What are the differential diagnoses for a patient presenting with symptoms suggestive of ST-Elevation Myocardial Infarction (STEMI)?

Differential Diagnosis of STEMI

Critical Life-Threatening Conditions to Rule Out Immediately

The most urgent priority when evaluating ST-segment elevation is to identify true STEMI requiring immediate reperfusion therapy, while simultaneously recognizing other potentially catastrophic causes including aortic dissection, massive pulmonary embolism, and acute pericarditis. 1

Cardiovascular Mimics

• Aortic dissection must be excluded immediately, particularly when ST-depression >0.1 mV appears in eight or more leads with ST elevation in aVR and/or V1, especially with hemodynamic compromise 1
• Acute pericarditis presents with widespread ST elevation (typically concave upward) with PR depression, distinguishing it from the convex ST elevation and reciprocal changes seen in STEMI 1
• Takotsubo (stress-induced) cardiomyopathy mimics STEMI with chest pain and ST elevation but shows transient apical/mid-ventricular ballooning on imaging, disproportionately low cardiac biomarkers relative to ventricular dysfunction, and patent coronary arteries on angiography 1
• Coronary vasospasm (Prinzmetal's angina) causes transient ST elevation that resolves spontaneously or with nitrates, with angiography showing no fixed obstructive lesions 2, 3

Pulmonary Causes

• Massive pulmonary embolism can present with ST elevation (exceedingly rare but reported), more commonly showing S1Q3T3 pattern, right axis deviation, or incomplete right bundle branch block; bedside echocardiography revealing right ventricular dilatation/dysfunction is invaluable for diagnosis 2, 4, 3
• Look specifically for anterolateral ST elevation as potential reciprocal changes from right ventricular strain in massive PE 4

Inflammatory/Infectious Conditions

• Focal myopericarditis (viral involvement of myocardium and pericardium) can precisely mimic STEMI with focal ST elevation and elevated cardiac enzymes, particularly in younger patients; this diagnosis is critical to avoid thrombolytic complications including intracranial bleeding, myocardial rupture, and hemorrhagic tamponade 5, 3
• Infective endocarditis with root abscess may present with ST elevation 3

Electrical/Conduction Abnormalities

• Brugada syndrome shows characteristic coved ST elevation in V1-V3 with right bundle branch block pattern 3
• Left bundle branch block (new or presumed new) requires treatment as STEMI equivalent 1
• Early repolarization demonstrates benign ST elevation, typically with notching at the J point 3

Structural Cardiac Conditions

• Left ventricular aneurysm (from prior transmural MI) shows persistent ST elevation in leads corresponding to the aneurysm location 3
• Coronary arteritis/aneurysm and spontaneous coronary artery dissection present with acute coronary syndrome features but different angiographic findings 6, 3

Metabolic/Systemic Causes

• Hyperkalemia produces peaked T waves progressing to ST elevation in severe cases 3
• Hypothermia causes characteristic Osborn (J) waves with ST elevation 3

Neurological Causes

• Subarachnoid hemorrhage can produce dramatic ST elevation and T-wave changes due to catecholamine surge 3

Diagnostic Approach Algorithm

Immediate Actions (Within 10 Minutes)

• Obtain 12-lead ECG and interpret for true STEMI criteria: ≥0.25 mV in men <40 years, ≥0.2 mV in men ≥40 years, or ≥0.15 mV in women in V2-V3; ≥0.1 mV in other leads at J point in two contiguous leads 1, 7
• Add posterior leads (V7-V9) if suspecting isolated posterior MI (ST depression in V1-V3 as dominant finding) 1
• Initiate continuous ECG monitoring with defibrillation capability 1

Physical Examination Red Flags

• Blood pressure differences between limbs suggests aortic dissection 6
• New systolic murmur may indicate mechanical complications or endocarditis 6
• Pericardial friction rub points toward pericarditis 1
• Signs of right heart failure (elevated JVP, peripheral edema) with hypotension suggests massive PE 2, 4

Bedside Echocardiography Indications

• Perform immediately when diagnosis uncertain to detect: regional wall motion abnormalities (occur within minutes of coronary occlusion), pericardial effusion, right ventricular dilatation/dysfunction (PE), ascending aortic dissection, or apical ballooning (Takotsubo) 1, 2
• Absence of wall motion abnormalities excludes major myocardial infarction 1

Laboratory Testing

• Obtain high-sensitivity cardiac troponin at presentation and repeat per validated algorithm (0h/1h or 0h/2h protocol) 1, 7
• Do not delay reperfusion therapy waiting for troponin results if ECG shows STEMI 1

Type 2 NSTEMI Considerations

• Identify supply-demand mismatch precipitants: severe hypertension, tachyarrhythmias, severe anemia, hypotension, respiratory failure, or coronary spasm causing troponin elevation without acute atherothrombosis 6
• Treatment focuses on correcting the underlying precipitating condition rather than immediate catheterization 6

Common Pitfalls to Avoid

• Never administer thrombolytics without confirming true STEMI, as focal myopericarditis patients risk catastrophic complications including hemorrhagic tamponade 5
• Do not dismiss tachycardia as excluding MI; sympathetic activation commonly causes tachycardia in acute MI and should heighten suspicion 7
• Recognize that normal ECG does not exclude MI; the ECG is seldom completely normal even early, but repeated recordings may be necessary 1
• Consider left main/multivessel disease when ST depression appears in ≥8 leads with ST elevation in aVR, requiring immediate angiography regardless of troponin 1, 7