BackgroundThe purpose of our study was to examine the association of sex steroid hormones (serum total testosterone, sex hormone-binding globulin (SHBG), and estradiol) with abdominal aortic calcification (AAC) and severe AAC (SAAC) among American adults over the age of 40.MethodsWe used the National Health and Nutrition Examination Survey (NHANES) data from 2013 to 2014 to conduct this study. Based on male and female, the association between sex steroid hormones and risk of AAC and SAAC was examined using multivariable logistic regression analysis and restricted cubic spline (RCS) plots.ResultsOur analysis included 2564 participants. The RCS plots showed a U-shaped curve association of estradiol with AAC, and SHBG and estradiol with the risk of SAAC in individuals who were male. Additionally, there was a negative association of serum total testosterone and SHBG with AAC risk and serum total testosterone with SAAC risk in individuals who were male. The estradiol and AAC risk also were shown to U-curve relationship in participants who were female. Finally, with the increase of serum total testosterone, the risk of AAC showed a trend of first increasing and then decreasing. The serum total testosterone, SHBG, and estradiol were inversely associated with SAAC risk, while SHBG was positively associated with AAC risk.ConclusionsOur findings suggest that sex steroid hormones play a role in known sex differences in AAC and SAAC in the American adult population over the age of 40.

ABSTRACT Background and Aims Among patients with acute myocardial infarction undergoing PCI, subsequent structural alterations of the left ventricle, including left ventricular remodeling (LVR) and left ventricular hypertrophy (LVH), may contribute to later heart failure. This study examined whether GLS measured early after reperfusion could help identify patients at increased risk for these post‐infarction changes. Methods A total of 131 patients with AMI who underwent primary PCI at our hospital between March 2023 and October 2024 were included. GLS was assessed within 7 days after PCI using two‐dimensional speckle‐tracking echocardiography. The primary endpoints were LVR and LVH assessed at 6–12 months of follow‐up. We used logistic regression to estimate the associations of GLS with the endpoints, applied restricted cubic splines (RCS) to explore possible nonlinear trends, and conducted subgroup analyses to assess the robustness of the results. Results Logistic regression analyses demonstrated that impaired GLS was independently associated with a higher risk of LVR. In tertile analyses, compared with patients in T1, representing better preserved LV systolic function, those in T3, representing more impaired LV systolic function, had significantly higher risks of LVR (OR = 7.51, 95% CI: 1.41–39.96, p = 0.02) and LVH (OR = 6.15, 95% CI: 1.40–27.04, p = 0.02). RCS analysis indicated linear associations between GLS and the risks of both LVR and LVH. ROC analysis showed that the optimal GLS cut‐off values for predicting LVR and LVH were −11.54% and −11.22%, with AUCs of 0.724 and 0.774, respectively. Conclusion Early impairment of GLS in patients with AMI after PCI was associated with subsequent LVR and LVH, suggesting that GLS may be useful for early risk stratification in this population.

Background:The objective of this investigation was to examine the correlation between intake of dietary vitamin K and lipid metabolism in cardiovascular disease populations. Methods:The data for this investigation were obtained from the National Health and Nutrition Examination Survey (NHANES) 2003-2014. The exposure variable was the total daily intake of dietary vitamin K (μg). Triglycerides (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) comprised the lipid indicators. To investigate the relationship between vitamin K intake and lipid metabolism, the following analyses were conducted: weighted multiple linear regression, smoothing curve fitting, generalized additive models, threshold analysis, subgroup analysis, and sensitivity analyses. Results:Ultimately, 1,543 participants aged 18 years or older were enrolled. The total daily intake of dietary vitamin K was found to be negatively correlated with TG (β: -15.57, 95% CI: -27.806, -3.333) and TC (β: -6.564, 95% CI: -12.252, -0.877). For each 1 ug increase in the total daily intake of dietary vitamin K, the LDL-C would decrease by 0.510 mg/dl (95% CI: -0.940, -0.078) when the total daily intake of dietary vitamin K was less than 23.7 ug. HDL-C was not influenced by total daily intake of dietary vitamin K. Furthermore, subgroup analyses and sensitivity analyses revealed that an increase in the total daily intake of dietary vitamin K was still negatively associated with TG, TC, and LDL. Conclusion:The consumption of foods with high vitamin K levels might contribute to the improvement of TC, TG, and LDL-C levels in CVD populations.

