CONTENTS
- Approach to STE
- STE in aVR (+/- V1) + diffuse STD
- Right precordial STE
- Anterior +/- inferior leads
- Inferior STE
- Diffuse STE with STD in aVR
(#1) consider if STE may be secondary to conduction abnormality/strain:
- LBBB or paced rhythm?
- LVH
- Hyperkalemia (can cause STE in V1-V3, usually downsloping)
- IVCD
- Tricyclic overdose or class IC antiarrhythmic
(#2) consider differential diagnosis based on the location of STE:
- Predominant STE in V1
- Right precordial STE
- Inferior STE
- Anterior +/- Inferior leads
- Benign diffuse STE pattern
(3) other possibilities
- Myocardial contusion
- Myocarditis
Several conditions are associated with diffuse STD as well as STE in aVR. Before moving down this list, scrutinize the ECG for any evidence of a focal OMI (e.g., STE beyond aVR +/- V1).
diffuse subendocardial ischemia
ECG findings in diffuse subendocardial ischemia
- [1] Diffuse STD, which is maximal in V4-V6 and lead II.
- [2] STE in aVR (and sometimes V1 as well).
- [3] There is no evidence of a focal OMI (e.g., no STE in leads other than aVR and sometimes V1).
- Subtle OMI may cause a slight focal STE, as well as a more obvious STD.
- Especially scrutinize leads aVL and III (either may be the sole lead to manifest with STE, thereby revealing an OMI). TWI in aVL could also support focal ischemia.
- [4] Absence of hyperacute T-waves (especially de Winter T-waves 📖).
- An anatomic distribution of hyperacute T-waves suggests an OMI.
- ⚠️ Focal and diffuse ischemia can co-exist (with two patterns layered upon one another).
clinical significance of diffuse subendocardial ischemia
- Diffuse subendocardial ischemia usually results from stenosis involving the left main coronary artery or multivessel coronary artery disease.
- Coronary arteries are not occluded; rather, there is poor perfusion throughout the heart.
- Clinically, the differential diagnosis includes the following entities:
- (1) Extensive nonocclusive MI (NOMI), such as stenosis of the left main coronary artery.
- (2) Severe chronic coronary artery stenoses plus physiological stress such as anemia or sepsis (this is commonly seen in medical ICU patients under marked physiological stress). In this situation, alleviating the physiological stress should cause prompt normalization of the ECG.
- ⚠️ Consider avoiding a P2Y12 inhibitor in these patients, as they are more likely to require CABG.
- ⚠️ There is frequently no wall motion abnormality on echocardiography because ischemia isn't transmural (it only involves the subendocardial surface). Therefore, preserved LV ejection fraction doesn't necessarily exclude coronary obstruction.
posterior OMI
- Posterior OMI vs. diffuse subendocardial ischemia is discussed here: 📖
anteroseptal MI
general features of anteroseptal MI:
- 🔑 ST vector is oriented superiorly:
- STE from V1-V3 or V1-V4.
- STE in aVR and aVL.
- STD in V5-V6.
- STD in inferior leads (especially III and aVF).
- 🔑 Loss of septal Q-waves in lateral leads.
- 🔑 RBBB is often seen (qR in V1).
- General features of anterior MI:
- 🔑 Hyperacute T-waves (bulky, +/- terminal QRS distortion).
- 🔑 Q-waves and/or loss of R-wave voltage (Q in V1 can be normal, but it shouldn't extend further).
sorting out anteroseptal MI versus diffuse subendocardial ischemia:
- (1) STE in anteroseptal MI tends to extend further along the precordium (usually V1-V3 or V1-V4). Alternatively, subendocardial ischemia usually only causes STE in V1 alone.
- (2) STD in anteroseptal MI tends to be less pronounced.
PE (usually massive PE) 📖
clues to PE in the context of diffuse STD with STE in aVR
- More STE:
- STE may extend a bit further than V1 (to involve V2).
- STE may occur in III and/or aVF.
