ObjectiveTo explore the correlations of high-density lipoprotein cholesterol (HDL-C)/low-density lipoprotein cholesterol (LDL-C) with myocardial infarction (MI), all-cause mortality, haemorrhagic stroke and ischaemic stroke, as well as the joint association of genetic susceptibility and HDL-C/LDL-C with the MI risk.Methods and resultsThis study selected 384 093 participants from the UK Biobank (UKB) database. First, restricted cubic splines indicated non-linear associations of HDL-C/LDL-C with MI, ischaemic stroke and all-cause mortality. Second, a Cox proportional-hazards model indicated that compared with HDL-C/LDL-C=0.4–0.6, HDL-C/LDL-C<0.4 and >0.6 were correlated with all-cause mortality (HR=0.97 for HDL-C/LDL-C<0.4, 95% CI=0.939 to 0.999, p<0.05; HR=1.21 for HDL-C/LDL-C>0.6, 95% CI=1.16 to 1.26, p<0.001) after full multivariable adjustment. HDL-C/LDL-C<0.4 was correlated with a higher MI risk (HR=1.36, 95% CI=1.28 to 1.44, p<0.05) and ischaemic stroke (HR=1.12, 95% CI=1.02 to 1.22, p<0.05) after full multivariable adjustment. HDL-C/LDL-C>0.6 was associated with higher risk haemorrhagic stroke risk after full multivariable adjustment (HR=1.25, 95% CI=1.03 to 1.52, p<0.05). Third, after calculating the coronary heart disease Genetic Risk Score (CHD-GRS) of each participant, the Cox proportional-hazards model indicated that compared with low CHD-GRS and HDL-C/LDL-C=0.4–0.6, participants with a combination of high CHD-GRS and HDL-C/LDL-C<0.4 were associated with the highest MI risk (HR=2.45, 95% CI=2.15 to 2.8, p<0.001). Participants with HDL-C/LDL-C<0.4 were correlated with a higher MI risk regardless of whether they had a high, intermediate or low CHD-GRS.ConclusionIn UKB participants, HDL-C/LDL-C ratio of 0.4–0.6 was correlated with lower MI risk, all-cause mortality, haemorrhagic stroke and ischaemic stroke. Participants with HDL-C/LDL-C<0.4 were correlated with a higher MI risk regardless of whether they had a high, intermediate or low CHD-GRS. The clinical significance and impact of HDL-C/LDL-C need to be further verified in future studies.
Background The association between body mass index (BMI) and Alzheimer's disease (AD) remains controversial. Genetic and environmental factors are now considered contributors to AD risk. However, little is known about the potential interaction between genetic risk and BMI on AD risk. Objective To study the causal relationship between BMI and AD, and the potential interaction between AD genetic risk and BMI on AD risk. Methods and Results Using the UK Biobank database, 475,813 participants were selected for an average follow-up time of more than 10 years. Main findings: 1) there was a nonlinear relationship between BMI and AD risk in participants aged 60 years or older (p for non-linear < 0.001), but not in participants aged 37–59 years (p for non-linear = 0.717) using restricted cubic splines; 2) for participants aged 60 years and older, compared with the BMI (23–30 kg/m2) group, the BMI (< 23 kg/m2) group was associated with a higher AD risk (HR = 1.585; 95% CI 1.304–1.928, p < 0.001) and the BMI (> 30 kg/m2) group was associated with a lower AD risk (HR = 0.741; 95% CI 0.618–0.888, p < 0.01) analyzed using the Cox proportional risk model; 3) participants with a combination of high AD genetic risk score (AD-GRS) and BMI (< 23 kg/m2) were associated with the highest AD risk (HR = 3.034; 95% CI 2.057–4.477, p < 0.001). In addition, compared with the BMI (< 23 kg/m2), the higher BMI was associated with a lower risk of AD in participants with the same intermediate or high AD-GRS; 4) there was a reverse causality between BMI and AD when analyzed using bidirectional Mendelian randomization (MR). Conclusion There was a reverse causality between BMI and AD analyzed using MR. For participants aged 60 years and older, the higher BMI was associated with a lower risk of AD in participants with the same intermediate or high AD genetic risk. BMI (23–30 kg/m2) may be a potential intervention for AD.
