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Background: It is unclear whether excessive salt intake accelerates the progression of cerebral small vessel disease (CSVD). The major objective of this study was to investigate the harmful effect of excessive salt intake on the progression of CSVD in older individuals. Methods: Between May 2007 and November 2010, 423 community-dwelling individuals aged 60 years and older were recruited from the Shandong area, China. Salt intake was estimated using 24-hour urine collection for 7 consecutive days at baseline. Participants were classified into low, mild, moderate and high groups according to the salt intake estimation. CSVD including white matter hyperintensities (WMHs), lacunes, microbleeds and an enlarged perivascular space (EPVS) were determined using brain magnetic resonance imaging. Results: During an average of five years of follow-up, the WMH volume and WMH-to-intracranial ratio were increased in the four groups. However, the increasing trends in the WMH volume and WMH-to-intracranial ratio were significantly faster in the higher salt intake groups compared with the lower salt intake groups (Padjusted < 0.001). The cumulative hazard ratios of new-incident WMHs (defined as those with Fazekas scale scores ≥ 2), new-incident lacunes, microbleeds or an EPVS, as well as composites of CSVD, were respectively 2.47, 2.50, 3.33, 2.70 and 2.89 for the mild group; 3.72, 3.74, 4.66, 4.01 and 4.49 for the moderate group; and 7.39, 5.82, 7.00, 6.40 and 6.61 for the high group, compared with the low group after adjustment for confounders (Padjusted < 0.001). The risk of new-incident WMHs, lacunes, microbleeds or an EPVS, and composites of CSVD was significantly increased with each 1-standard-deviation increment in salt intake (Padjusted < 0.001). Conclusion: Our data indicates that excessive salt intake is an important and independent contributor to the progression of CVSD in older adults. [ABSTRACT FROM AUTHOR]

Objective: Small and dense low-density lipoprotein (sdLDL) elevation may be among the most sensitive early biomarkers for nascent cardiovascular disease. This study, therefore, investigated the association between visit-to-visit changes in sdLDL and cerebral small vessel disease (CSVD) progression in older individuals, and the influence of Apolipoprotein E (APOE) genotype on this association. Methods: Between April 2007 and July 2009, 1,143 participants ≥60 years old were recruited from the Shandong region of China, and sdLDL was measured at baseline and at each follow-up visit. White matter hyperintensities (WMHs), lacunes, microbleeds, and enlarged perivascular spaces (EPVSs) were assessed by magnetic resonance imaging. The APOE genotype was determined and participants were stratified as ε 4- positive or ε 4- negative. Results: During an average follow-up of 86.0 months, 225 participants (19.7%) developed WMH progression, 193 (16.9%) lacune progression, 170 (14.9%) microbleed progression, and 185 (16.2%) EPVS progression. Compared with patients in the first (lowest) tertile of visit-to-visit mean sdLDL, those in the second and third tertiles demonstrated significantly greater risks of WMH progression (53.5 and 105.3% higher), lacune progression (53.3 and 60.8%), microbleed progression (47.2 and 127.6%), and EPVS progression (54.0 and 135.0%) after adjustment for confounders (all adjusted P values for trends <0.001). Compared with patients in the first tertile of visit-to-visit sdLDL SD, those in the second and third tertiles also demonstrated significantly greater risks of WMH progression (49.9% and 143.6%), lacune progression (75.3 and 178.0%), microbleed progression (12.7 and 64.7%), and EPVS progression (41.7 and 114.6%) after adjustment (all P < 0.001). There were significant and positive visit-to-visit mean sdLDL × visit-to-visit sdLDL SD, visit-to-visit mean sdLD×ε 4 -positive, visit-to-visit sdLDL SD×ε 4 -positive, and visit-to-visit mean sdLDL×visit-to-visit sdLDL SD×ε 4 -positive interactions influencing CSVD progression after confounder adjustment (all P < 0.05). Conclusion: Large and variable visit-to-visit changes in sdLDL are independent predictors of aggressive CSVD progression, and this association is strongly influenced by APOE ε 4 allele genotype. [ABSTRACT FROM AUTHOR]