- TWI:
- Most notably in the right precordial leads.
- Inferior leads: (TWI in III) > (TWI in aVF).
- Terminal right axis deviation:
- Prominent S-I (>1-1.5 mm).
- RSR' may occur in V1 (partial RBBB).
hypokalemia or digoxin
hypokalemia 📖
- 🔑 Q-TU prolongation with broad, bifid TU-waves.
- 🔑 Diffuse downsloping/scooped STD:
- It may produce a down-up morphology.
- Often greatest in the left precordial leads.
- 🔑 Prominent, peaked P-waves in inferior leads.
digoxin 📖
- It may cause diffuse STD with exactly the same distribution as subendocardial ischemia (example below).
- 🔑 Scooped ST depression (which may cause a down-up T-wave configuration).
- 🔑 Short QT interval. 📖
- 🔑 Unusual rhythms 2/2 increased automaticity & AV blockade:
- Accelerated junctional rhythm (+/- AF).
- Ectopic atrial tach with block.
- AF with slow ventricular rate.
- AF with 3rd-degree block.
reverse takotsubo cardiomyopathy 📖
- This looks a LOT like diffuse subendocardial ischemia and will often be misdiagnosed as such until echocardiography is performed.
- Some clues that may suggest reverse takotsubo rather than diffuse subendocardial ischemia:
- 1) Maximal STD in Takotsubo seems to be more ~V3-V4, whereas ischemia seems to be more ~V4-V5.
- 2) Low voltage in I and aVL can be suggestive (if present).
- 3) QT prolongation gives it a “flatter” and less malignant look than ischemia.
exaggerated atrial repolarization
- It may mimic diffuse STD.
- Creates up-sloping, benign-appearing STD, which is diffuse.
- This seems especially notable in the context of a lung hyperinflation pattern.
criteria for right precordial predominant STE pattern:
- (1) Relative STE is most prominent in V1 and/or V2.
- 💡 Severity of STE is always judged in comparison to the QRS complex size.
- (2) Absence of diffuse STD with STE in aVR pattern (this is discussed separately above: ⚡️).
causes of right precordial predominant STE pattern:
- Anteroseptal MI. ⚡️
- Isolated RVMI. ⚡️
- IMI plus RVMI. ⚡️
- Aslanger pattern. ⚡️
- PE. ⚡️
- Hyperkalemia. ⚡️
- Brugada. ⚡️
(#1/7) anteroseptal MI (proximal LAD)
- 🔑 ST vector is oriented superiorly:
- STE from V1-V3 or V1-V4.
- STE in aVR and aVL.
- STD in V5-V6.
- STD in inferior leads (especially III and aVF).
- 🔑 Loss of septal Q-waves in lateral leads.
- 🔑 RBBB is often seen (qR in V1).
- General features of anterior MI:
- 🔑 Hyperacute T-waves (bulky, +/- terminal QRS distortion).
- 🔑 Q-waves and/or loss of R-wave voltage (Q in V1 can be normal, but it shouldn't extend further).
(#2/7) isolated RVMI (pseudo-anteroseptal MI)
- 🔑 STE distribution:
- 🔑 Absence of reciprocal ST depressions in V5-V6 favors RVMI (as opposed to anteroseptal MI).
- 🔑 Absence of STE in aVR or aVL supports RVMI if seen (however, STE in aVR can occur in RVMI with simultaneous subendocardial ischemia involving other myocardial walls). (27918805)
- ⚠️ Consider obtaining right-sided ECG leads.
causes of isolated RVMI
- [1] Isolated occlusion of the right ventricular marginal branch of the RCA (this is important to suspect because the lesion is easily overlooked during cardiac catheterization if attention is incorrectly focused on the left anterior descending artery).
- [2] RCA occlusion occurs without inferior wall ischemia because the RCA is nondominant, because of collateralization, or due to CABG with a bypass graft.
