What are the non-myocardial infarction (heart attack) causes of ST changes on an electrocardiogram (ECG)?

Non-Myocardial Infarction Causes of ST Changes on ECG

ST changes on ECG can result from numerous cardiac and non-cardiac conditions beyond acute myocardial infarction, with the most critical to recognize being pericarditis, left ventricular hypertrophy, bundle branch blocks, electrolyte abnormalities, and drug effects—particularly digitalis.

Cardiac Causes (Non-Ischemic)

Pericarditis and Myopericarditis

• Widespread ST-segment elevation across multiple leads (or PR depression) represents the classic ECG pattern, though this occurs in less than 60% of cases 1
• ST elevation in pericarditis results from epicardial inflammation with current flowing from the epicardium through the great vessels and atria back into the heart 2
• Spodick's sign (downsloping T-P segment) occurs in 29% of pericarditis cases but can appear in 5% of STEMI patients, making it helpful but not definitive 3
• PR depression is more specific for pericarditis and helps distinguish it from MI 3
• ECG changes may be absent initially or evolve rapidly during the disease course 1, 4

Cardiomyopathy

• Both dilated and hypertrophic cardiomyopathy can produce ST-segment and T-wave abnormalities 5
• Takotsubo (apical ballooning) cardiomyopathy causes ST elevation mimicking anterior STEMI 5

Left Ventricular Hypertrophy

• Produces secondary repolarization abnormalities with ST-segment changes 5
• Patients with LVH and ST changes represent the highest risk group for adverse outcomes, even higher than those with primary ST deviation 5

Left Ventricular Aneurysm

• Causes chronic or evolutionary ST-segment elevation that persists from previous infarction 5
• Comparison with prior ECGs is essential to identify this pattern 5

Prinzmetal's (Variant) Angina

• Produces transient ST-segment elevation during coronary vasospasm episodes 5
• ST elevation resolves when spasm terminates, distinguishing it from persistent STEMI 5

Myocarditis

• Can produce ST elevation and T-wave changes similar to pericarditis 5
• ECG changes occur in 60.7% of myocarditis cases versus 24.5% in isolated pericarditis 4

Valvular Heart Disease

• May produce non-specific ST-T wave changes 5

Conduction Abnormalities (Secondary Repolarization Changes)

Bundle Branch Blocks

• Both right and left bundle branch block cause secondary ST-T wave abnormalities due to altered depolarization sequence 5
• Patients with bundle branch block and chest pain are at highest risk for adverse outcomes 5

Ventricular Pacing

• Paced rhythms produce secondary repolarization abnormalities that mimic ischemia 5
• Makes ST-segment monitoring invalid in most paced patients 5

Wolff-Parkinson-White Syndrome

• Ventricular preexcitation causes secondary ST-segment changes 5

Normal Variants

Early Repolarization Pattern

• Widespread ST-segment elevation at the J point with QRS slurring or notching 5
• Characteristic concave upsloping with prominent T waves in ≥2 contiguous leads 5
• More common in young Black males 5

Brugada Syndrome

• Right bundle branch block pattern with ST elevation in V1-V3 5
• High risk for ventricular arrhythmias despite absence of chest pain 5

Electrolyte Abnormalities

Hyperkalemia

• Produces prominent J point elevation with peaked T waves and QRS widening 5
• Creates a "baseline" waveform that may trigger false ST alarms when resolving 5

Hypocalcemia and Other Electrolyte Disturbances

• Can affect repolarization and cause primary ST-T wave changes 5

Drug and Toxin Effects

Digitalis

• Causes characteristic "scoop" or "soup ladle" ST-segment depression 5
• FDA labeling confirms digitalis produces ST-segment depression and PR prolongation at therapeutic doses 6
• These changes reflect expected drug effect, not toxicity 6

Tricyclic Antidepressants

• Cause deep T-wave inversion 5, 7

Phenothiazines

• Produce deep T-wave inversion similar to tricyclics 5, 7

Non-Cardiac Causes

Central Nervous System Events

• Intracranial hemorrhage and other CNS pathology cause deep T-wave inversion with QT prolongation 5, 7

Pulmonary Embolism

• Can produce T-wave inversions and right ventricular strain pattern 5

Hypothermia

• Produces Osborn waves (prominent J point elevation) mimicking ST elevation 5
• ST changes resolve with rewarming, potentially triggering false alarms 5

Post-Defibrillation

• Up to 25% of patients show ST elevation after defibrillation 5
• Usually decreases within 5 minutes 5

Critical Diagnostic Approach

Essential Comparisons

• Always compare with prior ECGs when available, particularly in patients with LVH or previous MI 5
• Obtain ECG during symptoms and after resolution to identify dynamic changes 5

High-Risk Confounding Patterns Requiring Urgent Evaluation

• Bundle branch block, paced rhythm, or LVH with chest pain represent highest mortality risk 5
• These patients require immediate troponin measurement and aggressive evaluation despite ECG ambiguity 5

Key Distinguishing Features for Pericarditis vs. STEMI

• ST depression (except in V1/aVR): OR 31 for STEMI 3
• Greater ST elevation in lead III than II: OR 21 for STEMI 3
• Absence of PR depression: OR 12 for STEMI 3
• Widespread ST elevation in multiple territories favors pericarditis over single-vessel MI 5

Common Pitfalls to Avoid

• A completely normal ECG does not exclude ACS—5% of patients with normal ECGs have MI or unstable angina 5
• Non-specific ST-T changes (<1 mm) are often seen in patients ultimately ruled out for ACS 5
• Left circumflex occlusion may produce non-diagnostic 12-lead ECG despite acute STEMI 5
• Consider posterior leads (V7-V9) and right ventricular leads (V4R-V6R) when standard 12-lead is non-diagnostic with high clinical suspicion 5