View clinical trials related to Cardiomyocyte Apoptosis.
Filter by:Retrograde cardioplegia during heart surgery is associated with inadequate myocardial protection. In experimental animal study retrograde cardioplegia induces more cardiomyocyte apoptosis when compared to antegrade cardioplegia. 20 volunteer patients under going elective aortic valve surgery will be divided in to two groups: 10 patients receiving only antegrade cardioplegia and 10 patients receiving only retrograde cardioplegia. Pre- and post-operatively cardiac MRI and cardiac ultrasound will be performed. During the surgery ventricular muscle samples will be taken in order to assess cardiomyocyte apoptosis. Aims of the study: 1. whether the cardiomyocyte apoptosis is significantly more induced after retrograde cardioplegia than antegrade cardioplegia, 2. whether the amount of apoptotic cardiomyocytes correlates to conventional markers of myocardial injury after cardiac surgery, 3. whether the extent of irreversible myocardial damage by apoptosis correlates to post-ischemic contractile dysfunction after cardiac surgery, as measured with echocardiography, 4. whether the amount of cardiomyocyte apoptosis correlates to long term outcome and cardiac function as measured with MRI.
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).