Original Article:
The rise and fall of aspirin in the primary prevention of cardiovascular disease
Inbar Raber MD, et al.
The Lancet, 2019, 393(10186), 2155-2167.
10.1016/S0140-6736(19)30541-0
Acetylsalicylic acid (ASA), also known as aspirin, is a nonsteroidal anti-inflammatory drug (NSAID) used to reduce pain, fever, and/or inflammation, and as an antithrombotic agent. Aspirin is one of the most commonly used drugs worldwide and is generally considered effective for the secondary prevention of cardiovascular disease. In this review, the authors summarize aspirin's mechanism of action, review the history and contemporary trials evaluating the drug, and reflect on the future direction of aspirin in the prevention of cardiovascular disease. Here, we focus on the mechanism of action of aspirin.
Mechanism of action
> Acetylsalicylic acid binds to, and irreversibly inhibits, cyclooxygenase (COX), which exists as two isoforms in humans: COX-1 and COX-2. COX-1 is involved in platelet aggregation through production of thromboxanes. COX-2 is involved in the upregulation of prostaglandins that have vasodilator and anti-aggregatory actions. Both isoenzymes are associated with protection of the gastric mucosa.
> In experimental settings, low-dose aspirin (75 mg or 81 mg) inhibits COX-1 and disrupts the production of thromboxane (Tx)A2, thereby reducing platelet aggregation and formation of a thrombus.
> Higher aspirin doses inhibit COX-2 leading to reduced production of prostacyclin (PGI2) and prostaglandin E (PGE), which is responsible for aspirin’s analgesic and antipyretic effects but can cause vasoconstriction, renal dysfunction, hyponatraematosis.
> For patients with cardiovascular disease, doses of aspirin as low as 75 mg/day might suffice to block both COX systems for 24 h or longer.
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Chemicals Related in the Paper:
Catalog Number | Product Name | Structure | CAS Number | Price |
---|---|---|---|---|
ACM50782 | Acetylsalicylic Acid | 50-78-2 | Price |