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Cardiovascular disease (CVD) remains one of the primary causes of morbidity and mortality worldwide. Classic cardiovascular risk factors, such as hypertension, diabetes mellitus (DM), hyperlipidemia, and smoking, have been well identified and given increased attention in clinical practice. However, the incidence and prevalence of CVD remains high, especially in developing countries. Therefore, there has been more attention to non-traditional CVD risk factors such as gut microbiota, sleep disorders, dietary structure, and psychosocial factors in their important roles in the development of CVD. In this review we summarize the association of non-traditional risk factors with CVD with the aim of further reducing the risk of CVD.

Background The gut microbiota provides health benefits in humans by producing short-chain fatty acids (SCFAs), whose deficiency causes multiple disorders and inflammatory diseases. However, gut bacteria producing SCFAs in patients with atrial fibrillation (AF), an arrhythmia with increasing prevalence, have not been reported. To investigate major gut microbial organisms related to SCFA synthesis, SCFAs-associated KEGG orthologues (KOs), enzymatic genes, and potential producers were examined according to metagenomic data-mining in a northern Chinese cohort comprising 50 non-AF control and 50 AF patients. Results Compared with non-AF controls, individuals with AF had marked differences in microbial genes involved in SCFA-related synthesis, including 125 KOs and 5 SCFAs-related enzymatic genes. Furthermore, there were 10 species that harbored SCFA-synthesis related enzymatic genes, and were markedly decreased in the gut of AF patients. Notably, discriminative features about SCFA-synthesis related function, including 8 KOs (K01752, K01738, K00175, K03737, K01006, K01653, K01647 and K15023), 4 genes ( menI , tesB , yciA and CO dehydrogenase acetyl-CoA synthase complex ) and 2 species ( Coprococcus catus and Firmicutes bacterium CAG:103 ), were selected as key factors based on LASSO analysis. Furthermore, PLS-SEM analysis showed that 72.8 and 91.14 % of the overall effects on gut microbiota diversity and key species on AF, respectively, were mediated by the key KOs. Meanwhile, 46.31 % of the total effects of SCFA-synthesis related function on left atrial enlargement was mediated by hsCRP. Upon incorporation of clinical properties in AF, the KO score was still significantly associated with AF incidence (OR = 0.004, P = 0.001). Conclusions The current study revealed that dysbiotic gut microbiota in AF is coupled with disrupted SCFA-synthesis related genes, characterized by decreased abundances of KEGG orthologues, synthesis enzymatic genes and harboring species.

Atrial fibrillation has been identified to be associated with disordered gut microbiota. Notably, atrial fibrillation is a progressive disease and could be categorized as paroxysmal and persistent based on the duration of the episodes. The persistent atrial fibrillation patients are accompanied by higher risk of stroke and lower success rate of rhythm control. However, the microbial signatures of different categories of atrial fibrillation patients remain unknown. We sought to determine whether disordered gut microbiota occurs in the self-terminating PAF or intestinal flora develops dynamically during atrial fibrillation progression. We found that different types of atrial fibrillation show a limited degree of gut microbiota shift. Gut microbiota dysbiosis has already occurred in mild stages of atrial fibrillation, which might act as an early modulator of disease, and therefore may be regarded as a potential target to postpone atrial fibrillation progression. Dysbiotic gut microbiota (GM) and disordered metabolic patterns are known to be involved in the clinical expression of atrial fibrillation (AF). However, little evidence has been reported in characterizing the specific changes in fecal microbiota in paroxysmal AF (PAF) and persistent AF (psAF). To provide a comprehensive understanding of GM dysbiosis in AF types, we assessed the GM signatures of 30 PAF patients, 20 psAF patients, and 50 non-AF controls based on metagenomic and metabolomic analyses. Compared with control subjects, similar changes of GM were identified in PAF and psAF patients, with elevated microbial diversity and similar alteration in the microbiota composition. PAF and psAF patients shared the majority of differential taxa compared with non-AF controls. Moreover, the similarity was also illuminated in microbial function and associated metabolic alterations. Additionally, minor disparity was observed in PAF compared with psAF. Several distinctive taxa between PAF and psAF were correlated with certain metabolites and atrial diameter, which might play a role in the pathogenesis of atrial remodeling. Our findings characterized the presence of many common features in GM shared by PAF and psAF, which occurred at the self-terminating PAF. Preventative and therapeutic measures targeting GM for early intervention to postpone the progression of AF are highly warranted. IMPORTANCE Atrial fibrillation has been identified to be associated with disordered gut microbiota. Notably, atrial fibrillation is a progressive disease and could be categorized as paroxysmal and persistent based on the duration of the episodes. The persistent atrial fibrillation patients are accompanied by higher risk of stroke and lower success rate of rhythm control. However, the microbial signatures of different categories of atrial fibrillation patients remain unknown. We sought to determine whether disordered gut microbiota occurs in the self-terminating PAF or intestinal flora develops dynamically during atrial fibrillation progression. We found that different types of atrial fibrillation show a limited degree of gut microbiota shift. Gut microbiota dysbiosis has already occurred in mild stages of atrial fibrillation, which might act as an early modulator of disease, and therefore may be regarded as a potential target to postpone atrial fibrillation progression.

