STEMI mimics


  • ST segment elevation (defined as 1mm in two contiguous leads or any Left Bundle Branch Block (LBBB) configuration meeting Sgarbossa criteria) is a myocardial injury pattern until proven otherwise
  • When STEMI is unlikely, there are several other etiologies of ST elevation that can be considered
  • If myocardial ischemia is suspected but not (yet) evident, serial ECG’s are helpful, as only 72% of patients will receive the diagnosis of STEMI within the first 1.5 hrs[1]


The mnemonic “ELEVATION”, can help you remember STEMI mimics

  • Electrolytes (Hyperkalemia)
  • Left Bundle Branch Block
  • Early Repolarization
  • Ventricular Hypertrophy (Left)
  • Aneurysm (Ventricular)
  • Thailand (Brugada Syndrome)
  • Inflammation (Pericarditis)
  • Osborne (J) Waves
  • Non-Ischemic Vasospasm


Electrolytes (Hyperkalemia)

  • T waves are peaked without any concave-down (tombstone) ST elevation
  • T waves of hyperkalemia should be tall, symmetrical, pointed, and narrow
  • Untreated hyperkalemia will progress to a sinuventricular rhythm or a sine wave

Left Bundle Branch Block

  • LBBB as well as any LBBB configuration (ex: RV pacing) can result in ST segment elevation, usually < 5mm
  • Use Sgarbossa Criteria to determine if there is a concurrent infarct
  • In addition, may look for Cabrera’s sign or Chapman’s sign if infarct is suspected, though both are specific but poorly sensitive
  • RBBB does not typically give ST elevation, therefore in cases of RBBB, the usual STEMI rules apply

Early Repolarization

  • Normal variant often seen in young athletes
  • Synonymous with J-point elevation (though not to be confused with a J-wave) i.e. elevation of the point where the QRS usually meets the isoelectric line
  • Some studies suggest an increased risk of VF in these patients, though the lifetime risk remains unclear

Ventricular Hypertrophy (Left Ventricular Hypertrophy)

  • LVH typically with ‘strain’ pattern: in these cases, the ST elevation should only be in V1-3, be concave-up (i.e. not a tombstone morphology), be discordant with the deep S wave, and not be elevated >2mm

Aneurysm (Ventricular Aneurysm)

  • After an MI, the walls of the ventricles can become aneurysmal and manifest on the surface 12 lead as persistent ST elevation in the territory of the old infarct
  • Q waves (from the previous MI) should be present in the leads with persistent ST elevation
  • An echo is required for the final confirmation
  • Takotsubo cardiomyopathy (broken heart syndrome) will present similarly.

Thailand (Brugada Syndrome)

  • Cause by a mutation in a cardiac sodium channel (mostly SCN5A), was first described in Thailand in 1992
  • May be responsible for 4-5% of all sudden cardiac deaths
  • 3 described ECG types - Types 1 and 2 more commonly give ST elevation while type 3 has a “saddle back” appearance without ST elevation
  • Brugada pattern can be pharmacologically induced (ex: antiarrhythmics such as sodium channel blockers), precipitated by illness or fever, or be intermittent (will commonly see an incomplete RBBB pattern)

Inflammation (Pericarditis)

  • Look for diffuse ST elevation
  • PR depression is typically only seen in viral pericarditis, though the teaching is that this is a classic electrocardiographic sign of pericarditis
  • In acute pericarditis, there might be PR elevation and ST depression in aVR only, but this is poorly sensitive
  • Consider the diagnosis of STEMI in favor of pericarditis when: there is ST depression anywhere (except for V1, aVR), ST elevation height in III>II, there is a convex/horizontal ST elevation morphology, or when there are new Q waves
  • If predominantly inferior elevation, depression in aVL is very sensitive for STEMI[2]

Osborn (J) wave

  • Hypothermia, usually <30 C is associated with the presence of Osborn J waves
  • Positive deflections at the J point.
  • Bradycardia (including AV block) and atrial fibrillation are also common in moderate and severe hypothermia
  • Hypothermic patients are at risk for VF

Non-Ischemic Vasospasm

  • True ST elevation, in the sense that the ST elevation pattern is that of an injury current, but has a different mechanism and a different management
  • Cocaine-induced ST elevation secondary to vasospasm should be treated with benzodiazepines and nitrates as needed
  • While it is possible to have a STEMI from a ruptured plaque and subsequent clot formation in a patient with cocaine toxicity, it is helpful to risk stratify patients with a suspected STEMI by age, risk-factors, etc
  • It may be impossible to tell by surface ECG (and therefore without a left heart catheterization) if the ST elevation is due to cocaine toxicity or due to plaque rupture

See Also


  1. Riley RF, Newby LK, Don CW, et al. Diagnostic time course, treatment, and in-hospital outcomes for STEMI patients presenting with non-diagnostic initial ECG: A report from the Aheadache mission: lifeline program. Am Heart J. 2013; 165(1):50–56.
  2. Bischof JE, Worrall C, Thompson P, et al. ST depression in lead aVL differentiates inferior ST-elevation myocardial infarction from pericarditis. Am J Emerg Med. 2016; 34(2):149-154.