Objective: This study analyzed the association of gastric acid secretion inhibitors (GASIs) [including proton pump inhibitors (PPIs) and histamine 2 receptor antagonists (H2RAs)] with the occurrence of ventilator-associated pneumonia (VAP) and in-hospital mortality in patients who received invasive mechanical ventilation (IMV).Method: Patients who received IMV and used GASI were included based on records in the MIMIC-IV database. The relationships of GASIs with VAP and the in-hospital mortality were determined using univariate and multivariate logistic regression analyses. Also, the effects of GASIs in some subgroups of the population were further analyzed.Results: A total of 18,669 patients were enrolled, including 9191 patients on H2RAs only, 6921 patients on PPIs only, and 2557 were on a combination of the two drugs. Applying logistic regression to the univariate and multivariate models revealed that compared with H2RAs, PPIs had no significant effect on the incidence of VAP, and the combination of H2RAs and PPIs was a risk factor for VAP. Compared with H2RAs, univariate logistic regression revealed that, PPIs and combine the two drugs were both risk factors for in-hospital mortality, but multivariate logistic regression showed that they were not significantly associated with in-hospital mortality. In subgroup analysis, there were interaction in different subgroups of age, PCO2, myocardial infarct, congestive heart failure (P for interaction<0.05).Conclusion: Compared with H2RAs, PPIs did not have a significant association with either VAP or in-hospital mortality; the combination of H2RAs and PPIs was risk factor for VAP, but did not have a significantly associated with in-hospital mortality.
Background: Dysphagia is common in elderly patients with dementia and is one of the common clinical geriatric syndromes. It imposes a heavy burden on patients and their caregivers and is becoming an important public health problem. This study examined the association between dysphagia in older dementia patients in the ICU and the subsequent adverse health outcomes they experience. Patients and Methods: A retrospective analysis of adults (≥65 years) with dementia in ICUs of a Boston tertiary academic medical center was conducted. Using the International Classification of Diseases' Ninth and Tenth Revisions, dementia patients were identified. The study cohort comprised 1009 patients, median age 84.82 years, 56.6% female, predominantly White (72.9%). Patients were grouped based on swallowing function: dysphagia (n=282) and no-dysphagia (n=727). Dysphagia was identified via positive bedside swallowing screening. Primary outcomes were 90-and 180-day mortality, secondary outcomes included aspiration pneumonia, pressure injury, and delirium. Cohort characteristics were compared using the Wilcoxon rank-sum and chi-square tests. Dysphagia and outcomes correlations were examined via Kaplan-Meier survival analysis, Cox proportional-hazards regression models, logistic regression models, and subgroup analysis. Results: After adjusting for covariates, the results from multivariate Cox proportional-hazards regression indicated that dysphagia was significantly associated with increased 90-day (HR=1.36, 95% CI=1.07-1.73, E-value=1.78) and 180-day (HR=1.47, 95% CI=1.18-1.82, E-value=1.94) mortality; the multifactorial logistic regression results indicated that dysphagia was associated with significant increases in pressure injury (OR=1.58, 95% CI=1.11-2.23, E-value=1.83) and aspiration pneumonia occurrence (OR=4.04, 95% CI=2.72-6.01, E-value=7.54), but was not significantly associated with delirium prevalence (OR=1.27, 95% CI=0.93-1.74). Conclusion: Dysphagia is likely to increase the risk of adverse health outcomes in older adults with dementia in ICU, and these adverse outcomes mostly include 90-and 180-day mortality, aspiration pneumonia, and pressure injury.
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