Type 2 diabetes (T2D) presents a growing global health burden, with early identification of high-risk individuals remaining a critical challenge. The modified cardiometabolic index (MCMI), which integrates visceral fat, lipid ratios, and glucose measures, has emerged as a promising alternative, offering a more comprehensive assessment of metabolic risk. However, no large-scale cohort study has directly assessed the long-term predictive performance of the MCMI for incident T2D, particularly in normoglycemic populations. This study investigates the 12-year predictive performance of the MCMI for incident T2D and compares its efficacy with that of the triglyceride-glucose (TyG) index. In this longitudinal cohort study, 15,453 adults with normal baseline glucose were selected from the NAGALA study. The associations of the MCMI and the TyG index with T2D risk were examined using Cox regression models and restricted cubic spline (RCS) analysis. Predictive performance was compared through receiver operating characteristic (ROC) analysis, and subgroup analyses assessed consistency across different populations. Among participants, 373 (2.41

Abstract Background The presence of depression related to an increased risk of all-cause and cardiovascular disease (CVD) mortality has been reported. However, studies conducted on certain specific depressive symptoms are scarce. Our purpose was to assess the effect of both depressive symptoms scores and certain specific depressive symptoms on all-cause and CVD mortality. Methods In the present cohort study, all participants, aged 18 years or older, were enrolled in the National Health and Nutrition Examination Survey (NHANES) from 2005 to 2014. Depressive symptoms score was assessed using the validated 9-item Patient Health Questionnaire Depression Scale (PHQ-9), which ranges from 0 to 27, with a PHQ-9 score ≥ 10 diagnosed as depression. The outcome events were all-cause and CVD mortality, which were followed up from 2005 to 2014. The associations of both depressive symptoms score and certain specific depressive symptoms with all-cause and CVD mortality were examined by weighted multivariable proportional hazards models. Results A total of 26,028 participants aged ≥ 18 years were included in the statistical analysis, including 12,813 (49.2%) males and 13,215 (50.8%) females, with a mean (SD) age of 47.34 (18.86) years. During the 9.32 (3.20) years of mean (SD) follow-up, 3261 deaths were recorded, of which 826 were cardiovascular deaths. All-cause mortality was 16.87/1000 person-years in subjects with depression. In terms of CVD mortality, these figures were 4.53/1000 person-years. In the full model (model 3), elevated depressive symptoms scores were independently associated with an increased risk of all-cause mortality (Highest depression symptom score group: adjusted hazard ratio, 1.63; 95% CI 1.44–1.85) and CVD mortality (Highest depression symptom score group: adjusted hazard ratio, 1.73; 95% CI 1.34–2.24). All 9 specific depressive symptoms that make up the PHQ-9 were related to an increased risk of all-cause mortality. However, only 3 symptoms, including trouble sleeping or sleeping too much, poor appetite or overeating, and suicidal ideation, were no significantly associated with an increased risk of CVD mortality. Conclusions The elevated depressive symptoms scores were strongly associated with an increased risk of all-cause and CVD mortality in US adults. Furthermore, all 9 specific depressive symptoms were associated with high all-cause mortality. However, trouble sleeping or sleeping too much, poor appetite or overeating, and suicidal ideation might not increase the risk of CVD mortality.

