BackgroundThe heart is an important target organ for the harmful effects of high dietary salt intake. However, the effects and associations of high salt intake on myocardial viability, cardiac function changes, and myocardial remodeling are unclear.MethodsA total of 3,810 participants aged 60 years and older were eligible and enrolled from April 2008 to November 2010 and from August 2019 to November 2019 in the Shandong area of China. Salt intake was estimated using 24-h urine collection consecutively for 7 days. Myocardial strain rates, cardiac function and structure, and serum high-sensitivity C-reactive protein (hsCRP) levels were assessed. Participants were classified into low (n = 643), mild (n = 989), moderate (n = 1,245), and high (n = 933) groups, corresponding to < 6, 6–9, 9–12, and >12 g/day of salt intake, respectively, depending on the salt intake estimation.ResultsThe global early diastolic strain rate (SRe) and late diastolic strain rate (SRa) in the high group were 1.58 ± 0.26, 1.38 ± 0.24. respectively, and significantly lower compared with the low, mild, and moderate groups (all P < 0.05). The global systolic strain rate (SRs) in the high group was −1.24 ± 0.24, and it was higher than those in the low, mild, and moderate groups (all P < 0.05). Salt intake was independently and positively correlated with global SRs, Tei index, and the parameters of left ventricular structure separately; negatively correlated with global SRe and SRa, left ventricular short axis shortening rate, left ventricular ejection fraction after adjusting for confounders (all Padjusted < 0.001). Hayes process analyses demonstrated that the mediating effects of hsCRP on global SRe, SRa, and SRs; Tei index; and left ventricular remodeling index were −0.013 (95% CI: −0.015 to −0.010), −0.010 (−0.012 to −0.008), 0.008 (0.006–0.010), 0.005 (0.003–0.006), and 0.010 (0.009–0.012), respectively (all Padjusted < 0.001).ConclusionOur data indicate that excess salt intake is independently associated with the impairment in myocardial viability and cardiac function, as well as myocardial remodeling. Chronic inflammation might play a mediating role in the association between high salt intake and cardiac function damage and myocardial remodeling.
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.
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