Objective To assess the clustering of cardiovascular risk factors and their effects on target organ damage in elderly patients with hypertension .Methods 421 treated elderly hypertension patients were divided into 5 groups based on the number of risk factors :hypertension without additional risk factor (group A ,25 cases) ,and the other 4 groups were complicated with 1 (group B ,76 cases) ,2(group C ,127 cases) ,3(group D ,128 cases)and ≥ 4 (group E ,65 cases) risk factors .The structure and function of heart and carotid artery were examined by ultrasonography in order to evaluate the damage of target organ and the morbidity .Re-sults The patient groups with three or more risk factors showed significantly higher levels of BMI ,plasma glucose ,triglyceride , LDL-C cholesterol ,serum creatinine and serum uric acid ,and needed greater number of antihypertensive drugs ,compared with other groups(P<0 .05) .The patient groups with two or more risk factors showed significantly higher levels of LVMI ,IMT and MAU/Cr compared with group A(P<0 .05) ,and significantly lower levels of the creatinine clearance (P<0 .05) .In addition ,they showed significantly higher incidences of coronary heart disease and cerebrovascular disease and chronic kidney disease compared with group A (P<0 .05) .Conclusion These results suggest that the hypertensive patients with clustering risk factors required greater number of antihypertensive drugs .The more additional risk factors exit ,the more target organ damages and higher morbidity occur ,and more intensive intervension are required to control not only blood pressure but also other complicated risk factors .

Isolated perfused rat hearts were subjected to regional ischemia followed by reperfusion and then tested for responsiveness to acetylcholine (Ach) and nitroglycerin (NTG). The effects of L-Arginine (L-Arg) and NG-monomethyl-L-Arg (L-NMMA) on the endothelium-dependent (ED) and independent (EI) vasodilator were also observed. It was found that both 15 and 30min ischemia followed reperfusion resulted in a decrease in ED vasodilation of Ach. ED vasodilation gradually renewed after 90min reperfusion in the 15min ischemic group, not in the 30min ischemic group. No significant decrease in EI vasodilation of NTG in all groups. L-Arg accelerated the renewing of ED vasodilation of Ach in the 15 min ischemia-reperfusion group, not in the 30min ischemia-reperfusion group. L-NMMA was an inverse action. The results indicate that brief ischemia followed by reperfusion can induce coronary endothelium dysfunction which may be related to the decrease of endothelium derived relaxing factor.