new ECG

Case 4: 45yo with three hours of chest pain; normal vitals.

Case 5: 75yo HTN/pacer with 4 hours chest pain and nausea; normal vitals; old then new

Case 6: 50yo with acute epigastric pain; normal vitals; ECG then repeat with posterior leads

Case 7: 55yo with one day of intermittent chest pain, now constant for 30 minutes; old then new ECG

Case 8: 70yo with 30 minutes of exertional chest pain; Old then serial ECGs

Case 9: 75yo with 2 hours of chest pain radiating to the arms; normal vitals; old then new ECG

Case 10: 40yo chronic kidney disease, with vomiting; normal vitals; old then new ECG

Occlusion MI and the revival of hyperacute T-waves

T waves represent ventricular repolarization. They are normally upright (except for aVR, V1 and sometimes III), with a concave and asymmetric morphology (gradual rise and quick descent), and a height proportional to their QRS complex (with T amplitude usually <5mm in limb leads and <10mm in precordial leads). There are many causes of tall T-waves[1] but the most common are:

  1. Normal variant, including early repolarization
  2. Secondary to abnormal depolarization
    1. LBBB: deep/wide anterior S waves followed by ST elevation and tall T wave
    2. LVH: deep/narrow anterior S waves followed by ST elevation and tall T wave
  3. Primary repolarization abnormality
    1. Hyperkalemia: “peaked T waves” are diffuse, look pinched (narrow base and sharp symmetric peak), and are associated with other signs of hyperkalemia (eg bradycardia, junctional rhythm, long PR, wide QRS)
    2. Occlusion MI: “hyperacute T waves” are regional, look inflated (broad base,rounded peak, and large relative to QRS), and are associated with other signs of occlusion MI (loss of R wave, new Q wave, ST elevation, reciprocal ST depression)

The hallmarks of hyperacute T waves have been described for a century:

  1. First sign of occlusion: in 1918, the first experimental study on ECGs in acute coronary occlusion noted that, “immediately following the ligation the T-waves became more prominent…in some instances it exceeded the height of the R wave.”[2]
  2. Precede ST elevation, but can also be associated with ST depression: In 1947, a series of case reports noted that, “high T-waves were the outstanding feature in the earliest stage of myocardial infarction, when elevation of S-T and significant changes of QRS were absent,” including, “in one instance huge upright T waves were associated with marked depression of S-T.”[3]
  3. Defined relative to QRS and associated with reciprocal change: in 1982 the term “hyperacute T waves” was defined as a “relative increase in T-wave positivity due to transmural myocardial ischemia” and it was noted that “the T waves may be only relatively, and not absolutely increased in amplitude. Occasionally with acute infarction, the reciprocal ST segment depressions may actually exceed the amplitude of primary, hyperacute changes. Only careful inspection will disclose the primary locus of injury in such cases.”[4]

The early STEMI guidelines incorporated this knowledge, explaining that “in the very early phase of acute infarction, giant, hyperacute T-waves may be present with no ST-segment elevation,” and that “it is appropriate to administer thrombolytic therapy. Thus, it should be clear that certain cases require experienced interpretation of the ECG before withholding reperfusion therapy.”[5] But as the STEMI paradigm took hold it, its exclusive focus on ST elevation criteria displaced other findings of acute coronary occlusion including hyperacute T-waves. The only mention in the current American STEMI guidelines is that “rarely, hyperacute T-wave changes may be observed in the very early phase of STEMI, before the development of ST elevation”[6]. This implies hyperacute T-waves are both infrequent and inconsequential, and that they’ll rapidly and inevitably give way to diagnostic ST elevation. But STEMI criteria lacks sensitivity for acute coronary occlusion, a dynamic process that can fluctuate between total occlusion and partial reperfusion. In this context, hyperacute T-waves can help identify subtle occlusions that don’t meet STEMI criteria, including those with dynamic occlusion. As a recent review explained, “STE might be preceded by (or if immediately after reperfusion and resolution of chest pain, followed by) large ‘hyperacute’ T-waves, which might thus be a subtle finding of early acute thrombotic occlusion.”[7]

The newer European STEMI guidelines consider hyperacute T waves in the absence of ST elevation as an indication for PCI [8], and deWinter has revived the pattern of upsloping ST depression and hyperacute T-waves first described by Dressler in 1947.[9] Hyperacute T-waves and reciprocal STD can help identify subtle inferior or lateral OMI that do not meet STEMI criteria, differentiate LAD occlusion from early repolarization, and differentiate old LV aneurysm (T/QRS<0.36) from anterior QS waves with new OMI (T/QRS>0.36).[10] Signs of OMI can double the sensitivity of  STEMI criteria for acute coronary occlusion, with preserved specificity, and can identify STEMI(-)OMI patients who experience preventable delays to reperfusion.[11]

