Can Acute Coronary Syndrome (ACS) occur secondary to plaque disruption?

Acute Coronary Syndrome and Plaque Disruption

Yes, Acute Coronary Syndrome (ACS) primarily occurs secondary to plaque disruption in the coronary arteries. According to multiple authoritative guidelines, plaque disruption is the fundamental pathophysiological mechanism that triggers the cascade of events leading to ACS 1, 2.

Pathophysiology of ACS Secondary to Plaque Disruption

The development of ACS follows a clear pathophysiological sequence:

1. Plaque Formation and Progression:

   • Initial accumulation of extracellular lipid in the arterial intima
   • Evolution to fibro-fatty stage
   • Progressive weakening of the fibrous cap 1

2. Plaque Disruption:

   • Occurs through two primary mechanisms:
     • Plaque rupture: More common in men, involves secretion of proteolytic enzymes by macrophages that weaken the fibrous cap 2
     • Plaque erosion: More common in women, characterized by surface erosion without deep rupture 2

3. Thrombosis Formation:

   • Disruption exposes thrombogenic material to circulating blood
   • Leads to platelet aggregation and thrombus formation
   • The degree of thrombosis determines the clinical presentation 1

Clinical Spectrum Following Plaque Disruption

The clinical manifestation depends on the extent of coronary occlusion following plaque disruption:

• Unstable Angina (UA):

  • Caused by nonocclusive thrombus on disrupted plaque
  • Transient myocardial ischemia with diminished flow
  • No significant myonecrosis (negative cardiac biomarkers) 2
  • More likely to involve platelet-rich (whitish) thrombus 3
  • More frequently associated with downstream plaque disruption sites 4

• NSTEMI:

  • Partially occluded coronary artery
  • Subendocardial ischemia
  • Elevated biomarkers of myonecrosis
  • Usually results in non-Q-wave MI 2

• STEMI:

  • Completely occluded coronary vessel
  • Transmural myocardial ischemia and infarction
  • Elevated biomarkers of myonecrosis
  • Usually results in Q-wave MI 2
  • More likely to involve fibrin-rich (red) thrombus 3
  • More frequently associated with upstream plaque disruption sites 4

Other Mechanisms of ACS

While plaque disruption is the predominant mechanism, other causes of ACS include:

1. Dynamic obstruction: Coronary spasm or vasoconstriction of epicardial and/or microvascular vessels 1
2. Progressive mechanical obstruction: Severe narrowing without spasm or thrombus 1
3. Coronary arterial inflammation 1
4. Coronary artery dissection: Particularly in peripartal women 1
5. Secondary UA: Precipitated by conditions extrinsic to the coronary arterial bed that increase myocardial oxygen demand or reduce supply 1

Clinical Implications

Understanding that ACS occurs secondary to plaque disruption has important clinical implications:

• Therapeutic targets: Antiplatelet and anticoagulant therapies target the thrombotic process, while lipid-lowering therapies aim to stabilize vulnerable plaques 2
• Risk stratification: Patients with evidence of plaque disruption are at higher risk for recurrent events
• Prevention strategies: Focus on plaque stabilization through risk factor modification 5

Important Caveats

• The clinical presentation of ACS depends not only on the degree of plaque disruption but also on the balance between coronary blood supply and myocardial oxygen demand 3
• The location of plaque disruption (upstream vs. downstream) may influence whether a patient presents with UA or AMI 4
• Individual patient factors (collateral circulation, pre-existing coronary disease) can modify the clinical presentation following plaque disruption