Objective : To investigate the effect of telmisartan, rosuvastatin, or their combination on dementia and to understand the impact of apolipoprotein E (APOE) genotype on the effect of the medications in older patients with hypertension. Methods : This is a double-blind, randomized, and placebo-controlled trial using a 2 × 2 factorial design. Between April 2008 and November 2010, 1,244 hypertensive patients aged ≥60 years without cognitive impairment were recruited from communities in six cities in Shandong area, China. Patients were randomized into telmisartan and rosuvastatin administration after a 2-week washout period. APOE genotype was identified at the baseline. Possible dementia was determined using the combination of the global cognitive function and Assessment of the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE). Results : Over an average follow-up of 7 [interquartile range (IQR): 6.7–7.2] years, telmisartan and rosuvastatin significantly reduced the cognitive impairment progression and the incidence of dementia. There was a synergistic interaction between telmisartan and rosuvastatin to reduce the cognitive impairment and the incidence of dementia (P adjusted < 0.001). The cognitive impairment progression and the risk of dementia were higher in the hypertensive patients with APOE ε4 allele than in those without APOE ε4 allele. Rosuvastatin medication significantly alleviated the cognitive impairment progression and the risks of dementia in patients with APOE ε4 allele. Conclusion : The combination of telmisartan and rosuvastatin might be an effective prevention and/or treatment strategy for cognitive impairment and dementia, especially in hypertensive patients with the APOE ε4 allele. Clinical Trial Registration: www.ClinicalTrials.gov, ChiCTR.org.cn, identifier ChiCTR-IOR-17013557. Registered on April 12, 2017 – Retrospectively registered, http://www.chictr.org.cn/showproj.aspx?proj=23121 [ABSTRACT FROM AUTHOR]

• High sodium intake is associated with an increased risk of new-onset AF. • High sodium intake enhances the association between hyperglycemia and new-onset AF. • A sodium-restricted diet result in a multiplier effect on reducing the risk of AF. Studies investigating the association between sodium intake and new-onset atrial fibrillation (AF) have come to controversial results. This study aimed to assess the effect of excessive sodium intake on new-onset AF in individuals with hyperglycemia. Between April 2007 and November 2011, 2841 community-dwelling individuals aged 60 years and older were recruited from the Shandong area, China. Dietary sodium intake was estimated using 24-hour urine collection within seven consecutive days. Fasting plasma glucose (FPG) and glycated hemoglobin (HbA1c) were assessed. New-onset AF was diagnosed using ICD-10 with codes I48 (I48.0 – I48.9) during follow-up. The findings were that excessive sodium intake significantly and independently increased the risk of new-onset AF in older adults with hyperglycemia: hazard ratio (HR) 1.525 [95% confidence interval 1.147;2.029] adjusted P = 0.004. The risk of new-onset AF increased by 29.3% (HR 1.293 [1.108;1.509] adjusted P = 0.001) with a one-standard deviation increase in sodium intake. Excessive sodium intake synergistically interacted with hyperglycemia on the increased risk of new-onset AF (HR 1.599 [1.342;1.905] adjusted P < 0.001 for FPG and HR 1.516 [1.271;1.808] adjusted P < 0.001 for HbA1c). Our findings indicate that excessive sodium intake independently enhances the risk of new-onset AF among patients with hyperglycemia. A sodium-restricted diet may perhaps result in a multiplier effect on reducing the risk of new-onset AF. [ABSTRACT FROM AUTHOR]

Economy has developed rapidly in China, and the clustering of cardiovascular risk factors in subjects increased remarkably over the past two decades. However, no data are available regarding the temporal prevalence of hyperuricemia and its correlates in this rapidly developing area, especially in the inland area. The cross-sectional survey was based on a random sample of 4,218 residents aged 35-64 years in the Jinan area. Hyperuricemia was defined as serum uric acid ≥416 μmol/L in men and ≥357 μmol/L in women. Subjects underwent physical examination and fasting blood testing. Complete data were available for analysis from 1,979 men and 2,062 women. The age-adjusted prevalence of hyperuricemia was 6.4 % for men and 2.1 % for women. The prevalence of hyperuricemia was greater in urban (6.7 %) than in rural areas (1.7 %) of Jinan city. Multivariate logistic regression models revealed hyperuricemia associated with hypertriglyceridemia [men: odds ratio (OR) = 6.101, 95 % confidence interval (CI) 4.064-9.159; women: OR = 7.103, 95 % CI 3.578-14.099] and high serum creatinine level (men: OR = 2.603, 95 % CI 1.602-4.230; women: OR = 5.237, 95 % CI 2.667-10.284). Hyperuricemia was also significantly associated with male sex, urban residence, hypertension, obesity, and hypercholesterolemia. Age (1-year increase) was negatively associated with hyperuricemia in men but positively associated with hyperuricemia in women. In conclusion, the prevalence of hyperuricemia is higher in urban than rural areas of Jinan, China. Male sex, urban residence, hypertension, obesity, hypercholesterolemia, hypertriglyceridemia, and high serum creatinine level contributed to hyperuricemia in this population. [ABSTRACT FROM AUTHOR]