Updates on NSAIDs in patients with and without coronary artery disease: pitfalls, interactions and cardiovascular outcomes

Abstract

NSAIDs are used worldwide by more than 30 million people everyday, given their anti-inflammatory, analgesic and antipyretic effects. NSAIDs are approved for several common adult diseases, including acute and chronic musculoskeletal or inflammatory disease, osteoarthritis, rheumatoid arthritis and other arthritic conditions, as well as for children with juvenile idiopathic arthritis. Importantly, the population commonly taking NSAIDs is that of older individuals who also represent the population with the highest risk for cardiovascular (CV) and gastrointestinal adverse effects. In recent years, a growing body of evidence regarding potential risks from chronic use of NSAIDs has emerged. The aim of this review is to update the available data concerning chronic use of NSAIDs in patients with and without CV disease by analyzing the mechanisms of action, the interference of specific NSAIDs with the established CV protective role of low-dose aspirin, and the potential increased risk of myocardial infarction, stroke, hypertension, heart failure and atrial fibrillation.

Keywords::

• aspirin interaction
• atrial fibrillation
• cardiovascular disease
• heart failure
• hypertension
• myocardial infarction
• non-steroidal anti-inflammatory drugs
• risk
• stroke

Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.

Key issues

• NSAIDs are worldwide used everyday, given their anti-inflammatory, analgesic and antipyretic effects.

• People commonly taking NSAIDs are older individuals, who also represent the population with the highest risk for cardiovascular (CV) disease and gastrointestinal (GI) adverse effects.

• The main mechanism of action of NSAIDs is the inhibition of COX, the enzyme responsible for the conversion of arachidonic acid to prostaglandins, translating into pain relief and also alteration of platelet aggregation, GI mucosal integrity, endothelium physiology, vasodilatation and renal flow regulation.

• NSAIDs’ usage increases the risk of GI complication and antagonizes the irreversible platelet inhibition (particularly ibuprofen and naproxen) of low-dose aspirin being the basis of its well-established CV protective role.

• NSAIDs’ chronic usage has been associated in several studies to an increased risk of myocardial infarction, stroke and combined CV adverse events.

• NSAIDs’ use has been related to both worsening and new onset of heart failure.

• NSAIDs have been included among the drugs able to induce hypertension and potentially causing resistant hypertension mainly due to their effect of sodium and water retention.

• A growing body of evidence underlines the potential relationship between NSAIDs’ chronic use and atrial fibrillation.

• The use of NSAIDs should be limited to cases in which they are strictly indicated and needed, always considering the balance between risks and benefits and what specific NSAID could be useful and less dangerous in a particular patient.

• When necessary, NSAIDs should be used at the lowest effective doses and for the shortest possible duration.

Notes