Effect of low HDL combined with hypertriglyceridemia in coronary artery disease patients on PGI2 biological activity in relation to lipid regulating treatment
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The purpose of this study was to investigate the effect of low high-density-lipoprotein (HDL) combined with hypertriglyceridemia in coronary artery disease (CAD) patients on prostaglandin I2(PGI2) biological activity in relation to lipid regulating treatment. The inhibitory rate of PGI2 on ADP-induced platelet aggregation was used as the index for PGI2 biological activity. Twenty health individuals served as normal controls. CAD group consisted of 20 patients with low HDL combined with hypertriglyceridemia. The results showed that, before the treatment, the stabilizing effect on PGI2 activity decreased significantly in CAD group when compared with the control group (P <0.01). One month after the treatment, HDL level in CAD group increased significantly and TG level significantly decreased (P <0.001). The different effect on PGI2 activity was no longer found between CAD group and control group (P > 0. 05), further confirming the protecting effect of HDL on PGI2 biological activity. Low HDL is considered as an important risk factor of CAD, therefore, impaired PGI2 biological activity and increased platelet aggregation might be responsible mechanisms. Furthermore, raising HDL level by lipid regulating treatment could restore the protective effect of HDL on PGI2 and might be helpful in the prevention of the acute coronary syndrome.
Key wordshigh-density-lipoprotein hypertriglyceridemia prostaglandin I2 coronary artery disease
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- 5.Badimon J J, Fuster V, Badimon Let al. Role of high density lipoprotein in the regression of atherosclerosis. Circulation, 1992, 70: 733Google Scholar
- 7.Teresa E D. A clinical perspective on the management of patients with coronary heart disease and those at high risk. Lipid, 1995, 9: 1Google Scholar
- 8.Szekers L, Pataricza J, Szilkvassy Zet al. Cardioprotection: Endogenous protective mechanism promoted by prostacyclin. Basic Res Cardiol, 1991, 86,(Supll 3): 215Google Scholar