Omacor
Omacor is the trade name of a patented complex, including ethyl esters of fatty polyunsaturated Omega-3 acids (up to 90% of the total composition). The drug also contains eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which are essential fatty acids. The EPA to DHA ratio is 1.2/1. The mechanism of action of Omacor is that eicosapentaenoic and docosahexaenoic acids are a poor substrate for enzymes responsible for the production of triglycerides (ultra-low density cholesterol) in the liver, thus increasing their concentration to a level characteristic of healthy people leads to the normalization of lipid metabolism by reducing the amount of triglycerides produced.
Figure 1 - Omacor is used for cholesterol
Omacor is used to reduce ultra-low-density cholesterol. The mechanism of action of Omacor is to improve lipid metabolism at three levels:
- Omega-3 fatty polyunsaturated acids are transported to the liver, where they form part of various types of lipoproteins, and are subsequently transported to peripheral fat depots;
- Phospholipids of cell membranes are replaced by phospholipids of lipoproteins - polyunsaturated fatty acids in this situation play the role of precursors of different types of eicosanoids;
- Fatty acids serve as a source of replenishing the energy balance in the body - its release occurs through their oxidation.
The concentration of Omega-3 fatty acids in Omacor corresponds to their natural level in the phospholipids of cell membranes.
Very low-density cholesterol is an endogenous lipid that is responsible for transporting fats from fat stores into the bloodstream in the form of fatty acids. When they are oxidized, energy is released. Dysfunction of VLDL (very low density lipids) leads to an increase in the proportion of endogenous triglycerides compared to individuals without such dysfunction. In turn, this can lead to the development of various cardiovascular diseases.
Figure 2 - Prepatha helps reduce cholesterol and weight loss
The drug is used to reduce cholesterol levels, in weight loss diets, to reduce the risk of recurrent myocardial infarction and stroke. Studies have shown that taking 1 milligram of the drug for 3-4 years significantly reduces the level of “bad” cholesterol. Taking Omacor reduces the production of endogenous lipids in the liver, which helps improve the condition of patients with impaired function of endogenous lipid metabolism.
A positive effect of the drug in normalizing blood pressure was noted.
Omacor is used as an adjuvant treatment of myocardial infarction, complementing other standard therapies - for example, the use of statins, antithrombocidal agents, beta blockers, angiotensin-modifying enzyme inhibitors.
In the treatment of endogenous hypertriglyceridemia, Omacor is prescribed if the desired effect cannot be achieved by maintaining a special diet. The drug is used both as monotherapy and in combination with statins.
The product is produced in the form of capsules filled with oils.
Take Omacor 1 capsule for breakfast and dinner orally in case of treatment of hypertriglyceridemia, 1 capsule per day for patients who have suffered a myocardial infarction. If necessary, the amount of the drug can be increased by the attending physician to the amount of daily Omacor intake to 4 capsules per day. It is especially recommended for patients with severe hypertriglyceridemia, for whom fibrates are contraindicated.
Data from clinical studies indicate that regular use of this drug for a long period, more than one year, significantly reduces the risk of developing coronary heart disease and other diseases of the cardiovascular system.
Capsules are taken whole, without opening or chewing, with the required amount of water. The effectiveness of the drug does not depend on food intake, however, if you experience discomfort in the stomach, it is better to combine taking Omacor with food.
Figure 3 — Before taking Omacor, you should consult your doctor
It is recommended to always take the drug at the same time to increase its effectiveness. You must strictly follow your doctor's instructions regarding dosage and frequency of administration. Before starting to take the drug, you should tell your doctor if the patient has or has had liver disease.
This medicine changes the way other medicines work, and you should not take other medicines without first consulting your doctor or pharmacist. Omacor may enhance the effect of oral anticoagulants. Your doctor may recommend a special diet that you should follow to increase the effectiveness of this medication.
If a patient taking Omacor is pregnant or thinks she may become pregnant during treatment, she should tell her doctor. You should also inform about breastfeeding your baby during the course of treatment.
The medicine may cause heartburn and nausea. If you experience any other symptoms that a person taking Omacor believes may be caused by the drug, you should report this to your doctor.
The drug is prescribed with caution to persons with hypersensitivity or allergies to fish.
Since taking Omacor in higher dosages (4 capsules per day) can increase blood clotting time, this factor is taken into account when treating individuals at risk of bleeding, for example, during surgery, bleeding injuries, etc.
When treating with high doses of the drug, the need to control blood pressure in patients, especially in those suffering from any form of liver failure, should be taken into account.
The drug is not prescribed to patients with elevated levels of exogenous triglycerides, i.e. lipids from food. It is not used to treat patients with uncompensated diabetes.
Omacor can be replaced with medications containing Omega-3 fatty acids, but it should be taken into account that the content of eicosapentaenoic and docosahexaenoic acids gives the drug great value.
Omacor, 1000 mg, capsules, 28 pcs.
Abbott, Netherlands
Price from 1530₽
There are contraindications. Specialist consultation is required.
Instructions for use of OMACOR®
Lipid-lowering drug. Contains omega-3 polyunsaturated fatty acids - eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which are essential fatty acids.
Omacor reduces the content of triglycerides as a result of a decrease in the concentration of VLDL, in addition, it affects hemostasis and blood pressure.
