BMC Cardiovascular Disorders最新文献

Background: Cardiovascular disease (CVD) is a major global health concern with increasing incident cases and deaths. Homocysteine (Hcy) has been investigated for its potential association with CVD, researchers have debated the extent to which Hcy should be considered a risk factor for cardiovascular diseases, as only 50% of CVD can be explained by classical risk factors.

Methods: We conducted a prospective cohort study using NHANES 1999-2006 data, analyzing 1,739 US patients aged at least 30 with CVD. Cox proportional hazards regression and restricted cubic splines were used to examine the relationship between Hcy levels and mortality, adjusting for covariates.

Result: A total of 1,739 participants with cardiovascular disease (CVD) were enrolled, with a median follow-up period of 126 months. Among them, 1,194 participants died, including 501 deaths due to cardiovascular causes. After adjusting for covariates, the hazard ratios (HR) and 95% confidence intervals (CI) for CVD mortality at different levels of homocysteine (Hcy) (T1 (< 9.3), T2 (9.3-12.5), T3 (> 12.5)) were 1.26 (0.92, 1.73) (T2), and 1.69 (1.14, 2.51) (T3) (P for trend = 0.0086). The HR and 95% CI for all-cause mortality at different levels of Hcy were 1.22 (1.05, 1.42) (T2) and 1.64 (1.29, 2.09) (T3) (P for trend < 0.0001). Elevated Hcy levels were associated with increased risks of all-cause mortality and CVD deaths, even at levels below the conventional threshold. The nonlinear relationship was observed, with inflection points at 14.5 µmol/L for all-cause mortality and 14.6 µmol/L for CVD mortality. Subgroup analyses revealed interactions with age, serum vitamin B12, and smoking.

Conclusion: Our study supports the notion that elevated Hcy levels are associated with higher all-cause and CVD mortality risks in CVD participants. The impact of Hcy on health outcomes can be observed at lower concentrations than previously thought.

Myocardial ischemia-reperfusion (I/R) injury caused by revascularization treatment is the leading cause of cardiac damage aggravation in ischemic heart disease. Increasing evidence has unraveled the crucial role of pyroptosis in myocardial I/R injury. Of note, lactylation has been validated to be participated in modulating pyroptosis. Hence, this study was aimed to elaborate the potential and mechanism of lactylation in myocardial I/R damage. We established the cell model of I/R through inducing hypoxia/reoxygenation (H/R) of H9c2 cells. It was uncovered that H/R stimulation drove cardiomyocyte pyroptosis and upregulated total lactylation level. Further, we demonstrated that promoting lactylation contributed to H/R-evoked pyroptosis, whereas silencing LDHA led to the opposite results. More than that, LDHA was confirmed to facilitate lactylation of NLRP3 at K245 site and increase its protein stability. Our findings indicated that activation of NLRP3 abolished the function of LDHA deficiency in H/R-treated H9c2 cells. In concert with the aforementioned outcomes, knockout of LDHA attenuated the infarct size and myocardial damage in I/R mice and upregulation of NLRP3 counteracted the effects of LDHA knockout on I/R-evoked injury in vivo. To summarize, the current research provided persuasive evidence that LDHA promoted myocardial I/R damage via enhancing NLRP3 lactylation to induce cardiomyocyte pyroptosis.

Objectives: Cardiovascular disease (CVD) is the leading cause of death in China. This study compared ethnic disparities and lifestyle determinants in the prevalence of CVD (hypertension, coronary heart disease [CHD], and stroke) among older adults of the Han majority and Ha Ni ethnic minority in rural southwest China, to provide evidence for preventing and controlling CVD among older-adult minority communities.

Methods: A multi-stage stratified random sampling method was used to select 1,413 Han majority participants and 1,402 Ha Ni ethnic minority participants aged ≥ 60 years in rural Southwest China. Data on general demographic characteristics, behavioral lifestyle, and self-reported diagnostic information for patients with CHD and stroke were collected using a standardized questionnaire. The height, weight, waist circumference, and blood pressure of each participant were recorded. The relationship between lifestyle factors and CVD was analyzed using multivariate logistic regression.