- [3] Prior inferior MI has already occurred. (27367171)
(#3/7) combined IMI + RVMI
- 🔑 Core features of IMI:
- Inferior STE (may be subtle)
- STD in aVL.
- 🔑 Features implicating the RCA:
- Bradycardia/blocks.
- STE in III > STE in II.
- STD in Lead I.
- 🔑 Features of RV ischemia:
- STE of ≧0.5 mm in V1 (although STE can occasionally extend out to V3).
(#4/7) Aslanger pattern
- Criteria:
- (a) STE in V1 > STE in V2.
- (b) STE in lead III, but not in other inferior leads.
- (c) STD with a terminally positive T-wave in any of leads V4-V6 (but no STD in V2).
- Aslanger pattern is due to a combination of OMI involving the LCX or RCA plus simultaneous diffuse subendocardial ischemia (e.g., due to triple vessel disease). Diffuse subendocardial ischemia causes ST depression in leads II and aVF that camouflages the inferior OMI. (32526537)
(#5/7) pulmonary embolism
- Discussed here: 📖
(#6/7) hyperkalemia
- 🔑 Infarct mimic (STE in V1-V2; often triangular STE diving into TWI).
- STE in (V1 > V2), aVR, sometimes III.
- Triangular STE morphology dives into TWI.
- 🔑 Peaked T-waves.
- 🔑 P-waves widen, PR increases, and eventually, P-waves disappear.
- 🔑 Bradycardia, blocks, and/or pauses.
- 🔑 QRS widening (may mimic RBBB or VT; can be >200 ms).
- 🔑 Terminal right axis deviation (large S-I +/- S-V6; RSR' in V1).
(#7/7) Brugada I pattern 📖
right precordial leads
- V1 and/or V2 with: {RSR' pattern –> coved/straight STE –> TWI}.
- r' wave isn't well defined (but rather, it is very blunted).
⚠️ Brugada I can be indistinguishable from anterior MI:
- Brugada I may cause STE in aVL.
- Brugada I may cause STD in lateral precordial leads and inferior leads.
If Brugada I is due to a sodium-channel blocker, you may also see:
- Axis deviation:
- Prominent R-wave in aVR.
- Terminal S-wave in I.
- QRS prolongation (can mimic RBBB).
anterior aneurysm
key features of anterior aneurysm
- 🔑 Typically, there are deep Q-waves in V1-V4.
- Usually, at least one QS wave within V1-V4.
- Sometimes there is very poor R-wave progression, with rS in the left precordial leads (V4 – V6).
- rSr' may be seen (El-Sherif sign).
- 🔑 STE: Coved STE in V1-V4 (persistent STE >1 month after MI suggests aneurysm).
- 🔑 Often shallow TWI. This may have a biphasic, up-down morphology that looks like Wellens A. 📖
differential diagnosis
- Acute anterior MI.
- LVH.
features favoring an anterior OMI (rather than chronic aneurysm)
- Disproportionate upright T-wave in V1-V4:
- An upright T-wave >36% of the size of the QRS complex suggests ischemia. (15915398)
- Unequivocally hyperacute morphology of an upright T-wave supports active ischemia.
- Other features of acute anterior OMI, for example:
- If STE in leads without deep Q-waves (especially aVL).
- Reciprocal STD (e.g., inferior leads or left precordial leads).
- (More on ECG findings in anterior MI: 📖)
key diagnostic maneuvers
- Obtaining old ECGs. Morphology should be roughly stable over time (noting that tachycardia may slightly increase the ST elevation).
- Obtaining old echo or CT scan data. Note that echo may not always show an actual aneurysm (but old echocardiograms should show a wall motion abnormality).
- Obtaining a new echocardiogram: thinning of the left ventricular wall supports the diagnosis of aneurysm.
anterior OMI 📖
- 🔑 Hyperacute T-waves (bulky, +/- terminal QRS distortion).
- 🔑 STE in anterior leads, especially if:
- STE >5 mm.
- Convex, coved STE.
- 🔑 Q-waves and/or loss of R-wave voltage (Q in V1 can be normal, but it shouldn't extend further).
