Is the CV risk associated with NSAIDs specific to certain drugs? Observational and RCT data suggest that all NSAIDs are associated with some level of CV risk, especially in high-risk populations (e.g., prior CV event or calculated CV risk score >20%). Some studies have shown that naproxen has a neutral or even mildly protective effect on …
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Is the heart disease risk associated with NSAIDs seen only after years of consistent use? While many studies support a dose-response relationship between NSAIDs and CV risk, there is also existing data to suggest that CV risk may be evident following exposure to NSAIDs in as little as 30 days. Some of these studies were …
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CV effects of NSAIDs Nonselective NSAIDs inhibit COX-1 and COX-2 enzymes to varying degrees. However, even among those offering significant levels of COX-1 inhibition, none have consistently shown the same level of cardioprotection afforded by ASA. This may stem from concurrent inhibition of the COX-2 enzyme, unsustained COX-1 inhibition due to the reversible nature of …
CV effects of ASA ASA is a well-established therapy for secondary prevention of myocardial infarction (MI) in patients with known CAD. This is accomplished through inhibition of COX-1 and subsequent decline in TXA 2 , a potent platelet activator. It is an ideal agent for several reasons: (1) COX-1, but not COX-2; is expressed in mature platelets; …
What NSAIDs to be used in mild renal compromise? The nonacetylated salicylates are poor COX inhibitors and may have less effect on GFR. The hope was that the selective COX-2 inhibitors would have less renal effects than the traditional NSAIDs. However, COX-2 is found in the glomeruli and renal vasculature. COX-2 appears to be the dominant contributor …
How nephrotoxic are NSAIDs? PGs can vasodilate renal arteries, increase sodium loss, and increase renin release. They have relatively little impact on the renal system in euvolemic patients with normal renal function. However, in renal insufficiency or hypovolemic states, PGs are important in maintaining adequate glomerular flow and pressure. Nephrotoxic effects of NSAIDs include: • Vasoconstriction, …
How to decrease the incidence of NSAID induced gastric and duodenal ulcers in high risk individuals? 1. When appropriate, use alternative analgesics or topical NSAID formulations. 2. Use the lowest dose and frequency of NSAID possible. • Nonselective COX inhibitors, COX-2 selective inhibitors, and ASA have all demonstrated a linear dose-response relationship with GI side effects. 3. If NSAIDs …