Current Cardiology Reviews最新文献

Research into drugs that can enhance cardiovascular health has been sparked by the rising prevalence of cardiovascular illnesses (CVDs). In addition to its anti-inflammatory and antioxidant qualities, Resveratrol (RES) is well known for its capacity to increase endothelial NO synthase (eNOS) activity. This page summarises RES's wide effects on energy metabolism, resilience to stress, exercise mimicking, circadian rhythm, lifespan control, and microbiome composition. This article addresses the poor and contradictory results shown in preclinical and clinical trials provides an update on the cardiovascular preventive properties of RES. The activation of AMP-activated protein kinase (AMPK), silent information regulator 1 (SIRT1), and natural antioxidant enzymes is associated with some of the positive effects of RES on the cardiovascular system. A microarray data summary indicates a strong correlation between the heart's reaction to calorie restriction and the transcriptional responses to RES. RES has been demonstrated to reduce contractile dysfunction, cardiac remodelling, and hypertrophy in several animal models of heart failure. Its preventive properties are believed to be due to several molecular pathways, including the suppression of prohypertrophic signalling molecules, enhancement of cardiac Ca2+ handling, control of autophagy, and decreases in inflammation. RES thus has the potential to be used in several novel therapeutic approaches for treating diseases such as atherosclerosis, ischemia/reperfusion damage, metabolic syndrome, heart failure, and inflammatory changes associated with ageing.

Mitochondrial dysfunction plays a crucial role in the pathogenesis of various cardiac diseases, including heart failure, ischemic cardiomyopathy, and drug-induced cardiotoxicity. Mitochondria are essential for cellular energy production, calcium homeostasis, redox balance, and apoptotic regulation, making their proper function vital for cardiac health. Dysfunctional mitochondria contribute to excessive reactive oxygen species (ROS) production, impaired ATP synthesis, and disruption of mitochondrial dynamics, leading to cardiomyocyte damage and cell death. Emerging research highlights mitochondrial dynamics, including fission, fusion, mitophagy, and biogenesis, as critical determinants of cardiac homeostasis. Perturbations in these processes exacerbate myocardial injury and heart failure progression. Additionally, chemotherapy-induced cardiotoxicity, primarily from anthracyclines, is closely linked to mitochondrial damage, underscoring the need for targeted therapeutic strategies. Pharmacological interventions, such as antioxidants, mitochondrial-targeted drugs, and cardioprotective agents, have shown promise in mitigating mitochondrial dysfunction-related cardiac toxicity. Furthermore, lifestyle modifications, including exercise and dietary interventions, are being explored to enhance mitochondrial resilience in cardiac tissues. Advanced imaging techniques and biomarker-based diagnostics are improving the early detection of mitochondrial dysfunction in cardiac diseases. Emerging therapeutic strategies, such as mitochondrial transplantation, gene therapy, and precision medicine approaches, hold potential for targeted intervention. Despite these advances, challenges remain in translating mitochondrial-targeted therapies into clinical practice due to complexities in mitochondrial regulation and inter-organ communication. Future research should focus on optimizing mitochondrial-targeted interventions, improving diagnostic precision, and exploring novel molecular pathways to mitigate cardiac mitochondrial dysfunction. A comprehensive understanding of mitochondrial pathophysiology in cardiac diseases will pave the way for innovative treatment strategies aimed at preserving cardiac function and reducing the burden of heart failure.

Cardiovascular diseases (CVDs) are the leading cause of death worldwide and include a range of conditions affecting the heart and vascular system. There is a growing priority on identifying and validating biomarkers for CVDs to increase early diagnosis and survival rates. Within this framework of research, there has been a notable increase in interest in resolvins, a class of specialized pro-resolving mediators. Resolvins are well-known for their capacity to promote tissue healing and reduce inflammation. They are categorized into three series: Dseries (RvD1 to RvD6), T-series (RvT1 to RvT4), and E-series (RvE1 to RvE4). These molecules are produced through biochemical pathways involving enzymes such as lipoxygenase (LOX), cyclooxygenase (COX), and cytochrome P450 (CYP). These enzymes utilize precursor molecules like docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA), and docosapentaenoic acid (DPA). This review addresses a critical gap in the literature by evaluating the potential of resolvins as biomarkers for the diagnosis and prognosis of cardiovascular diseases. By synthesizing existing knowledge on their production pathways and receptors, it highlights the implications of altered resolvins levels in disease mechanisms and offers new perspectives on their clinical relevance.

Background: Fluoropyrimidine (FP) is a key cancer treatment but often causes side effects, notably cardiotoxicity. This cardiotoxicity can present as angina, arrhythmia, dyspnea, and palpitations, requiring urgent cardiologist attention. The etiology, management, and frequency of FP-induced cardiotoxicity are still unknown despite long-term use.