- 🔑 Reciprocal changes may occur with anteroseptal or high lateral MI (involving inferior leads and/or V5-V6).
pericarditis ⚡️
- 🔑 STE:
- Concave or saddle-shaped, often following J-point elevation.
- STE is greatest in II and V5-V6.
- STD in aVR.
- No reciprocal STD (especially in aVL).
- 🔑 Upright, relatively small T-waves (in V6, STE is >25% height of the T-wave).
- 🔑 PR depression (~80% sensitive, but nonspecific).
early repolarization ⚡️
- 🔑 Usually men (75%), <50-70 years old.
- 🔑 Widespread STE (greatest in V3-V4; often limb leads esp. II).
- 🔑 Notching/slurring at the J-point is followed by concave STE.
- 🔑 T-waves are usually tall and asymmetric, with STE in V6 <25% of the T-wave height (but benign TWI is possible).
- 🔑 R-waves and generally tall.
- 🔑 Often associated with STD in aVR.
Takotsubo cardiomyopathy 📖
- 🔑 STE is often maximal in V3-V5 but can be diffuse (including II).
- 🔑 Lack STE in V1 (~80% sensitive & specific for differentiation from anterior MI). (36074030)
- 🔑 aVR usually has STD.
- 🔑 No reciprocal STD or Q-waves.
- 🔑 QT may be dramatically prolonged.
myocarditis ⚡️
- Variable findings.
- Consider in patients not fitting other patterns or based on clinical context.
- It can coexist with pericarditis (myopericarditis).
- Causes of inferior STE are discussed in the IMI chapter here: 📖
differential diagnosis
- [1] Consider OMI. 📖
- [2] Remaining differential diagnosis:
[1] consider OMI 📖
red flags for MI
- 🚩 Malignant morphology (e.g., STE is flat or convex, frankly hyperacute T-waves).
- 🚩 STE >5 mm.
- 🚩 STE in aVR.
- 🚩 STD in the lateral precordial leads, I, or aVL.
- 🚩 STD in aVR:
- Pericarditis: should not have STD in aVL. (26542793)
- Early repolarization: May have STD in aVR if QRS complex is negative.
- 🚩 STD in inferior leads:
- Early repolarization may have a minimal amount of inferior STD, for example, <1 mm of summed STD in II, III, and aVF.
- Pericarditis: STD in lead III occurs in 14% of patients. (4726240)
- 🚩 Loss of normal R-wave height and R-wave transition.
- 🚩 New Q-waves in V2-V4 (note that Q-waves may occur in post-MI pericarditis).
- 🚩 Invasive T-waves cause terminal QRS distortion in V2-V4.
- 🚩 TWI in V2-V6 (unless this fits the pattern of benign T-wave inversion).
- ⚠️ Combination diagnoses are possible. Precordial leads may show obvious ER, but there may also be an inferior OMI. Benignity in part of the ECG doesn't exclude an OMI elsewhere in the ECG.
- ⚠️ Obtain a STAT bedside echocardiogram. If the above red flags are absent and the bedside echocardiogram reveals preserved LVEF without any wall motion abnormalities, a multi-territory OMI is largely excluded.
MI may cause diffuse STE without reciprocal change in a few situations, as outlined below:
[#1/2] wrap-around LAD
- LAD supplies anterior and inferior walls.
- Occlusion causes STE in anterior and inferior distribution without reciprocal STD.
[#2/3] anterolateral MI
- STE occurs predominantly in the anterior and lateral territories (including I, aVL).
- STE may spill over into Lead II as well.
ER vs. pericarditis vs. myopericarditis vs. Takotsubo cardiomyopathy
[1] distribution of STE
- Pericarditis:
- Maximal precordial STE in V5-V6.
- Virtually always STE in limb leads (usually greatest in II).
- STD in V1 favors pericarditis (STD in V1 seen in ~1/3 of patients with pericarditis, almost never seen in benign early repolarization).
