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Can COX-2 inhibitor-induced increase in cardiovascular disease risk be modified by essential fatty acids?
J Assoc Physicians India. 2005 Jul; 53:623-7.JA

Abstract

Selective COX-2 inhibitors increase the risk of myocardial infarction and stroke. This has been attributed to their ability to inhibit endothelial COX-2 derived prostacyclin (PGI2) but not platelet COX-1 derived thromboxane A2 (TXA2). On the other hand, aspirin blocks both COX-1 and COX-2 enzymes without decreasing PGI2 but blocks TXA2 synthesis that explains its beneficial action in the prevention of coronary heart disease (CHD). The inhibitory action of aspirin on COX-1 and COX-2 enzymes enhances the tissue concentrations of dihomo-gamma-linolenic acid (DGLA), arachidonic acid, eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). These fatty acids form precursors to PGE1, PGI2, PGI3, lipoxins (LXs), and resolvins that have anti-inflammatory actions. In contrast, increase in the concentrations of DGLA, AA, EPA, and DHA is much less with specific COX-2 inhibitors since they do not block the formation of eicosanoids through COX-1 pathway. COX-2 inhibitors interfere with the formation of LXs and resolvins that have neuroprotective and cardioprotective actions. EPA and PGI2 have anti-arrhythmic action. EPA, DHA, and AA augment eNO formation that prevents atherosclerosis. This suggests that COX-2 inhibitors increase cardiovascular and stroke risk by interfering with the formation of eNO, PGI2, LXs, and resolvins and implies that combining EFAs with COX-2 inhibitors could prevent these complications.

Authors+Show Affiliations

UND Life Sciences, #205, 2477 Overlook Road, Cleveland Heights, OH 44106, USA.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

16190133

Citation

Das, U N.. "Can COX-2 Inhibitor-induced Increase in Cardiovascular Disease Risk Be Modified By Essential Fatty Acids?" The Journal of the Association of Physicians of India, vol. 53, 2005, pp. 623-7.
Das UN. Can COX-2 inhibitor-induced increase in cardiovascular disease risk be modified by essential fatty acids? J Assoc Physicians India. 2005;53:623-7.
Das, U. N. (2005). Can COX-2 inhibitor-induced increase in cardiovascular disease risk be modified by essential fatty acids? The Journal of the Association of Physicians of India, 53, 623-7.
Das UN. Can COX-2 Inhibitor-induced Increase in Cardiovascular Disease Risk Be Modified By Essential Fatty Acids. J Assoc Physicians India. 2005;53:623-7. PubMed PMID: 16190133.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Can COX-2 inhibitor-induced increase in cardiovascular disease risk be modified by essential fatty acids? A1 - Das,U N, PY - 2005/9/30/pubmed PY - 2005/11/4/medline PY - 2005/9/30/entrez SP - 623 EP - 7 JF - The Journal of the Association of Physicians of India JO - J Assoc Physicians India VL - 53 N2 - Selective COX-2 inhibitors increase the risk of myocardial infarction and stroke. This has been attributed to their ability to inhibit endothelial COX-2 derived prostacyclin (PGI2) but not platelet COX-1 derived thromboxane A2 (TXA2). On the other hand, aspirin blocks both COX-1 and COX-2 enzymes without decreasing PGI2 but blocks TXA2 synthesis that explains its beneficial action in the prevention of coronary heart disease (CHD). The inhibitory action of aspirin on COX-1 and COX-2 enzymes enhances the tissue concentrations of dihomo-gamma-linolenic acid (DGLA), arachidonic acid, eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). These fatty acids form precursors to PGE1, PGI2, PGI3, lipoxins (LXs), and resolvins that have anti-inflammatory actions. In contrast, increase in the concentrations of DGLA, AA, EPA, and DHA is much less with specific COX-2 inhibitors since they do not block the formation of eicosanoids through COX-1 pathway. COX-2 inhibitors interfere with the formation of LXs and resolvins that have neuroprotective and cardioprotective actions. EPA and PGI2 have anti-arrhythmic action. EPA, DHA, and AA augment eNO formation that prevents atherosclerosis. This suggests that COX-2 inhibitors increase cardiovascular and stroke risk by interfering with the formation of eNO, PGI2, LXs, and resolvins and implies that combining EFAs with COX-2 inhibitors could prevent these complications. SN - 0004-5772 UR - https://www.unboundmedicine.com/medline/citation/16190133/Can_COX_2_inhibitor_induced_increase_in_cardiovascular_disease_risk_be_modified_by_essential_fatty_acids L2 - https://antibodies.cancer.gov/detail/CPTC-TIMP1-2 DB - PRIME DP - Unbound Medicine ER -