Objective: The article aims to provide an overview of the pathogenic occurrence, cardiac event risk factor, possible underlying mechanism of FP-cardiotoxicity, diagnostics, and therapeutic approach for the corrective management of this clinical condition.

Methods: review was performed by searching extensively for various existing literature search PubMed, Web of science and Scopus using suitable keywords to find articles that support our review study.

Result: FP induced cardiotoxicity results in morbidness and fatality in patient undergoing the treatment. Thus, an effective management system must be standardized to effectively treat and prevent this clinical condition.

Conclusion: the cardiotoxic event following 5-FU has been lesser-known clinical entity with limited study on its pathophysiology and management. In the diagnosis procedure, each patient undergoing FP treatment ought to have early symptom identity, risk categorization, and therapy individualized based on benefit-risk ratio.

Cardiovascular diseases (CVD) are the leading cause of death worldwide, creating the need for new therapeutic strategies targeting the pathological processes involved. Mitochondria, which comprise one-third of cardiac cell volume, maybe a potential therapeutic target for CVD. Known primarily for energy production, mitochondria are also involved in other processes including intermediary metabolism, mitophagy, calcium homeostasis, and regulation of cell apoptosis. Mitochondrial function is closely linked to morphology, which is altered through mitochondrial dynamics, including processes such as fission and fusion, which ensure that the energy needs of the cell are met. Recent data indicate that mitochondrial dysfunction is involved in the pathophysiology of several CVDs, including cardiac hypertrophy, heart failure, ischemia/reperfusion injury, and cardiac fibrosis. Furthermore, mitochondrial dysfunction is associated with oxidative stress related to atherosclerosis, hypertension, and pulmonary hypertension. In this review, we first briefly present the physiological mechanisms of mitochondrial function in the heart and then summarize the current knowledge on the impact of mitochondrial dysfunction on CVD. And finally, we highlight the evidence from in vitro, in vivo, and clinical studies of the cardioprotective effects of drugs that preserve mitochondrial function in CVD. It is hoped that this review may provide new insights into the need to discover new pharmacological targets with direct actions on mitochondria that may provide combined therapeutic strategies to optimally treat these pathologies.

Introduction: Percutaneous atrial septal defects (ASD) closure with fluoroscopy guidance is the standard procedure. However, fluoroscopy poses stochastic and deterministic risks for small infants and children. Zero fluoroscopy ASD closure is an alternative, yet its feasibility and safety compared to fluoroscopy remain unclear. Therefore, this study compares outcomes using standardized fluoroscopy and zero fluoroscopy methods for transcatheter ASD closure.

Methods: Four databases (PubMed, ProQuest, Google Scholar, Wiley) were used to search literature published before July 2023. The main results were the success rate and the complications. Outcomes were processed using the DerSimonian-Laird random-effects model of proportional meta-analysis to determine the overall proportion.

Results: A total of 68 cohort studies (8,989 patients) were included in this meta-analysis. Overall, percutaneous ASD closure was successfully performed in 97% of patients (95%CI: 96-98%) based on 59 studies (8,989 patients), of which fluoroscopy accounted for 97% (95%CI: 96- 98%) based on 51 studies (7,760 patients) and non-fluoroscopy for 98% (95%CI: 96-100%)] based on 8 studies (1,229 patients). Device embolization, AV block, and other arrhythmias did not differ significantly between the two groups. However, the percentage difference in residual leaks between the two groups was quite vast, with 5% in the non-fluoroscopy group and 12% in the fluoroscopy group.

Conclusion: Percutaneous ASD closure with zero fluoroscopy is safe and effective, as evidenced by the high success rate, and is non-inferior to the standardized fluoroscopy method.

Recent endeavors have led to the exploration of Machine Learning (ML) to enhance the detection and accurate diagnosis of heart pathologies. This is due to the growing need to improve efficiency in diagnostics and hasten the process of delivering treatment. Several institutions have actively assessed the possibility of creating algorithms for advancing our understanding of atrial fibrillation (AF), a common form of sustained arrhythmia. This means that artificial intelligence is now being used to analyze electrocardiogram (ECG) data. The data is typically extracted from large patient databases and then subsequently used to train and test the algorithm with the help of neural networks. Machine learning has been used to effectively detect atrial fibrillation with more accuracy than clinical experts, and if applied to clinical practice, it will aid in early diagnosis and management of the condition and thus reduce thromboembolic complications of the disease. In this text, a review of the application of machine learning in the analysis and detection of atrial fibrillation, a comparison of the outcomes (sensitivity, specificity, and accuracy), and the framework and methods of the studies conducted have been presented.

Introduction: The concomitant use of PPIs with antiplatelet therapy remains controversial due to potential drug interactions affecting clinical outcomes. While PPIs are recommended for gastroprotection in patients receiving antiplatelet therapy, concerns persist regarding their impact on antiplatelet efficacy, particularly with dual antiplatelet therapy (DAPT).

