Non-steroidal anti-inflammatory drug-induced cardiovascular adverse events: a meta-analysis

Gunter, Bryan; Butler, Kristen A.; Wallace, Rick L.; Smith, Steven M.; Harirforoosh, Sam

doi:10.1111/jcpt.12484

Cited by 119 publications

(83 citation statements)

References 55 publications

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“…To further elucidate the reason behind the differences in the observed degree of CV risk between various NSAIDs, more focus should be placed on studies scrutinizing their exact pharmacokinetic and pharmacodynamic properties [38]. …”

Section: Reviewmentioning

confidence: 99%

Cardiovascular Risk of Nonsteroidal Anti-Inflammatory Drugs: An Under-Recognized Public Health Issue

Varga

Sabzwari

Vargova

2017

Cureus

124

120

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Nonsteroidal anti-inflammatory drugs (NSAIDs) are drugs with analgesic, anti-inflammatory, and antipyretic activity. Their effect is achieved by the reduction in synthesis of prostanoids. Inhibition of prostanoids is responsible for a substantial risk of adverse effects. The risk of side effects affecting the gastrointestinal tract and kidneys has long been known. The possibilities of blood pressure elevation and the development of congestive heart failure are also widely recognized. Increased incidence of acute myocardial infarction in clinical trials with rofecoxib drew attention to the potential cardiotoxicity of selective cyclooxygenase-2 inhibitors, and similarly, concerns have been raised regarding the cardiovascular safety of non-selective NSAIDs. The safety of NSAIDs with regards to cardiovascular events has been studied in recent years in a large number of retrospective and prospective clinical studies and meta-analyses. The results indicate that cardiotoxicity is a class effect, but the magnitude of the risk is widely variable between individual NSAID drugs. This article aims to summarize the available data on the risk of adverse cardiovascular events with NSAIDs, the clinical impact of these events and possible underlying mechanisms.

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Section: Reviewmentioning

confidence: 99%

Cardiovascular Risk of Nonsteroidal Anti-Inflammatory Drugs: An Under-Recognized Public Health Issue

Varga

Sabzwari

Vargova

2017

Cureus

124

120

View full text Add to dashboard Cite

show abstract

“…ˆ High GI risk includes a history of peptic ulcer disease or upper GI bleeding; high CV risk includes unstable angina or myocardial infarction. *Naproxen might be preferred for patients with high CV and low GI risk if not taking aspirin [14,18‐20,22,27]. If the patient is on low‐dose aspirin and an NSAID is being prescribed for short‐term use, it is recommended to administer the 2 medications at different times in attempt to decrease interference with aspirin's antiplatelet effect [36].…”

Section: Conclusion and Author Recommendationsmentioning

confidence: 99%

Safety Considerations in Prescription of NSAIDs for Musculoskeletal Pain: A Narrative Review

Hatt

Vijapura

Maitin

et al. 2018

PM&R

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Nonsteroidal anti-inflammatory drugs (NSAIDs) are frequently prescribed for the treatment of painful musculoskeletal conditions. When prescribing oral NSAIDs, clinicians must consider coexisting cardiovascular, cerebrovascular, gastrointestinal, and renal disease because oral NSAIDs are associated with a broad spectrum of adverse effects on these systems. The different safety profiles of NSAIDs can be attributed to differences in the extent to which the drug inhibits cyclo-oxygenase-1 vs -2 and their potential for drug-drug interactions. This narrative review intends to guide the clinician in prescribing oral NSAIDs while taking into consideration these comorbid conditions and drug interactions.

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“…Compared to other cyclooxygenase-2 inhibitors, celecoxib is associated with a lower cardiovascular risk (Solomon et al, 2004; Hirayama et al, 2014; Nissen et al, 2016; Gunter et al, 2017). Though the mechanism is unclear, animal studies suggest that COX-2-inhibition plays a role in attenuating the effects of Angiotensin II (AngII; Wu et al, 2005; Martínez-Revelles et al, 2013) the effector molecule of the renin angiotensin system (RAS), which plays a central role in the pathophysiology of hypertension, an important risk factor for cardiovascular disease (Touyz and Schiffrin, 2004; Mehta and Griendling, 2007).…”

Section: Introductionmentioning

confidence: 99%

Cyclooxygenase-2 Inhibition Limits Angiotensin II-Induced DNA Oxidation and Protein Nitration in Humans

et al. 2017

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Compared to other cyclooxygenase-2 inhibitors, celecoxib is associated with a lower cardiovascular risk, though the mechanism remains unclear. Angiotensin II is an important mediator of oxidative stress in the pathophysiology of vascular disease. Cyclooxygenase-2 may modify the effects of angiotensin II though this has never been studied in humans. The purpose of the study was to test the effects of selective cyclooxygenase-2 inhibition on plasma measures of oxidative stress, the vasoconstrictor endothelin-1, and nitric oxide metabolites, both at baseline and in respose to Angiotensin II challenge in healthy humans. Measures of 8-hydroxydeoxyguanosine, advanced oxidation protein products, nitrotyrosine, endothelin-1, and nitric oxide metabolites were assessed from plasma samples drawn at baseline and in response to graded angiotensin II infusion (3 ng/kg/min × 30 min, 6 ng/kg/min × 30 min) before and after 14 days of cyclooxygenase-2 inhibition in 14 healthy subjects (eight male, six female) in high salt balance, a state of maximal renin angiotensin system suppression. Angiotensin II infusion significantly increased plasma oxidative stress compared to baseline (8-hydroxydeoxyguanosine; +17%; advanced oxidation protein products; +16%), nitrotyrosine (+76%). Furthermore, levels of endothelin-1 levels were significantly increased (+115%) and nitric oxide metabolites were significantly decreased (−20%). Cycloxygenase-2 inhibition significantly limited the increase in 8-hydroxydeoxyguanosine, nitrotyrosine and the decrease in nitric oxide metabolites induced by angiotensin II infusion, though no changes in advanced oxidation protein products and endothelin-1 concentrations were observed. Cyclooxygenase-2 inhibition with celecoxib partially limited the angiotensin II-mediated increases in markers of oxidative stress in humans, offering a potential physiological pathway for the improved cardiovascular risk profile of this drug.

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Non-steroidal anti-inflammatory drug-induced cardiovascular adverse events: a meta-analysis

Cited by 119 publications

References 55 publications

Cardiovascular Risk of Nonsteroidal Anti-Inflammatory Drugs: An Under-Recognized Public Health Issue

Cardiovascular Risk of Nonsteroidal Anti-Inflammatory Drugs: An Under-Recognized Public Health Issue

Safety Considerations in Prescription of NSAIDs for Musculoskeletal Pain: A Narrative Review

Cyclooxygenase-2 Inhibition Limits Angiotensin II-Induced DNA Oxidation and Protein Nitration in Humans

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