To investigate the predictive value of baseline platelet count and its short-term dynamic changes in the prognosis of patients with acute heart failure (AHF) in the intensive care unit. Patients diagnosed with AHF in the medical information mart for intensive care III and their clinical data were retrospectively filtered. Patients were divided into survivor and non-survivor groups based on their prognosis during hospitalization, and differences in baseline data between groups were compared. Logistic regression models and restricted cubic spline (RCS) plots were performed to evaluate the relationship between baseline platelet counts and in-hospital mortality. Changes and trends in platelet counts were compared between the survivor and non-survivor groups after adjusting for confounders with the generalized additive mixing model (GAMM). A total of 2930 critical patients with acute heart failure were included, of which 2720 were survivors and 210 were non-survivors. Multiple logistic regression models revealed that baseline platelet count was an independent factor in hospital mortality (OR 0.997, 95% CI 0.994–0.999, P-value = 0.018). The RCS plot demonstrated a U-shaped dose–response relationship between baseline platelet count and in-hospital mortality. GAMM analysis suggested that the platelet counts decreased and then increased in the survivor group and gradually decreased in the non-survivor group, with a gradual increase of difference between two groups. After adjusting for confounders, the mean daily increase was −6.014 (95% CI −7.076–4.953, P-value < 0.001). Baseline platelet demonstrated a U-shaped dose–response relationship with adverse outcomes in critical patients with AHF. Early elevation of platelet was correlated with higher in-hospital mortality, indicating that tracking early changes in platelet might help determine the short-term prognosis of critical patients with AHF.

The purpose of this study was to explore the use of aspirin in conjunction with various statins for cardiovascular disease (CVD) prevention in the general population of the United States (U.S.). A total of 3778 people from the National Health and Nutrition Examination Surveys from 2011 to 2018 were included in our analysis. After adjusting for sociodemographic and common cardiovascular risk factors, we used multivariable logistic regression analysis to determine aspirin should be combined with which type of statin for better CVD preventive effects. Subgroup analyses were carried out subsequently. In comparison to the aspirin use alone, the odds ratios with 95% confidence intervals for CVD were 0.43 (0.33, 0.57), 0.69 (0.42, 1.13), 0.44 (0.31, 0.62), 0.34 (0.23, 0.50) and 0.64 (0.49, 0.84) for the combination use of aspirin and atorvastatin, lovastatin, pravastatin, rosuvastatin as well as simvastatin, respectively, in the fully-adjusted model. Aspirin combined with rosuvastatin was more effective in the prevention of individual CVD, including congestive heart failure, coronary heart disease, angina pectoris and heart attack, than aspirin combined with other statins. In conclusion, statins combined with aspirin have a clear advantage over aspirin alone in preventing CVD. In addition, when various sex, age, and fitness levels were considered, as well as with and without diabetes mellitus, the combination usage of aspirin and rosuvastatin had the greatest CVD preventive effects than aspirin coupled with other statins.

BACKGROUND:Serum uric acid (SUA) has been shown to increase all-cause mortality from cardiovascular disease. However, limited studies have examined the mediating effect of dyslipidemia, hyperglycemia, or hypertension on the association between SUA and all-cause mortality in patients with congestive heart failure (CHF). METHODS:Participants in the present investigation were 620 US adults with CHF from the NHANES database (1999-2014). The relationship between SUA and all-cause mortality was evaluated utilizing multivariable Cox proportional hazards models. Additionally, the nonlinearity between SUA and mortality was investigated utilizing Restricted Cubic Splines (RCS) and 2-piecewise Cox proportional hazards models. Finally, the mediating role of cardiometabolic factors on the relationship between SUA and all-cause mortality was investigated utilizing the mediation analysis. RESULTS:During a mean follow-up of 7.6 years, 391 (63.1%) all-cause deaths occurred. Furthermore, we found a U-shaped association between SUA and all-cause mortality. The inflection point for the RCS curve was found at a SUA level of 363 umol/L. The hazard ratios (95% confidence intervals) for all-cause mortality were 0.998 (0.995-1.000) and 1.003 (1.002-1.005) to the left and right of the inflection point, respectively. This U-shaped association was also observed in both subgroups of sex and age. Moreover, the effect of SUA on all-cause mortality was not mediated by hypertension, hyperglycemia, or dyslipidemia (all P-values>0.05). CONCLUSION:The association between SUA level and all-cause mortality followed a U-shaped curve, and this association was not mediated by hypertension, hyperglycemia, or dyslipidemia.

