PT - JOURNAL ARTICLE AU - Yan Xiong AU - Yan Xiong TI - e0375 Long-term enhanced external counterpulsation repairs platelet membrane fluidity and alleviates lipid peroxidation in patients with stable angina pectoris AID - 10.1136/hrt.2010.208967.375 DP - 2010 Oct 01 TA - Heart PG - A116--A116 VI - 96 IP - Suppl 3 4099 - http://heart.bmj.com/content/96/Suppl_3/A116.2.short 4100 - http://heart.bmj.com/content/96/Suppl_3/A116.2.full SO - Heart2010 Oct 01; 96 AB - Objective To explore the effect of long-term enhanced external counterpulsation (EECP) on platelet membrane fluidity (PMF) and lipid peroxidation in patients with stable angina pectoris. Methods Long-term EECP was performed on 30 patients with stable angina pectoris, 1 h once a day for 36 days. Platelets were harvested from all patients pre-EECP (before EECP), during EECP (EECP for 18 h) and post-EECP (EECP for 36 h). Fluorescence polarisability P′ was measured by fluorescence spectrophotometer. Meanwhile, the levels of lipid peroxidation and plasma lipids including total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C), were measured. Results Compared with pre-EECP, PMF was repaired significantly in patients with stable angina pectoris, no matter EECP performed for 18 h or for 36 h (0.337±0.053), (0.257±0.042) vs (0.543±0.066), respectively, (p<0.05). Similarly, lipid peroxidation levels were also alleviated obviously (0.427±0.053) μmol/l, (0.302±0.046) μmol/l vs (0.712±0.126) μmol/l, respectively, (p<0.05). Moreover, it seems a more significant change in both PMF and lipid peroxidation when EECP performed for 36 h than for 18 h. On the contrary, there was no significant change in the levels of plasma lipids (TC, TG, LDL-C, HDL-C). A direct negative correlation was observed between PMF and the levels of lipid peroxidation. Conclusion This result demonstrates that Long-term EECP can alleviate lipid peroxidation and restore or repair PMF in patients with stable angina pectoris, contributing to postponing atherogenesis.