Results: Han majority older adults had a higher prevalence of CHD (6.4% vs. 3.6%) and stroke (7.9% vs. 2.9%) than their Ha Ni minority counterparts (P < 0.01). Han majority participants had a markedly higher prevalence of obesity, central obesity, and physical inactivity than their Ha Ni ethnic minority counterparts (9.2%, 48.3%, and 55.1% vs. 3.4%, 19.1%, and 49.2%, respectively, P < 0.01). By contrast, Ha Ni ethnic minority participants had a higher prevalence of current drinking than Han majority participants (31.2% vs. 14.4%, P < 0.01). Among Han majority and Ha Ni ethnic minority older adults, participants with central obesity (OR = 2.09, 95% CI: 1.62-2.69 vs. OR = 2.66, 95% CI: 1.88-3.76) had a higher risk of hypertension, participants with obesity (OR = 1.99, 95% CI: 1.02-3.67 vs. OR = 3.66, 95% CI: 1.39-9.66) were more likely to suffer from CHD, and participants with physical inactivity (OR = 1.88, 95% CI: 1.18-2.98 vs. OR = 2.29, 95% CI: 1.13-4.64) had a higher probability of suffering from stroke. Furthermore, Current drinking status increased the risk of CHD (OR = 2.31, 95% CI: 1.05-5.08), but decreased the risk of stroke (OR = 0.33, 95% CI: 0.13-0.83) in Ha Ni ethnic minority participants.

Conclusion: CHD and stroke are more prevalent among the Han majority older adults in rural Southwest China, and lifestyle factors significantly influence CVD.

Background: The spontaneous echo contrast (SEC) in patients with atrial fibrillation (AF) indicates a prethrombic state that ultimately progresses into thrombus formation. A comprehensive understanding of specific plasma metabolomics characteristics may protect AF patients from thrombus, particularly in the early stage.

Objectives: Through the investigation of metabolic pathways, we endeavor to uncover the metabolomic characteristics associated with SEC states, and to examine the differential metabolites by which may exert their influence on thrombotic states.

Methods: Patients with AF were enrolled, and the participants were divided into three groups based on the results of the echocardiogram: non-SEC, low-SEC and high-SEC group. Samples were collected and subjected to non-targeted metabolomics analysis. The analytical process included data quality control, metabolite difference analysis, component analysis, Kegg cluster analysis, etc. RESULTS: Our metabolic phenotype revealed a clear differential metabolic pattern between the SEC and non-SEC. Specifically, we identified 35 and 142 significantly differential metabolites in venous and atrial plasma, respectively, suggesting that SEC may be involved in pervasive metabolic dysregulation and that the degree of metabolic dysregulation in atrial plasma is more severe than that in venous blood.

Conclusion: Patients with SEC have a significantly different metabolic pattern compared to those without SEC. Our work promoted the understanding of mechanism of the occurrence and development of SEC, facilitated the screening of the target metabolites for its therapeutic intervention, and provided evidence for the prevention and treatment of SEC or thrombosis in AF. Our work also provided new directions for subsequent research in related fields. In conclusion, our study not only provides a theoretical basis for understanding the occurrence and development of SEC in AF, but also provides recommendations for the daily diet of AF patients with SEC, such as a balanced intake of essential amino acids, avoiding excessive intake of benzoic acid, and intake of appropriate inositol.

Clinical trial number: Not applicable.

Background: The NLRP3 inflammasome, a pivotal mechanism regulating inflammatory responses and featuring the pyrin domain containing 3 (NLRP3) within the NOD-like receptor family, is widely recognized as a central pathogenic factor in cardiovascular diseases. The present study endeavors to delve into the correlation and potential interplay between the rs10754558 polymorphism of NLRP3 and the predisposition to hypertension among the Chinese adult population.

Methods: All the participants who came from a community in Bengbu, China were investigated by being interviewed with a questionnaire. Overall, 354 paired case-control participants were analyzed. Genomic DNA was extracted from 5ml venous blood using the Tiangen DNA extraction kit. The rs10754558 polymorphism of the NLRP3 gene was genotyped by TaqMan allelic discrimination real-time PCR.The association between the rs10754558 polymorphism and hypertension risk was investigated by a logistic regression analysis. Furthermore, an additive interaction analysis was conducted using related indicators, including the relative excess risk due to interaction (RERI), attributable proportion due to interaction (AP), and synergy index (SI).