Background Periodontitis is a periodontal inflammatory disease closely related to hypertension. However, the role of age and systemic inflammation is unclear. This study examined the effect of age and systemic inflammation on the association between severity of periodontitis and blood pressure in periodontitis patients. Methods This cross-sectional clinical study included periodontitis patients treated at Beijing Chaoyang Hospital, Capital Medical University from January 2020 to July 2023. Patients with periodontitis were included using inclusion and exclusion criteria, and data on basic information, blood pressure, periodontal examination indicators, and biochemical examination indicators were collected. Patients were grouped by blood pressure, and differences in basic information, blood indexes, and periodontal examination indexes between the two groups were compared by independent sample T-test. With PBOP as independent variables, systolic blood pressure (SBP) and diastolic blood pressure as dependent variables, and several indexes as covariables, the relationship between them was studied by linear regression. The interaction was used to explore the relationship between age and systemic inflammation in periodontitis and hypertension. Results A total of 144 patients with periodontitis were enrolled. In fully adjusted analyses, the percentage of site with bleeding on probing (PBOP) was significantly associated with SBP (B = 10.08, p  = 0.027) in the overall group. In patients 50 years or older, but not in those younger than 50, PBOP remained significantly associated with SBP ( p  = 0.018 for interaction). The strength of association between PBOP and SBP was greater in patients with higher systemic immune-inflammation index. The regression coefficients of PBOP in the systemic immune-inflammation index ≥ 400 and < 400 groups were 16.61 (95% CI, 3.32–29.90; p  = 0.015) and 13.69 (95% CI, 1.15–26.23; p  = 0.033), respectively ( p  = 0.047 for interaction). Similar results were observed in the systemic inflammation response index ≥ 9 and < 9 groups (B = 17.04 (95% CI, 2.66–31.42, p  = 0.021) and 13.98 (95% CI, 1.94–26.01, p  = 0.024 respectively; p  = 0.028 for interaction). Conclusions This study indicates a significant association between the severity of periodontitis and SBP, which was modified by age and systemic inflammation.

Background: Studies on the association between body mass index (BMI) and death risk among patients with hypertension are limited, and the results are inconsistent. We investigated the association between BMI and cardiovascular disease (CVD) and all-cause mortality among hypertensive patients in a population of Beijing, China. Methods: We conducted a prospective cohort study of 2535 patients with hypertension aged 40 to 91 years from Beijing, China. Participants with a history of CVD at baseline were excluded from analysis. Cox proportional hazards regression models were used to estimate the association of different levels of BMI stratification with CVD and all-cause mortality. Results: During a mean follow-up of 8.1 years, 486 deaths were identified, including 233 cases of CVD death. The multivariable-adjusted hazards ratios for all-cause mortality associated with BMI levels (<20, 20-22, 22-24, 24-26 [reference group], 26-28, 28-30, and ≥30 kg/m2) were 2.03 (95% confidence interval [CI], 1.48-2.78), 1.61 (95% CI, 1.18-2.20), 1.30 (95% CI, 0.95-1.78), 1.00 (reference), 1.12 (95% CI, 0.77-1.64), 1.33 (95% CI, 0.90-1.95), and 1.66 (95% CI, 1.10-2.49), respectively. When stratified by age, sex, or smoking status, the U-shaped association was still present in each subgroup (P > 0.05 for all interactions). Regarding the association of BMI with CVD mortality, a U-shaped trend was also observed. Conclusions: The present study showed a U-shaped association of BMI with CVD and all-cause mortality among patients with hypertension. A lowest risk of all-cause mortality was found among hypertensive patients with BMI between 24 and 26 kg/m2.

