Optimal suppression of thromboxane a2formation by aspirin during percutaneous transluminal coronary angioplasty: no additional effect of a selective cyclooxygenase-2 inhibitor

Kearney, Dermot; Byrne, Anthony; Crean, Peter; Cox, Dermot; Fitzgerald, Desmond J.

doi:10.1016/j.jacc.2003.09.041

Cited by 29 publications

(5 citation statements)

References 40 publications

(60 reference statements)

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“…In accordance with the above described rather low selectivity of this Coxib for inhibiting COX-2, celecoxib (800mg, single dose after 4 hours) also significantly reduced Tx-M in this study (by about 28%, ibuprofen caused a maximum reduction of more than 95% of Tx-M) [75]. A significant decrease of PGI-M after delivery of other selective inhibitors of Cox-2 in vivo has repeatedly been observed in animal or human models [64,[83][84][85].…”

Section: Selective Cox-2 Inhibitorssupporting

confidence: 87%

Cyclooxygenase Inhibition and Atherothrombosis

Sohn¹,

Krötz

2006

CDT

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Cyclooxygenases represent a major target of pharmaceutical therapy. Cyclooxygenase inhibitors are applied in order to reduce inflammation, to relieve from pain, or to prevent atherothrombotic complications in cardiovascular disease. Inhibition of platelet aggregation by aspirin, which is due to inhibition of platelet cyclooxygenase-dependent formation of thromboxane A2, is a cheap, safe and effective strategy to prevent myocardial infarction or stroke and is thus the most established strategy of secondary prevention of atherothrombotic disease. However, the existence of several isoforms of the cyclooxygenase enzyme, their tissue-specific expression patterns, their spatial and functional association with enzymes that further degrade the major cyclooxygenase products and the specific pharmacological properties of substances that have the potential of inhibiting cyclooxygenase make the ultimate physiological effects of a specific cyclooxygenase inhibitor a highly sophisticated pharmacological question. Specific inhibitors of the cyclooxygenase-2 isoform (COX-2) have at first promised to represent a major improvement of pharmaceutical therapy, but later have been suggested to enhance the risk of atherothrombotic events in vivo. This has led to the withdrawal of some of these substances from global markets and also initiated a discussion as to whether some non-selective cyclooxygenase inhibitors (non-steroidal anti-inflammatory drugs, NSAID), such as naproxen would also have an antithrombotic effect in vivo. This review summarizes current pathophysiological and clinical knowledge about the effects on atherothrombosis of drugs that target cyclooxygenases either as specific inhibitors of a cyclooxygenase isoform, or as non-specific cyclooxygenase inhibitors. It specifically discusses the question, whether all selective COX-2 inhibitors may have an intrinsic risk of enhancing the risk of atherothrombosis.

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Section: Selective Cox-2 Inhibitorssupporting

confidence: 87%

Cyclooxygenase Inhibition and Atherothrombosis

Sohn¹,

Krötz

2006

CDT

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“…Interestingly, and in accordance with its rather low selectivity for COX-2, one dose of celecoxib (800 mg, assessed at 4 h) also caused a statistically significant reduction of about 28% for one of two Tx-M that were measured (ibuprofen caused a maximum reduction of more than 95% of Tx-M) [56]. Reduction of PGI-M by other selective inhibitors of COX-2 has repeatedly been observed in animal or human models [57,58,59,60]. …”

Section: Influence Of Selective Cox-2 Inhibitors On Vascular Formatiomentioning

confidence: 92%

Selective COX-2 Inhibitors and Risk of Myocardial Infarction

Krötz¹,

Schiele²,

Klauß³

et al. 2005

J Vasc Res

110

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Selective inhibitors of cyclooxygenase-2 (COX-2, ‘coxibs’) are highly effective anti-inflammatory and analgesic drugs that exert their action by preventing the formation of prostanoids. Recently some coxibs, which were designed to exploit the advantageous effects of non-steroidal anti-inflammatory drugs while evading their side effects, have been reported to increase the risk of myo cardial infarction and atherothrombotic events. This has led to the withdrawal of rofecoxib from global markets, and warnings have been issued by drug authorities about similar events during the use of celecoxib or valdecoxib/parecoxib, bringing about questions of an inherent atherothrombotic risk of all coxibs and consequences that should be drawn by health care professionals. These questions need to be addressed in light of the known effects of selective inhibition of COX-2 on the cardiovascular system. Although COX-2, in contrast to the cyclooxygenase-1 (COX-1) isoform, is regarded as an inducible enzyme that only has a role in pathophysiological processes like pain and inflammation, experimental and clinical studies have shown that COX-2 is constitutively expressed in tissues like the kidney or vascular endothelium, where it executes important physiological functions. COX-2-dependent formation of prostanoids not only results in the mediation of pain or inflammatory signals but also in the maintenance of vascular integrity. Especially prostacyclin (PGI₂), which exerts vasodilatory and antiplatelet properties, is formed to a significant extent by COX-2, and its levels are reduced to less than half of normal when COX-2 is inhibited. This review outlines the rationale for the development of selective COX-2 inhibitors and the pathophysiological consequences of selective inhibition of COX-2 with special regard to vasoactive prostaglandins. It describes coxibs that are current ly available, evaluates the current knowledge on the risk of atherothrombotic events associated with their intake and critically discusses the consequences that should be drawn from these insights.

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“…To date, the best-known COX-1- and COX-2-targeted inhibitors are nonsteroidal anti-inflammatory drugs (NSAIDS), such as aspirin, celecoxib, and rofecoxib, which are used to relieve pain, fever, and inflammation with additional benefits of treating or preventing heart attacks, strokes, or chest pain. 354 The COX-2 inhibitor celecoxib reversed endothelial dysfunction and improved brachial artery flow–mediated dilation in patients with hypertension but had an adverse effect on prostacyclin production and increased blood pressure and thrombosis risk. 337,347 Furthermore, the functional range of COX-1 inhibition by aspirin was compromised by ibuprofen in patients with osteoarthritis and stable ischemic heart disease.…”

Section: Potential Applications Of the Aa Pathway In Clinical Transla...mentioning

confidence: 99%

Emerging Roles and Therapeutic Applications of Arachidonic Acid Pathways in Cardiometabolic Diseases

Hu,

Li,

Cheng

et al. 2024

Circulation Research

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Cardiometabolic disease has become a major health burden worldwide, with sharply increasing prevalence but highly limited therapeutic interventions. Emerging evidence has revealed that arachidonic acid derivatives and pathway factors link metabolic disorders to cardiovascular risks and intimately participate in the progression and severity of cardiometabolic diseases. In this review, we systemically summarized and updated the biological functions of arachidonic acid pathways in cardiometabolic diseases, mainly focusing on heart failure, hypertension, atherosclerosis, nonalcoholic fatty liver disease, obesity, and diabetes. We further discussed the cellular and molecular mechanisms of arachidonic acid pathway–mediated regulation of cardiometabolic diseases and highlighted the emerging clinical advances to improve these pathological conditions by targeting arachidonic acid metabolites and pathway factors.

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Optimal suppression of thromboxane a2formation by aspirin during percutaneous transluminal coronary angioplasty: no additional effect of a selective cyclooxygenase-2 inhibitor

Cited by 29 publications

References 40 publications

Cyclooxygenase Inhibition and Atherothrombosis

Cyclooxygenase Inhibition and Atherothrombosis

Selective COX-2 Inhibitors and Risk of Myocardial Infarction

Emerging Roles and Therapeutic Applications of Arachidonic Acid Pathways in Cardiometabolic Diseases

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