Objective Association between neutrophil-to-lymphocyte ratio (NLR) on admission and poor prognosis in patients with acute heart failure (AHF) has been well established. However, the relationship between dynamic changes in NLR and in-hospital mortality in AHF patients has not been studied. Our purpose was to determine if an early change in NLR within the first week after AHF patients was admitted to intensive care unit (ICU) was associated with in-hospital mortality. Methods Data from the medical information mart for intensive care IV (the MIMIC-IV) database was analyzed. The effect of baseline NLR on in-hospital mortality in critical patients with AHF was evaluated utilizing smooth curve fitting and multivariable logistic regression analysis. Moreover, comparison of the dynamic change in NLR among survivors and non-survivors was performed using the generalized additive mixed model (GAMM). Results There were 1169 participants who took part in the present study, 986 of whom were in-hospital survivors and 183 of whom were in-hospital non-survivors. The smooth curve fitting revealed a positive relationship between baseline NLR and in-hospital mortality, and multivariable logistic regression analysis indicated that baseline NLR was an independent risk factor for in-hospital mortality (OR 1.04, 95% CI 1.02,1.07, P-value = 0.001). After adjusting for confounders, GAMM showed that the difference in NLR between survivors and non-survivors grew gradually during the first week after ICU admission, and the difference grew by an average of 0.51 per day (beta = 0.51, 95% CI 0.45-0.56, P-value <0.001). Conclusions Baseline NLR was associated with poor prognosis in critical patients with AHF. Early rises in NLR were linked to higher in-hospital mortality, which suggests that keeping track of how NLR early changes might help identify short-term prognosis of critical patients with AHF.

BACKGROUND:Myocardial ischemia/reperfusion (I/R) injury is common during the treatment of cardiovascular diseases. Neuronal PAS Domain Protein 2 (NPAS2) is one of the core genes that control the rhythm of the biological clock. NPAS2 also regulates the biological rhythm.RESULTS:The rat I/R model showed that the expression of NPAS2 decreased with the increase of reperfusion time. Overexpressing NPAS2 adenovirus (ad-NPAS2) was injected into IR rat which demonstrated that ad-NPAS2 ameliorated rats I/R injury. A hypoxia/reoxygenation (H/R) model in rat cardiomyocytes showed that ad-NPAS2 inhibited cardiomyocyte apoptosis. Co-Immunoprecipitation results showed that there is an interaction between NPAS2 and Cry2. Knockdown of Cry2 aggravated the cardiomyocyte apoptosis induced by H/R. Additionally, NPAS2 directly act on the promoter region of CX3CL1. Knockdown of CX3CL1 reverse the protective effect of ad-NPAS2 on rat myocardial ischemia-reperfusion injury and H/R-induced cardiomyocyte apoptosis. CX3CL1 also regulates autophagy through the downstream AKT/mTOR pathway.CONCLUSIONS:research demonstrated that overexpression of NPAS2 interacts with Cry2 and promotes the transcriptional activity of CX3CL1. Moreover, overexpression of NPAS2 regulates the downstream AKT/mTOR pathway to inhibit autophagy in order to improve rat cardiac I/R injury.

Permanent left bundle branch area pacing (LBBP) is a promising physiological pacing technique that has emerged in recent years. However, LBBP is almost exclusively clinically applied in adult patients. The feasibility and safety of the use of LBBP in children have not been well-assessed. Here, we report the case of a 6-year-old child with a third-degree atrioventricular block after surgical aortic valve replacement who successfully received a permanent LBBP.

Background Familial dilated cardiomyopathy (FDCM) is most commonly inherited as an autosomal dominant trait. TheLamin A/C(LMNA) gene variants have been identified to be associated with DCM, conductive system disorders, type 2 Emery-Dreifuss muscular dystrophy and several other disorders. Here, we reported a novel variant in theLMNAgene that might be related to FDCM. Case presentation A 30-year-old young man was hospitalized for chest tightness, extreme fatigue, palpitation and impaired activity tolerance. He had clinical characteristics including cardiac dilatation, atrial tachyarrhythmia, severe conductive system disorders, and dyskinesia of both upper limbs and the neck. Genetic sequence analysis indicated that the patient carried a novel c.1325 T>C heterozygousLMNAgene variant. Catheter ablation and cardiac resynchronization therapy with pacing function (CRT-P) were performed to treat the arrhythmia. Conclusion The variant c.1325 T>C is a novel variant in theLMNAgene that has not been previously reported. Young patients with DCM, conductive system disorders and skeletal myopathy should be alert to the possibility ofLMNAgene variant. Cardiac resynchronization therapy (CRT) may be a reasonable choice for patient carrying aLMNAgene variant with third-degree atrioventricular block even if the left ventricular ejection fraction is preserved in order to prevent the deterioration of cardiac function caused by right ventricular pacing dependency.