Aims: To establish a nomogram-scoring model for evaluating the risk of death in patients with critical cardiovascular disease after continuous renal replacement therapy (CRRT) in a coronary care unit (CCU). Methods: This retrospective cohort study included data collected on 172 patients, in whom CRRT was initiated in the CCU between January 2017 and June 2021. Predictors of mortality were selected using an adaptive least absolute shrinkage and selection operator logistic model and used to construct a nomogram. The nomogram was evaluated using the concordance index (C-index) and Hosmer–Lemeshow test. Results: The number of patients who died in-hospital after CRRT was 91 (52.9%). The results of the multivariate logistic regression analyses clarified that age, history of hypertension and/or coronary artery bypass grafting, a diagnosis of unstable angina pectoris or acute myocardial infarction, ejection fraction, systolic blood pressure, creatinine, neutrophil, and platelet counts before CRRT initiation were significant predictors of early mortality in patients treated with CRRT. The nomogram constructed on these predictors demonstrated significant discriminative power with an unadjusted C-index of 0.902 (95% CI: 0.858–0.945) and a bootstrap-corrected C-index of 0.875. Visual inspection showed a good agreement between actual and predicted probabilities (Hosmer–Lemeshow χ2 = 5.032, p-value = 0.754). Conclusions: Our nomogram based on nine readily available predictors is a reliable and convenient tool for identifying critical patients undergoing CRRT at risk of mortality in the CCU.

Background The exact relationship between 25-hydroxyvitamin D [25(OH) D] levels and small vessel disease (SVD) are not clear in China. The aim of this study was to determine such the association between 25(OH) D and SVD in China. Methods We retrospectively enrolled 106 patients with SVD and 115 controls between Jan 2017 and Dec 2017. All the subjects were categorized into three subgroups according to the level of 25 (OH) D: vitamin D deficiency (< 12 ng/ml), insufficiency (12–20 ng/ml) and sufficiency (> 20 ng/ml). Results Among 106 SVD patients, 80 (75.5%) were men and the mean age was 61.6 ± 13.2 years. The deficiency of 25(OH) D was observed in 76 (71.7%) of SVD patients and 47 (40.9%) of controls ( P  = 0.001). Compared with controls, patients with SVD were more likely to be male, a stroke history, smokers, with hyperlipidemia, higher systolic and diastolic blood pressure and low-density lipoprotein, and lower of 25(OH)D level ( P  < 0.05). Logistic regression analysis revealed the level of 25 (OH) D as an independent predictor of SVD ( OR 0.772, 95% CI 0.691–0.862, P  = 0.001). Compared with the sufficient 25 (OH) D group, the ORs of SVD in deficient and insufficient 25(OH)D group were 5.609 (95% CI 2.006–15.683) and 1.077 (95% CI : 0.338–3.428) after adjusting for potential confounders, respectively. In hypertensives with vitamin D deficient and insufficient group compared with sufficient group, the ORs of SVD increased to 9.738 (95% CI 2.398–39.540) and 1.108 (95% CI 0.232–5.280), respectively ( P interaction  = 0.001). Conclusion We found significant associations between SVD and 25(OH)D deficiency. The combined presence of hypertension and vitamin D deficiency increased the probability of developing SVD. Our findings will warrant further prospective studies in the future.

Chronic kidney disease (CKD) significantly increases the rate of adverse cardiovascular events in patients with coronary artery disease. In this study, we aimed to establish a risk score (RS) model to predict in-hospital mortality risk in patients with end-stage renal disease (ESRD) and acute myocardial infarction (AMI). A total of 113 consecutive patients with ESRD and AMI were retrospectively enrolled between January 1, 2015 and December 31, 2019. All patients received regular hemodialysis and were divided into two groups according to the prognosis during hospitalization. Univariable and multivariable logistic regression analyses were used to identify the risk factors of in-hospital mortality. A RS model was developed based on multiple regression analysis and was internally validated using 1000 bootstrap analysis. The receiver operating characteristic (ROC) curve was performed, and the area under curve (AUC) was analyzed to evaluate the performance of the RS model. AUCs were compared using the Z test. Thirty-three patients died during hospitalization, resulting in in-hospital mortality rate of 29.2%. After multivariate logistic regression, an RS model (0–8) was established based on five independent factors that were assigned with different points according to relative coefficients (coefficient of the index risk factor divided by the lowest coefficient among these five risk factors; rounded to closest integer): 1 for C-reactive protein (CRP) ≥ 14.2 mg/L and left ventricular ejection fraction (LVEF) ≤ V3%; 2 for age ≥ 65 years old, heart rate (HR) at admission ≥ 86 beats per minute (bpm) and d-dimer ≥ 2.4 mg/L FEU. The present RS model had a sensitivity of 85.7%, the specificity of 84%, and an accuracy of 78.1%. In ROC curve analysis, the model demonstrated a good discriminate power in predicting in-hospital mortality (AUC = 0.895, 95% CI 0.814–0.96; P < 0.001), which was significantly better than the predictive power of the Global Registry of Acute Coronary Events risk score (GRACE RS) (AUC = 0.754, 95% CI 0.641–0.868; P < 0.001 after Z test). A novel RS model, which was established to help predict in-hospital mortality of patients with ESRD and AMI, was easy to use and had higher accuracy than the GRACE RS.

