The Pathophysiology of White Plaque in NSTEMI
In NSTEMI, the plaque appears white due to the formation of a non-occlusive, platelet-rich "white thrombus" that develops on a disrupted atherosclerotic plaque, as opposed to the completely occlusive red thrombus seen in STEMI. 1
Plaque Disruption and Thrombus Formation in NSTEMI
The pathophysiology of NSTEMI involves several key processes:
Plaque Vulnerability and Disruption
White Thrombus Formation
Plaque Composition Differences
Clinical Implications of White Plaque in NSTEMI
Understanding the white plaque composition in NSTEMI has important clinical implications:
Diagnosis and Risk Stratification
Treatment Approach
- The platelet-rich nature of the white thrombus explains why antiplatelet therapy is particularly important in NSTEMI management 1
- Understanding that NSTEMI typically results from severe coronary artery narrowing, transient occlusion, or microembolization rather than complete occlusion guides treatment strategies 6
Distinguishing Features Between NSTEMI and STEMI Plaques
| Feature | NSTEMI (White Plaque) | STEMI |
|---|---|---|
| Occlusion | Subtotally occlusive | Completely occlusive [2] |
| Thrombus composition | Platelet-rich (white) | Fibrin-rich (red) [1] |
| Minimal luminal area | Larger | Smaller [3] |
| Lipid content | Less | More [3] |
| Rupture length | Shorter | Longer [3] |
| Calcium content | Variable | Often less [4] |
Common Pitfalls in Understanding NSTEMI Plaque
Misconception: Assuming NSTEMI is always less severe than STEMI
- Reality: NSTEMI can lead to significant myocardial damage and has important prognostic implications 2
Misconception: Focusing only on the culprit lesion
- Reality: Non-culprit vulnerable plaques also contribute to future risk 7
Misconception: Relying solely on calcium scoring for risk assessment
- Reality: The amount of non-calcified plaque is a better predictor of events after NSTEMI than calcium score 5
Understanding the white, platelet-rich nature of NSTEMI plaque helps guide appropriate antiplatelet and anticoagulant therapy to prevent further platelet aggregation and thrombus formation, ultimately improving patient outcomes.