Omacor reduces triglyceride synthesis in the liver, since EPA and DHA are weak substrates for enzymes responsible for triglyceride synthesis and inhibit the esterification of other fatty acids.
Increased beta-oxidation of fatty acids in liver peroxisomes also helps reduce triglyceride levels by reducing the amount of free fatty acids involved in their synthesis. Inhibition of triglyceride synthesis reduces VLDL levels.
In some patients with hypertriglyceridemia, Omacor increases LDL-cholesterol levels. HDL-C levels increase only slightly, much less than after fibrates, and not permanently.
The long-term lipid-lowering effect (after use for more than 1 year) is unknown. Moreover, there is no significant evidence that lowering triglyceride levels reduces the risk of developing CAD.
During therapy with Omacor, there is a decrease in the formation of thromboxane A2 and a slight increase in bleeding time. There were no significant effects on other coagulation factors.
An open multicenter randomized study GISSI-Prevenzione was conducted in Italy. 11,324 patients who had recently suffered a myocardial infarction (<3 months) and were receiving recommended prophylactic treatment with a Mediterranean diet were randomized to receive Omacor (n=2836), vitamin E (n=2830), Omacor and vitamin E (n= 2830) and in the control group (n=2828). The results of observation for 3.5 years when using Omacor at a dose of 1 g / day showed a decrease in the combined indicator, which included overall mortality, non-fatal myocardial infarction and non-fatal stroke (compared to the control group, the relative risk decreased by 15% [2-26] p = 0.0226 in patients who took Omacor, and by 10% [1-18] p=0.0482 - in patients who took Omacor with or without vitamin E). There was a reduction in the second prespecified endpoint of cardiovascular mortality, nonfatal myocardial infarction, and nonfatal stroke (relative risk reduction by 20% [5-32] p = 0.0082 compared with the control group in patients receiving Omacor as monotherapy , and by 11% [1-20] p=0.0526 in patients taking Omacor with or without vitamin E). Secondary analyzes of each component of the primary endpoint showed significant reductions in all-cause and cardiovascular mortality but no reduction in nonfatal cardiovascular events or fatal and nonfatal stroke.
Omacor, 28 pcs., 1000 mg, capsules
Omega-3 polyunsaturated fatty acids - eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) - are classified as essential fatty acids (NEFA). Omacor is active against plasma lipids, reducing the concentration of triglycerides as a result of reducing the concentration of very low density lipoproteins (VLDL). In addition, it actively affects blood pressure and hemostasis, reducing the synthesis of thromboxane A2 and slightly increasing blood clotting time. No significant effects on other coagulation factors were observed.
Omacor reduces the synthesis of triglycerides in the liver, since EPA and DHA are less active substrates for the enzymes responsible for the synthesis of triglycerides, and they inhibit the esterification of other fatty acids. A decrease in the concentration of triglycerides is facilitated by an increase in the number of peroxisomes β - oxidation of fatty acids (a decrease in the amount of free fatty acids available for the synthesis of triglycerides). Inhibition of this synthesis reduces VLDL levels. Omacor increases LDL cholesterol levels in some patients with hypertriglyceridemia. The increase in high-density lipoprotein (HDL) concentrations is minimal and significantly lower than after fibrates, and is not constant.
The duration of the lipid-lowering effect when taking Omacor for more than 1 year has not been studied. Otherwise, there is no convincing evidence that lowering triglyceride levels reduces the risk of coronary heart disease. GISSI-Prevenzione is a multicenter, randomized, open-label clinical trial involving patients after recent myocardial infarction (less than 3 months) treated with Omacor (n=2836) and those not treated with Omacor (n=2828).
The results obtained after 3.5 years of observation while taking Omacor 1 g per day showed a significant reduction in the criteria for the combined end point, including mortality from all causes, non-fatal myocardial infarction and stroke (relative risk reduction by 15% [2-26 ] p = 0.0226) in patients taking only Omacor compared to the control group. There was a reduction in the prespecified secondary endpoint of cardiovascular death, nonfatal myocardial infarction, and stroke (20% relative risk reduction [5-32] p = 0.0082) in patients receiving Omacor alone vs. with the control group. The GISSI-Heart Failure (GISSI-HF) study examined the effect of Omacor on reducing mortality and hospitalization due to cardiovascular disease in 6975 patients with chronic heart failure (NYHA functional class II-IV) receiving standard medical therapy. GISSI-HF was a randomized, double-blind, placebo-controlled study in which patients received 1 g of Omacor per day (n=3494) or placebo (n=3481) for an average of 3.9 years.
Results showed reductions in both endpoints, including all-cause death (9% relative risk reduction, p=0.041) and all-cause death and cardiovascular hospitalization (8% relative risk reduction, p=0.009). . A secondary analysis of the rate of initial hospitalization due to ventricular arrhythmias showed a relative risk reduction of 28% (p = 0.013) in the group receiving Omacor compared with the placebo group. A subanalysis showed a relative increase in left ventricular ejection fraction of 8.1%, 11.1%, and 11.5% at 1, 2, and 3 years, respectively, in the Omacor group, compared with 6.3%, 8 .2% and 9.9% in the placebo group (p=0.005).