Background: Some individuals who maintain desirable low-density lipoprotein cholesterol (LDL-C) levels still experience the progression of atherosclerosis, which may eventually lead to cardiovascular events. Non-high-density lipoprotein cholesterol (non-HDL-C) levels are quantified to assess residual risk in statin-treated patients with coronary heart disease. The study aimed to estimate the predictive performance of discordance between non-HDL-C and LDL-C on clinical prognosis in statin-treated patients with previous coronary artery bypass grafting (CABG). Methods: 468 statin-treated patients with previous CABG undergoing percutaneous coronary intervention (PCI) as a secondary coronary treatment due to acute coronary syndrome (ACS) were retrospectively enrolled in this study. The definition of major adverse cardiovascular events (MACEs) was a composite endpoint of cardiovascular death, recurring myocardial infarction, and a need for repeat revascularization. Cox proportional hazards modeling, restricted cubic splines regression, and discordance analysis were conducted to the association between all lipid parameters and the occurrence of MACEs. Discordant values were defined as LDL-C concentrations ≤1.8 mmol/L accompanied by non-HDL-C >2.6 mmol/L. Results: MACEs occurred in 95 patients over a median follow-up period of 744.5 days. Cox models demonstrated that increased concentrations of non-HDL-C and LDL-C levels were independent risk indicators of MACEs (p < 0.001). The restricted cubic spline analysis revealed a linear relationship between non-HDL-C concentrations and MACEs (p-nonlinear: 0.26), whereas a nonlinear relationship was observed between LDL-C concentrations and MACEs (p < 0.01). In the subgroup analysis, the spline curves revealed that the odds of the individuals with desirable LDL-C levels suffering MACEs emerged when non-HDL-C levels were above 2.07 mmol/L. Individuals who exhibited discordance involving high non-HDL-C/low LDL-C levels had an elevated risk of experiencing MACEs compared to those with concordantly low LDL-C and low non-HDL-C levels [hazard ratios (HRs) = 2.44, 95% confidence interval (CI) = 1.14–5.22, p = 0.02]. Conclusions: Non-HDL-C levels could predict the residual risk of MACEs in ACS patients with previous CABG and statin therapy that underwent percutaneous coronary intervention. A discordance between non-HDL-C and LDL-C in individuals with desirable LDL-C levels could be useful in identifying those with a residual risk of cardiovascular complications.

Background: Elevated heart rate (HR) is associated with cardiovascular mortality and other events associated with acute myocardial infarction (AMI). The heart rate after discharge is likely superior to reflect the deteriorating heart function, which negatively responds to normal physical activity. This study aimed to explore the effect of HR at the first outpatient visit on clinical outcomes. Methods: We retrospectively identified 605 patients with AMI. HRs at admission, discharge, and first outpatient visits were measured. The primary endpoint was defined as major adverse cardiovascular events (MACEs), including cardiovascular (CV) death, readmission for worsening heart failure, recurrent nonfatal myocardial infarction (MI), repeated coronary revascularization, and ischemic stroke. Results: During the follow-up period, 145 cases of MACE occurred, including 34 CV deaths, 31 recurrent MI, 89 revascularizations, 41 heart failures, and 4 strokes. The event group displayed an elevated HR at the first outpatient visit compared to the event-free group (p < 0.001). After adjustment for confounding risk factors, Cox models showed that the outpatient HR had the best correlation with MACE [Hazard ratio (HR) = 1.33, 95% confidence interval (CI) = 10.8–59.3, p < 0.01 for increments of 1 standard deviation (SD) in the outpatient HR) and CV mortality (HR = 1.18, 95% CI = 1.052–1.325, p < 0.01) compared with the other two HRs. The restricted spline model indicated that HR at the first post-discharge above 71 bpm was associated with CV mortality. Conclusions: Elevated HR at the first outpatient visit over a period of 2–4 weeks is related to the adverse outcomes of AMI and may identify AMI patients at higher risk of CV mortality.