BACKGROUND:Syncope is a perplexing challenge that often receives thorough evaluation, yet the diagnosis remains unclear. Usually, the emergency department is the first point at which patients present with syncope. However, diverse medical factors, including low diagnostic rates and inconsistent management by doctors, add to healthcare costs and delay diagnosis for syncope patients. METHODS:Patients who had been to the emergency department at least once but were not given a clear diagnosis of syncope were recruited into our study at the time they visited syncope clinic staffed by a multidisciplinary team. Complete medical histories and clinical examinations were conducted by both experienced cardiologists and neurologists. If patients were not given a conclusive diagnosis at the syncope clinic on the basis of outpatient examinations, they were admitted for further evaluation. RESULTS:A total of 209 consecutive patients claiming "syncope" visited the syncope clinic, yet only 167 patients were formally diagnosed with syncope. For these 167 patients, the mean age was 55.93 ± 17.40 years old, and 41.3% were male. The proportions of cardiac syncope, reflex syncope, orthostatic hypotension (OH), and syncope of uncertain etiology were 19.8%, 64.1%, 7.8%, and 8.4%, respectively. The diagnostic rate was 91.6%, and the hospitalization rate was 23.4%. Patients with reflex syncope and OH were younger than patients with cardiac syncope. Cardiac syncope tends to occur more frequently in males, while reflex syncope is more likely in females. CONCLUSIONS:The cooperation of professional cardiologists and neurologists will play an important role in improving diagnostic rates, lowering admission rates, and reducing medical costs.

比伐卢定作为新型的抗凝药物,直接作用于凝血酶的活性位点从而发挥抗凝作用.然而,目前对于急性冠脉综合征(acute coronary syndrome,ACS)患者在经皮冠脉介入术(percutaneous coronary intervention,PCI)围手术期的抗凝治疗中,若与传统的药物普通肝素进行比较,比伐卢定是否具有更安全、有效的显著优势目前尚无定论.本文以比伐卢定为主要分析对象,将其药理学特性及近5年国际上的临床研究进展综述如下.

患者男性,34岁.反复发作性心悸10余年,曾于外院行2次射频消融未成功,心动过速时维拉帕米静脉注射有效.入院心电图示窄QRS波(103 ms)心动过速,不完全右束支传导阻滞图形伴电轴右偏,可见房室分离,窦性夺获;电生理标测提示室性心动过速,在左后分支和左前分支区域行激动标测均未标测到理想靶点,遂逐步将标测导管移至左上间隔部,可记录到PP电位,室性心动过速时发生逆转,在此处消融成功,后在此处起搏所记录图形与室性心动过速图形完全一致,提示可能为局灶起源的微折返室性心动过速.

患者男性,55岁,因胸闷、心悸不适10年,加重1周入我院治疗.入院时心电图示窦性心律,可见部分频率为60～75次/分,P波消失,窄的畸形QRS波(88 ms),不完全左束支传导阻滞图形,缓慢起始,缓慢终止,与窦性心律交替出现,临床诊断为加速性室性自主心律(AIVR).动态心电图(Holter)检查显示室性早搏负荷为57％,经心脏超声、心肌酶学、冠状动脉造影、同位素心肌显像等检查排除器质性及继发性因素后决定行电生理检查.EnSite NAVX三维标测系统激动标测和起搏标测均提示AIVR起源于右室后侧壁,于此处标测到理想靶点(单极电图呈QS型且领先体表QRS波42 ms),行导管射频消融获得成功.术后患者症状改善,3个月后随访Holter未再出现AIVR.

