Causal association between serum 25-hydroxyvitamin D levels and right ventricular structure and function: A Mendelian randomization study.

BACKGROUND AND AIM: Deficient concentrations of vitamin D have been linked to several cardiovascular conditions, but the causal relationship between serum 25-hydroxyvitamin D (25(OH)D) levels and right ventricular structure and function remains unclear. Mendelian randomization (MR) was employed to inspect this association. METHODS AND RESULTS: Genetic instrumental variables associated with 25(OH)D levels were acquired from genome-wide association studies (GWAS) analyses. Summary statistics for right ventricular structure and function, including right ventricular end diastolic volume, right ventricular end systolic volume, right ventricular stroke volume, and right ventricular ejection fraction, were acquired from publicly available GWAS datasets. For the primary analysis, the inverse variance weighted (IVW) method was utilized in performing the MR analysis. Additionally, secondly analyses were conducted to estimate the robustness and consistency of the attained conclusions. The MR analysis did not reveal a considerable causal association between serum 25(OH)D levels and right ventricular end diastolic volume (ß: 0.112, 95% confident interval [CI]: -0.006 to 0.230, p = 0.063), right ventricular end systolic volume (ß: 0.102, 95% CI: -0.021 to 0.226, p = 0.105), right ventricular stroke volume (ß: 0.095, 95% CI: -0.018 to 0.207, p = 0.099), or right ventricular ejection fraction (ß: -0.005, 95% CI: -0.123 to 0.112, p = 0.928). CONCLUSIONS: Our findings did not reveal any substantial evidence supporting a causal relationship between serum 25(OH)D levels and the structure and function of the right ventricle. These findings suggest that serum 25(OH)D levels may not directly influence right ventricular parameters assessed.

Elevated mean arterial pressure is associated with a lower risk of mortality in acute kidney injury patients receiving continuous renal replacement therapy.

OBJECTIVE: maintenance of an appropriate mean arterial pressure (MAP) is important for critically ill patients. However, the association between MAP and prognosis in acute kidney injury (AKI) patients receiving continuous renal replacement therapy (CRRT) is thus far unclear. MATERIALS AND METHODS: a total of 1,144 AKI patients who had received CRRT between January 2009 and September 2016 were enrolled and their MAP was measured at CRRT initiation. Patients were categorized into four groups (Quartile 1: MAP < 67.3 mmHg; Quartile 2: 67.3 ≤ MAP < 76.7 mmHg; Quartile 3: 76.7 ≤ MAP < 86.3 mmHg; Quartile 4: MAP ≥ 86.3 mmHg), and 28- and 90-day mortality rates were compared. RESULTS: our results demonstrate that 204 (72.1%), 187 (63.4%), 174 (62.6%), and 145 (50.3%) deaths occurred in quartiles 1, 2, 3, and 4 within 28 days, respectively (p < 0.001). This trend also exists in 90-day mortality (Quartile 1: 81.3%; Quartile 2: 72.5%; Quartile 3: 72.3%; Quartile 4: 61.1%, p < 0.001). The Kaplan-Meier results indicate that higher MAP is associated with a reduction in 28- and 90-day mortality (both p < 0.001). After adjusting for potential confounders using Cox proportional hazard regression analysis, higher MAP was still associated with a decline in 28 - and 90-day mortality (both p < 0.001). CONCLUSION: MAP is a valuable parameter for predicting mortality in AKI patients who are receiving CRRT.

This study explored the relationship between mean arterial pressure and the risk of mortality in patients with acute kidney injury receiving continuous renal replacement therapy.Elevated mean arterial pressure is associated with a lower risk of mortality in acute kidney injury patients receiving continuous renal replacement therapy.

Systolic blood pressure is associated with abnormal alterations in brain cortical structure: Evidence from a Mendelian randomization study.

