Current Cardiology Reviews最新文献

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.

Platelets, tiny cell fragments measuring 2-4 μm in diameter without a nucleus, play a crucial role in blood clotting and maintaining vascular integrity. Abnormalities in platelets, whether genetic or acquired, are linked to bleeding disorders, increased risk of blood clots, and cardiovascular diseases. Advanced proteomic techniques offer profound insights into the roles of platelets in hemostasis and their involvement in processes such as inflammation, metastasis, and thrombosis. This knowledge is vital for drug development and identifying diagnostic markers for platelet activation. Platelet activation is an exceptionally rapid process characterized by various posttranslational modifications, including protein breakdown and phosphorylation. By utilizing multiomics technologies and biochemical methods, researchers can thoroughly investigate and define these posttranslational pathways. The absence of a nucleus in platelets significantly simplifies mass spectrometry-based proteomics and metabolomics, as there are fewer proteins to analyze, streamlining the identification process. Additionally, integrating multiomics approaches enables a comprehensive examination of the platelet proteome, lipidome, and metabolome, providing a holistic understanding of platelet biology. This multifaceted analysis is critical for elucidating the complex mechanisms underpinning platelet function and dysfunction. Ultimately, these insights are crucial for advancing therapeutic strategies and improving diagnostic tools for platelet-related disorders and cardiovascular diseases. The integration of multi-omics technologies is paving the way for a deeper understanding of platelet mechanisms, with significant implications for biomedical research and clinical applications.

Cardiovascular-kidney-metabolic (CKM) syndrome is the association between obesity, diabetes, CKD (chronic kidney disease), and cardiovascular disease. GDF-15 mainly acts through the GFRAL (Glial cell line-derived neurotrophic factor Family Receptor Alpha-Like) receptor. GDF-15 and GDFRAL complex act mainly through RET co-receptors, further activating Ras and phosphatidylinositol-3-kinase (PI3K)/Akt pathways through downstream signaling. GDF-15 decreases cardiac dysfunction and hypertrophy by inducing HIF-α (hypoxia-inducible factor-1α). It causes increased fractional shortening and a significant decrease in ventricular dilation through the induction of the SMAD 2/3. GDF-15 prevents hyperglycemia-induced apoptosis in diabetes mellitus. GDF-15 causes anorexia by influencing the central systems regulating metabolism and appetite. Therefore, targeting GDF-15 can be useful for the treatment of anorexia caused by cancer as well as the prevention of resulting weight loss. GDF-15 has an important role in predicting mortality in acute kidney injury. Its high levels are related to eGFR decline and also have a prognostic role in CKD patients. Growth differentiation factor-15 (GDF-15) is a vital biomarker for diagnosis, treatment, and prognosis of CKM syndrome. Elevated GDF-15 levels can be utilised as a biomarker to determine the suitable metformin dosage. In light chain amyloidosis, a raised level of GDF-15 predicts early death in heart failure and renal disease patients. In vivo, studies using GDF-15 analogs and antibodies against GFRAL to affect metabolic parameters and ventricular dilatation have shown potential for GDF-15-based therapeutic interventions. This review aims to study the role of GDF-15 in CKM syndrome and establish it as a CKM biomarker.