Pilot Study of Lovaza (Omega 3 Fatty Acids) to Improve Cardiac Antioxidant/Anti-inflammatory Profile Before Cardiac Surgery
This trial is active, not recruiting.
|Conditions||mitral valve regurgitation, left atrium dilatation and hypertrophy, mitochondrial dysfunction in the heart, cardiomyocyte apoptosis, cardiac inflammation|
|Sponsor||East Carolina University|
|Start date||January 2010|
|End date||October 2013|
|Trial size||24 participants|
|Trial identifier||NCT01046604, ECUomega3-01|
In the absence of treatment, severe mitral valve regurgitation (MR) results in left atrium (LA) dilatation and hypertrophy, followed ultimately by left ventricular dysfunction and heart failure. One promising intervention for the prevention of the deleterious effects of pressure overload-induced cardiac hypertrophy and heart failure is dietary supplementation with n-3 polyunsaturated fatty acids (PUFAs). However, the molecular targets and mechanisms by which n-3 PUFAs exert their effects are not completely defined. A possible target of n-3 PUFAs is the mitochondrial membrane which has broad implications given that mitochondrial dysfunction and altered metabolism have been associated with cardiac hypertrophy and heart failure. The investigators have recently identified significant mitochondrial dysfunction in the LA of patients with severe MR, as compared to their non-hypertrophied right atrium (RA). However, the investigators have not addressed the possibility that intervention with purified n-3 PUFAs (Lovaza) could improve mitochondrial function. From a mechanistic perspective, the investigators have observed in vitro that n-3 PUFAs accumulate predominately into the mitochondrial membrane of cardiomyocytes where the investigators believe they exert their effects on the biophysical organization of the membrane. Therefore, the CENTRAL HYPOTHESIS is that administering Lovaza to patients with severe MR will reduce apoptosis and improve mitochondrial function in LA (Aim 1). This change in mitochondrial function will be driven by significant biochemical and biophysical remodeling of the mitochondrial membrane (Aim 2).
|Endpoint classification||efficacy study|
|Intervention model||parallel assignment|
|Primary purpose||supportive care|
Specific Aim 1: To determine if Lovaza treatment reduces markers of inflammation and improves mitochondrial function in atrial myocardium
time frame: 15 months
Specific Aim 2: To determine if Lovaza treatment alters the biophysical and biochemical organization of cardiac mitochondrial membranes. The following questions will be addressed using the blood and cardiac tissue samples collected as described above:
time frame: 15 months
Male or female participants from 18 years up to 70 years old.
- Patients age 18+ undergoing minimally invasive mitral valve repair surgery will be enrolled in this study.
- Patients with chronic renal insufficiency
- Chronic obstructive pulmonary disease
- Previous myocardial infarction
- Left ventricular dysfunction (ejection fraction <40%)
- Use of anti-arrhythmic drugs other than beta blockers, and the presence of an implantable defibrillator.
- In addition, patients that have a high dietary intake of fish (≥ 2 servings/week) or have been taking n-3 PUFA supplements will be excluded.
- Also, patients that are allergic to fish or shellfish, or taking any anticoagulant/antiplatelet medications other than aspirin (e.g. Plavix, Coumadin) will be excluded from this study.
- Patients under the age of 18, and women who are pregnant will be excluded from this study.
|Official title||Mitigating Cardiac Inflammation and Oxidative Stress in Atrial Myocardium Via Short-term Lovaza Treatment Prior to Surgery|
|Principal investigator||Ethan J Anderson, PhD|
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