What is the classification of myocardial infarction (MI)?

Classification of Myocardial Infarction

Myocardial infarction is classified into five distinct types based on underlying pathophysiology, with Type 1 (spontaneous atherothrombotic MI) and Type 2 (supply-demand mismatch MI) being the most clinically relevant for spontaneous presentations, while Types 4 and 5 are procedure-related and Type 3 represents fatal MI without biomarker confirmation. 1, 2

The Five Types of MI

Type 1: Spontaneous Myocardial Infarction

• This is the classic MI caused by atherosclerotic plaque rupture, ulceration, fissuring, erosion, or dissection with resulting intraluminal thrombus in coronary arteries, leading to decreased myocardial blood flow or distal platelet emboli with myocyte necrosis. 1
• Accounts for 65-90% of all NSTEMI cases. 3
• Patients may have underlying severe coronary artery disease, though 5-20% may show non-obstructive or no CAD at angiography, particularly in women. 1

Type 2: Myocardial Infarction Secondary to Ischemic Imbalance

• Occurs when conditions other than coronary artery disease create an imbalance between myocardial oxygen supply and demand. 1, 2
• Common causes include coronary endothelial dysfunction, coronary artery spasm, coronary embolism, tachyarrhythmias or bradyarrhythmias, anemia, respiratory failure, hypotension, hypertension with or without left ventricular hypertrophy, and severe dehydration. 2, 4
• These patients typically have multiple comorbidities, and in-hospital mortality is not always cardiovascular-related. 3
• Critical distinction: Type 2 MI requires correction of the underlying precipitant (e.g., aggressive hydration for dehydration, treating anemia, controlling heart rate) rather than primary reperfusion therapy. 4

Type 3: Cardiac Death Due to MI

• Applies to patients who suffer cardiac death with symptoms suggestive of myocardial ischemia accompanied by presumed new ischemic ECG changes or new LBBB, but death occurred before cardiac biomarkers could be obtained or before they would be elevated. 1
• These patients should be classified as having had a fatal MI even if cardiac biomarker evidence is lacking. 1

Type 4a: PCI-Related Myocardial Infarction

• Defined by elevation of cardiac troponin values >5× the 99th percentile upper reference limit in patients with normal baseline values (or >20% rise if baseline values are elevated and stable or falling). 1, 2
• Requires additional evidence: symptoms of ischemia, new ischemic ECG changes, angiographic findings consistent with procedural complication, or imaging demonstration of new loss of viable myocardium or new regional wall motion abnormality. 1, 2

Type 4b: Stent Thrombosis-Associated MI

• Detected by coronary angiography or autopsy in the setting of myocardial ischemia with a rise and/or fall of cardiac biomarker values with at least one value above the 99th percentile URL. 1

Type 5: CABG-Related Myocardial Infarction

• Defined by elevation of cardiac biomarker values >10× the 99th percentile URL in patients with normal baseline cardiac troponin values. 1, 2
• Requires additional criteria: new pathological Q waves or new LBBB, angiographic documented new graft or native coronary artery occlusion, or imaging evidence of new loss of viable myocardium or new regional wall motion abnormality. 1, 2

Clinical ECG-Based Classification

STEMI vs NSTEMI

• MI is clinically classified based on ECG findings as ST-Elevation MI (STEMI) or Non-ST-Elevation MI (NSTEMI). 2
• New ST elevation at the J point in two contiguous leads with cut-points: ≥0.1 mV in all leads except V2-V3, where ≥0.2 mV in men ≥40 years, ≥0.25 mV in men <40 years, or ≥0.15 mV in women defines STEMI. 1
• Both Type 1 and Type 2 MI can present as either STEMI or NSTEMI. 3

Q-Wave vs Non-Q-Wave MI

• Q waves represent transmural infarction and are associated with larger infarct size, while non-Q-wave MI indicates subendocardial involvement. 2

Critical Clinical Pitfalls

Recognizing STEMI Equivalents

• Approximately 30% of NSTEMI patients have total coronary artery occlusion and represent high-risk STEMI equivalents requiring immediate invasive strategy (<2 hours). 5, 6
• STEMI equivalents include hyperacute T-wave changes, true posterior MI, multilead ST depression with ST elevation in lead aVR, and characteristic diagnostic criteria in the setting of left bundle branch block. 2

Atypical Presentations

• MI may present with atypical symptoms or even without symptoms, especially in women, elderly patients, diabetics, and post-operative or critically ill patients. 2
• Differentiation between true MI and other causes of myocardial injury is crucial for appropriate management. 2

Type 1 vs Type 2 Distinction

• It is essential to distinguish between Type 1 and Type 2 MI early in the clinical course because they require fundamentally different treatment approaches—Type 1 requires reperfusion therapy while Type 2 requires correction of the underlying supply-demand mismatch. 3