Current Cardiology Reviews最新文献

Left ventricular remodeling (LVR) refers to the changes in the size, shape, and function of the left ventricle, influenced by mechanical, neurohormonal, and genetic factors. These changes are directly linked to an increased risk of major adverse cardiac events (MACEs). Various parameters are used to assess cardiac geometry across different imaging modalities, with echocardiography being the most commonly employed technique for measuring left ventricular (LV) geometry. However, many echocardiographic evaluations of geometric changes primarily rely on two-dimensional (2D) methods, which overlook the true three-dimensional (3D) characteristics of the LV. While cardiac magnetic resonance (CMR) imaging is considered the gold standard for assessing LV volume, it has limitations, including accessibility issues, challenges in patients with cardiac devices, and longer examination times compared to standard echocardiography. In nuclear medicine, LV geometry can be analyzed using the shape index (SI) and eccentricity index (EI), which measure the sphericity and elongation of the left ventricle. Myocardial perfusion imaging (MPI) using SPECT or PET is inherently a 3D technique, making it particularly effective for accurately and consistently assessing LV size and shape parameters. In this context, LV metrics such as EI and SI can significantly enhance the range of quantitative assessments available through nuclear cardiology techniques, with particular value in identifying early LV remodeling in specific patient groups. This article explores the diagnostic significance of left ventricular geometric indices through various diagnostic methods, highlighting the important role of nuclear cardiology.

Leptin, a hormone produced by fat cells, is crucial for regulating energy equilibrium, managing body mass, and influencing metabolic and cardiovascular well-being. Leptin decreases appetite, boosts energy usage, and has a significant impact on glucose metabolism by primarily activating the JAK2/STAT3 signaling pathway in the hypothalamus. Obesity leads to the development of leptin resistance, which is marked by high levels of leptin in the bloodstream and a decreased responsiveness to its signals. This leads to increased food consumption, weight gain, and metabolic issues, such as type 2 diabetes (T2DM) and cardiovascular disease (CVD). This study explores the many roles of leptin in metabolic regulation, with a specific emphasis on its interaction with insulin and its impact on peripheral organs like the pancreas, liver, and muscles. Leptin resistance worsens chronic inflammation, oxidative stress, endothelial dysfunction, and insulin resistance, all of which are strongly linked to the development of cardiovascular disease (CVD). Moreover, there is a correlation between genetic variations in the leptin receptor (LEPR) gene and a higher susceptibility to stroke and other cardiovascular issues. Therapeutic interventions, such as leptin replacement therapy, have demonstrated potential in the treatment of congenital leptin insufficiency and lipodystrophy while also enhancing glycaemic control, lipid profiles, and neuroendocrine function. Recent studies have indicated that manipulating leptin levels or enhancing its responsiveness by specific treatments, such as chemical chaperones and inhibitors of negative regulators like SOCS3 and PTP1B, might potentially restore the efficacy of leptin.

Background: At a critical juncture in the ongoing fight against cardiovascular disease (CVD), healthcare professionals are striving for more informed and expedited decisionmaking. Artificial Intelligence (AI) promises to be a guiding light in this endeavor. The diagnosis of coronary artery disease has now become non-invasive and convenient, while wearable devices excel at promptly detecting life-threatening arrhythmias and treatments for heart failure.

Objective: This study aimed to highlight the applications of AI in cardiology with a particular focus on arrhythmias and its potential impact on healthcare for all through careful implementation and constant research efforts.

Methods: An extensive search strategy was implemented. The search was conducted in renowned electronic medical databases, including Medline, PubMed, Cochrane Library, and Google Scholar. Artificial Intelligence, cardiovascular diseases, arrhythmias, machine learning, and convolutional neural networks in cardiology were used as keywords for the search strategy.

Results: A total of 6876 records were retrieved from different electronic databases. Duplicates (N = 1356) were removed, resulting in 5520 records for screening. Based on predefined inclusion and exclusion criteria, 4683 articles were excluded. Following the full-text screening of the remaining 837 articles, a further 637 were excluded. Ultimately, 200 studies were included in this review.

Conclusion: AI represents not just a development but a cutting-edge force propelling the next evolution of cardiology. With its capacity to make precise predictions, facilitate non-invasive diagnosis, and personalize therapies, AI holds the potential to save lives and enhance healthcare quality on a global scale.

