In a previous post, I presented a case of Takotsubo non-ischemic cardiomyopathy that met “STEMI” criteria and was diagnosed by angiography. Let’s take a moment to discuss some other non-ischemic cause of ST elevation, otherwise known as “STEMI mimics.”
The differential of ‘STEMI’ from the OMI Manifesto
1) Benign Early Repolarization and Left Ventricular Hypertrophy
Early repolarization pattern, with a notch at the J-point in V4.
ST-elevation does not necessarily imply disease and is often found in the healthy population. Two studies of healthy male subjects found a prevalence of 91-93% for STE of at least 1mm in precordial leads (3,4). “Benign early repolarization” (BER) is theorized to be the mechanism for ST elevation in mid-precordial leads in healthy individuals. Besides the clinical picture, BER can be distinguished from OMI electrocardiographically by STE greatest in V4 with a notch at J point and a concave ST segment (2). Additionally, since BER is not secondary to coronary occlusion, the changes of BER may be seen across multiple vascular distributions. For example, inferior OMI results in STE III>II with reciprocal ST depression in aVL, but BER typically results in STE II>III without reciprocal ST depression in aVL (2). To further complicate matters, T wave inversion with associated STE in mid-precordial leads has also been noted to be a normal varia
Left: left ventricular hypertrophy. Right: acute MI.
nt of healthy individuals (5,6). In this instance, QT interval can provide a clue, as healthy individuals with this variant typically have short QT intervals, whereas those with acute ischemia may have prolonged QT (2). The mechanism behind this variant may be explained by a persistent Juvenile T-wave pattern (2).
Left ventricular hypertrophy (LVH) may produce STE as a result of deep S waves (2). In LVH the ST segment will also be concave.
2) Pericarditis
Left: pericarditis. Right: acute MI.
Pericarditis involves the subepicardial layer of ventricles, typically resulting in diffuse ST elevation across multiple coronary vascular territories (2). Unlike acute MI, the ST elevation of pericarditis typically does not exceed 5 mm (2). Pericarditis may also affect the subepicardial layer of the atria, with corresponding PR depression – this is rarely seen in acute MI.
3) Bundle branch blocks
Left: bundle branch block. Right: acute MI.
A new left bundle branch block alone is no longer considered a “STEMI equivalent.” While a new left bundle branch block implies a pathological process, the rate of acute MI with a new bundle branch block is only 2-4% which is the same rate as a patient with chest pain and an old left bundle branch block (7).
Further complicating the matter, bundle branch blocks inherently produce ST elevation and ST depression as a result of the respective block. This also applies to patients with paced rhythms which artificially produce bundle branch block pattern. As such, Sgarbossa (8) created criteria to recognize patterns more likely to be representative of acute ischemia. The Smith modification to the original Sgarbossa criteria was found to have a sensitivity of 80% and a specificity of 99% for acute MI (9).
4) Hyperkalemia
Left: hyperK Right: Acute MI.
Levine et al first noted the association between ST elevation and hyperkalemia in 1956 (10). Unlike OMI, the ST segment of hyperkalemia is noted to be downsloping whereas STEMI typically is upsloping or plateaued (2).
5) Pulmonary embolism
All medical students and residents are drilled with the phrase “S1Q3T3” as a reminder of the typical ECG pattern seen with pulmonary embolism. However, this is just a reminder that the ECG of PE can also resemble OMI with STE and/or T wave inversions in anteroseptal or inferior leads (11,12,13,14). RV injury from PE, may present with ST elevation in V1-V3 (representing anterior vector of injury) with or without ST depression in V4-V6 (15).
RV injury from PE may also present with ST elevation in aVR w/ diffuse ST depression, especially in patients with severe PE and those complicated by cardiogenic shock (16,17,18). This pattern may mimic OMI resulting from left main disease or multivessel disease as highlighted in the Fourth Univesival definition of Myocardial Infarction (19).
PE can be distinguished from OMI by a concomitant RV strain pattern (TWI in V1 and V2, III) (15). A closer inspection of an ECG may also demonstrate a rightward deviation of the terminal component of QRS vector (as depicted below 15).
Despite all of this, many of us will still not feel comfortable making the diagnosis with ECG alone. Especially in an unstable patient who cannot obtain a CTA, bedside ultrasound may help support your diagnosis by finding a McConnell sign or RV dilation. Still, perhaps despite your best efforts, you cannot obtain the four-chamber view or there is no ultrasound available. You can always dust off your stethoscope, listen to your patient, and trust your gestalt (20).
6) Post-MI Left Ventricular Aneurysm
Following acute anterior MI without adequate reperfusion, 60% of patients will develop LV aneurysm (LVA) which manifests as persistent ST elevation (21). While LVA may be detectable by formal echocardiogram, the presence of one does not rule out acute MI. Therefore the question becomes, what ECG findings can help differentiate between the two processes? Acute MI usually has larger T waves than LVA: “If any 1 lead in V1-V4 has a T wave amplitude to QRS amplitude ratio greater or equal to 0.36, then STEMI is predicted” (sensitivity of 91.5%, specificity 81.3%) (22).
7) Prinzmetal Angina
Prinzmetal angina (23) has ECG findings indistinguishable from acute coronary occlusion as both processes result in decreased blood supply from epicardial arteries. As Prinzmetal is secondary to spasm (24), the STE will resolve as spasm resolves, unlike the acute coronary occlusion which typically persists without intervention.
8) Transthoracic Cardioversion
Another transient, relatively benign cause of ST-elevation may result from transthoracic cardioversion. This phenomenon has been reported for both atrial (25) and ventricular (26) dysrhythmias and typically resolves without an increase in myocardial enzymes.
9) Takotsubo Cardiomyopathy
See this previous post.
Monday morning quarterback:
The decision to activate the cath lab is a difficult one, and know that you are not alone in having to make it. In fact, a study found that over 50% of cath lab activations are canceled (27). In the case we have presented earlier, the decision for emergent cath is supported by the literature. The AHA recommends (class IA) emergent cath within 2 hours for a patient with NSTEMI and electrical or hemodynamic instability (28). However, for those that are truly stable, it may be worthwhile to more carefully evaluate your patient, take a closer look at the ECG, and ask yourself: Is this presentation really consistent with an OMI? If the answer to the question is “no” or you have any doubt, take a breath and consider the “STEMI mimics” before activating the cath lab.
References
Robby
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