A 52-year-old man recovering from an acute myocardial infarction develops new-onset chest pain that is relieved by leaning forward. The pain is exacerbated with deep inspiration. The patient was admitted with acute inferior myocardial infarction 2 days ago and did not undergo revascularization due to his late presentation. Since admission, he has had no chest pain until this morning. On physical examination, a friction rub is present at the left sternal border. The patient is treated with a medication that inhibits COX-1 and COX-2 enzymes via irreversible acetylation, resulting in significant relief of his symptoms. Which of the following agents was most likely used in this patient?

Question

A 52-year-old man recovering from an acute myocardial infarction develops new-onset chest pain that is relieved by leaning forward.  The pain is exacerbated with deep inspiration.  The patient was admitted with acute inferior myocardial infarction 2 days ago and did not undergo revascularization due to his late presentation.  Since admission, he has had no chest pain until this morning.  On physical examination, a friction rub is present at the left sternal border.  The patient is treated with a medication that inhibits COX-1 and COX-2 enzymes via irreversible acetylation, resulting in significant relief of his symptoms.  Which of the following agents was most likely used in this patient?

Quizplus · Accepted Answer

11ec160b_3be7_2c92_9249_f56562451e22_MD0001_00 This patient's presentation of recent (within 1-3 days) myocardial infarction, pleuritic chest pain improved by leaning forward, and a friction rub on cardiac examination likely indicates peri-infarction pericarditis. Although most patients with peri-infarction pericarditis improve with supportive measures, those with sufficient or persistent symptoms are typically treated with aspirin in combination with colchicine. Aspirin (acetylsalicylic acid) is a nonsteroidal anti-inflammatory drug (NSAID) that irreversibly inhibits cyclooxygenase-1 and -2 (COX-1 and -2) enzymes via acetylation, preventing conversion of arachidonic acid to prostaglandins, prostacyclin, and thromboxane. COX-1 acetylation inhibits generation of thromboxane A₂ in platelets (antithrombotic effect). COX-2 acetylation blocks prostaglandin production in inflammatory cells (eg, activated lymphocytes, neutrophils), resulting in anti-inflammatory, antipyretic, and analgesic effects. (Choice A) Acetaminophen is an analgesic and antipyretic agent that reversibly inhibits COX enzymes (primarily in the central nervous system). It lacks anti-inflammatory properties due to its weak inhibition of COX in peripheral tissues. (Choice C) Budesonide is a glucocorticoid agent with potent anti-inflammatory activity. Corticosteroids reduce COX-2 expression and decrease synthesis of arachidonic acid via phospholipase A₂ inhibition. (Choice D) Celecoxib is a selective COX-2 inhibitor that provides anti-inflammatory benefits without interfering with the physiological functions of COX-1. In contrast to the non-selective NSAIDs, selective COX-2 inhibitors have no significant effect on platelet function and are associated with a lower incidence of gastrointestinal bleeding. However, selective COX-2 inhibition is associated with an increased incidence of thrombosis. (Choice E) Colchicine exerts its anti-inflammatory effects by inhibiting polymerization of beta-tubulin into microtubules, preventing migration and activation of neutrophils. (Choices F, G, and H) Diclofenac, ibuprofen, and indomethacin are NSAIDs that reversibly inhibit COX-1 and COX-2. Educational objective: Aspirin (acetylsalicylic acid) is a nonsteroidal anti-inflammatory drug (NSAID) that irreversibly inhibits cyclooxygenase-1 and -2 (COX-1 and -2) enzymes via acetylation. In contrast, other NSAIDs (eg, diclofenac, ibuprofen, indomethacin) reversibly inhibit COX-1 and COX-2. __________ References: Clinical pharmacology of non-steroidal anti-inflammatory drugs: A review. (http://www.ncbi.nlm.nih.gov/pubmed/22934743) What are all the things that aspirin does? (http://www.ncbi.nlm.nih.gov/pubmed/12969898)

A 52-Year-Old Man Recovering from an Acute Myocardial Infarction Develops