BACKGROUND: Hypertension has been recognized as a significant risk factor for cerebrovascular diseases and cognitive decline. However, the specific impact of hypertension, systolic/diastolic blood pressure, pulse pressure (PP) and mean arterial pressure (MAP) on brain cortical structure remains unclear. Mendelian randomization (MR) provides a robust approach to investigate the causal relationship between blood pressure components and brain cortical changes. METHODS: In this MR study, data from large-scale genome-wide association studies for blood pressure components and neuroimaging were utilized to conduct our analyses. We leveraged genetic variants associated specifically with hypertension (122,620 cases and 332,683 controls), systolic (469,767 individuals), diastolic (490,469 individuals) blood pressure, PP (810,865 individuals) and MAP (over 1 million individuals) to evaluate their effects on brain cortex surficial area (51,665 individuals) and cortex thickness (51,665 individuals). RESULTS: Our findings revealed a significant correlation between systolic blood pressure and abnormal reduction in brain cortex surficial area (ß=-1330.69, 95% confident interval [CI]: -2655.35 to -6.02, p = 0.0489); however, no significant relationship was found between systolic blood pressure and brain cortex thickness (ß=-0.0078, 95% CI: -0.0178 to 0.0022, p = 0.1287). Additionally, no significant associations were observed between hypertension (ß=-200.05, p = 0.6884; ß=-0.0051, p = 0.1179, respectively), diastolic blood pressure (ß=-460.63, p = 0.5160; ß=0.0047, p = 0.2448, respectively), PP (ß=1041.84, p = 0.3725; ß=-0.0112, p = 0.2212, respectively), MAP (ß=-18.84, p = 0.8841; ß=0.0002, p = 0.7654, respectively) and both brain cortex surficial area and brain cortex thickness. CONCLUSION: Our MR study provides evidence supporting the hypothesis that systolic blood pressure, rather than diastolic blood pressure, PP or MAP, is associated with abnormal changes in brain cortical structure.

Association between basal metabolic rate and cardio-metabolic risk factors: Evidence from a Mendelian Randomization study.

Background: Cardio-metabolic risk factors play a crucial role in the development of cardiovascular and metabolic diseases. Basal metabolic rate (BMR) is a fundamental physiological parameter that affects energy expenditure and might contribute to variations in these risk factors. However, the exact relationship between BMR and cardio-metabolic risk factors has remained unclear. Methods: We employed Mendelian Randomization (MR) analysis to explore the association between BMR (N: 534,045) and various cardio-metabolic risk factors, including body mass index (BMI, N: 681,275), fasting glucose (N: 200,622), high-density lipoprotein (HDL) cholesterol (N = 403,943), low-density lipoprotein (LDL) cholesterol (N = 431,167), total cholesterol (N: 344,278), and triglycerides (N: 441,016), C-reactive protein (N: 436,939), waist circumference (N: 232,101), systolic blood pressure (N: 810,865), diastolic blood pressure (N: 810,865), glycated haemoglobin (N: 389,889), and N-terminal prohormone brain natriuretic peptide (N: 21,758). We leveraged genetic variants strongly associated with BMR as instrumental variables to investigate potential causal relationships, with the primary analysis using the Inverse Variance Weighted (IVW) method. Results: Our MR analysis revealed compelling evidence of a causal link between BMR and specific cardio-metabolic risk factors. Specifically, genetically determined higher BMR was associated with an increased BMI (ß = 0.7538, 95% confidence interval [CI]: 0.6418 to 0.8659, p < 0.001), lower levels of HDL cholesterol (ß = -0.3293, 95% CI: 0.4474 to -0.2111, p < 0.001), higher levels of triglycerides (ß = 0.1472, 95% CI: 0.0370 to 0.2574, p = 0.0088), waist circumference (ß = 0.4416, 95% CI: 0.2949 to 0.5883, p < 0.001), and glycated haemoglobin (ß = 0.1037, 95% CI: 0.0080 to 0.1995, p = 0.0377). However, we did not observe any significant association between BMR and fasting glucose, LDL cholesterol, total cholesterol, C-reactive protein, systolic blood pressure, diastolic blood pressure, or N-terminal prohormone brain natriuretic peptide (all p-values>0.05). Conclusion: This MR study provides valuable insights into the relationship between BMR and cardio-metabolic risk factors. Understanding the causal links between BMR and these factors could have important implications for the development of targeted interventions and therapies.