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Coronary Artery Disease 1

Coronary artery disease
pathophysiology

Question

Vignette: A 55-year-old male with a history of hypertension and hyperlipidemia presents to the clinic with shortness of breath and chest pain. The patient describes the pain as "crushing" and radiating to the left arm. An EKG shows ST segment elevations in leads II, III, and aVF. The patient is diagnosed with an acute myocardial infarction and is promptly treated with thrombolytics. The patient's symptoms improve significantly after treatment. What is the most likely cause of this patient's myocardial infarction?

Choices

A) Decreased production of nitric oxide

B) Increased production of endothelin-1

C) Increased production of leukotrienes

D) Decreased production of prostacyclin

E) Increased production of thromboxane A2

Answer

E) Increased production of thromboxane A2

Explanation

This patient's symptoms and EKG findings are indicative of an acute myocardial infarction, most likely caused by a thrombus occluding a coronary artery. Thromboxane A2 is a potent vasoconstrictor and platelet aggregator, which promotes thrombosis. In the setting of atherosclerosis (as suggested by this patient's history of hypertension and hyperlipidemia), plaque rupture can expose subendothelial collagen and tissue factor, leading to platelet adhesion, aggregation, and thrombus formation. Aspirin, a common medication for the prevention of myocardial infarction, works by irreversibly inhibiting the cyclooxygenase enzyme and decreasing thromboxane A2 synthesis, thereby reducing platelet aggregation and thrombus formation. Therefore, increased production of thromboxane A2 is the most likely cause of this patient's myocardial infarction.

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