STEMI mimics

Background

• 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

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

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

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

• ST-Elevation Myocardial Infarction (STEMI)
• ST segment elevation
• STEMI equivalents

References

Authors

Max Hockstein, Neil Young, Ross Donaldson, Daniel Ostermayer