What is a myocardial infarction (MI) in adults with a history of cardiovascular disease?

Definition of Myocardial Infarction

Myocardial infarction (MI) is myocardial cell death caused by prolonged ischemia, diagnosed when cardiac biomarkers (preferably troponin) rise above the 99th percentile upper reference limit in the clinical setting of acute myocardial ischemia. 1

Pathophysiological Basis

• MI represents irreversible necrosis of cardiac myocytes resulting from a perfusion imbalance between oxygen supply and demand 2
• Cell death occurs through coagulation and/or contraction band necrosis, typically evolving through oncosis rather than apoptosis 1, 2
• Myocardial cell death is not immediate—it requires at least 20 minutes to begin and 2-4 hours or longer for complete necrosis of all at-risk myocytes 1, 2
• The time to complete necrosis depends on collateral circulation, persistent versus intermittent coronary occlusion, myocyte sensitivity to ischemia, and individual oxygen demand 2

Clinical Diagnostic Criteria

The diagnosis requires evidence of myocardial necrosis in a clinical setting consistent with acute myocardial ischemia, meeting any ONE of the following criteria: 1

• Detection of rise and/or fall of cardiac troponin (cTn) with at least one value above the 99th percentile URL PLUS at least one of: 1

  • Symptoms of ischemia
  • New or presumed new significant ST-segment–T wave changes or new left bundle branch block (LBBB)
  • Development of pathological Q waves on ECG
  • Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
  • Identification of intracoronary thrombus by angiography or autopsy

• Cardiac death with symptoms suggestive of myocardial ischemia and presumed new ischemic ECG changes or new LBBB, occurring before cardiac biomarkers were obtained or would be increased 1

Clinical Presentation

• Ischemic chest discomfort typically lasts at least 20 minutes and is diffuse, non-localized, non-positional, and unaffected by movement of the region 1, 2
• The discomfort may be accompanied by dyspnea, diaphoresis, nausea, or syncope 1, 2
• Critical pitfall: MI may present with atypical symptoms or be completely asymptomatic, detected only by ECG, biomarker elevations, or cardiac imaging 1, 3, 2
• Atypical presentations are particularly common in women, elderly patients, diabetics, and post-operative or critically ill patients 3

Classification Systems

By ECG Findings

• ST-Elevation MI (STEMI): New ST-segment elevation on ECG 3, 4
• Non-ST-Elevation MI (NSTEMI): Elevated biomarkers without ST-elevation 3, 4
• Q-wave MI versus Non-Q-wave MI: Distinguished by presence or absence of pathological Q waves, with Q waves representing transmural infarction and larger infarct size 3

By Pathophysiology (Five Types)

• Type 1 (Spontaneous MI): Related to atherosclerotic plaque rupture, ulceration, fissuring, erosion, or dissection with resulting intraluminal thrombus causing decreased myocardial blood flow or distal platelet emboli 3, 2
• Type 2 (Secondary MI): Ischemic imbalance from conditions other than coronary artery disease, including coronary spasm, embolism, arrhythmias, anemia, respiratory failure, hypotension, or hypertension 3, 2
• Type 3: Sudden cardiac death with symptoms suggestive of MI and new ECG changes or LBBB, but death occurred before biomarkers could be obtained 3, 2
• Type 4a (PCI-related MI): Troponin elevation >5× the 99th percentile URL in patients with normal baseline values, requiring additional evidence of ischemia, new ECG changes, angiographic complications, or imaging evidence of new myocardial loss 3, 2
• Type 5 (CABG-related MI): Cardiac biomarker elevation >10× the 99th percentile URL in patients with normal baseline values, plus new pathological Q waves, new LBBB, angiographic evidence of graft or native coronary artery occlusion, or imaging evidence of new myocardial loss 3, 2

By Temporal Pathology

• Acute MI (6 hours to 7 days): Characterized by polymorphonuclear leukocytes 1, 2
• Healing MI (7 to 28 days): Characterized by mononuclear cells and fibroblasts, absence of polymorphonuclear leukocytes 1, 2
• Healed MI (≥29 days): Manifested as scar tissue without cellular infiltration 1, 2

By Size

• Microscopic (focal necrosis) 1, 2
• Small (<10% of left ventricular myocardium) 1, 2
• Moderate (10-30% of LV myocardium) 1, 2
• Large (>30% of LV myocardium) 1, 2

Key Clinical Considerations

• Any amount of myocardial necrosis caused by ischemia should be labeled as MI, as even minimal damage detected by cardiac troponins implies impaired clinical outcome 2
• The clinical and ECG timing may not correspond exactly with pathological timing—ECG may show evolving ST-T changes and biomarkers may remain elevated when the infarct is pathologically in the healing phase 1, 2
• STEMI equivalents requiring prompt recognition include hyperacute T-wave changes, true posterior MI, multilead ST depression with ST elevation in lead aVR, and characteristic findings with left bundle branch block 3