American journal of cardiovascular disease最新文献

Objectives: To develop and evaluate deep learning models for predicting heart disease using the University of California, Irvine (UCI) heart disease dataset, and to contextualize model performance against classical machine learning approaches.

Method: Data were extracted from the University of California Irvine (UCI) heart disease dataset, including information from Cleveland, Hungary, Switzerland, and Long Beach V, collected in 1988. The dataset comprises 1,025 patients and 14 key attributes. Deep learning models were used to analyze the data and predict heart disease risk.

Results: The deep learning models demonstrated high accuracy in predicting heart disease risk. The Random Forest model achieved an accuracy of 99%. Significant predictors included exercise-induced angina and downsloping ST segments. The data revealed that 72% of females and 42% of males experienced heart attacks. There was a 79% chance that atypical angina and a 77% chance that non-anginal pain would lead to a heart attack. Exercise-induced angina had a 67% chance of resulting in a heart attack, while downsloping of the peak exercise ST segment had a 72% chance. Additionally, a 71% chance was observed for heart attacks in patients with no major coronary artery blockage (ca=0), and a 75% chance for those with a potentially reversible thalassemia-related defect (thal=2). Age groups 40-44 and 50-54 had a 76% and 61% risk of heart attacks, respectively.

Conclusion: Deep learning models can significantly enhance heart disease risk prediction, leading to improved treatment strategies. These findings can aid in early diagnosis and timely interventions, improving clinical outcomes for heart disease patients.

Cardiovascular diseases (CVDs) remain one of the leading causes of death worldwide. Although the well-known risk factors include hypertension, hyperglycemia, dyslipidemia and obesity, the latest studies implicate involvement of pathological mechanisms at the molecular level. Various cellular processes, including oxidative stress, inflammatory response, mitochondrial dysfunction, and ferroptosis, are regarded as contributors to the initiation and progression of CVDs. Ubiquitination, a post-translational modification essential for the maintenance of protein homeostasis, influences the pathogenesis of CVD through regulating protein degradation, signal transduction and cellular functionality. The enzymes E1, E2 and several E3 ligases (e.g., TRAF6, TRIM21, TRIM35) participate in autophagy, inflammation and cardiac remodelling, while deubiquitinating enzymes (DUBs) (e.g., USP25, OTUB1) modulate cardiac function by stabilizing calcium pumps or regulating key signalling molecules. For example, ubiquitination of TRPC3 Ca²⁺ channels prevents them from functioning closely with phospholipase C; excessive accumulation of TRPC3 lowers cardiac contractility. On the other hand, new protein degradation technologies like Proteolysis-Targeting Chimera (PROTAC) are promising for precise selective down-regulation of disease-related proteins. This study will systematically summarize the molecular mechanisms of ubiquitination in CVDs and its potential therapeutics to provide theoretical support for mechanistic research and the development of new targeted drugs.

Objectives: Heart transplantation remains the last resort for patients with end-stage heart failure. The clinical and hemodynamic profiles of these patients may differ depending on the underlying etiology of cardiomyopathy. This study aimed to evaluate pre-transplant hemodynamic characteristics in patients with ischemic versus non-ischemic cardiomyopathy.

Methods: We conducted a retrospective analysis of 170 adult patients who underwent orthotopic heart transplantation at a single center. Patients were categorized based on the etiology of heart failure as either ischemic or non-ischemic cardiomyopathy. Preoperative hemodynamic and echocardiographic parameters were compared between the groups.

Results: Of the 170 patients, 45.2% had ischemic cardiomyopathy. These patients were significantly older than those with non-ischemic cardiomyopathy (53.2 vs. 46.7 years, P<0.01). However, no significant differences were observed between the two groups in pulmonary capillary wedge pressure (17.9 ± 8.0 vs. 17.4 ± 9.5 mmHg), mean pulmonary artery pressure (29.4 ± 10.9 vs. 27.3 ± 12.6 mmHg), or left ventricular ejection fraction (21.4 ± 10.8% vs. 23.3 ± 12.5%).

Conclusion: While ischemic cardiomyopathy patients were older, their preoperative hemodynamic and echocardiographic profiles were closely similar to those with non-ischemic cardiomyopathy.

