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Omacor (prescription omega-3-acid ethyl esters 90): From severe rhythm disorders to hypertriglyceridemia.
Adv Ther. 2009 Jul; 26(7):675-90.AT

Abstract

Despite progress made in post-myocardial infarction (MI) revascularization and background therapy for the failing heart, the prevention of adverse cardiac remodeling associated with severe rhythm disorders remains an important drug target. Part of the remodeling can be counteracted by modulating the activity of ion channels and exchangers by omega-3 acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). In the GISSI-Prevenzione and GISSI-HF trials, omega-3 fatty acids were administered as ethyl esters (Omacor Solvay Pharmaceuticals) and not as triglycerides present in fish oil. Ethyl esters result in a sustained intestinal absorption of EPA and DHA and require various purification steps during production, thereby minimizing the content of environmental toxins. Also the rather high (38%) DHA content of Omacor should not be ignored since in rats with low dose intake of omega-3 acids, DHA but not EPA inhibited ischemia-induced arrhythmias. In patients on multiple tablets, 840 mg EPA+DHA in one capsule is preferred to increase compliance. It is not justified to refer to Omacor as "n-3 polyunsaturated fatty acid supplementation" or even "fish oil" and, based on controlled clinical trials, there is no evidence that fish oil could be a substitute of Omacor. To avoid further confusion, guidelines should be precise and refer to the medication, eg, as in NICE guideline CG48: "Omega-3-acid ethyl esters treatment licensed for secondary prevention post-MI." The anti-arrhythmogenic action of Omacor should be seen in the context of implantable cardioverter-defibrillator trials (DINAMIT, IRIS) where non-sudden death was increased and total mortality unaltered. However, Omacor administered in the GISSI-HF trial reduced the incidence of severe arrhythmic events and mortality. Also in the GISSI-Prevenzione trial, arrhythmic death and mortality were reduced. At higher dosages (daily, 3-4 g) Omacor exhibits more pronounced cardiovascular benefits and, as a licensed indication, improves hypertriglyceridemia and related lipid parameters.

Authors+Show Affiliations

Experimental Cardiology Laboratory, Heart Center, Department of Internal Medicine and Cardiology, Philipps University of Marburg, 35043 Marburg, Germany. Rupp@staff.uni-marburg.de

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

19629408

Citation

Rupp, Heinz. "Omacor (prescription Omega-3-acid Ethyl Esters 90): From Severe Rhythm Disorders to Hypertriglyceridemia." Advances in Therapy, vol. 26, no. 7, 2009, pp. 675-90.
Rupp H. Omacor (prescription omega-3-acid ethyl esters 90): From severe rhythm disorders to hypertriglyceridemia. Adv Ther. 2009;26(7):675-90.
Rupp, H. (2009). Omacor (prescription omega-3-acid ethyl esters 90): From severe rhythm disorders to hypertriglyceridemia. Advances in Therapy, 26(7), 675-90. https://doi.org/10.1007/s12325-009-0045-2
Rupp H. Omacor (prescription Omega-3-acid Ethyl Esters 90): From Severe Rhythm Disorders to Hypertriglyceridemia. Adv Ther. 2009;26(7):675-90. PubMed PMID: 19629408.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Omacor (prescription omega-3-acid ethyl esters 90): From severe rhythm disorders to hypertriglyceridemia. A1 - Rupp,Heinz, Y1 - 2009/07/27/ PY - 2009/06/26/received PY - 2009/7/25/entrez PY - 2009/7/25/pubmed PY - 2009/12/17/medline SP - 675 EP - 90 JF - Advances in therapy JO - Adv Ther VL - 26 IS - 7 N2 - Despite progress made in post-myocardial infarction (MI) revascularization and background therapy for the failing heart, the prevention of adverse cardiac remodeling associated with severe rhythm disorders remains an important drug target. Part of the remodeling can be counteracted by modulating the activity of ion channels and exchangers by omega-3 acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). In the GISSI-Prevenzione and GISSI-HF trials, omega-3 fatty acids were administered as ethyl esters (Omacor Solvay Pharmaceuticals) and not as triglycerides present in fish oil. Ethyl esters result in a sustained intestinal absorption of EPA and DHA and require various purification steps during production, thereby minimizing the content of environmental toxins. Also the rather high (38%) DHA content of Omacor should not be ignored since in rats with low dose intake of omega-3 acids, DHA but not EPA inhibited ischemia-induced arrhythmias. In patients on multiple tablets, 840 mg EPA+DHA in one capsule is preferred to increase compliance. It is not justified to refer to Omacor as "n-3 polyunsaturated fatty acid supplementation" or even "fish oil" and, based on controlled clinical trials, there is no evidence that fish oil could be a substitute of Omacor. To avoid further confusion, guidelines should be precise and refer to the medication, eg, as in NICE guideline CG48: "Omega-3-acid ethyl esters treatment licensed for secondary prevention post-MI." The anti-arrhythmogenic action of Omacor should be seen in the context of implantable cardioverter-defibrillator trials (DINAMIT, IRIS) where non-sudden death was increased and total mortality unaltered. However, Omacor administered in the GISSI-HF trial reduced the incidence of severe arrhythmic events and mortality. Also in the GISSI-Prevenzione trial, arrhythmic death and mortality were reduced. At higher dosages (daily, 3-4 g) Omacor exhibits more pronounced cardiovascular benefits and, as a licensed indication, improves hypertriglyceridemia and related lipid parameters. SN - 0741-238X UR - https://www.unboundmedicine.com/medline/citation/19629408/Omacor__prescription_omega_3_acid_ethyl_esters_90_:_From_severe_rhythm_disorders_to_hypertriglyceridemia_ L2 - https://dx.doi.org/10.1007/s12325-009-0045-2 DB - PRIME DP - Unbound Medicine ER -