Cardiology Research and Practice最新文献

Background: Alkaline phosphatase to albumin ratio (APAR) is an emerging prognostic indicator for sepsis, cancer, and coronary artery disease. However, the predictive value of APAR in patients with atrial fibrillation (AF) has not been investigated yet. Therefore, this study aims to explore the association between APAR and the risk of mortality in critically ill patients with AF.

Methods: The data of AF patients were extracted from the Medical Information Mart for Intensive Care-IV (MIMIC-IV) database. Patients with AF were divided into three groups according to the APAR tertiles. Study outcomes were defined as 28-day and 365-day all-cause mortality. The Kaplan-Meier analysis was conducted to compare the survival rates between groups. Cox proportional hazards regression and restricted cubic spline (RCS) were used to investigate the association between APAR and all-cause mortality. Receiver operating characteristic (ROC) curve analysis was utilized to evaluate the predictive value of APAR for study outcomes.

Results: A total of 1105 critically ill patients with AF were enrolled in the study. The Kaplan-Meier analysis demonstrated that patients with the highest APAR had the lowest survival rate. The Cox regression analysis indicated that the highest APAR tertile was significantly associated with 28-day (HR, 1.64 [95% CI 1.20-2.25]; p=0.002) and 365-day (HR, 1.87 [95% CI 1.47-2.39]; p < 0.001) all-cause mortality. Nonlinear relationships between APAR and 28-day and 365-day all-cause mortality were illustrated based on the RCS curves. The areas under the ROC curves for predicting 28-day and 365-day all-cause mortality were 0.617 and 0.642, respectively.

Conclusions: Our research suggested that APAR was a simple biomarker for the prognosis in patients with AF.

Background: This study explored the potential role of FT3 in predicting long-term heart failure (HF) in patients with acute myocardial infarction (AMI), so as to provide relevant information about the Chinese population.

Methods: This was an observational, retrospective, single-center study of consecutive patients with AMI enrolled at the Affiliated Hospital of Yangzhou University. The patients were divided into the HF group or the non-HF group according to the occurrence of HF after AMI. Cox proportional hazards regression models identified factors independently associated with long-term HF. The patients were segregated into two groups by the median level of FT3 (4.63 pmol/L): the Group 1 (< 4.63 pmol/L) and the Group 2 (> 4.63 pmol/L), and the Kaplan-Meier survival analysis was used to estimate the HF-free survival between the two groups. The receiver operating characteristic (ROC) curves were used to evaluate the predictive performance of FT3 on long-term HF among patients with AMI.

Results: A total of 269 AMI patients were included. Multivariable Cox regression analysis indicated that age (p < 0.001), FT3 (p=0.030), and LVEF (p < 0.001) were independent prognostic factors for long-term HF after AMI. The Kaplan-Meier survival analysis revealed a significantly lower HF-free survival rate in patients with lower FT3 levels (p < 0.01). The ROC analysis revealed that FT3 exhibited good predictive performance for long-term HF after AMI, with an AUC of 0.736 (p < 0.01).

Conclusions: Lower levels of FT3, even within the normal range, not only serve as independent risk factors for long-term HF after AMI but also predict a higher incidence of it.

Background: Determining the normal ranges of the aortic dimension is essential in various populations. In this study, we aim to define the normal ranges for the sinus of Valsalva (SoV), the sinotubular junction (STJ), and the ascending aorta (AA) diameters using the Imam Khomeini Hospital Complex (IKHC) data registry of Iranian adults.

Methods: This study was conducted on 2269 adult participants with left ventricular ejection fraction (LVEF) of more than 50%. Echocardiographic measurements were taken at the SoV, STJ, and AA levels. Subjects with any valvular stenosis and more than moderate insufficiency were excluded.

Results: The normal range of SoV was found to be 24.5-38.9 mm in males and 21.7-34.9 mm in females. Additionally, the STJ diameters ranged from 19.7 to 32.5 mm and 18.0 to 29.6 mm in males and females, respectively. The AA measurements showed significant differences between sexes, ranging from 23.74 to 38.02 mm in males and 21.45 to 36.53 mm in females. Results also indicated that for every 10-year increase in age, the diameters of SoV, STJ, and AA increased by approximately 1.0, 0.8, and 1.6 mm, respectively.