Results: Participants carrying the GG genotype were more likely to develop hypertension than participants carrying the CC genotype (adjusted odds ratio [OR]: 2.16, 95% confidence interval [CI]: 1.33-3.52). A significant additive interaction between the NLRP3 polymorphism and obesity status concerning the risk of hypertension was observed, as estimated by all indicators: RERI (1.12, 95% CI: 0.70-1.5), AP (0.34, 95% CI: 0.14-0.53), and SI (1.92, 95% CI: 1.03-3.59). The values of RERI (1.74, 95% CI: 0.37-3.11), AP (0.46, 95% CI: 0.21-0.70), and SI (2.62, 95% CI: 1.18-5.83) showed that a significant interaction between the rs10754558 polymorphism and a family history of hypertension.

Conclusions: Our findings indicate a significant association between the NLRP3 rs10754558 polymorphism and the risk of hypertension in Chinese adults. Moreover, a notable additive interaction emerges between NLRP3 polymorphisms and obesity status, further amplifying the risk of hypertension.

Background: Anemia represents a commonly reported comorbidity in patients diagnosed with heart failure (HF), related with a higher risk of unfavorable outcomes such as recurrent hospitalizations and mortality. There is a lack of evidence in Latin America regarding this topic. Our aim was to evaluate the prognostic value of the diagnosis of anemia in patients from the Colombian Heart Failure Registry (RECOLFACA).

Methods: RECOLFACA registry included adult ambulatory patients with HF in 60 medical centers in Colombia during 2017-2019. Baseline characteristics of patients diagnosed with anemia and those without anemia were compared. The main outcome was all-cause mortality. A Cox proportional hazards regression model was used to evaluate the factors linked to the main outcome in patients with anemia. A statistically significant p-value was < 0.05.

Results: From the 2528 patients included in RECOLFACA, 2409 had at least one available hemoglobin value, and 726 (30.1%) corresponded to a diagnosis of anemia. Patients with anemia were significantly older, and had a higher prevalence of comorbidities, especially hypertension, type 2 diabetes, and chronic kidney disease (CKD). Patients without anemia had significantly lower mortality rate of 0.30 per 1000 person-years (95% CI 0.26-0.35), compared to patients diagnosed with anemia who had a mortality rate of 0.42 per 1000 person-years (95% CI 0.26-0.98) (p < 0.001). Lastly, the multivariate model results showed that the presence of an anemia diagnosis was associated with a significantly greater risk of mortality (HR 1.48; 95% CI 1.06, 2.05, p < 0.001).

Conclusions: Anemia represents a highly prevalent comorbidity in patients with HF in Colombia and is also related with higher mortality in ambulatory patients during follow-up period. Our results highlight the relevance of anemia in the pathophysiology of HF. Nevertheless, due to its observational nature, out study results must be validated and further explored in future studies to elucidate the potential underlying mechanisms of this association.

Isolation of adult mouse cardiomyocytes is an essential technique for advancing our understanding of cardiac physiology and pathology, and for developing therapeutic strategies to improve cardiac health. Traditionally, cardiomyocytes are isolated from adult mouse hearts using the Langendorff perfusion method in which the heart is excised, cannulated, and retrogradely perfused through the aorta. While this method is highly effective for isolating cardiomyocytes, it requires specialized equipment and technical expertise. To address the challenges of the Langendorff perfusion method, researchers have developed a Langendorff-free technique for isolating cardiomyocytes. This Langendorff-free technique involves anterograde perfusion through the coronary vasculature by clamping the aorta and intraventricular injection. This method simplifies the experimental setup by decreasing the need for specialized equipment and eliminating the need for cannulation of the heart. Here, we introduce an updated Langendorff-free method for isolating adult mice cardiomyocytes that builds on the Langendorff-free protocols developed previously. In this method, the aorta is clamped in situ, and the heart is perfused using a peristaltic pump, water bath, and an injection needle. This simplicity makes cardiomyocyte isolation more accessible for researchers who are new to cardiomyocyte isolation or are working with limited resources. In this report, we provide a step-by-step description of our optimized protocol. In addition, we present example studies of analyzing mitochondrial structural and functional characteristics in untreated isolated cardiomyocytes and cardiomyocytes treated with the acute inflammatory stimulus lipopolysaccharide (LPS).