- Early repolarization:
- Maximal precordial STE in ~V3-V4.
- STE is sometimes in inferior leads (especially II).
- Myopericarditis is more unpredictable.
- Takotsubo:
- STE is often maximal in V3-V5, but can be diffuse (including II).
- Lack STE in V1 (~80% sensitive & specific for differentiation from anterior MI). (36074030)
[2] T-wave morphology
- Pericarditis:
- STE is >25% of the T-wave height.
- Dramatic STE (e.g., >5 mm) may suggest a component of myocarditis as well.
- Benign early repolarization:
- T-waves are often tall and asymmetric (slow upstroke & fast downstroke).
- STE is <25% of the T-wave height.
- Takotsubo:
- QT interval may be markedly prolonged.
- Prominent T-waves may be typically seen throughout the ECG.
[3] consider unequivocal PR depression
- This favors pericarditis or perimyocarditis.
- 💡 Unequivocal PR depression with STE that doesn't fit pericarditis suggests myopericarditis.
(J-waves don't really help)
- Commonly occur in ER (so they may favor this diagnosis somewhat).
- Can occur in MI.
- Can occur in myocarditis.
- Can occur in Takotsubo cardiomyopathy.
- Not generally seen in isolated pericarditis.
⚠️ When in doubt about the diagnosis, start with the diffuse STE algorithm here: ⚡️
key features of early repolarization
- 🔑 Usually men (75%), <50-70 years old.
- 🔑 Widespread STE (greatest in V3-V4; often limb leads esp. II).
- 🔑 Notching/slurring at the J-point is followed by concave STE.
- 🔑 T-waves are usually tall and asymmetric, with STE in V6 <25% of the T-wave height (although benign TWI is possible).
- 🔑 R-waves and generally tall.
- 🔑 Often associated with STD in aVR.
- Related algorithms:
STE
- Morphology:
- Notch or slur at the end of the R-wave.
- Often followed by concave ST elevation.
- Distribution:
- V2-V5, greatest in ~V3-V4.
- Often STE in inferior leads (especially in lead II).
- (This is one cause of a benign diffuse STE pattern.)
- STE <5 mm.
T-waves
- Tall & asymmetric T-waves are usually seen (with a slower upstroke and fast downstroke). This helps differentiate early repolarization from:
- Pericarditis – which has shorter T-waves.
- MI can have hyperacute T-waves (which are fatter and more symmetric).
benign TWI may occur in the context of early repolarization
- 🔑 Typical morphology:
- [i] Tall R-wave, with minimal/no S-wave.
- [ii] Often J-waves.
- [iii] Usually, some STE.
- [iv] ST segment has a gentle upslope, which creates an up –> down configuration.
- [v] TWI is often shallow.
- [vi] QT is usually short (e.g., QTc < ~425 ms).
- 🔑 Distribution:
- Benign TWI extends out more laterally (~V3-V6) than Wellens (~V2-V5).
- Inferior leads typically have TWI.
- 🔑 TWI is relatively stable over time.
- (DDx of biphasic up–>down TWI in precordial leads: 📖)
proposed definition of early repolarization
- Various authors use the term “early repolarization” to refer to a variety of ECG patterns. In 2015 a group of authors proposed a consensus definition of ER, requiring the following attributes: (26205599)
- [1] End-QRS notch or slur on the downslope of a prominent R-wave.
- If there is a notch, it should lie entirely above the baseline.
- If there is a slur, the onset of the slur must be above baseline.
- [2] The peak of the notch or slur (Jp) is ≧1 mV in two or more contiguous leads (excluding V1-V3).
- [3] QRS duration is <120 ms (measuring leads without notching/slurring).
- This definition makes no requirement regarding the ST segment.
- There is a risk of malignant arrhythmia, but it is small (e.g., ~1/10,000). Stratification of the risk of arrhythmia may include:
- Upsloping ST segment is more benign.
- Flat or downsloping ST segment may associated with malignant arrhythmias.
