Myocardial functional and metabolic parameters in heart failure following chronic high fat feeding

Abstract

Heart failure (HF) is a complex process that remains to be fully understood, but involves multiple factors. Excess dietary fat is a risk factor for cardiovascular disease, but the role of fatty acids in HF progression has yet to be defined. Lipid accumulation in non-adipose tissue is known to cause a number of pathological events implicating fatty acids in cardiac pathology progression. However, the relationship between dietary lipid and contractile dysfunction is complicated; recent data from human and animal studies suggest dietary fat may be protective following infarction. Previous work in our laboratory using coronary artery ligation demonstrates that rats fed high fat after cardiac injury results in less contractile dysfunction and increased mitochondrial respiration despite increased tissue triglyceride. These results suggest an alteration in substrate utilization that benefits the injured heart. The current study aimed to characterize the impact of high fat on cardiac performance and substrate utilization in rats using a working heart perfusion model. Cardiac output, oxygen consumption (MVO2), and glucose oxidation were measured. Under normal conditions, HF animals had decreased MVO2 with no change in glucose oxidation. However, high fat feeding resulted in increased MVO2 with lower glucose oxidation in sham (SH) and HF animals. Under conditions of increased workload, HF animals had lower cardiac output, MVO2, and glucose oxidation. Furthermore, both SH and HF animals fed high fat had lower cardiac output and glucose oxidation than their respective controls fed normal chow. These results suggest that high dietary fat may not alter cardiac function under normal conditions, but may be deleterious for contractile and metabolic function during increased physiological stress.