General FAQ's

What outcome data is available for Omacor?

For secondary prevention post MI refer to the GISSI-P Study below

Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial GISSI-Prevenzione Investigators.2

Background
There was conflicting evidence on the benefits of foods rich in vitamin E (a-tocopherol), n-3 polyunsaturated fatty acids (PUFA), and their pharmacological substitutes. This paper investigated the effects of 1g per day of omega-3 ethyl esters in patients who had had a myocardial infarction.1

Methods
From October 1993 to September 1995 11 324 patients surviving a recent (<3 months) myocardial infarction were randomly assigned to supplements of n-3 PUFA (1 g daily, n=2836), vitamin E (300 mg daily, n=2830), both (n=2830), or none (control, n=2828) for 3·5 years. The primary combined efficacy endpoint was death, non-fatal MI and stroke. Secondary endpoints included all fatal events, cardiovascular deaths and sudden death. This was analysed as both a 2 way factorial (combining vitamin E and omega-3) and a 4 way factorial separating the 4 arms.

Results

  • Two way analysis showed a significant 10% relative decrease in risk for the primary endpoints of: death, non-fatal stroke (1.3% absolute risk reduction) and a non-significant decrease in risk for cardiovascular death, non-fatal MI and non-fatal stroke (1.1% absolute risk reduction)
  • The four way analysis showed a significant relative decrease in relative risk for the combined primary endpoints of death, non-fatal MI and non-fatal stroke of 15% (2.3% absolute risk reduction) and 20% for cardiovascular death, non-fatal MI and non-fatal stroke (2.2% absolute risk reduction)
  • Analysis of Omacor showed a significant relative decrease in secondary endpoints for mortality; 20% for total deaths (2.1% absolute risk reduction), 30% for cardiovascular deaths (2% absolute risk reduction) and 45% (1.6% absolute risk reduction) for sudden deaths

Conclusion by Authors
Dietary supplementation with n-3 PUFA led to a clinically important and statistically significant benefit. Vitamin E had no benefit. Its effect on fatal cardiovascular events require further exploration.

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What is the clinical guidance on omega-3 fatty acid?

NICE guideline on post-MI therapy

Patients should be advised to consume at least 7g of omega-3 fatty acids per week from two to four portions of fish5

  • For patients who have had an MI within 3 months and who are not achieving 7g of omega-3 fatty acids per week, consider providing at least 1g daily of omega-3-acid ethyl esters treatment licensed for secondary prevention post MI for up to 4 years

Joint British Societies (JBS2) guidelines (JBS2) on prevention of CHD and other lipid lowering treatments recommend omega-3-acid ethyl esters (Omacor)6

ESC (European Society of Cardiology)7

  • Recommends the increased consumption of omega-3 fatty acid (oily fish)
  • Supplementation with 1g fish oil in patients with a low intake of oily fish

AHA (American Heart Association) recommends ~1g/day of EPA and DHA (the amount in each Omacor capsule) for patients with CHD8

SMC (Scottish Medicines Consortium) recommends Omacor as acceptable for general use in NHS Scotland as an additional treatment for secondary prevention of MI9

How much fish would patients need to eat to meet the NICE recommendations?

Download PDF


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How does Omacor differ from other products (including OTC)?

None of the other products have;

  • A licence for secondary prevention post MI
  • 460mg EPA & 380mg DHA per capsule
  • Undergoes a patented purification process
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Is there a dose effect?

One Omacor capsule daily was used in the GISSI-Prevenzione trial and showed significant efficacy in the secondary prevention after myocardial infarction, with a 20% relative reduction in deaths (2.1% absolute risk reduction) and a 45% relative reduction in sudden deaths (1.6% absolute risk reduction). Higher doses have not been investigated for this indication.

The dose for hypertriglyceridaemia is 2-4 g, titrated according to clinical response.

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Which patients will benefit from Omacor?

Any patient who has had an MI and patients with types IV and IIB/III endogenous hypertriglyceridaemia.

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What are the side effects?

The frequencies of adverse reactions are ranked according to the following:

common (> 1/100, < 1/10)
uncommon (>1/1000 < 1/100)
rare (>1/10000, < 1/1000)
very rare ( < 1/10000), including isolated reports.

Infections and infestations:
Uncommon: gastroenteritis

Immune system disorders:
Uncommon: hypersensitivity

Metabolism and nutrition disorders:
Rare: hyperglycaemia

Nervous system disorders:
Uncommon: dizziness, dysgeusia
Rare: headache

Vascular disorders:
Very rare: hypotension

Respiratory thoracic and mediastinal disorders:
Very rare: nasal dryness

Gastrointestinal disorders:
Common: dyspepsia, nausea
Uncommon: abdominal pain, gastrointestinal disorders, gastritis, abdominal pain upper
Rare: gastrointestinal pain,
Very rare: lower gastrointestinal haemorrhage

Hepatobiliary disorders:
Rare: hepatic disorders

Skin and subcutaneous tissue disorders:
Rare: acne, rash pruritic
Very rare: urticaria

General disorders and administration site conditions:
Rare: Ill-defined disorders
Investigations:
Very rare: white blood count increased, blood lactate dehydrogenase increased. Moderate elevation of transaminases has been reported in patients with hypertriglyceridaemia.

Omacor SmPC

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What are the interactions with Omacor?

Interaction with other medicinal products and other forms of interaction (please also see warnings below).

Oral anticoagulants: Omacor has been given in conjunction with warfarin without haemorrhagic complications. However, the prothrombin time must be checked when Omacor is combined with warfarin or when treatment with Omacor is stopped.

Special warnings and precautions for use

Warnings
Because of the moderate increase in bleeding time (with the high dosage, i.e. 4 capsules), patients receiving anticoagulant therapy must be monitored and the dosage of anticoagulant adjusted if necessary. Use of this medication does not eliminate the need for the surveillance usually required for patients of this type.

Make allowance for the increased bleeding time in patients at high risk of haemorrhage (because of severe trauma, surgery, etc).

In the absence of efficacy and safety data, use of this medication in children is not recommended.

Omacor is not indicated in exogenous hypertriglyceridaemia (type 1 hyperchylomicronaemia). There is only limited experience in secondary endogenous hypertriglyceridaemia (especially uncontrolled diabetes).

There is no experience regarding hypertriglyceridaemia in combination with fibrates.

Special precaution
Regular monitoring of hepatic function (ASAT and ALAT) is required in patients with hepatic impairment (in particular with the high dosage, i.e. 4 capsules).

Omacor SmPC

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What is the mode of action?

Myocardial scaring after myocardial infarction is one of the most important substrates for re-entrant ventricular arrhythmias. The presence of surviving myocotes inside necrotic zones, separated by electrically inactive tissue, allows re-entrant circuits.10

The presence of free omega-3 fatty acids helped to prevent the generation and propagation of arrhythmic action potentials in animal studies by Leaf et al.11

Hyperpolarised cells are less likely to respond to an aberrant signal and may reduce the likelihood of arrhythmias in damaged tissue post-MI.11

Omega-3 fatty acids inhibit triggered arrhythmias in isolated human myocytes.12

In summary although the actions of Omacor are multi-factorial and not straight forward, in the context of reducing sudden death post MI animal studies show omega-3 fatty acids appear to stabilize the cardiac myocyte membrane and thus make the ventricle less susceptible to re-entry arrhythmias.

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Are there any precautions for renal impairment?

No special dosage adjustments are required with renal impairment. Our SPC states that there is only limited information regarding use of Omacor in patients with renal impairment

Omacor SmPC

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Are there any precautions for hepatic impairment?

Special precaution.

Regular monitoring of hepatic function (ASAT and ALAT) is required in patients with hepatic impairment (in particular with the high dosage, i.e. 4 capsules).

Omacor SmPC

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Can Omacor be used during pregnancy and/or lactation?

Pregnancy

There is no adequate data from the use of Omacor in pregnant women.

Studies in animals have not shown reproductive toxicity. The potential risk for humans is unknown and therefore Omacor should not be used during pregnancy unless clearly necessary.

Lactation

There is no data on the excretion of Omacor in animal and human milk. Omacor should not be used during lactation.

Omacor SmPC

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Why should patients continue to take Omacor?

Patients are given Omacor because they have recently had a heart attack or they suffer from hypertriglyceridaemia. By continuing to take Omacor daily, along with any other treatments prescribed and recommendations on healthy eating and exercise, patients will give themselves the best possible chance of living a full life.

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Availability & usage

How should Omacor be used?

  • Together with other medicines for treatment after a heart attack
  • To treat certain forms of increased triglycerides (fats) in the blood after changes to the diet have not worked.
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References:

  1. Omacor SmPC
  2. GISSI-P. Lancet 1999; 354: 447-455.
  3. 4S. Lancet 1994; 344: 1383-1389.
  4. Antiplatelet Trialists' Collaboration. Br Med J 1994; 308: 81-106.
  5. NICE Guideline. Post Myocardial Infarction. Secondary Prevention in primary and secondary care for patients following a myocardial infarction. Royal College of General Practitioners. May 2007.
  6. Joint British Societies. Heart 2005; 91(suppl v): v1-v52.
  7. Van der Wharf et al. Eur Heart J 2008; 29: 2909-2945.
  8. Kris-Etherton et al. Circulation 2002; 106: 2747-2757.
  9. Scottish Medicines Consortium. 90% omega-3 acid ethyl esters. Summary of Recommendations. Glasgow, 2002.
  10. Bayes-de-Luna A et al. Cardiovasc Drugs Ther 1994; 8(Suppl 2): 335-343.
  11. Leaf A et al. Circulation 2003; 107: 2646-2652.
  12. Den Ruijiter HM et al. Circulation 2008; 117: 536-544.
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