Atherosclerosis最新文献

Background and aims: It remains uncertain whether pericoronary adipose tissue attenuation (PCATa) is associated with clinical outcome in patients with nonobstructive coronary artery disease (CAD). We aim to investigate the incremental prognostic value of PCATa beyond clinical and coronary computed tomographic angiography (CCTA) features in patients with nonobstructive CAD.

Methods: Consecutive patients with chest pain suspected of CAD referred for CCTA from January 2017 to December 2018 were prospectively included. Multivariable Cox proportional hazard regression analysis was employed to identify the predictive factors for major adverse cardiovascular events (MACE), while the receiver operating characteristics (ROC) curve was utilized to assess the discriminatory capacity of PCATa. Kaplan-Meier curves were ultilized to visually represent event-free survival and were compared using Log-rank tests among groups stratified by high-risk plaque (HRP) and PCATa.

Results: Of the 1614 patients (mean age 59.0 years, 55.6 % male) with nonobstructive CAD, 68 (4.2 %) suffered MACE during a median follow-up of 28.6 months. After multivariable adjustment, PCATa was identified as an independent predictor (HR: 1.060, 95%CI: 1.025-1.096, p = 0.001). The inclusion of PCATa significantly enhanced the discrimination capacity [AUC:0.72 (0.66-0.78), p = 0.041] and risk reclassification (NRI = 1.99, p < 0.001; IDI = 0.93, p < 0.001) beyond the influence of clinical and CCTA factors. In the presence of HRP, a higher PCATa was found to be associated with a relatively higher risk of MACE compared to a lower PCATa (HR: 2.45, 95%CI: 1.09-5.52, p = 0.031).

Conclusions: PCATa is positively correlated with adverse outcome in patients with nonobstructive CAD, and it offers incremental predictive value beyond clinical variables and CCTA characteristics.

Background and aims: Knowledge about the association between oral microbiome diversity within individuals and cardiovascular disease (CVD) and non-CVD mortality is scarce. Besides, variation by sex and racial and ethnic groups, and the potential mediators of these associations remain unclear. We aimed to investigate the associations of oral microbiome alpha diversity with all-cause, CVD, and non-CVD mortality, and the interaction effects of sex and racial and ethnic groups and potential mediators in the associations.

Methods: The National Health and Nutrition Examination Survey (NHANES) is a population-based observational study, conducted periodically in Mexican American, Other Hispanic, Non-Hispanic (NH) White, NH Black, and other racial/ethnic participants. We linked 2009-12 survey data of 8199 adults to the mortality data until 2019. By analyzing RNA gene sequences from oral rinse samples, microbiome alpha diversity within individuals was assessed using operational taxonomic unit (OTU) richness. Potential mediators included obesity, diabetes mellitus, dyslipidemia, hypertension, and periodontitis. Multivariable Cox proportional hazards regression and causal mediation analysis were used.

Results: Baseline mean ± standard deviation (SD) age was 42.1 ± 15.1 years. Over a median follow-up of 9.1 years, 405 all-cause mortality occurred (CVD, 105; non-CVD, 300). Each 1-SD increment in OTU richness was inversely associated with all-cause mortality (hazard ratio [HR] 0.92, 95 % confidence interval [CI] 0.90-0.95), CVD mortality (HR, 0.92; 95 % CI, 0.90-0.95), and non-CVD mortality (HR, 0.92; 95 % CI, 0.90-0.95). With evidence of significant racial and ethnic groups-interaction (p <0.05), these associations were evident in Mexican American, NH White, and others racial/ethnic participants. None of the potential mediators significantly mediated the associations of OTU richness with all-cause, CVD, and non-CVD mortality.

Conclusions: Lower oral microbiome alpha diversity is associated with higher risk for all-cause, CVD, and non-CVD mortality, and the associations are varied by racial and ethnic groups.

