What causes STEMI (ST-Elevation Myocardial Infarction) changes on EKG (Electrocardiogram) other than arterial occlusion in patients with or without a history of cardiac conditions or risk factors?

Non-Occlusive Causes of STEMI-Pattern ECG Changes

Yes, multiple cardiac and non-cardiac conditions can produce ST-segment elevation mimicking STEMI without arterial occlusion, and recognizing these is critical to avoid inappropriate reperfusion therapy and identify the true underlying pathology. 1, 2

Cardiac Causes of ST Elevation Without Arterial Occlusion

Takotsubo (Stress) Cardiomyopathy

• Produces ST elevation mimicking anterior STEMI but without coronary occlusion 1, 2
• Triggered by physical or emotional stress with transient apical or mid-left ventricular ballooning 1
• ECG changes are usually modest and do not correlate with the severity of ventricular dysfunction 1
• Disproportionately low cardiac biomarkers relative to the degree of ventricular dysfunction 1
• Emergency angiography shows no significant culprit stenosis or intracoronary thrombi 1

Acute Pericarditis

• Causes diffuse ST elevation across multiple leads without reciprocal ST depression 1
• Typically accompanied by PR depression in chest leads (38% of non-ischemic ST elevation cases) 3
• Pericardial friction rub may be present on examination 1

Myocarditis

• Produces ST elevation with inflammatory myocardial injury rather than ischemic occlusion 1
• Can present with chest pain and elevated troponins mimicking acute MI 1

Left Ventricular Aneurysm

• Persistent ST elevation in leads corresponding to prior infarction territory 1
• Represents chronic finding from previous transmural MI with wall thinning 1
• Comparison with prior ECGs is essential to identify this pattern 1

Left Ventricular Hypertrophy (LVH)

• Produces secondary repolarization abnormalities with ST-segment changes 2
• Patients with LVH and ST changes represent the highest risk group for adverse outcomes, even higher than those with primary ST deviation 2

Conduction Abnormalities

Left Bundle Branch Block (LBBB)

• Causes secondary ST-T wave abnormalities due to altered depolarization sequence 1, 2
• Makes identification of acute MI extremely challenging 1
• Patients with bundle branch block and chest pain are at highest risk for adverse outcomes 2

Right Bundle Branch Block (RBBB)

• Produces secondary ST changes, particularly in right precordial leads 2
• New RBBB with anterior STEMI indicates critical proximal LAD occlusion with extensive myocardial involvement and worse prognosis 4

Wolff-Parkinson-White Syndrome

• Pre-excitation pattern can produce ST-segment abnormalities 1

Normal Variants

Early Repolarization Pattern

• Widespread ST-segment elevation at the J point with QRS slurring or notching 1, 2
• More common in young Black males 1, 2
• Generally benign and requires no intervention in asymptomatic individuals 5
• Critical to distinguish from acute STEMI to avoid inappropriate thrombolytic therapy or primary angioplasty 5

Vasospastic Causes

Prinzmetal's (Vasospastic) Angina

• Transient coronary artery spasm produces ST elevation without fixed occlusion 1
• ST elevation resolves when spasm terminates 1

Non-Cardiac Causes

Central Nervous System Events

• Intracranial hemorrhage, stroke, or other CNS pathology can cause deep T-wave inversion 1
• Neurogenic ST changes occur without coronary pathology 1

Pulmonary Embolism

• Produces T-wave inversions and right ventricular strain pattern 2
• Can show ST elevation in right-sided leads 2

Hypothermia

• Produces Osborn waves (prominent J point elevation) mimicking ST elevation 2

Drug and Toxin Effects

Tricyclic Antidepressants

• Cause deep T-wave inversion 1

Phenothiazines

• Can produce ST-T wave abnormalities 1

Digitalis

• Causes characteristic "scoop" or "soup ladle" ST-segment depression 2

Electrolyte Abnormalities

Hyperkalemia

• Produces prominent J point elevation with peaked T waves and QRS widening 2

Hypocalcemia

• Affects repolarization and can cause primary ST-T wave changes 2

Critical Distinguishing Features

Favoring True STEMI (Arterial Occlusion):

• Reciprocal ST depression: In anterior ST elevation, ST depression ≥0.025 mV in lead II occurred in 40% of STEMI but 0% of non-ischemic cases 3
• In inferior ST elevation, ST depression ≥0.025 mV in lead I was present in 83% of STEMI but 0% of non-ischemic cases 3
• Terminal QRS distortion more prevalent in STEMI (40%) than non-ischemic ST elevation (7%) 3
• Convex ST elevation occurred in 22% of STEMI versus 9% of non-ischemic cases 3

Favoring Non-Ischemic Causes:

• Chest-lead PR depression uncommon in STEMI (12%) compared to non-ischemic cases (38%) 3
• ST depression in aVR associated with non-ischemic diagnosis 3
• Diffuse ST elevation without reciprocal changes suggests pericarditis 3

Essential Clinical Approach

Immediate Actions:

• Obtain serial ECGs at 15-30 minute intervals if initial ECG is non-diagnostic 1
• Measure cardiac troponins immediately and repeat at appropriate intervals 5
• Always compare with prior ECG tracings when available 1, 2
• Assess for dynamic ECG changes during symptoms 5

Critical Pitfalls to Avoid:

• Do not confuse benign early repolarization with acute STEMI, as inappropriate thrombolytic therapy carries unnecessary hazards 5
• Do not rely on ECG alone—bundle branch block, paced rhythm, or LVH with chest pain represent highest mortality risk requiring immediate troponin measurement despite ECG ambiguity 2
• Do not dismiss ST elevation in the setting of chest pain without considering Takotsubo cardiomyopathy, which requires emergency angiography to exclude MI 1
• Approximately 4% of acute MI patients show ST elevation isolated to posterior chest leads (V7-V9) "hidden" from standard 12-lead ECG 5