A 65-year-old woman with diabetes and dyslipidemia presents with acute-onset chest pain and dyspnea. Troponin is elevated, and ECG shows ST depression in multiple leads without ST elevation. She is diagnosed with NSTEMI. Which is the most common underlying pathological mechanism responsible for NSTEMI?

Question

Accepted Answer

B. Plaque rupture with partial thrombotic occlusion. ## Pathological Mechanisms of NSTEMI **Key Point:** Plaque rupture with partial or intermittent thrombotic occlusion is the most common pathological mechanism in NSTEMI, accounting for approximately 70–80% of cases. ### Comparison of NSTEMI Pathological Mechanisms | Mechanism | Frequency | Pathology | Angiographic Finding | |---|---|---|---| | **Plaque rupture + partial thrombosis** | **70–80%** | **Atherosclerotic plaque erosion/rupture with mural thrombus** | **Irregular stenosis, TIMI flow 2–3** | | Vasospasm (Prinzmetal) | 5–10% | Coronary artery spasm without fixed lesion | Normal or minimal stenosis | | Spontaneous coronary artery dissection (SCAD) | 1–4% | Intimal tear with intramural hematoma | Intimal flap, haziness | | Coronary embolism | <1% | Thrombus from LV or atrial source | Distal occlusion, no proximal lesion | **High-Yield:** The defining difference between STEMI and NSTEMI is the degree of coronary occlusion: STEMI involves complete occlusion (→ transmural infarction, ST elevation), while NSTEMI involves partial or intermittent occlusion (→ subendocardial ischemia, ST depression/T-wave changes). ### Pathophysiology of Plaque Rupture in NSTEMI ```mermaid flowchart TD A[Atherosclerotic plaque with lipid core]:::outcome --> B[Plaque rupture or erosion]:::action B --> C[Exposure of thrombogenic material]:::action C --> D[Partial thrombotic occlusion]:::action D --> E{Coronary flow restored?}:::decision E -->|Yes, intermittent| F[Subendocardial ischemia]:::outcome E -->|No, persistent| G[Transmural ischemia]:::outcome F --> H[ST depression, T-wave inversion]:::outcome G --> I[ST elevation]:::outcome ``` **Clinical Pearl:** Plaque rupture is triggered by: - Mechanical stress (increased wall shear stress) - Inflammatory infiltration (macrophages, T cells) - Thin fibrous cap overlying a large lipid core - These features are seen in "vulnerable plaques" on intravascular ultrasound or optical coherence tomography. **Warning:** Do not confuse NSTEMI mechanisms with STEMI. Vasospasm (Prinzmetal angina) can cause ST elevation transiently but is a separate entity and accounts for <10% of acute coronary syndromes. **Mnemonic:** **PACT** — Plaque rupture (most common), Arterial dissection, Coronary embolism, Thrombosis (in order of frequency in ACS).

Answer

A. Coronary vasospasm without atherosclerotic disease

Answer

C. Spontaneous coronary artery dissection

Answer

D. Coronary embolism from a cardiac source

Explanation

Pathological Mechanisms of NSTEMI

Comparison of NSTEMI Pathological Mechanisms

Pathophysiology of Plaque Rupture in NSTEMI

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Mechanism	Frequency	Pathology	Angiographic Finding
Plaque rupture + partial thrombosis	70–80%	Atherosclerotic plaque erosion/rupture with mural thrombus	Irregular stenosis, TIMI flow 2–3
Vasospasm (Prinzmetal)	5–10%	Coronary artery spasm without fixed lesion	Normal or minimal stenosis
Spontaneous coronary artery dissection (SCAD)	1–4%	Intimal tear with intramural hematoma	Intimal flap, haziness
Coronary embolism	<1%	Thrombus from LV or atrial source	Distal occlusion, no proximal lesion