Aims: The aim of this study is to evaluate the safety profiles of antiplatelet-proton pump inhibitors (PPIs) combinations and assess the clinical implications of their concurrent use in real-world settings through pharmacovigilance data analysis.

Objectives: The objective of this study is to analyze and compare the thrombo-embolic risk profiles of various antiplatelet-PPI combinations using the FDA Adverse Event Reporting System database.

Methods: We conducted a comprehensive analysis of the FDA Adverse Event Reporting System (FAERS) database to evaluate the thrombo-embolic risk associated with antiplatelet-PPI combinations. The reporting odds ratio (ROR) and information component were calculated to detect safety signals. The interaction signal score (INTSS) was used to assess the protective or harmful effects of adding acetylsalicylic acid to clopidogrel-PPI combinations.

Results and discussion: Analysis revealed significant safety signals for thrombo-embolic events with clopidogrel-rabeprazole (ROR: 62.67, 95% CI: 38.38-102.32) and clopidogrel-omeprazole (ROR: 6.87, 95% CI: 4.89-9.66) combinations. DAPT-PPI combinations showed comparable safety profiles to monotherapy-PPI combinations. The INTSS analysis suggested a potential protective effect of acetylsalicylic acid when added to clopidogrel-PPI combinations. Genderspecific analysis revealed female predominance in monotherapy complications and male predominance in combination therapy events. Clinical outcomes, including mortality and hospitalization rates, were comparable between groups.

Conclusion: This pharmacovigilance analysis suggests that while DAPT-PPI combinations demonstrate acceptable safety profiles, careful consideration should be given to PPI selection, particularly given the unexpected safety signals with rabeprazole and confirmed risks with omeprazole. The addition of acetylsalicylic acid to clopidogrel-PPI combinations may offer protective effects against thrombo-embolic events. These findings support individualized riskbenefit assessment in selecting antiplatelet-PPI combinations while ensuring adequate gastroprotection for high-risk patients.

Atherosclerosis and associated cardiovascular diseases are the leading causes of illness and mortality worldwide. The development of atherosclerosis is a complex process involving oxidative stress, surplus lipid deposition and retention, endothelial dysfunction, and chronic inflammation. Developing novel anti-atherogenic and repurposing existing drugs requires the use of suitable animal models to characterise the fundamental mechanisms underlying atherosclerosis initiation and progression and to evaluate potential therapeutic effects. Commonly used rodent models, however, are not always appropriate, and other models may be required to translate these discoveries into valuable preventive and treatment agents for human applications. Recent advances in gene-editing tools for large animals have allowed the creation of animals that develop atherosclerosis faster and more similarly to humans in terms of lesion localisation and histopathology. In this review, we discuss the major advantages and drawbacks of the main non-rodent animal models of atherosclerosis, particularly rabbits, pigs, zebrafish, and non-human primates. Moreover, we review the application of recently invented novel therapeutic methods and agents, and repurposed existing drugs (such as antidiabetic and anticancer) for atherosclerosis treatment, the efficacy of which is verified on non-rodent animal models of atherosclerosis. In total, the proper selection of a suitable animal model of atherosclerosis facilitates reproducible and rigorous translational research in repurposing of existing drugs, discovering new therapeutic strategies, and validating novel anti-atherosclerotic drugs.

Heart failure remains a significant global health challenge, necessitating continuous advancements in management strategies to improve patient outcomes. This review aimed to elucidate the current scenario of heart failure and its management in the modern era, focusing on integrating medical therapy and implantable device interventions. According to guidelines, medical treatment remains the primary method of treating heart failure. Such medications include ACE inhibitors, neprilysin-angiotensin receptor inhibitors, beta-blockers, angiotensin II receptor blockers, mineralocorticoid receptor antagonists, and blockers of sodium-glucose co-transporter- 2. These pharmacologic agents have demonstrated efficacy in decreasing mortality and morbidity in patients. The advent of implantable devices has revolutionized treatment, providing substantial benefits in specific patient populations. Cardiac resynchronization therapy has emerged as a pivotal intervention for patients with reduced ejection fraction and dyssynchronous ventricular contraction, effectively enhancing cardiac function and quality of life. Furthermore, left bundle branch area pacing improvements provide fascinating alternatives to traditional cardiac resynchronization therapy. The essential significance of device-based therapies is further highlighted by the function of implanted cardioverter-defibrillators in preventing unexpected cardiac deaths in high-risk patients. Furthermore, integrating remote monitoring technologies and novel device innovations continues to enhance the precision and efficacy of heart failure management. This review comprehensively examines current guidelines and evidence supporting the use of these therapies, addressing their synergistic potential and the practical considerations for their implementation, while synthesizing recent advancements in pharmacologic and device-based interventions.