血管紧张索受体-脑啡肽酶抑制剂(ARNI)是近年来心力衰竭治疗上最重要的发现,目前国内外ARNI的使用率仍很低.本文就ARNI的研发背景、作用机制以及临床研究结果等方面作一全面阐述.

Background/Aims: Increased endoplasmic reticulum (ER) stress contributes to development of cardiorenal syndrome (CRS), and Silent Information Regulator 1 (SIRT1), a class III histone deacetylase, may have protective effects on heart and renal disease, by reducing ER stress. We aimed to determine if SIRT1 alleviates CRS through ER stress reduction. Methods: Wild type mice (n=37), mice with cardiac-specific SIRT1 knockout (n=29), or overexpression (n=29), and corresponding controls, were randomized into four groups: sham MI (myocardial infarction) +sham STNx (subtotal nephrectomy); MI+sham STNx; sham MI+STNx; and MI+STNx. To establish the CRS model, subtotal nephrectomy (5/6 nephrectomy, SNTx) and myocardial infarction (MI) (induced by ligation of the left anterior descending (LAD) coronary artery) were performed successively to establish CRS model. At week 8, the mice were sacrificed after sequential echocardiographic and hemodynamic studies, and then pathology and Western-blot analysis were performed. Results: Neither MI nor STNx alone significantly influenced the other healthy organ. However, in MI groups, STNx led to more severe cardiac structural and functional deterioration, with increased remodeling, increased BNP levels, and decreased EF, Max +dp/dt, and Max -dp/dt values than in sham MI +STNx groups. Conversely, in STNx groups, MI led to renal structural and functional deterioration, with more severe morphologic changes, augmented desmin and decreased nephrin expression, and increased BUN, SCr and UCAR levels. In MI+STNx groups, SIRT1 knockout led to more severe cardiac structural and functional deterioration, with higher Masson-staining score and BNP levels, and lower EF, FS, Max +dp/dt, and Max -dp/dt values; while SIRT1 overexpression had the opposite attenuating effects. In kidney, SIRT1 knockout resulted in greater structural and functional deterioration, as evidenced by more severe morphologic changes, higher levels of UACR, BUN and SCr, and increased desmin and TGF-β expression, while SIRT1 overexpression resulted in less severe morphologic changes and increased nephrin expression without significant influence on BUN or SCr levels. The SIRT1 knockout but not overexpression resulted in increased myocardial expression of CHOP and GRP78. Cardiac-specific SIRT1 knockout or overexpression resulted in increased or decreased renal expression of CHOP, Bax, and p53 respectively. Conclusions: Myocardial SIRT1 activation appears protective to both heart and kidney in CRS models, probably through modulation of ER stress.

Introduction The mortality due to cardiogenic shock complicating acute myocardial infarction (AMI) is high even in patients with early revascularization. Infusion of low dose recombinant human brain natriuretic peptide (rhBNP) at the time of AMI is well tolerated and could improve cardiac function. Objective The objective of this study was to evaluate the hemodynamic effects of rhBNP in AMI patients revascularized by emergency percutaneous coronary intervention (PCI) who developed cardiogenic shock. Methods A total of 48 patients with acute ST segment elevation myocardial infarction (STEMI) complicated by cardiogenic shock and whose hemodynamic status was improved following emergency PCI were enrolled. Patients were randomly assigned to rhBNP (n=25) and control (n=23) groups. In addition to standard therapy, study group individuals received rhBNP by continuous infusion at 0.005 µg kg−1 min−1 for 72 hours. Results Baseline characteristics, medications, and peak of cardiac troponin I (cTnI) were similar between both groups. rhBNP treatment resulted in consistently improved pulmonary capillary wedge pressure (PCWP) compared to the control group. Respectively, 7 and 9 patients died in experimental and control groups. No drug-related serious adverse events occurred in either group. Conclusion When added to standard care in stable patients with cardiogenic shock complicating anterior STEMI, low dose rhBNP improves PCWP and is well tolerated.