Acute mi

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"myocardial infarction" AND pathophysiology

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Acute Myocardial Infarction - Pathophysiology & Types

Definition

At the cellular level, an acute MI is myocardial cell death with necrosis of the myocardium. The Fourth Universal Definition of Myocardial Infarction (ACC/ESC) distinguishes two related terms:

Myocardial injury: elevated cardiac troponin with at least one value above the 99th percentile upper reference limit (URL), with a rise or fall indicating acuity.
Myocardial infarction: acute myocardial injury (elevated troponin > 99th percentile URL) PLUS at least one of:
- Symptoms of myocardial ischemia
- New ischemic ECG changes (ST/T changes or new pathologic Q waves)
- Imaging evidence of new loss of viable myocardium or regional wall motion abnormality
- Angiographic or autopsy evidence of coronary thrombus

(ROSEN's Emergency Medicine, p. 996)

Pathophysiology

1. Oxygen Supply-Demand Imbalance

The core mechanism is inadequate coronary perfusion relative to myocardial oxygen demand. Myocardial oxygen consumption is determined by:

Heart rate
Afterload
Contractility
Wall tension

Coronary stenosis typically does not cause resting ischemia until obstruction exceeds 95% of the vessel lumen. Below this threshold, ischemia may still occur with physiologic stress and increased demand. (ROSEN's, p. 996)

2. Atherosclerosis and Plaque Biology

Coronary artery disease (CAD) develops through thickening and obstruction of the arterial lumen by atherosclerotic plaques. Two plaque types are relevant:

Plaque Type	Features	Risk
Fibrous (stable)	Thick fibrous cap, small lipid core, minimal inflammation	Causes stable angina; unlikely to rupture
Fibro-lipid (vulnerable)	Thin fibrous cap (<55 µm), large lipid-rich necrotic core, abundant macrophages, marked inflammation	High risk of rupture

The fibrous cap's mechanical stability is proportional to its collagen content. Inflammation destabilizes plaques by increasing metalloprotease-mediated collagen degradation and reducing smooth muscle cell collagen synthesis. Adrenergic stimulation (e.g., physical exertion, intense emotions) can also increase shear forces and trigger rupture. (Robbins & Kumar Basic Pathology, p. 322)

Stable vs. vulnerable atherosclerotic plaque - Robbins & Kumar Basic Pathology

3. Plaque Rupture / Erosion - The Triggering Event

Rupture of the fibrous cap (most commonly at its shoulder regions) exposes the thrombogenic necrotic core to luminal blood. This initiates a cascade:

Plaque disruption - rupture, erosion, or fissuring of the fibrous cap
Platelet activation - platelets adhere to exposed subendothelial collagen and plaque contents
White thrombus formation - platelet-rich thrombus forms at the rupture site
Red thrombus propagation - fibrin-rich thrombus extends proximally and distally
Luminal occlusion - partial (NSTEMI/UA) or complete (STEMI)
Myocardial necrosis - irreversible cell death downstream

Note: plaques responsible for AMI are often not significantly stenotic beforehand - a catastrophic event can arise from a previously asymptomatic, non-flow-limiting plaque. (Robbins & Kumar, p. 322; Fuster and Hurst's The Heart, 15th ed.)

Atherosclerotic plaque rupture: (A) rupture without thrombus; (B) acute coronary thrombosis superimposed on disrupted fibrous cap - Robbins & Kumar Basic Pathology

4. STEMI vs. NSTEMI

Feature	STEMI	NSTEMI/UA
Coronary occlusion	Complete, total	Partial / subtotal
Extent of infarction	Transmural (full-wall thickness)	Subendocardial
ECG	ST-segment elevation	ST depression, T-wave changes, or normal
Troponin	Elevated (rise and fall)	Elevated (NSTEMI) / normal (UA)

STEMI results from acute, total occlusion of an epicardial coronary artery - most often due to plaque rupture/erosion with complete thrombotic occlusion. The older terms "transmural" vs. "non-transmural" or "Q-wave" vs. "non-Q-wave" MI are no longer preferred because they imperfectly reflect the coronary event and its pathology. (Washington Manual of Medical Therapeutics; ROSEN's, p. 997)

Types of AMI - The Fourth Universal Classification

The five types reflect the clinical mechanism behind the infarction:

Type 1 - Spontaneous MI (True ACS)

Caused by a primary coronary event: atherosclerotic plaque rupture, erosion, fissuring, or dissection, with accompanying thrombus formation and/or vasospasm. This is the classic ACS mechanism - platelet and coagulation inhibition are the cornerstone of management.

Type 2 - Secondary MI (Supply-Demand Mismatch)

MI secondary to ischemia from increased oxygen demand or decreased supply, unrelated to primary plaque rupture. Examples:

Coronary artery spasm
Coronary embolism
Severe anemia
Sustained tachyarrhythmia or bradyarrhythmia
Significant systemic hypotension (any cause)

Management focuses on identifying and treating the underlying imbalance, not simply antiplatelet therapy.

Type 3 - Sudden Cardiac Death Before Biomarker Sampling

Unexpected cardiac death with symptoms suggesting ischemia plus presumably new ST elevation or new LBBB, with fresh coronary thrombus found on angiography or autopsy - but death occurs before blood sampling can confirm elevated biomarkers.

Type 4 - PCI-Related MI

MI associated with percutaneous coronary intervention:

In patients with normal baseline troponin, any elevation above the 99th percentile URL indicates periprocedural myocardial necrosis
Values >3× the 99th percentile URL define PCI-related MI
A subtype (Type 4b) includes stent thrombosis

Type 5 - CABG-Related MI

MI associated with coronary artery bypass grafting:

In patients with normal baseline troponin, any elevation above the 99th percentile URL indicates periprocedural necrosis
Values >5× the 99th percentile URL PLUS at least one of the following defines CABG-related MI:
- New pathologic Q waves or new LBBB
- Angiographically documented new graft or native coronary artery occlusion
- Imaging evidence of new loss of viable myocardium

(ROSEN's Emergency Medicine, p. 996-997; Sabiston Textbook of Surgery)

Summary Diagram

Mechanism	Pathway
Vulnerable plaque	Large lipid core + thin cap + inflammation
Plaque rupture/erosion	Shear stress, adrenergic surge, proteases
Platelet activation	Exposed collagen + tissue factor
Thrombus	White (platelet) → Red (fibrin)
Partial occlusion	NSTEMI / Unstable Angina
Complete occlusion	STEMI
Myocardial ischemia >20-40 min	Irreversible necrosis (coagulative)

Sources:

ROSEN's Emergency Medicine, 9th ed., p. 995-997
Robbins & Kumar Basic Pathology, p. 322
Fuster and Hurst's The Heart, 15th ed., Ch. 16
Washington Manual of Medical Therapeutics, p. 146
Sabiston Textbook of Surgery

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