Pharmacogenomics has transformed the way we approach the treatment of the most common diseases worldwide, especially cardiovascular. In this article, we highlight the main categories of drugs involved in major cardiovascular diseases (CVD), related genetic variability and their effects on metabolism in each case of contrastive operability. This not only explains disparities in treatment outcomes but also unfolds customised management based on genomic studies to improve efficiency and limit side effects. Genetic variations have been identified that impact the efficacy, safety, and adverse effects of drugs commonly used in the treatment of CVDs, such as Angiotensin converting Enzyme Inhibitor (ACEI), Angiotensin Receptor Blocker (ARBs), calcium channel blockers, antiplatelet agents, diuretics, statins, beta-blockers, and anticoagulants. It discusses the impact of genetic polymorphisms on drug metabolism, efficacy, and adverse reactions, highlighting the importance of genetic testing in optimizing treatment outcomes. Pharmacogenomics holds immense potential for revolutionizing the management of CVDs by enabling personalized medicine approaches tailored to individual genetic profiles. However, challenges such as clinical implementation, cost-effectiveness, and ethical considerations need to be addressed to completely incorporate pharmacogenomic testing into standard clinical practice. Continued research and clinical diligence are required for the utilization of pharmacogenomics to improve therapeutic outcomes and reduce the burden of CVD globally.

Introduction: Chronic ischemic heart failure is a major global health issue despite advancements in therapy. Stem cell (SC) therapy has emerged as a potential treatment, but its effectiveness remains uncertain. This study aimed to systematically review and meta-analyze the current evidence on SC therapy's efficacy.

Methods: We conducted a comprehensive literature search in PubMed, Embase, and Cochrane databases up to April 2024. We included randomized controlled trials (RCTs) with blinded designs, focusing on patients with heart failure with reduced ejection fraction (HFrEF) treated with mesenchymal stem cells compared to placebo or sham interventions via percutaneous endomyocardial catheter systems. Data extraction, performed independently by two authors, focused on safety and efficacy variables. The meta-analysis used a random-effects model, with sensitivity analyses to address study heterogeneity.

Results: Twenty studies were included in the meta-analysis. Significant improvements were observed in the stem cell group for left ventricular end-systolic volume (LVESV) (pooled effect size -7.59, 95% CI [-12.28 to -2.89], P=0.002) and stress SPECT outcomes (pooled effect size - 5.33, 95% CI [-6.73 to -3.93], P<0.00001). Sensitivity analysis reduced heterogeneity in left ventricular end-diastolic function (LVEDF) (P=0.01, I²=54%) and revealed a significant benefit for stem cell therapy (pooled effect size -3.87, 95% CI [-6.77 to -0.97], P=0.009). No significant effects were observed for left ventricular ejection fraction (LVEF) or myocardial oxygen consumption (MVO2). Functional improvements in New York Heart Association (NYHA) classification were noted (OR=4.22, 95% CI [1.14-15.68], P=0.03), though no significant differences were found in safety outcomes, including major cardiovascular events, mortality, or rehospitalization rates.

Conclusion: Transendocardial SC therapy shows promise in improving certain cardiac parameters, though its impact on LVEF and MVO2 remains inconclusive, indicating the need for further research.

Objective: The usage of doxorubicin (DOX), an antineoplastic drug that is frequently used for the cure of cancer, is restricted to maximal doses due to its cardiac toxicity. Reactive oxygen species produced by DOX result in lipid peroxidation and organ failure, ultimately resulting in cardiomyopathy. Due to its high polyphenol content, virgin rice bran oil (VRBO) is a diet nutritional supplement with a strong antioxidant. This study aimed to assess the potential defense of VRBO against DOX-induced cardiotoxicity.

Methods: VRBO and DOX injections were administered to thirty male Wistar rats for 42 days after being randomly assigned to five groups.

Results: The study demonstrated the cardioprotective effects of VRBO against doxorubicin (DOX)-induced cardiotoxicity. VRBO (0.71 and 1.42 ml/kg) significantly improved the heart-tobody weight ratio, reduced elevated serum CK-MB and LDH levels by 18.4% and 52.7%, respectively, and increased HDL by 43.1%. ECG parameters also improved, with reductions in QT interval (19%), ST interval (28%), and QRS complex (15%). VRBO enhanced systolic blood pressure (up to 21%) and heart rate (7.1%). Antioxidant markers showed notable recovery, with MDA levels reduced by 66.1%, while GSH, SOD, and catalase levels increased by 129.4%, 158.2%, and 84.8%, respectively.

