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Our Pacesetters ensure that we can chart the course for a cure for those who live with arthritis. Our Signature partners make their mark by helping us identify new and meaningful resources for people with arthritis. NSAIDs may impair renal function in patients with a decreased effective circulating volume by inhibiting prostaglandin synthesis.
Consequently, water and sodium retention, and decreases in renal blood flow and glomerular filtration rate may occur, affecting the unstable cardiovascular homeostasis in these patients. In patients with pre-existing heart failure, this may lead to cardiac decompensation. The same study highlighted the differences between various coxibs. Significant increases in blood pressure were found with rofecoxib and etoricoxib, while the effect of celecoxib on blood pressure appeared to be minimal.
The risk of NSAID-mediated BP increase in patients with pharmacologically controlled hypertension also depends on the antihypertensive drug used by the patient. The effect of beta-blockers and various renin-angiotensin-aldosterone system RAAS inhibitors seems to be influenced the most [ 40 , 42 ].
The most likely reason is that NSAIDs under normal circumstances inhibit the production of renin as a compensatory mechanism for the retention of water and sodium caused by them and also by direct COX-2 inhibition. If RAAS is inhibited chronically by the antihypertensive regimen used by the patient, the previously described compensatory mechanism can't help to avoid an increase in the blood pressure [ 43 ]. Most patients with severe rheumatoid arthritis and osteoarthritis are elderly and often have multiple co-morbidities, including hypertension treated with antihypertensive drugs.
Under these circumstances the safe and effective treatment of their symptoms is problematic [ 44 ]. In a pilot study by Varga, et al. Inhibition of prostanoid production in the kidney may reduce glomerular filtration and excretion of sodium and water. NSAIDs are therefore associated with risk of hypervolemia and worsening heart failure.
The study by Heerdink, et al. The authors did not find a significant difference between individual NSAIDs, which suggests a class effect. The highest risk of heart failure decompensation was present within the first days of treatment initiation and gradually decreased to the level of placebo after a month. NSAID users were found to have a relative risk of 2. In patients with established CV disease, the RR was noticeably higher Mamdani, et al.
The relative risk in users of non-selective agents was 1. Celecoxib was not associated with increased risk. The level of risk displays a large variability between individual drugs in the group and seems to be affected by the baseline cardiovascular risk of patients, although CV ADRs can develop even in individuals without a pre-existing CV condition. It appears that the absolute degree of COX-2 inhibition and not COX-2 selectivity is responsible for the increased risk.
Differences in pharmacokinetics might also play a role. Patients with congestive heart failure are at risk of the disease decompensation while taking NSAIDs.
The risk is highest in patients taking diuretics, especially during the first few weeks of NSAID treatment. In conclusion, it should be stressed that candidates for long-term administration of NSAIDs are commonly elderly patients, who often suffer from arterial hypertension, CHF and coronary artery disease. Adequate monitoring for signs and symptoms of adverse effects with proper patient education are required to increase patient safety during NSAID therapy. The duration of NSAID treatment should be limited as much as the clinical situation allows and only the minimal effective dose should be used.
Cureus is not responsible for the scientific accuracy or reliability of data or conclusions published herein.
All content published within Cureus is intended only for educational, research and reference purposes. Additionally, articles published within Cureus should not be deemed a suitable substitute for the advice of a qualified health care professional.
Do not disregard or avoid professional medical advice due to content published within Cureus. The authors have declared that no competing interests exist. National Center for Biotechnology Information , U. Journal List Cureus v. Published online Apr 8. Author information Article notes Copyright and License information Disclaimer. Corresponding author. Zoltan Varga moc. Received Feb 24; Accepted Apr 8.
This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. This article has been cited by other articles in PMC. Abstract Nonsteroidal anti-inflammatory drugs NSAIDs are drugs with analgesic, anti-inflammatory, and antipyretic activity. Keywords: non-steroidal anti-inflammatory drugs, cardiovascular risk, adverse effect, cardiovascular event, arterial hypertension, heart failure.
Non-selective COX-1 and COX-2 inhibitors: acetylsalicylic acid, ibuprofen, diclofenac, ketoprofen, indomethacin, naproxen Preferential COX-2 inhibitors: meloxicam, nimesulide, etodolac Selective COX-2 inhibitors: celecoxib, rofecoxib, etoricoxib, valdecoxib. Open in a separate window. Gastrointestinal erosions and ulcers of gastric mucosa, nausea, vomiting, bloating, diarrhea, constipation Renal reduced glomerular filtration rate, Na and water retention, pitting edema, hyperkalemia, kidney failure, interstitial nephritis Cardiovascular thrombotic events, increased blood pressure, congestive heart failure, palpitations Central nervous system headache, fatigue, insomnia, vertigo, seizures Other bleeding, asthma attacks, Reye's syndrome, urticaria, neutropenia.
Thrombotic events After introduction of the first coxibs to clinical practice, multiple large, randomized clinical trials were organized to assess their gastrointestinal tolerability. Table 3 Overview of the results of Trelle, et al.
Table 5 Relative risk of cardiovascular events with preferential and selective COX-2 inhibitors compared to controls in a meta-analysis McGettigan and Henry. Possible mechanisms for the increased risk of thrombotic events The first theory trying to explain the risk of thrombotic events of selective COX-2 inhibitors was based on the assumption that COX-2 in the vessel wall was an important source of prostacyclin, whereas COX-1 was responsible for the production of thromboxane in platelets.
Increase in arterial blood pressure NSAIDs can cause sodium and water retention, as well as reduce formation of the vasodilator prostacyclin in the vessel wall.
Heart failure Inhibition of prostanoid production in the kidney may reduce glomerular filtration and excretion of sodium and water. Footnotes The authors have declared that no competing interests exist.
References 1. Use of non-steroidal anti-inflammatory drugs that elevate cardiovascular risk: an examination of sales and essential medicines lists in low-, middle-, and high-income countries. McGettigan P, Henry D. PLoS Med. Recent advances in medical diagnosis and treatment. Douthwaite AH. Acute oliguric renal failure induced by indomethacin: possible mechanism. Ann Intern Med. Effects of prostaglandin synthesis inhibition on blood pressure and humoral factors in exercising, sodium-deplete normal man.
J Hypertens. Prostaglandins in congestive heart failure and the effects of nonsteroidal anti-inflammatory drugs. Cannon PJ. Am J Med. Comparison of upper gastrointestinal toxicity of rofecoxib and naproxen in patients with rheumatoid arthritis. New Engl J Med. Risk of upper gastrointestinal bleeding and perforation associated with individual non-steroidal anti-inflammatory drugs.
Association of upper gastrointestinal toxicity of non-steroidal anti-inflammatory drugs with continued exposure: cohort study. Effects of nabumetone, celecoxib, and ibuprofen on blood pressure control in hypertensive patients on angiotensin converting enzyme inhibitors. Am J Hypertens. Comparison of rofecoxib, celecoxib, and naproxen on renal function in elderly subjects receiving a normal salt diet. Clin Pharmacol Ther. Ibuprofen-associated renal impairment in a large general internal medicine practice.
Am J Med Sci. Selective cyclooxygenase-2 COX-2 inhibitors and potential risk of cardiovascular events. Mukherjee D. Biochem Pharmacol. Gastrointestinal toxicity with celecoxib vs nonsteroidal anti-inflammatory drugs for osteoarthritis and rheumatoid arthritis: the CLASS study: a randomized controlled trial.
Celecoxib Long-term Arthritis Safety Study. Association between naproxen use and protection against acute myocardial infarction. Arch Intern Med.
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