Language
Country/Area
No result found
The double-edged sword of COX-2 inhibitors: Why may they trigger cardiovascular events?
In modern medicine, the use of pain management and anti-inflammatory drugs is quite common. Among them, cyclooxygenase-2 (COX-2) inhibitors are widely favored due to their advantages in targeted therapy. However, the side effects of these drugs, especially the risk of cardiovascular events, have caused significant concern in the medical community. COX-2 is an enzyme expressed primarily in inflammatory tissues and is responsible for converting arachidonic acid into prostaglandins that are critical for many physiological and pathological processes.
COX-2 inhibitors are designed to reduce inflammation and pain, but their cardiovascular risks have become a major paradox in the medical community.
Biology and functions of COX-2
Cyclooxygenase-2 is the only enzyme among the three cyclooxygenases whose expression level is low under normal conditions. When the body is in a state of inflammation, its expression increases significantly. COX-2 is primarily responsible for converting arachidonic acid into prostaglandin H2 (PGH2), which is further converted into a variety of bioactive substances, including prostaglandin E2 (PGE2), which play a role in processes required for inflammation.
The separate regulation of COX-2 makes it a target for many new drugs, especially selective COX-2 inhibitors ("coxibs").
Risks of COX-2 inhibitors
Despite their utility in reducing inflammation and pain, clinical data suggest that COX-2 inhibitors may increase the risk of cardiovascular events. This is primarily because COX-2 inhibitors selectively reduce prostaglandin I2 (prostacyclin) in vascular endothelial cells, while PGE2 dilates blood vessels and prevents platelet aggregation.
The mechanism for this risk is that selective COX-2 inhibitors, while reducing pain caused by inflammation, also inhibit the production of prostaglandins that help maintain cardiovascular health.
How to balance patient risk
Physicians should carefully consider the patient's cardiovascular health when prescribing COX-2 inhibitors. The risks of using this class of drugs may be more significant in patients with a history of cardiovascular disease. Therefore, doctors may choose a more conservative treatment plan or closely monitor cardiovascular status after taking medications.
Conclusion
The alarming cardiovascular risks posed by COX-2 inhibitors reveal that many drugs are not infallible in treating inflammation. While we enjoy the relief these drugs bring, we should also face up to their potential harm. We may need to think about: In the process of pursuing pain relief, have we neglected the maintenance of cardiovascular health?
