Abstract 15216: Thermal Therapy Prevented the Transition from Cardiac Hypertrophy to Heart Failure
Introduction Long-term cardiac hypertrophy causes heart failure. One of the mechanisms of this transition from hypertrophy to heart failure is collapse of hypoxic response and angiogenesis. Heat shock protein 27 (HSP27) was found to act as an anti-apoptotic protein and its phosphorylation is responsible for the protection of cells against heat stress. There is a report that HSP27 regulates p53 expression, which contributes to down-regulate angiogenic factors through hypoxia inducible factor-1α(HIF-1α). We have reported that thermal therapy improves cardiac and vascular function in patients with chronic heart failure. However, the effect of this therapy on cardiac hypertrophy is unknown.
Methods and Results Cardiac hypertrophy was induced by transverse aortic constriction (TAC) in C57BL/6 mice. At 2 weeks after TAC, all mice were examined by echocardiography and showed left ventricular hypertrophy. Mice were randomly divided into thermal therapy or untreated group. Thermal therapy group received thermal therapy using an experimental far infrared dry sauna, which elevates the core temperature by 1 degree Celsius for 30 minutes, daily for 4 weeks. Sham operated mice were used as control. At 6 weeks after TAC, body weight, heart rate and blood pressure did not differ in three groups. Echocardiography showed that left ventricular fractional shortening of thermal therapy group was significantly larger than that of untreated group (Sham vs. Untreated vs. Thermal; 50.0±1.7 vs. 36.7±1.3 vs. 46.2±0.5, P>0.01, n=6 each). Heart weight/tibia length ratio of thermal therapy group was significantly smaller than that of untreated group (6.7±0.1 vs. 9.7±0.5 vs. 7.9±0.2, P>0.01, n=9 each). Western blot showed that thermal therapy increased phosphorylation of HSP27 and reduced p53. Thermal therapy also increased HIF-1α and vascular endothelial growth factor at 6 weeks after TAC. Capillary/myofiber ratio was larger in thermal therapy group than that in untreated group (1.71±0.05 vs. 2.04±0.04 vs. 2.41±0.10, P>0.01, n=4 each).
Conclusion Thermal therapy prevented the transition from cardiac hypertrophy to heart failure in mice. As the mechanism, thermal therapy up-regulated phosphorylation of HSP27 and reduced p53, which maintained angiogenesis in heart.
- © 2012 by American Heart Association, Inc.