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Background and purpose This study aims to investigate whether changes in lifestyle, added to the antihypertensive treatment, could translate to changes in cardiovascular (CV) morbidity and mortality in hypertensive patients. Methods Between October 2007 and November 2008, men or women (50–79 years) were enrolled randomly in this study when their BP was 140/90–179/109 mmHg with a 2-weeks run-in stage firstly. All participants had at least one additional CV risk factor, indicated by a history of stroke, myocardial infarction (MI), etc. Results 12,245 (90.4%) patients were eligible for our analysis. We assigned them to the lifestyle intervention group (5225) or to control group (7020). In the end of the study, weight loss at least 1 kg of the participants of the intervention group of accounted for 33.2%, control group was 24.9 (P < 0.001). Salt intake more than 6 g of the participants accounted for 29.4% in the intervention group, 38.4% in the control group (P < 0.001). The composite CV events which include non-fatal stroke, MI and CV death, happened in 133 (2.2%) participants of intervention group and 177 (2.4%) in the control group. However, the improvement of composite CV events reduced 55% (adjusted HR = 0.45, 95% CI: [0.32,0.63]), and decreased by 55% (HR = 0.45, 95% CI: [0.37,0.63]) for all CV events. Conclusions The effect of advised only lifestyle intervention used in our study is minor for CV prevention. However, the effect of improvement of lifestyle on CV prevention is indisputable even in hypertensives who receive a-hypertension drug treatment. [ABSTRACT FROM AUTHOR]

Abstract: Aim of the study: To investigate the effects of the ethanol extract from Portulaca oleracea (EEPO) on hypoxia models mice and to find the possible mechanism of its anti-hypoxic actions so as to elucidate the anti-hypoxia activity and provide scientific basis for the clinical use of Portulaca oleracea. Materials and methods: EEPO was evaluated on anti-hypoxic activity in several hypoxia mice models, including closed normobaric hypoxia and sodium nitrite or potassium cyanide toxicosis. To verify the possible mechanism(s), we detected the activities of pyruvate kinase (PK), phosphofructokinase (PFK), lactate dehydrogenase (LDH) and the level of adenosine triphosphate (ATP) in mice cortices. Results: Given orally, the EEPO at doses of 100, 200, 400mg/kg could dose-dependently enhance the survival time of mice in both of the normobaric and chemical hypoxia models. The activity of the glycolysis enzymes and the level of ATP were higher than those of the control. In the pentobarbital sodium-induced sleeping time test and the open-field test, EEPO neither significantly enhanced the pentobarbital sodium-induced sleeping time nor impaired the motor performance, indicating that the observed anti-hypoxic activity was unlikely due to sedation or motor abnormality. Conclusions: These results demonstrated that the EEPO possessed notable anti-hypoxic activity, which might be related to promoting the activity of the key enzymes in glycolysis and improving the level of ATP in hypoxic mice. [Copyright &y& Elsevier]