Do Unstable Angina and Non-ST-Elevation Myocardial Infarction (NSTEMI) both occur due to a non-occlusive thrombus over a disrupted plaque?

Pathophysiology of Unstable Angina and NSTEMI

Yes, both Unstable Angina (UA) and Non-ST-Elevation Myocardial Infarction (NSTEMI) primarily occur due to a non-occlusive thrombus over a disrupted atherosclerotic plaque. 1

Common Pathophysiological Mechanism

The pathophysiology of both UA and NSTEMI centers around:

• Plaque disruption: Inflammation in the arterial wall leads to plaque destabilization, rupture or erosion 1
• Thrombus formation: A thrombus develops on the disrupted plaque, causing coronary artery narrowing 1
• Non-occlusive nature: The thrombus is usually non-occlusive, unlike in STEMI where complete occlusion occurs 1
• Microembolization: Platelet aggregates and plaque components can embolize distally 1

Key Differences Between UA and NSTEMI

Despite sharing the same pathophysiological mechanism, UA and NSTEMI differ in one critical aspect:

Feature	Unstable Angina	NSTEMI
Cardiac Biomarkers	Normal	Elevated
Myocardial Necrosis	Absent	Present
ECG Changes	May show ischemic changes or be normal	ST depression, T-wave inversion, or normal

The distinction between UA and NSTEMI is made based on the presence or absence of myocardial necrosis as detected by cardiac biomarkers (troponin) 2. In NSTEMI, microembolization of platelet aggregates and plaque components leads to myocardial cell death and troponin release, while in UA, the ischemia is not severe enough to cause detectable myocardial necrosis 1.

Alternative Mechanisms

While non-occlusive thrombus is the most common cause, other mechanisms can also lead to UA/NSTEMI:

1. Dynamic obstruction: Coronary spasm or vasoconstriction of epicardial or microvascular vessels 1
2. Progressive mechanical obstruction: Severe narrowing without thrombus or spasm 1
3. Coronary arterial inflammation: Inflammatory processes affecting the coronary arteries 1
4. Secondary UA: Extrinsic factors increasing myocardial oxygen demand or decreasing supply 1
5. Coronary artery dissection: Rare cause, more common in peripartal women 1

Clinical Implications

Understanding this pathophysiology has important clinical implications:

• Antiplatelet and antithrombotic therapy: Forms the cornerstone of treatment for both conditions 2
• Risk stratification: The extent of plaque disruption and thrombus formation influences prognosis 2
• Treatment approach: While UA has a better short-term prognosis than NSTEMI, both require aggressive management to prevent progression to complete vessel occlusion 2

Common Pitfalls in Understanding UA/NSTEMI

• Assuming complete occlusion: Unlike STEMI, UA/NSTEMI typically involves subtotal occlusion. However, an occlusive thrombus can cause UA/NSTEMI if extensive collateral circulation is present 1
• Overlooking multiple mechanisms: Multiple pathophysiological processes may coexist in the same patient 1
• Failing to recognize atypical presentations: Particularly common in women, elderly patients, and those with diabetes 2

The distinction between UA and NSTEMI is ultimately determined by the presence or absence of myocardial necrosis markers, not by differences in the underlying pathophysiological process, which is predominantly a non-occlusive thrombus over a disrupted plaque in both conditions.