STEMI mimics

Background

  • ST segment elevation is myocardial injury until proven otherwise
    • 1mm in two contiguous leads or Left Bundle Branch Block (LBBB) configuration meeting Sgarbossa criteria
  • When STEMI is unlikely based on symptoms and demographics, consider other etiologies of ST elevation
    • Serial EKGs helpful in observing evolution of STEMI pattern
      • Only 72% of patients with STEMI receive diagnosis in first 1.5h [1]

Mnemonic

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

ELEVATION

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
  • Elevation in this case should be concave and greatest in precordial leads

Ventricular Hypertrophy (Left Ventricular Hypertrophy)

  • LVH typically with ‘strain’ pattern
  • ST elevation should be:
    • In V1 - V3 only
    • Concave
    • Discordant with deep S wave
    • Not more than 2 mm elevated

Aneurysm (Ventricular Aneurysm)

  • After MI, walls of ventricles can become aneurysmal
    • Manifests as persistent ST elevation in territory of old infarct
    • Q waves should be present in the leads with persistent ST elevation
  • Echo is required for the final confirmation
  • Takotsubo cardiomyopathy (broken heart syndrome) presents similarly

Thailand (Brugada Syndrome)

  • Cardiac sodium channel mutation (usually SCN5A) 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
    • Type 3 has “saddle back” appearance without ST elevation
  • Can be pharmacologically unveiled (ex: antiarrhythmics such as sodium channel blockers), precipitated by illness or fever, or be intermittent (will commonly see an incomplete RBBB pattern)

Inflammation (Pericarditis)

  • Diffuse ST elevation
    • In acute presentation, there may be PR elevation and ST depression in aVR only, but this is poorly sensitive
  • PR depression classically taught as EKG sign of pericarditis but may only occur in viral pericarditis
  • 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

References

  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.