Inflammation plays a pivotal in the occurrence and development of coronary heart disease (CHD). We aim to investigate the association between the Dietary Inflammatory Index (DII) and CHD in the present study. In this cross-sectional study, adult participants from the National Health and Nutrition Examination Survey (NHANES) (1999–2018) were enrolled. The social demographic information, lifestyle factors, blood biochemical measurements, dietary information, and CHD status of all the participants were systematically collected. Multivariable logistic regression was adopted to investigate the association between the risk of CHD and the DII. Besides, restricted cubic spline (RCS) analysis was used to explore whether there was a nonlinear association of the DII and CHD. Subgroup analysis stratified by sex, age, race/ethnicity, and BMI was conducted to evaluate the association of the DII and CHD among different populations. A total of 45,306 adults from NHANES (1999–2018) were included. Compared with individuals without CHD, the DIIs of the participants with CHD were significantly elevated. A positive association was observed between the DII and CHD in multivariable logistic analysis after adjusting for age, sex, race/ethnicity, education levels, smoking, drinking, diabetes, hypertension, and body mass index (BMI). Results of RCS analysis suggested a nonlinear relationship between the DII and CHD. In addition, the increment of the DII had a greater impact on female individuals compared with male individuals. The DII is closely associated with the risk of CHD. For better prevention and treatment of CHD, more attention should be paid to controlling dietary inflammation.

Choline is an essential nutrient for human body, but dietary choline is metabolized into the hazard metabolite for the cardiovascular system. Because of the conflicting results between dietary choline intake and cardiovascular disease (CVD) risk in previous studies, we aimed to investigate this in US adults. Non-pregnant participants and those aged >20 years from National Health and Nutrition Examination Survey 2011–2016, with CVD assessment and reliable dietary recall status, were included. The dietary choline intake was assessed as a mean value of two total dietary choline intakes, including dietary choline intake and supplemental choline intake, in 24-h dietary recall interviews. The association between dietary choline intake and the presence of CVD was examined using logistic regression. We enrolled 14,323 participants. The participants without CVD had substantially higher dietary choline intakes (318.4 mg/d vs. 297.2 mg/d) compared to those with CVD (p < 0.05). After multivariable adjustments, the highest quartile of dietary choline intake was associated with a lower CVD risk, OR 0.693, 95%CI [0.520, 0.923], when compared to the lowest quartile. Consistent results were also found for stroke. Subgroup analyses also supported these, especially in participants aged ≥60 years and in those with BMI < 30 kg/m². We found that a higher dietary choline intake was associated with a lower CVD risk, especially the risk of stroke. Further clinical trials are needed in order to confirm this finding and to provide dietary suggestions for the appropriate amount of choline intake.

Aims: Diabetic cardiomyopathy (DCM) is an ill-defined entity. This study aims to explore the clinical characteristics and prognosis of diabetic patients that disparately develop heart failure (HF) with preserved ejection fraction (HFpEF) other than HF with reduced ejection fraction (HFrEF). Patients and Methods: A total of 911 patients diagnosed with diabetes mellitus were identified in the ChiHFpEF cohort (NCT05278026). DCM was defined as diabetic patients diagnosed with HF, absent from flow obstructive coronary artery disease (CAD), uncontrolled refractory hypertension and hemodynamics significant heart valvular diseases, arrhythmia and congenital heart diseases. The primary endpoint was a composite of all-cause death and rehospitalization due to HF. Results: As compared to DCM-HFrEF patients, DCM-HFpEF patients had a longer duration of diabetes, were older and more noticeable in hypertension and non-obstructive CAD. After a median follow-up of 45.5 months, survival analysis showed that DCM-HFpEF patients had a better composite endpoint. Cox regression implicated that non-obstructive CAD was a negative (HR 0.101, 95% CI 0.028–0.373, p = 0.001) predictor for the composite endpoint of DCM-HFrEF patients. Age was a positive predictor for the composite endpoint of DCM-HFpEF patients (HR 1.044, 95% CI 1.007–1.082, p = 0.018). Conclusion: DCM-HFpEF is a disparate entity from DCM-HFrEF. Additional phenomic studies are needed to explore the molecular mechanisms and develop targeted therapies.

Background: Atherosclerosis preferentially develops at arterial regions exposed to low shear stress (LSS), highlighting the critical role of local hemodynamic forces in disease initiation and progression. Emerging evidence indicates that endothelial lipid metabolism is a key determinant of vascular homeostasis; however, whether LSS directly regulates endothelial lipid droplets’ (LDs) dynamics remains unclear. In particular, the mechano-transduction pathways linking shear stress to lysosome-mediated lipid processing within the endothelium have yet to be defined. Methods: Complementary in vitro flow systems and in vivo atheroprone models were employed to examine the effects of LSS on endothelial lipid metabolism. Endothelial LDs accumulation, lysosome-dependent lipophagy, and atherosclerotic lesion development were systematically assessed under LSS conditions. Mechanistically, molecular profiling and rapamycin-mediated functional rescue were conducted to delineate the role of the KLF4/TFEB/ATP1A1 signaling axis in LSS-induced impairment of lysosome-dependent lipophagy. Results: We found that LSS induced pathological accumulation of LDs in vascular endothelial cells, accompanied by a marked suppression of lysosome-dependent lipophagy. Elucidation of the mechanism showed that LSS downregulated the shear-responsive transcription factor KLF4, resulting in aberrant phosphorylation of transcription factor EB (TFEB) and impaired TFEB nuclear translocation. Consequently, the TFEB transcriptional program governing lysosomal function was disrupted, including reduced expression of the TFEB target ATP1A1, leading to defective lysosomal acidification and blockade of lipid autophagic flux. Restoration of the KLF4/TFEB/ATP1A1 axis reactivated lipophagy, alleviated endothelial lipid burden, and significantly attenuated atherosclerotic lesion development. Conclusions: Our findings demonstrate that disruption of the KLF4/TFEB/ATP1A1 signaling pathway mediates LSS-induced impairment of endothelial lipophagy, thereby driving pathological LDs accumulation. This highlights the potential of restoring this axis as a therapeutic strategy to attenuate atherosclerotic progression.