Cardiovascular diseases (CVDs) remain the leading cause of death worldwide, and efficient drug delivery (DD) is critical for treatment success. The use of external electric (EF) and magnetic fields (MF) offers a promising approach to enhance targeted drug transport in vascular systems. This study investigates the effect of combined electric and magnetic fields (EMF) on blood flow and drug delivery (DD) in a cardiovascular tube model. The governing equations for momentum, energy, and concentration were formulated using magneto-hydrodynamics (MHD) theory with slip boundary conditions and external electromagnetic forces (EEF). Similarity transformations reduced the equations to ordinary differential form (ODEs), which were solved numerically using MATLAB code. Increasing magnetic field strength reduced flow resistance while improving drug penetration, whereas the electric field (EF) enhanced solute dispersion via electro-osmotic effects (EOE). The combined effect significantly improved concentration profiles along the tube. Conclusion: The findings suggest that external electromagnetic fields (EEF) can optimize drug delivery (DD) efficiency, providing a theoretical framework for advanced cardiovascular therapies.

Type 2 diabetes mellitus predisposes patients to abnormally increased atherosclerotic cardiovascular disease risk and deteriorated lower extremity functional status. Objective: To evaluate the effect of combined application of moderate to high intensity interval training and low frequency pulsed electromagnetic therapy on atherosclerotic cardiovascular disease risk and lower extremity function in older adults with type 2 diabetes mellitus. Fifty-four patients (age 45-60 years) with type 2 diabetes mellitus were randomly allocated into four groups: group A underwent moderate to high intensity interval training plus low frequency pulsed electromagnetic therapy for 8 weeks (n=13), group B received low frequency pulsed electromagnetic therapy (n=14), group C underwent moderate to high intensity interval training (n=13), and group D were the controls (n=14). The 10-year atherosclerotic cardiovascular disease risk was evaluated using the Atherosclerotic Cardiovascular Disease Risk Estimator Plus tool, while lower extremity function was assessed using the Short Physical Performance Battery. Statistical comparisons were conducted within and between groups using SPSS 20. A P-value <0.05 was considered statistically significant. After 8 weeks, the atherosclerotic cardiovascular disease risk significantly decreased by -10.91% (P<0.001) and -6.66% (P<0.001) in groups A and C, respectively, non-significantly decreased by -0.16% (P=0.43) in group B, and non-significantly increased by 1.35% (P=0.24) in group D. The lower extremity function significantly increased by 64.62% (P<0.001), 27.48% (P=0.001), and 48.49% (P<0.001) in groups A, B, and C, respectively. There was a non-significant increase of 0.5% (P=0.73) in group D. In conclusion, the combined application of moderate-to-high-intensity interval training and low-frequency pulsed electromagnetic therapy programmes was effective in improving atherosclerotic cardiovascular disease risk and lower extremity function in older adults with type 2 diabetes mellitus. Furthermore, the moderate-to-high-intensity interval training programme is more effective than low-frequency pulsed electromagnetic therapy in improving atherosclerotic cardiovascular disease risk and lower extremity function in patients with type 2 diabetes mellitus.

This is letter to the editor: we point to a statistical error in a recent article published in the journal by Movahed MR, Soltani Moghadam A. A normal and particularly small (<35 mm) left atrial size measured during echocardiography suggests low likelihood of moderate or severe left ventricular systolic dysfunction, which may have resulted in a biased conclusion.

Each year, cardiovascular diseases (CVDs) claim millions of lives worldwide, making them one of the biggest causes of deaths globally. More often than not, the inflammatory response is the principal disease mechanism behind the onset and development of CVDs. The study seeks to elucidate the mechanistic role of pyroptosis in CVDs and to summarize the current progress of potential therapeutic strategies targeting pyroptotic pathways. Pyroptosis is a form of PCD, which is inflammatory and mediated through an inflammasome and gasdermin complex. In the past few years, it has emerged as a crucial mechanism possibly explaining protracted inflammation and tissue damage. There is evidence suggesting that pyroptosis contributes to multiple CVDs. Indeed, it may induce disruption of endothelial barrier and plaque instability in atherosclerosis (AS). Also, it may aggravate ischemia-reperfusion injury (IRI) and reduce repair processes in case of myocardial infarction (MI). Finally, it may drive ventricular remodeling and functional impairment in heart failure (HF). Cell death and immune activation are further aggravated by a vicious cycle between pyroptosis and inflammation. Recent studies indicate that therapeutic interventions focused on key molecules, including the NLRP3 inflammasome, caspase-1, and gasdermin D (GSDMD), along with combination therapies consisting of antioxidants and inflammation inhibitors, exhibit significant cardioprotective effects. Additionally, one's diet, exercise and other lifestyle choices impact pyroptotic pathways and influence the risk of CVD. We should include pyroptosis as a form of cell death in future research only. Further, it would be necessary to identify reliable biomarkers for all of these forms of cell death for their therapeutic mechanisms.

