Cardiology Research and Practice最新文献

Objective: To explore the feasibility of continuous low-dose isoproterenol (ISP) in identifying atrial fibrillation (AF) triggers under conscious sedation and to investigate the association between unmappable triggers and postablation recurrence.

Methods: In 50 PAF patients (Group 1), standardized ISP infusion (2-4 μg/min) was administered to provoke triggers, followed by adenosine triphosphate (ATP) challenge (30-40 mg) if no arrhythmia was induced. A matched control cohort (n = 96, Group 2) was selected based on baseline characteristics. Pulmonary vein isolation (PVI) was performed in all patients. Those with mappable triggers underwent additional ablation based on triggers. Additional ablation for other patient was guided by operators' discretion.

Results: In Group 1, provocative testing identified mappable triggers in 35 patients (Group 1A: 34 PV triggers and 10 non-PV triggers) and unmappable triggers in 5 (Group 1B), with 10 patients showing no inducible arrhythmia (Group 1C). After 12-month follow-up, Group 1B showed significantly higher recurrence than all other groups (60.0% vs. Group 1A: 5.7%, Group 1C: 0%, and Group 2: 14.6%; p < 0.05).

Conclusions: Continuous low-dose ISP challenge provides a pragmatic approach for intraprocedural AF trigger identification, particularly under conscious sedation. The high recurrence rate in patients with unmappable triggers underscores the imperative for advanced mapping modalities to precisely localize arrhythmogenic foci origins.

Introduction: Angiogenesis is a critical adaptation to regular physical exercise, primarily driven by hypoxia-inducible factor-1 alpha (HIF-1α). However, prolonged exercise has been associated with the downregulation of HIF-1α, potentially mediated by increased expression of its negative regulators, prolyl hydroxylase domain (PHD) and factor-inhibiting HIF-1 (FIH).

Objectives: This study aimed to investigate the effects of short-term (acute) and long-term (chronic) moderate-intensity exercise on HIF-1α, PHD, and FIH mRNA expression in Wistar rat hearts.

Methods: Twenty Wistar rats (age: 8 weeks, body weight: 200-250 g) were divided into four groups: acute control (AC) (15 days) (n = 5), acute exercise (AE) (15 days) (n = 5), chronic control (CC) (8 weeks) (n = 5), and chronic exercise (CE) (8 weeks) (n = 5). The exercise groups underwent moderate-intensity treadmill exercise with 20 m/min for 30 min each day for 5 times a week. At the end of the experiment, rats were sacrificed 1 h (acute group) and 24 h (chronic group) after exercise using isoflurane anesthesia, followed by cervical dislocation. Left ventricular heart muscle samples were collected for mRNA expression analysis of HIF-1α, PHD, and FIH using real-time PCR.

Results: Exercise significantly altered the expression of HIF-1α, PHD, and FIH. HIF-1α mRNA was significantly higher in the AE group versus AC (AC vs AE, p=0.006) and in the CE group versus CC (CC vs CE, p=0.004). PHD expression likewise increased with exercise (AE vs AC, p=0.001; CE vs CC, p ≤ 0.001). In contrast, FIH showed no significant differences (acute p=0.472; chronic p=0.095). Exploratory one-way analyses confirmed overall group effects for HIF-1α (p ≤ 0.001) and PHD (p=0.016), but not for FIH (p=0.105).

Conclusion: Chronic moderate-intensity exercise upregulates the expression of HIF-1α negative regulators (PHD and FIH) in the myocardium, suggesting a shift from acute hypoxia-driven responses to oxygen-dependent regulation. These findings offer insight into the molecular adaptations of cardiac tissue to prolonged exercise and their potential role in angiogenesis regulation.

Background: Andersen-Tawil syndrome (ATS) is a rare inheritable potassium channelopathy, accompanied by ventricular arrhythmias due to long QT intervals, muscle weakness, and dysmorphic features. Next-generation sequencing can identify the genetic causes of the phenotype.

Methods: Whole-exome sequencing (WES) was performed on a 12-year-old girl with long QT syndrome and dysmorphic features. Sanger sequencing was subsequently used to confirm the variant and perform segregation analysis in the proband and all available family members.

Results: WES identified a novel homozygous likely pathogenic missense variant (chr17, c.G598A, p.V200M; hg19; NM_017755.5) in KCNJ2 in the proband. Some of her family members were heterozygous for the variant but remained asymptomatic with no cardiac manifestation.

Conclusions: We propose that patients with dysmorphic skeletal findings and cardiac arrhythmias be evaluated via NGS for possible genetic variants.

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.