Association between blood pressure level and incidence of carotid artery plaque in middle-aged and elderly people / 中华心血管病杂志

<p><b>OBJECTIVE</b>To explore the association between blood pressure level and incidence of carotid arterial plaque in middle-aged and elderly people.</p><p><b>METHODS</b>A total of 5852 individuals were randomly stratified from the 101 510 health examination survey participants in Tangshan Kailuan Company community during 2006-2007. A total of 5440 people (age above 40 years old, free of stroke, TIA and myocardial infarction) were enrolled in the final analysis. A questionnaire survey, blood biochemical analysis and carotid artery ultrasound examination were finished by trained medical staff. Sixteen individuals without carotid artery plaques information and 35 individuals without blood pressure information were excluded. Finally, a total of 5389 participants [3235 male, mean age: (54.7 ± 11.8) years] were analyzed. According to 2010 Chinese guideline to prevention and treatment of hypertension and blood pressure level classification, participants were divided into normotensive group (n = 1377), high normal blood pressure group (n = 1971) and hypertensive group (n = 2041). Multivariate logistic regression analysis was used to determine the risk factors of the carotid artery plaques.</p><p><b>RESULTS</b>Age, male gender, BMI, IMT, TG, FBG, smoking and alcohol drinking rate were significantly higher in high normal blood pressure group than in normotensive group (all P < 0.05), LDL-C, HDL-C, hs-CRP and TC were similar between these two groups. Incidence of carotid artery plaques in normotensive, high normal blood pressure and hypertensive groups was 24.8%, 37.4%, 60.2% respectively. The risk of carotid artery plaques was increased to 38% and 163% in high normal and hypertensive groups compared to normotensive group, the OR ratio was 1.38 (95%CI: 1.15-1.66) and 2.63 (95%CI: 2.18-3.18), respectively. After adjusting gender, age, smoking, alcohol consumption, TG, TC, HDL-C, FBG, hs-CRP and BMI, the risk of developing carotid artery plague was increased in proportion to increasing blood pressure and the OR value was 1.24 (95%CI:1.01-1.52) , 1.69 (95%CI:1.34-2.15) and 2.66 (95%CI:2.20-3.21) in high normal group I [SBP/DBP 121-129/80-84 mm Hg(1 mm Hg = 0.133 kPa)] and high normal group II (SBP/DBP 130-139/85-89 mm Hg) and hypertensive group, respectively.</p><p><b>CONCLUSIONS</b>The cardiovascular risk factors and prevalence of carotid artery plague increase in proportion to blood pressure level in this cohort. The detection rate of carotid artery plague is already significantly increased in individuals with high normal blood pressure.</p>

Association between blood pressure level and the development of memory dysfunction in patients with hypertension / 中华心血管病杂志

<p><b>OBJECTIVE</b>It is known that hypertension may be implicated the development of memory dysfunction. Our study tests the hypothesis that prevalence of memory dysfunction is closely linked with the level of SBP (systolic blood pressure) and DBP (diastolic blood pressure) in hypertension patients.</p><p><b>METHODS</b>Non-stroke hypertension patients aged 18-75 years (n = 196, age 54 ± 10, 101 male) with diagnosed hypertension for more than one year were included. Memory function was measured by the Rivermead Behavioral Memory Test Second Edition (RBMTII, 2003). The general information was obtained through questionnaire.</p><p><b>RESULTS</b>RBMTII total score, the ability of recall name, remember storing article, recall faces, delayed route memory and orientation score were significantly decreased in proportion with increasing blood pressure (P < 0.05: hypertension III vs. II and I). RBMTII total score, the ability of recall name, and recall faces were significantly lower in hypertension II group compared to hypertension I group (P < 0.05). The age, male gender, years of hypertension, level of SBP and BMI were risk factors of memory dysfunction while the years of education was protective factor of memory dysfunction. The morbidity of memory dysfunction in patients with hypertension was higher and more serious with increasing blood pressure level (χ(2) = 10.389, P < 0.01).</p><p><b>CONCLUSIONS</b>Our results suggest that blood pressure is positively related to increased risk of memory dysfunction. The age, male gender, years of hypertension, level of SBP and BMI are risk factors of memory dysfunction while the years of education is protective factor of memory dysfunction.</p>

Protective effects of edaravone on diffuse brain injury in rats / 世界急诊医学杂志（英文）

BACKGROUND: Edaravone can alleviate brain injury and improve neurological functions and symptoms. This study aimed to investigate the effect of edaravone on the p38Mitogen-activated protein kinases/Caspase-3 (p38MAPK /Caspase-3) pathway after diffuse brain injury (DBI) in rats. METHODS: DBI models were established according to the description of Marmarou's method. A total of 250 rats were divided (random number) into four groups: control group (CG, n=45), model group (MG, n=77), low-dose edaravone group (n=67, dosage 5 mg/kg) and high-dose edaravone group (n=61, dosage 10 mg/kg). After 1, 6, 24, 48, and 72 hours after injury, brain tissues were collected. The changes of neuron morphous in the hippocampal region were observed through Nissl staining. The expression levels of phosphorylated p38MAPK and caspase-3 were detected by immunohistochemistry and Western blotting respectively. Learning and memory function were tested with Morris water maze from the 3rd to 7th day after injury. RESULTS: Some neurons had histopathologic changes of necrosis and apoptosis in the model group compared with the control group. The phosphorylated p38MAPK expressions increased at 1, 6, 4, and 48 hours (P<0.05), but no significant difference was observed at 72 hours (0.54±0.19 vs. 0.40±0.14, P>0.05). Caspase-3 expressions increased at 6, 24, 48, and 72 hours respectively (P<0.05), but there was no significant difference at 1 hour (0.59±0.29 vs. 0.40±0.17, P>0.05). From the 3rd to 6th day during the Morris water maze test, the latency to find the platform was significantly prolonged (P<0.05) and times of rats crossing the platform was decreased on the 7th day (2.28±1.18 vs. 8.20±1.52, P<0.05). The phosphorylated p38MAPK expressions decreased at 6, 24 and 48 hours respectively in the low dose edaravone group compared with the model group (P<0.05), whereas no significant difference was seen at 1 hour (1.66±0.80 vs. 1.85±0.86, P>0.05). Caspase-3 expression decreased at 6, 24, 48, and 72 hours (P<0.05). The latency to find the platform was significantly shortened (P<0.05), and times of rats crossing the platform increased (4.17±1.15 vs. 2.28±1.18, P<0.05). The above mentioned parameters changed more significantly in the high-dose edaravone group than in the low-dose edaravone group. CONCLUSION: Edaravone can alleviate brain tissue damage after DBI, inhibit p38MAP signal activation after early injury, reduce the expression of caspase-3, and promote the recovery of neurological function in the late period.