⚠️ When in doubt about the diagnosis, start with the diffuse STE algorithm here: ⚡️
key features of pericarditis
- 🔑 STE:
- Concave or saddle-shaped.
- STE is greatest in II and V5-V6.
- STD in aVR.
- No reciprocal STD (especially in aVL).
- 🔑 Upright, relatively small T-waves (in V6, STE is >25% height of the T-wave).
- 🔑 PR depression.
STE
- Morphology:
- Concave or saddle-shaped.
- STE <5 mm.
- Distribution is usually diffuse:
- Precordial leads: usually greatest in V5-V6.
- Limb leads: Typically greatest in lead II.
STD is allowed in:
- STD in V1 and aVR often occurs in pericarditis.
- STD in lead III occurs in 14% of patients with pericarditis. (4726240)
T-waves
- (1) T-waves are initially upright (when ST segments are elevated).
- (2) T waves should be relatively small:
- ST/T wave ratio is usually >25%.
- Prominent T-waves (ST/T ratio <24%) may suggest:
- Benign early repolarization.
- Hyperacute T-waves.
- Myopericarditis.
- After STE resolves, diffuse TWI develops (everywhere except aVR, V1).
PR depression
- Defining PR depression:
- PR depression is best seen in the inferior leads and V4-V6.
- In pericarditis, PR depression should occur everywhere – except for aVR and occasionally V1.
- PR depression should be unequivocal (e.g., >0.5-0.8 mm) to be called pathological. (Charles MA et al. Arch Int Med 1973;131:657; 31778001).
- PR depression is ~80% sensitive to pericarditis. It may be the initial and sole ECG finding. (Braunwald 12e)
- PR depression is not entirely specific. Other causes include:
- Atrial infarction, usually in the context of inferior MI. PR depression may be more anatomically restricted in myocardial ischemia as compared to pericarditis. (O'Keefe 2021)
- Perimyocarditis (discussed below).
- Chronic pulmonary disease.
- Takotsubo cardiomyopathy.
- Pseudodepression due to atrial flutter or Parkinsonian tremor. (O'Keefe 2021)
- ⚠️ In the presence of PR depression, consider using the TP segment as the baseline to judge ST elevation or depression. Marked PR depression may create pseudo-deviations of the ST segments!
effusion
- If present, large effusion may cause additional findings (e.g., low voltage).
stages of pericarditis
- All stages are often not seen. Evolution through these stages occurs more slowly than with MI (over days).
- Stage 1: STE; PR depression.
- This is usually how patients present (seen in >80% of cases).
- T waves rarely invert while ST is still elevated.
- Q-waves should not occur.
- Stage 2: Pseudonormalization.
- Stage 3: TWI with or without STD; PR normalization: Occurs days-weeks later
- It may resemble “diffuse ischemia” or the Wellens picture.
- This can remain indefinitely but generally goes away within a few months.
- Stage 4: Normalization.
related differential algorithms
- ECG findings:
- Diagnostic algorithms:
- Lateral OMI 📖
what is PIRP?
- This may occur following a transmural infarction that extends to the epicardium, causing regional pericarditis.
- As such, PIRP will happen in the context of a full-thickness, Q-wave infarction.
- The clinical significance is that PIRP may portend a risk of myocardial wall rupture or ventricular septal defect.
ECG findings in PIRP
- [#1] Large, transmural Q-wave MI with persistent STE.
- In some ways, this is a prerequisite for PIRP.
- Persistent STE for >48-72 hours after MI suggests PIRP. (de Luna 2022)
- These patients may often have features of ventricular aneurysm.
- [#2] Positive T-waves where they are not expected:
- (a) Persistently positive (upright) T-waves >48 hours after MI onset.
- (b) T-waves initially invert due to reperfusion. However, they subsequently flip back to being upright ~48-72 hours after MI onset (faster than this transition normally occurs).
- The differential diagnosis here is pseudo-normalization due to re-infarction.