Back to the cases

Case 1: Tall T waves from early repolarization

  • Heart rate/rhythm: sinus bradycardia
  • Electrical conduction: normal intervals, incidental U waves V1-4
  • Axis: normal
  • R-wave: normal progression, high voltage
  • Tension: high voltage can be normal for age, no sign of LVH strain pattern
  • ST/T: concave STE and tall asymmetric T waves proportional to QRS, with J waves V3-4

Impression: early repolarization. Meets STEMI criteria with 3mm STE in V1-2, but the STE and T waves are proportional to large QRS complexes, and there are no signs of LAD occlusion (e.g. anterior Q, terminal QRS distortion, STE>5mm, non-concave STE, TWI, or reciprocal change). Negative workup.

Case 2: Tall T waves secondary to LBBB

  • H: sinus tach
  • E: LBBB
  • A: normal axis
  • R: delayed R wave progression from LBBB
  • T: can’t assess LVH
  • S: anterior STE and tall T waves proportional to massive voltages

Impression: LBBB with proportional repolarization changes. Had cath lab activated because met traditional Sgarbossa criteria (5mm STE in V2-3) but modified Sgarbossa negative (V2 STE/S = 7=45 = 0.16; V3 STE/S = 7/55 = 0.13; both < 0.25). No obstructive lesions and symptoms improved with treatment of COPD. Discharge ECG with normal heart rate had less prominent STE and tall T-waves, still proportional to large complexes.

Case 3: T-wave changes secondary to LVH

  • H: NSR
  • E: normal intervals
  • A: normal axis
  • R: normal R wave progression, large voltages
  • T: LVH with strain
  • S: anterior STE/tall T and inferolateral STD/TWI secondary to large voltages

Impression: LVH with strain. Had cath lab activated but normal coronaries.

Case 4: LVH + hyperacute T-waves from anterior OMI

  • H: NSR
  • E: normal conduction
  • A: normal axis
  • R: large voltages, normal progression
  • T: LVH
  • S: concave STE and tall T waves V2-3 can be normal in LVH, but especially in V3 this is disproportionate (with 5mm of STE and a T wave larger than the entire QRS complex)

Impression: LVH + OMI. Cath lab activated: ECG-to-Activation time 10 minutes, 99% mid LAD occlusion, first Trop I was 400 and peak 38,000.

Repeat ECG: reperfusion T-wave inversion

Case 5: hyperacute T-waves from inferior OMI

  • H: atrial paced rhythm
  • E: normal conduction
  • A: normal axis
  • R: normal R wave progression
  • T: no LVH
  • S: hyperacute T-waves inferior (not tall in absolute terms but much larger than baseline and relative to the QRS, and with an inflated appearance with ST straightening and a rounded peak) and lateral (still relatively small but with a straighened ST), both with mild terminal T-wave inversion.  Reciprocal STD I/aVL  confirms inferior OMI, and V2 STD/TWI from posterior involvement

Impression: inferoposterior OMI. Didn’t meet STEMI criteria. ECG repeated 90 minutes later when first trop I came back at 160:

Still no ST elevation, less hyperacute T-waves (more concave) but no reperfusion T wave inversion, and still inferior reciprocal change and now posterior reciprocal change extends to V3. Cath lab activated: ECG-to-Activation time 148 minutes, 99% RCA occlusion, peak trop I = 45,000. Discharge ECG had inferior Q waves and taller R wave in V2, inferolateral reperfusion TWI, and resolution of infero-posterior reciprocal changes:

Case 6: normal variant T-waves

  • H: NSR
  • E: normal
  • A: borderline R axis
  • R: normal progression
  • T: no hypertrophy
  • S: inferior T waves are tall relative to the QRS but don’t look inflated (no broad base and rounded peak), and there is no reciprocal STD in aVL (which makes inferior OMI very unlikely)

Impression: normal variant T-waves. Cath lab activated but normal coronaries.

Case 7: hyperacute T-waves from lateral OMI

  • H: NSR
  • E: normal conduction
  • A: normal axis
  • R: new Q wave in V2-3
  • T: no hypertrophy
  • S: obvious inferior TWI is reciprocal to subtle hyperacute T-waves I/AVL (now larger and more rounded than baseline) and V2 (now relatively large compared to reduced QRS)

Impression: first diagonal OMI.(hyperacute T in I/aVL/V2 with inferior reciprocal change). But pain resolved after nitro, repeat ECG:

Resolution of hyperacute T-waves and inferior reciprocal changes. First trop I was 26 (borderline normal), but due to dynamic changes was admitted as “unstable angina.” Cath: 95% D1 occlusion, peak trop 2,500. Discharge ECG: recovery of anterior R waves, reperfusion TWI in I/aVL, V2-4.