Background: Cardiovascular diseases (CVD) are among the most prevalent and preventable chronic diseases in the 21st century The global burden of disease: 2004 update. The Report in Sections. A person's risk of developing CVD can be reduced by adopting healthy lifestyles, spiritual and religious practices The American Heart Association Life's Simple 7 in African Americans of the Jackson Heart Study. Fasting as a spiritual practice is not exempted from these benefits. Most world's religions recommend a period of fasting. The obligatory Ramadan fasting in Islam may provide an interesting opportunity to reduce food intake and increase physical activity. The main objective of this study is to investigate the effect of Ramadan fasting on cardiovascular risk factors on healthy adult Muslims.

Method: The study was pre/post-test single arm intervention conducted at the staff clinic of Family Medicine department, AKTH, and Northwest, Nigeria. Kano. The study recruited healthy adults 18yrs and above not on any medications that can affect metabolic profiles consecutively from two weeks before Ramadan fasting of 2018 and the last week of Ramadan of the same year. The questionnaire included information on sociodemographic, clinical parameters and Lifestyle pattern.

Result: Thirty healthy volunteers were included in this study, 25 males (83.3%) and 5 females (16.7%). The mean age was 38.23 ± 6.35(SD). Twenty-five participants were married (83.3%) with 4 singles (13.3%) and 1 divorcee (3.3%). During Ramadan fasting, weight reduced (67.90 ± 11.61 versus 66.53 ± 12.13 4th week of Ramadan p-value < 0.002) Body Mass Index (22.89 ± 3.63 versus 4th week of Ramadan 22.38 ± 3.64 p-value < 0.002) and systolic blood pressure (120.33 ± 19.91versus 4th week of Ramadan 115.33 ± 14.32 p-value 0.003) reduced significantly compared to baseline. The waist circumference, pulse rate, fasting blood sugar and cholesterol were reduced but were not statistically significant.

Conclusion: The result from this study suggested that Ramadan fasting may be a useful means of reducing burden of cardiovascular diseases, as the improved cardiovascular risk factors associated with fasting may translate into a significant health benefit.

Objective: To measure the plasma levels of human cartilage intermediate layer protein 1 (CILP1) in patients with diabetic cardiomyopathy (DCM), and to investigate its association with the occurrence of major adverse cardiovascular events (MACE) in DCM.

Methods: A total of 336 diabetic patients were enrolled and assigned into two groups based on the presence or absence of DCM (DCM group and N-DCM group). The baseline clinical data including glutamic-pyruvic transaminase (ALT), glutamic oxaloacetic acid transferase (AST), albumin, serum creatinine, glycosylated hemoglobin (HbA1c), C-reactive protein (CRP), and N-terminal pro brain natriuretic peptide (NT-proBNP) were recorded. Subsequently, plasma levels of CILP1 at admission were detected by the enzyme linked immunosorbent assay (ELISA) method. Echocardiographic parameters were also acquired for all patients. The association of CILP1 with LVEF, LVDD and CRP was determined. In addition, the occurrence of MACE was examined during the 12-month follow-up in the DCM group.

Results: The concentration of CILP1 in the DCM group was higher than in the N-DCM group [1329.97 (1157.14, 1494.36) ng/L vs. 789.00 (665.75, 937.06) ng/L, P < 0.05], higher in the MACE group than in the non-MACE group [1777.23 (1532.83, 2341.26)ng/L vs. 885.00 (722.40, 1224.91) ng/L, P < 0.05). Correlation analysis revealed that CILP1 expression was associated with LVEF, CRP and LVDD (r = -0.58, 0.29 and 0.44, respectively, P < 0.05). Analysis of a nomogram demonstrated that CILP1, sex, age, BMI, LVEF and LVDD could predict the occurrence of MACE in DCM patients at 12 months (P < 0.05). The plasma levels of CILP1 were independently associated with a stronger discriminating power for DCM. Furthermore, inclusion of CILP1 as a covariate in the model caused a significant improvement in risk estimation compared with traditional risk factors for DCM [BASIC: AUC: 0.556, 95%CI: 0.501-0.610; BASIC + CILP1: AUC: 0.913, 95%CI: 0.877-0.941, P < 0.05] and MACE [BASIC: AUC: 0.710, 95%CI: 0.616-0.792; BASIC + CILP1: AUC: 0.871, 95%CI: 0.794-0.928, P < 0.05].

Conclusions: The serum concentration of CILP1 was increased in DCM patients. Elevated fasting plasma CILP1 levels was a robust diagnostic marker of DCM and was independently associated with an increased risk of MACE.