- (Echocardiography showing pericardial effusion could support the diagnosis of PIRP. If a moderate/large effusion is found, myocardial wall rupture must also be considered.) 🌊
overall performance
- ECG is abnormal in ~85% of patients. (33176455)
rhythm
- Sinus tachycardia is the most common.
- Bradyarrhythmias due to heart block may occur. In the context of myocarditis, advanced heart block should suggest cardiac sarcoidosis, Lyme disease, or immunotherapy-associated myocarditis. (38763214)
- Atrial fibrillation may occur.
- VT is an uncommon initial manifestation but often occurs during follow-up. (VT may suggest giant cell myocarditis or sarcoidosis). (Gaggin 2021)
- PVCs occur in about 25%. Polymorphic PVCs may suggest myocarditis. (37589159)
intervals
- Heart block may be seen:
- Prominent conduction abnormalities may suggest Lyme disease, immune checkpoint inhibitors, giant cell myocarditis, or sarcoidosis. (37014337)
- Heart block is rare in lymphocytic myocarditis. (Gaggin 2021)
- QRS prolongation may occur, often due to LBBB.
- QT prolongation (poor prognostic factor due to its association with arrhythmias).
low voltage may occur:
- This may result from a pericardial effusion.
- This may happen in the absence of a pericardial effusion.
STE
- General aspects of STE in myocarditis:
- Pericarditis-like pattern:
- Seen in perimyocarditis.
- J-point elevation and upward concavity may be seen. (31778001)
- MI-like pattern:
Q-waves may occur (~20%) but are usually not very deep.
- Q-waves may disappear over time, so they don't necessarily indicate necrosis. (31778001)
- However, Q-waves are a poor prognostic feature, especially when associated with STE. (31778001)
PR depression
- PR depression is generally absent in pure myocarditis.
- If seen, PR depression may suggest a diagnosis of perimyocarditis (rather than myocardial infarction).
- PR depression in perimyocarditis is similar to that seen in pericarditis, as discussed in the section above. ⚡️
J-waves
- J-waves may occur (creating an appearance that resembles early repolarization).
- On CMR, J-waves may correlate with epicardial inflammation (rather than transmural inflammation). In the context of myocarditis, J-waves don't seem to portend a high arrhythmia risk, although available studies are small. (30879333)
TWI
- Occurs in ~25% of patients with myocarditis.
- TWI seems to be a late feature of myocarditis (evolving over several days following admission). (31778001)
differentiation from MI
- ⚠️ Differentiation between MI and myocarditis is frequently impossible (especially based on a single ECG). If there is STE and the diagnosis is unclear, emergent cardiac catheterization may be required to exclude occlusive MI.
- Some hints:
- (1) Myocarditis evolves more slowly than MI, so serial ECGs tend to be more static.
- (2) PR depression may suggest perimyocarditis.
- (3) STE in a global distribution may favor myocarditis or perimyocarditis.
- (4) Lack of reciprocal STD may favor myocarditis.
- (5) On echo, myocarditis tends to cause diffuse wall motion abnormality (whereas MI is more focal).
among patients with known myocarditis
poor prognostic features
- QRS >120 ms.
- Prolonged QT interval.
- Second or third-degree AV block.
- Ventricular arrhythmias.
- Q-waves.
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References
- 26205599 Macfarlane PW, Antzelevitch C, Haissaguerre M, Huikuri HV, Potse M, Rosso R, Sacher F, Tikkanen JT, Wellens H, Yan GX. The Early Repolarization Pattern: A Consensus Paper. J Am Coll Cardiol. 2015 Jul 28;66(4):470-7. doi: 10.1016/j.jacc.2015.05.033 [PubMed]
- 27367171 Harnett DT, LaHaye SA, Wilkinson JS. Isolated Right Ventricular Myocardial Infarction: A Sheep in Wolf's Clothing. JAMA Intern Med. 2016 Aug 1;176(8):1207-10. doi: 10.1001/jamainternmed.2016.3085 [PubMed]
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