Conclusion: This study provided detailed echocardiographic reference values for aortic dimensions in the Iranian population and compared them across various age groups, genders, and body mass index (BMI) categories. Also, the findings emphasize the impact of aging on aortic values. The limited external validity of our single-center, hospital-based study suggests that future multicenter research is necessary to confirm our findings and improve their generalizability.

Purpose: Mitochondrial biogenesis is an important factor affecting the development of acute myocardial infarction. MAP/MARK4, a member of the MAP serine/threonine kinase (MARK) family, is involved in a variety of physiological processes. The aim of this study was to investigate the role of microtubule affinity-regulating kinase 4 (MARK4) in regulating mitochondrial biogenesis in rats with myocardial infarction.

Methods: One week after the left anterior descending, coronary artery was ligated to establish a myocardial infarction model, and MARK4 expression was knocked down in mice. In the fifth week, changes in cardiac function and structure, the myocardial BNP and ATP content, mitochondrial ultrastructure, and the mitochondrial membrane potential and reactive oxygen species levels were observed and detected, and the levels of AMPKα and mitochondrial biogenesis- and apoptosis-related proteins were detected using western blot analysis.

Results: We found that downregulating the expression of MARK4 in rats with myocardial infarction improved cardiac function, alleviated cardiac pathological injury and restored damaged mitochondrial membrane potential, effectively inhibited myocardial apoptosis and restored the myocardial energy supply, and promoted mitochondrial biosynthesis by increasing AMPKα phosphorylation. However, the addition of an AMPKα inhibitor after MARK4 knockdown did not affect mitochondrial biosynthesis in cardiomyocytes, indicating that the inhibition of MARK4 expression may be a promising therapeutic target for myocardial infarction.

Conclusion: Inhibition of MARK4 expression in rats with myocardial infarction plays a cardioprotective role and promotes mitochondrial biogenesis by promoting AMPKα phosphorylation.

Background: Sudden death in young athletes is a serious concern, and appropriate, noninvasive, and easily implementable screening of at-risk individuals is imperative.

Objectives: This study aimed to identify potential risk factors associated with sudden cardiac arrest (SCA) in collegiate athletes.

Methods: In this cross-sectional observational study, we conducted an online survey of college student athletes who were part of Japanese university sports organizations associated with the Japanese Collegiate Athletic Association (UNIVAS) between June 2022 and October 2022. The questionnaire collected information on prior cardiac arrest and personal and family medical history.

Results: A total of 10,861 athletes (median age: 19.9 years; female: 37.2%) answered the questionnaire. Six athletes (three males and three females) reported a history of cardiac arrest. Of the six patients, two had a history of arrhythmia and four had a history of syncope. Arrhythmia and syncope were significantly more common in athletes with SCA (p < 0.01). Similarly, a family history of heart failure, arrhythmia, or syncope was significantly more common in patients with SCA (p < 0.01), and a history of previous syncope significantly increased the odds ratio for the occurrence of SCA (odds ratio: 41.98; 95% confidence interval: 5.99-293.83, p < 0.01).

Conclusions: A history of syncope significantly increases the risk of SCA in young athletes. Further research is needed to stratify the risks for SCA and create standardized protocols.

Background: The mechanism of estrogen-mediated myocardial protection remains incompletely understood. Our previous studies have shown that estrogen replacement therapy can modulate the expression of NLRP3 and alleviate inflammation in ovariectomized mice, while NLRP3 has been implicated in mediating cell pyroptosis. This study aimed to investigate the potential protective effects of 17β-estrogen (E2) on myocardial ischemia/reperfusion (I/R) injury by inhibiting NLRP3 inflammasome-mediated pyroptosis.