Objectives: Permanent pacemakers are widely used to manage symptomatic bradyarrhythmias and conduction disorders; however, their impact on hospitalization outcomes, such as length of stay, in patients with acute decompensated diastolic heart failure remains unclear. This study aimed to assess whether prior pacemaker implantation independently affects hospital length of stay using data from the 2018-2019 National Inpatient Sample database.

Methods: A total of 14,523 adult patients hospitalized with acute diastolic heart failure were identified, including 855 with a history of pacemaker implantation. Propensity score matching was conducted to adjust for baseline differences, and competing risks regression was performed to account for the competing risk of in-hospital mortality.

Results: Before matching, pacemaker recipients were older and had a higher burden of comorbidities; unadjusted analysis showed a modest but statistically significant association with shorter length of stay (sHR = 1.075; 95% CI: 1.010-1.144; P = 0.023). After matching, this association was attenuated and no longer significant (sHR = 1.081; 95% CI: 0.992-1.178; P = 0.077). Comorbid conditions, particularly chronic kidney disease, liver disease, and pulmonary hypertension, were stronger predictors of prolonged hospitalization.

Conclusions: These findings suggest that pacemaker status alone does not independently affect the length of stay in patients hospitalized with acute diastolic heart failure, highlighting the importance of managing comorbidities to potentially reduce hospital length of stay in this vulnerable population, although further studies are warranted to confirm these observations.

Ferroptosis is a novel form of programmed cell death characterized by iron-dependent lipid peroxidation (LPO). It has been widely demonstrated in the last years to play a crucial pathogenic role in ischemia-reperfusion injury (IRI). The pathological basis for ferroptosis is established through disturbances in energy metabolism, iron homeostasis and mitochondrial injury during ischemic phase. During the following period of reperfusion, the surge in reactive oxygen species (ROS), along with the liberation of inflammatory mediators, and the aggravation of LPO, will further stimulate peroxidase 4 (GPX4) inactivation and augment iron load in the cells, which will greatly intensify bodily tissue injury. Ferroptosis, which operates through intricate cross-regulation with oxidative stress, immune-inflammatory responses, and autophagy, forms a multi-tiered positive feedback loop that actively contributes to injury-repair imbalance IRI pathogenesis across various organs, including the heart, brain, liver and kidney. Studies show that tissue damage and recovery can be improved by targeting system Xc^-, GPX4, ACSL4, TfR1, and NCOA4 in the body. This review summarizes the mechanisms, organ-specific manifestations, and current therapeutic strategies of ferroptosis in IRI. It is helpful for the theoretical foundation and potential direction of clinical targeted therapy.

Objectives: The cardiac sodium channel Nav1.5, encoded by the SCN5A gene, is crucial for the generation and propagation of cardiac action potential. While SCN5A mutations have been linked to familial atrial fibrillation (AF), the functional impact of certain mutations remains unclear. This study aims to identify new SCN5A mutation associated with AF and investigate the mechanism of the mutation dysregulation of SCN5A channel function underlying AF.

Methods: We identified a three-generation African American family with a history of familial AF. Functional characterization of an SCN5A mutation was performed using whole-cell patch-clamp recordings in HEK cells expressing the recombinant mutant channels.

Results: The proband, along with his mother and maternal grandmother, all presented with early-onset symptomatic paroxysmal AF, which co-segregated with the SCN5A-N470K mutation. The N470K mutation exhibited different electrophysiological properties when compared to the wild-type channel. Functional evaluation of the SCN5A-N470K variant revealed an increased peak sodium current, a hyperpolarizing shift in the voltage-dependence of steady-state activation, and a depolarizing shift in voltage-dependent inactivation. Additionally, N470K mutation did not produce significantly larger persistent current.

Conclusion: The SCN5A-N470K mutation represents a gain-of-function alteration characterized by increased peak sodium current, and enhanced window current defined by the overlap of voltage-dependent inactivation and activation curves. These changes may alter myocardial excitability or conduction, providing a plausible mechanism by which the SCN5A-N470K mutation increases susceptibility to AF in this African American family.