Conclusion: A cardioprotective benefit was found at middle and higher VRBO dosages. In order to demonstrate the effectiveness of VRBO as a cardioprotective medication, further research on dosage response and bioavailability is required.

Cardiovascular diseases remain a significant reason for illness and death globally. Although certain interleukins have been extensively researched about cardiovascular disease (CVD), new findings have identified unique members of the interleukin family that could potentially play a role in cardiovascular well-being and ailments. This review discusses the current understanding of the role of these recently identified interleukins, such as IL-27, IL-31, IL-32, IL-33, and the IL-28 group (IL-28A, IL-28B, IL-29), in the development of cardiovascular diseases. Every interleukin has various impacts achieved through particular receptors and signaling pathways that affect inflammatory processes, differentiation of immune cells, and the functioning of blood vessels. IL-27 controls the development of inflammatory Th17 cells and might decrease inflammation in atherosclerosis. IL-31 plays a role in the interaction between the immune system and nerves, as well as in itching. IL-32 enhances the generation of inflammatory proteins and has been linked to coronary artery disease. IL-33 has beneficial effects on the cardiovascular system, whereas its imitation receptor sST2 could potentially be used as a biomarker. Additional studies are needed to investigate the antiviral and immune-system regulating effects of the IL-28 group in cardiovascular diseases. In general, explaining the ways in which new interleukins contribute to the progression of cardiovascular diseases can help discover fresh targets for therapy and new approaches toward enhancing the prevention and treatment of heart disorders. Additional research on the way these cytokines engage with established disease pathways is necessary.

Background: Dyspnea and exertional intolerance are the most common clinical manifestations of Heart Failure (HF). One of the possible mechanisms of both symptoms in HF patients is weakness of the inspiratory muscles.

Aim: Because the diaphragm is the main inspiratory muscle, this review aimed to investigate the contribution of diaphragmatic function to the genesis of dyspnea or exercise intolerance in HF patients.

Methods: Original articles, clinical trials, and cohort or case-control studies published between January 2003 and March 2023 were included. The population, variables, and outcome strategy were the basis of this review, including studies that assessed HF patients, diaphragmatic function, and dyspnea or exercise tolerance. The PubMed/MEDLINE, Embase, and BVS/LILACS databases were searched.

Results: A total of 353 articles were identified from electronic databases. After removing duplicate articles and screening based on titles, abstracts, and full texts, nine articles were included in the qualitative synthesis of this review. These studies were quite heterogeneous in their methodologies; however, most, except two, demonstrated an association among diaphragmatic dysfunction, dyspnea, and exertional intolerance in HF patients.

Conclusion: Although few studies have assessed the contribution of diaphragmatic function to dyspnea and exertional intolerance in HF individuals, the vast majority of articles included in this review found such an association, especially when diaphragmatic function was assessed using ultrasound.

Background: Supraventricular tachycardia (SVT) is very common in daily clinical practice, especially in the emergency department, with rapid onset and urgent management. The review highlights the recent genetic predispositions and mechanisms in SVT.

Methods: Through analysis of epidemiology, familial clustering, and gene mutations of the relevant literature，the review elucidates the genetic properties and potential pathophysiology of SVT.

Results: There are many pathophysiological mechanisms related to atrioventricular node reentrant tachycardia (AVNRT) and atrioventricular reentrant tachycardia (AVRT). Currently, there is relatively little research on inappropriate sinus tachycardia (IST), atrial tachycardia (AT), and congenital junctional ectopic tachycardia (CJET). It seems that every type of SVT has gene mutations in ion channels, with three types of SVT having gene mutations in signaling pathways, and others including gene mutations in beta-adrenergic-receptor autoantibodies, autonomic nervous system, and AV node structure.

Conclusion: SVT has certain genetic characteristics and is often associated with other heart diseases. From the analysis of mutated genes in SVT, it appears to be a type of cardiac ion channel disease. Unlike common ion channel diseases, it is more insidious and more susceptible to external factors. The confirmation of the genetic basis of SVT provides direction for future hazard stratification assessment and gene targeted therapy drug research.