Methods and results: Using an ovariectomy (OVX) mouse model of myocardial I/R, our findings revealed that E2 replacement therapy led to a significant reduction in infarct size and pyroptosis levels, accompanied by a decrease in the expressions of key pyroptosis-related proteins including TXNIP, NLRP3, cleaved Caspase-1, ASC, IL-1β, and GSDMD. In vitro experiments with H/R cardiomyocytes further supported these observations, as E2 treatment improved cell viability and reduced pyroptosis-related protein levels. Conversely, coadministration of the estrogen receptor antagonist ICI 182780 reversed the protective effects of E2. Additionally, treatment with the NLRP3 inhibitor Bay11-7082 and the Caspase-1 inhibitor AC-YVAD-CMK also attenuated pyroptosis.

Conclusions: Collectively, these results suggest that estrogen may alleviate myocardial I/R injury by inhibiting pyroptosis through the ER/TXNIP/NLRP3/Caspase-1 pathway, offering insights into potential therapeutic strategies for cardiac ischemic injury.

Background: Recent studies have identified an association between the fibrinogen-to-albumin ratio (FAR) and the prognosis of coronary heart disease; however, evidence regarding its significance in heart failure patients remains limited. This study aims to examine the relationship between the FAR and short-term mortality among individuals with heart failure. Methods: In this retrospective cohort study, we conducted an analysis of clinical data from patients with heart failure who were hospitalized at Zigong Fourth People's Hospital from December 2016 to June 2019. The primary exposure variable was the FAR, while the outcomes of interest were mortality rates at 28 days and 3 months. Multivariate logistic regression evaluated FAR's independent association with short-term mortality, with predictive accuracy assessed via ROC curves and subgroup consistency through stratified analyses. Furthermore, smooth curve fitting was utilized to investigate the linear relationship, and a series of sensitivity analyses were conducted to validate the robustness of the findings. Results: The analysis included 1880 participants, of whom 58.1% were females and 54.1% were aged 60-80 years. Our study showed that a one standard deviation rise in the FAR was linked to a 45% increase in 28-day mortality (OR = 1.45, 95% CI = 1.02-2.06, p=0.04) after adjusting for potential confounding factors. The 28-day mortality rate was markedly elevated in the high FAR group (FAR > 0.126) compared to the low FAR group (OR = 4.01, 95% CI = 1.17-13.82, p=0.028). Comparable findings were noted at the 3-month mark. There were no significant interactions found in the subgroup analysis. A linear association was identified between FAR and short-term mortality. The optimal FAR cutoff value for predicting 28-day mortality was 0.156 (sensitivity 68.0%, specificity 59.4%, AUC = 0.654), while for 3-month mortality, it was 0.156 (sensitivity 68.0%, specificity 58.3%, AUC = 0.647). Sensitivity analyses corroborated the robustness of our findings. Conclusion: A positive correlation exists between the FAR and short-term mortality among Chinese patients with heart failure. These findings underscore the necessity for further investigation into the underlying pathophysiological mechanisms and potential therapeutic interventions associated with FAR in the context of heart failure.

Background: Congestive heart failure (CHF) requires continuous monitoring, especially during exacerbation phases. Pulse oximetry, commonly used for critical patient surveillance, has shown diagnostic potential in acute heart failure. In this exploratory pilot study, we investigated oxygen saturation (SpO₂) data and respiratory sounds from CHF patients to uncover their relationship and to assess the potential of respiratory sound intensity in telehealth or self-monitoring systems, with a view toward future predictive applications. Methods: The relationship between SpO₂ and acoustic intensity was explored by collecting physiological and acoustic data, including infrasound, from 25 CHF patients using an electronic pickup device. These patients had been enrolled in a larger clinical trial that aimed to explore disease exacerbation across various chronic diseases. Four patients experienced exacerbation phases (SpO₂ < 92%), and for each phase, we computed Pearson correlations in two frequency ranges (audible, audible + infrasound). Eight prespecified correlations were assessed, with unadjusted and adjusted p values (Bonferroni, FDR) and effect sizes reported. Results: Significant negative correlations between specific acoustic frequency ranges and SpO₂ variations were found in several patients. In all four patients, inclusion of the infrasound range increased the correlation magnitude compared to the audible range alone, with lower p values in all cases. Adjusted analyses retained significance in Patients 2 and 4 across both frequency ranges. Conclusion: This pilot work identifies consistent moderate-to-strong negative correlations between acoustic intensity and SpO₂ during CHF exacerbations. While not confirmatory, these results support the potential of acoustic intensity as a candidate indicator for early detection, warranting validation in larger studies and predictive modeling frameworks. Trial Registration: EUDAMED Clinical Investigation (CIV) Identification: CIV-NO-21-10-037926.

