Pilot Study of Lovaza (Omega 3 Fatty Acids) to Improve Heart Function in Patients With Mitral Valve Disease

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).