Myocardial Energetics as a Target for Treatment of Ischemic Heart Disease: A Translational Approach From Patient to Mitochondria
Myocardial Energetics as a Target for Treatment of Ischemic Heart Disease: A Translational Approach From Patient to Mitochondria
Trimetazidine (1-[2,3,4-trimethoxybenzyl] piperazine dihydrochloride) is a clinically effective antianginal agent. Despite these clinical successes, the understanding of trimetazidine's mechanism of action remains incomplete, particularly influence of trimetazidine on mitochondrial function in isolated human cardiomyocytes. The investigators will perform this study to seek possible differences in mitochondrial respiration related to standard preoperative enrolled trimetazidine therapy.
Background:
Different types of medication are used for treatment of ischemic heart disease. One of recently developed drugs is trimetazidine. Although it clinical benefits are clear, mechanism by which this occurs is as yet undefined. In few animal studies authors try to define what effects trimetazidine has on both fatty acid and glucose metabolism in heart. Data collected from human cardiomyocytes are rare. Available data suggest that trimetazidine may act as a potent inhibitor of beta oxidation, with no significant effect on glucose oxidation.
Objective:
Primary objective: collection of mitochondrial respiration data using human heart ventricular samples. Secondary objective: define possible differences in mitochondrial respiration depending on preoperative trimetazidine usage.
Methods:
Regularly scheduled patients for coronary artery bypass grafting surgery who accept to participate in study will be enrolled in further protocol. Patients with inclusion criteria and without exclusion criteria will be enrolled in the study. At the end of operation, surgeon will take biopsy sample of left ventricle for mitochondrial function and metabolic activity analysis.
Inclusion Criteria:
Exclusion Criteria: