Cardiovascular pathology – Atherosclerosis most directly increases the risk of which blood-related event?

Introduction / Context:
Atherosclerosis is characterized by lipid-rich plaques within arterial walls. Plaque instability and rupture expose prothrombotic material to the bloodstream, precipitating acute thrombus formation. Recognizing clotting as the key immediate complication clarifies why atherosclerosis underlies myocardial infarction and ischemic stroke.

Given Data / Assumptions:

• Atherosclerotic plaques can become inflamed and rupture.
• Exposure of tissue factor and subendothelial matrix triggers the coagulation cascade and platelet aggregation.
• Occlusive thrombi reduce or stop downstream blood flow.

Concept / Approach:
The pathogenic sequence involves endothelial dysfunction, plaque growth, and potential rupture. Thrombus formation at the rupture site may partially or completely occlude the artery, causing acute ischemia. This is a clotting phenomenon, not “blood thinning” or generalized viscosity changes.

Step-by-Step Solution:

Verification / Alternative check:
Clinical imaging and pathology show fresh thrombi over disrupted plaques in acute coronary syndromes; antiplatelet and anticoagulant therapies reduce event rates.

Why Other Options Are Wrong:

• Blood thinning: opposite effect; atherothrombosis promotes clotting.
• Uniform “thickening” of blood is not a principal consequence of plaques.
• Hemolysis is not a hallmark consequence of atherosclerotic lesions.

Common Pitfalls:
Equating chronic plaque stenosis with viscosity changes; the acute risk is thrombus formation after plaque rupture.

Final Answer:
Thrombotic blood clot formation at sites of plaque rupture