Case 8: hyperacute and then deWinter T-waves from anterior OMI

  • H: NSR
  • E: normal conduction
  • A: normal axis
  • R: loss of R wave in V2, new Q in V3
  • T: no LVH
  • S: hyperacute T-waves in V2 (smaller amplitude than baseline but now broader and double the size of the reduced QRS) and V3 (now as big as the R wave), and then DeWinter T-wave V3-4 (STD + hyperacute T wave)

Impression: STEMI(-)OMI from LAD occlusion. Cath lab activated: ECG-to-Activation time 34 minutes, 100% mid LAD occlusion, first Trop I negative and peak 50,000. Discharge ECG: deeper anterior Q waves with reperfusion T-wave inversion

Case 9: acute Q wave + hyperacute T-wave from anterior OMI

  • H: sinus tach
  • E: normal conduction
  • A: normal axis
  • R: new anterior Q waves
  • T: no hypertrophy
  • S: anterior hyperacute T waves (wide, broad and large relative to the QRS, with T/QRS>0.36 in V2-3), and inferolateral reciprocal STD

Impression: acute Q waves with hyperacute T-waves, which differentiate it from LV aneurysm. Cath lab activated: ECG-to-Activation time 8 minutes, 95% proximal LAD occlusion, first trop I was 2,000 and peak 50,000. Repeat ECG had ongoing anterior Q waves, resolution of hyperacute T-waves (now T/QRS<0.36), and resolution of reciprocal changes:

Case 10: peaked T-waves from hyperkalemia

  • H: NSR
  • E: normal conduction
  • A: normal axis
  • R: normal R wave progression
  • T: no hypertrophy
  • S: diffuse peaked T-waves (look pinched, with a narrow base and sharp peak)

Impression: hyperkalemia (7.7). Treated with calcium, insulin/D50 and dialysis, with resolution of hyperacute T-waves:

Take home points on hyperacute T-waves and occlusion MI

  1. Tall T-waves can be a normal variants (including early repolarization), secondary to abnormal depolarization (LBBB, LVH), or a primary repolarization abnormality (hyperkalemia, occlusion MI)
  2. “Peaked T-waves” from hyperkalemia are diffuse, look pinched (narrow base, sharp peak), and are associated with other signs of hyperkalemia (brady, junctional rhythm, long PR, wide QRS)
  3. “Hyperacute T-waves” from OMI are regional, look inflated (wide base, round peak, large relative to the QRS), and are associated with other signs of occlusion like acute Q/loss of R waves, STE or reciprocal STD
  4. Variants of hyperacute T-waves include: upsloping STD + hyperacute T wave (deWinter T wave), and anterior QS waves with hyperacute T-waves (T/QRS>0.36, which differentiates from LV aneurysm)

References for ECG Cases 21: Hyperacute T-waves and Occlusion MI

  1. Somers MP, Brady WJ, Perron AD, et al. The prominent T wave: electrocardiographic differential diagnosis. Am J Emerg Med 2002 May;20(3):243-51
  2. Smith F. The ligation of coronary arteries with electrocardiographic study. 1918 Ann Noninvas Electrocardiol 2004 Jan;9(1):80-93
  3. Dressler W, Roesler H. High T waves in the earliest stage of myocardial infarction. Am Heart J 1947 Nov;34(5):627-45
  4. Ary Goldberger. Hyperacute T waves revisited. Am Heart J 1982;104(4):888-890
  5. Ryan TJ, Anderson JL, Antman EM, et al. ACC/AHA guidelines for the management of patients with acute myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Acute Myocardial Infarction). JACC Nov 1 1996;28(5):1328-428
  6. O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. JACC January 29, 2013;61(4):378-140
  7. 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
  8. Ibanez M, James S, Agewall S, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-elevation: the Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J 2018;39:119-177
  9. Littman L. The Dressler – de Winter sign of acute proximal LAD occlusion. J of Electrocardiol 2018;51:138-139
  10. Smith SW. T/QRS ratio best distinguishes ventricular aneurysm from anterior myocardial infarction. Am J of Emerg Med 2005;23:279-287
  11. Meyers HP, Bracey 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 Apr;33:100767
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