Background: Bioresorbable coronary stents (BRS) were designed with the aim of reducing the risk of late adverse events of permanent drug-eluting stents (DES) by dissolving once vessel patency had been restored and the requirement for acute mechanical support resolved. Bioresorbable poly-L-lactic acid (PLLA) scaffold designs, while initially appearing as promising technology, were unsuccessful in widespread clinical use due to an observed high rate of late stent thrombosis. Magnesium-based BRS (MgBRS) have provided an alternative to this original design and have shown promise in early-phase clinical trials. This review aims to address the clinical question: How does the current safety and efficacy evidence for MgBRS in all patients requiring percutaneous coronary intervention compare with the randomised data assessing PLLA-BRS and contemporary DES? Methods: Two parallel systematic reviews were performed using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, utilising MEDLINE, EMBASE and Web of Science: the first assessing clinical outcomes of all observational and randomised MgBRS trials, the second assessing clinical outcomes of PLLA-BRS versus DES in randomised clinical trials. The primary safety and efficacy outcomes collected were cardiac death, target vessel failure (TVF) and stent thrombosis. Results: A total of 3582 MgBRS patients (24 trials), 6370 PLLA-BRS and 5413 DES patients (16 trials) were included for analysis. Cardiac death was similar across all three stent designs in all time intervals. MgBRS performed similarly to contemporary DES and superiorly to PLLA-BRS at 12- and 24-month intervals with regard to TVF and stent thrombosis. Longer follow-up was suggestive of a poorer performance of MgBRS relative to DES, although with limited patient numbers. Conclusion: MgBRS appear to perform similarly to DES and superiorly to PLLA-BRS at 12 and 24 months in regard to key clinical safety and efficacy measures. Further randomised studies are required before recommending this technology for widespread clinical use over DES.

Objective: This study investigates the reparative effect of electroacupuncture on myocardial fibrosis (MF) in mice and explores its impact on intestinal flora and metabolism profile. This examines an investigation into the biological mechanisms underlying electroacupuncture's efficacy in treating MF in mice. Methods: Twenty-four male Kunming mice (27-34 g) were randomized into three groups: normal control (NC, n = 8), MF model (MF, n = 8), and electroacupuncture treatment (EA, n = 8). MF and EA groups received daily subcutaneous ISO injections (25 mg/kg) at the nape for 5 days; NC mice received saline. The EA group underwent 14 days of EA at PC6 (Neiguan). Cardiac function, intestinal flora, and metabolites were assessed post-treatment. Results: EA significantly reduced cardiac weight index (CWI), collagen volume fraction (CVF), and serum procollagen III N-terminal propeptide (PIIINP) and improved left ventricular ejection fraction (LVEF) and shortening fraction (LVFS) (p < 0.05). Gut microbiota analysis revealed distinct composition shifts: EA restored Bacteroidota abundance and lowered Firmicutes/Bacteroidota ratios, resembling NC profiles. Notably, differential bacteria (e.g., Staphylococcus lentus, Xylanophilum) correlated with PIIINP, CVF, and cardiac function. Metabolomics identified reduced TMAO, phenylalanine, acetone, and lactic acid in EA vs. MF (p < 0.05). Negative correlations included Stricto-1 vs. phenylalanine and Rodentium vs. acetone. Conclusion: EA ameliorates ISO-induced MF in mice by modulating gut microbiota structure and metabolic profiles, suggesting a microbiota-metabolite axis mediates its therapeutic effects.