A 58-year-old man with a 10-year history of type 2 diabetes mellitus and hypertension presents with acute onset chest pain and dyspnea. ECG shows ST elevation in leads II, III, and aVF. Troponin I is 2.8 ng/mL (normal <0.04 ng/mL). He is taken for emergency coronary angiography, which reveals a thrombus in the right coronary artery. Aspiration thrombectomy is performed and the thrombus is sent for histopathology. Microscopy shows platelet-rich thrombus with minimal fibrin. What is the most likely mechanism underlying thrombus formation in this patient?

Explanation

## Acute Coronary Thrombosis: Pathophysiology **Key Point:** Acute ST-elevation MI is caused by rupture of an atherosclerotic plaque, exposing subendothelial collagen and von Willebrand factor (vWF), which triggers platelet adhesion, activation, and aggregation → platelet-rich (white) thrombus formation. ## Mechanism of Plaque Rupture & Thrombosis 1. **Plaque rupture** → exposure of lipid-rich necrotic core and tissue factor 2. **Platelet adhesion** → vWF and collagen bind to platelet glycoprotein Ib and integrin α2β1 3. **Platelet activation** → release of ADP, serotonin, thromboxane A₂ (TXA₂) 4. **Platelet aggregation** → cross-linking via fibrinogen bridges (integrin αIIbβ3) 5. **Thrombin generation** → amplification of coagulation cascade 6. **Result** → platelet-rich thrombus (white thrombus) ## Histopathology Interpretation | Thrombus Type | Composition | Cause | Location | |---|---|---|---| | **White (platelet-rich)** | Platelets + minimal fibrin | Arterial flow, plaque rupture | Coronary, cerebral arteries | | **Red (fibrin-rich)** | Fibrin + RBCs + WBCs | Venous stasis, low flow | Veins, cardiac chambers | | **Mixed** | Platelets + fibrin + RBCs | Transition zones | Thrombus tail | **High-Yield:** The **platelet-rich composition** of this thrombus is the diagnostic clue — it indicates arterial thrombosis from plaque rupture, NOT venous stasis or hypercoagulability. ## Clinical Pearl **Diabetes accelerates atherosclerosis** via endothelial dysfunction, increased oxidative stress, and enhanced platelet reactivity. However, the acute thrombotic event is still triggered by plaque rupture with platelet-mediated thrombosis, not by diabetes-induced hypercoagulability alone. ## Pathophysiology Flowchart ```mermaid flowchart TD A[Atherosclerotic plaque in RCA]:::outcome --> B[Plaque rupture: lipid core + TF exposure]:::urgent B --> C[Subendothelial collagen + vWF exposed]:::outcome C --> D[Platelet adhesion via GPIb and integrin α2β1]:::action D --> E[Platelet activation: ADP, serotonin, TXA2 release]:::action E --> F[Platelet aggregation: αIIbβ3-fibrinogen cross-linking]:::action F --> G[Platelet-rich white thrombus formation]:::outcome G --> H[RCA occlusion → STEMI inferior wall]:::urgent ``` [cite:Harrison 21e Ch 295, Robbins 10e Ch 4]