Cholesterol feeding (0.5%) in rabbits induced systolic and diastolic dysfunction and increased the ratio of MHC-beta to MHC-alpha mRNA 5-fold, independent of vascular disease.
BACKGROUND: Although hypercholesterolemia is a well-established risk factor for coronary artery disease, little is known regarding its direct effects on cardiac function. METHODS AND RESULTS: We examined the effects of cholesterol feeding (0.5%) on cardiac function in rabbits. After 10 weeks, both systolic shortening and diastolic relaxation rates were impaired without any change in aortic pressure or ventricular hypertrophy. However, sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA)-2 mRNA levels were reduced within 4 days after initiation of cholesterol feeding. After this effect, SERCA-2 protein and SERCA-mediated Ca uptake into sarcoplasmic reticulum vesicles were impaired, and the ratio of MHC-beta to MHC-alpha mRNA increased 5-fold. Suppression of the SERCA-2 message correlated temporally with enrichment of the cardiac sarcolemma with cholesterol. CONCLUSIONS: These data demonstrate that dietary hypercholesterolemia induces a "cholesterol cardiomyopathy" characterized by systolic and diastolic dysfunction. These alterations were independent of vascular disease and demonstrate a dietary link to cardiac dysfunction.
Huang et al. (Tue,) conducted a other in Hypercholesterolemia. Cholesterol feeding was evaluated on Cardiac function (systolic shortening and diastolic relaxation rates). Cholesterol feeding (0.5%) in rabbits induced systolic and diastolic dysfunction and increased the ratio of MHC-beta to MHC-alpha mRNA 5-fold, independent of vascular disease.
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