MicroRNAs (miRNAs) are short non-coding RNAs, that regulate gene-expression at post-transcriptional level. Unlike other RNA species, blood miRNAs circulate in a highly stable form, either within extracellular vesicles or bound to proteins. In recent years, circulatory miRNA profiles have been proposed as potential biomarkers for multitude of pathologies, including essential hypertension. However, the evidence of miRNA biomarker potential is limited, mainly due to the scarcity of profiling studies associating miRNA levels with hypertension. Furthermore, most of these studies have been performed with preselected miRNA pool, limiting their discovery potential. Here, we summarize the results of the unbiased profiling studies and additionally discuss findings from targeted miRNA analysis. Only miR-30e has been found to be associated with hypertension in more than one unbiased study. The targeted analyses highlight the association of miR-1, -21, -34a, -92a, -122, -126, -143, -145, -605, -623, -1299, as well as let-7 and miR-30 families with hypertension. Current literature indicates that some of these miRNAs are involved in hypertension-associated vascular dysfunction and the development of atherosclerosis, suggesting a novel mechanism for cardiovascular disease risk posed by hypertension. All in all, studies associating hypertension with circulatory miRNA profiles are scarce, with several limitations affecting the comparability of the studies. This review discusses the functions and potential mechanisms linking the identified miRNAs to hypertension and underscores the need for further research.

Background and aims: The interaction between full-spectrum chronic kidney disease (CKD) and atrial fibrillation (AF) on ischemic stroke and all-cause mortality risk, particularly in stage 4 and 5 CKD, remains undetermined.

Methods: This matched cohort study identified incident AF patients using the International Classification of Disease codes and electrocardiograms from the Clinical Research Data Repository of China Medical University Hospital between 2003 and 2020. For each AF patient, we selected four controls without AF and matched them by age, sex, eGFR within 10 mL/min/1.73 m², end-stage kidney disease (ESKD) vintage, and diagnosis year. Multivariable Cox proportional hazard models were utilized to assess the interaction between AF and CKD on three-year ischemic stroke and all-cause mortality outcomes.

Results: Within a total of 10,155 patients and 39,439 controls, incidence rates were 3.03 % and 1.48 % for ischemic stroke and 15.6 % and 9.53 % for overall mortality, respectively. In AF, the stroke risk was the highest among patients with stage 4 and 5-ND (non-dialysis) CKD with adjusted hazard ratio (aHR) of 3.31 (95 % CI, 2.46-4.45) and 2.73 (1.88-3.96), respectively. The mortality risk difference varied between 45% and 177 % with the highest difference noted in ESKD (aHR 3.36 [95 % CI, 2.84-3.98] in AF vs. 1.59 [95 % CI, 1.28-1.96] in non-AF; interaction p < 0.001). Anticoagulation therapy significantly lowered the mortality risk among patients with AF and advanced CKD (3-way interaction p < 0.001).

Conclusions: The risk of ischemic stroke and overall mortality was particularly high among patients with concurrent AF and stage 4 and 5-ND CKD, underscoring the urgent evidence to optimize prognosis.

Background: Remnant cholesterol (RC), defined as non-HDL-non-LDL cholesterol, has attracted recent scientific interest as a candidate lipid factor for residual cardiovascular risk. Despite a rising amount of epidemiologic information, there are imprecisions because most available data arise from non-fasting, frozen and calculated values.

Methods: We enrolled 1474 consecutive patients with angiographically proven CAD, and measured RC in strictly fasting, non-frozen samples with a direct assay for LDL-C. Prospectively, all-cause mortality, cardiovascular mortality, and major adverse cardiovascular events (MACE) were recorded over a mean follow-up period of 11.6 ± 5.0 years, covering 17098 patient years.

Results: During follow-up, CAD patients had a rate of all-cause mortality of 52.2 % (n = 769), of cardiovascular mortality of 20.6 % (n = 303), and an incidence of major adverse cardiovascular events (MACE) of 39.1 % (n = 576). Prospectively, RC was associated with all-cause mortality (HR 1.12 [1.03-1.23], p = 0.009), cardiovascular mortality (HR 1.20 [1.06-1.36], p = 0.005), and MACE (HR 1.10 [1.01-1.21], p = 0.033) in Cox regression analyses across various levels of adjustment (age, sex, smoking, LDL-C, HDL-C, hypertension, T2DM, and BMI). Findings did not differ between women and men. Furthermore, there was no discernible influence of statin treatment.

Conclusions: From our data we conclude that RC is associated with future all-cause mortality, cardiovascular mortality and MACE in patients with established coronary artery disease. Proper pre-analytic and analytic methods provided, RC represents a reliable indicator of residual risk.