Current Cardiology Reviews最新文献

Phytoestrogens are plant-derived compounds resembling human estrogen and have recently gained attention due to their potential role in improving cardiovascular health. These compounds exert their effects through various mechanisms, including interactions with estrogen receptors, growth factor receptors, inflammatory mediators, thrombogenic reactions, and apoptotic pathways. This results in cardioprotective effects like modulating endothelial function, decreasing vessel tone, reducing inflammation, altering lipid profiles, and influencing arrhythmogenesis. Recent studies indicate the intricate and multidimensional association between phytoestrogens and cardiovascular disease. Despite the overwhelming evidence that phytoestrogen intake lowers the risk of myocardial infarction (MI), prevents atherosclerosis, improves cardiac function, prevents hypertension, and reduces the risk of arrhythmias, there have been studies that show contradictory outcomes. For this reason, the therapeutic use of phytoestrogens for the treatment of cardiovascular diseases, which appears to be extremely promising, should be handled cautiously, considering the individual variances, dosage, and the specific components of phytoestrogens. This review consolidates findings on the effects of phytoestrogens on the heart and blood vessels, explores the mechanisms behind these interactions, and seeks to determine the best methods for using phytoestrogens as a supplement in managing and preventing cardiovascular disease. By understanding these aspects, we can better evaluate the potential of phytoestrogens in cardiovascular health and develop guidelines for their safe and effective use.

High-altitude regions pose distinctive challenges for cardiovascular health because of decreased oxygen levels, reduced barometric pressure, and colder temperatures. Approximately 82 million people live above 2400 meters, while over 100 million people visit these heights annually. Individuals ascending rapidly or those with pre-existing cardiovascular conditions are particularly vulnerable to altitude-related illnesses, including Acute Mountain Sickness (AMS) and Chronic Mountain Sickness (CMS). The cardiovascular system struggles to adapt to hypoxic stress, which can lead to arrhythmias, systemic hypertension, and right ventricular failure. Pathophysiologically, high-altitude exposure triggers immediate increases in cardiac output and heart rate, often due to enhanced sympathetic activity. Over time, acclimatisation involves complex changes, such as reduced stroke volume and increased blood volume. The pulmonary vasculature also undergoes significant alterations, including hypoxic pulmonary vasoconstriction and vascular remodelling, contributing to conditions, like pulmonary hypertension and high-altitude pulmonary edema. Genetic adaptations in populations living at high altitudes, such as gene variations linked to hypoxia response, further influence these physiological processes. Regarding cardiovascular disease risk, stable coronary artery disease patients generally do not face significant adverse outcomes at altitudes up to 3500 meters. However, those with unstable angina or recent cardiac interventions should avoid high-altitude exposure to prevent exacerbation. Remarkably, high-altitude living correlates with reduced cardiovascular mortality rates, possibly due to improved air quality and hypoxia-induced adaptations. Additionally, there is a higher incidence of congenital heart disease among children born at high altitudes, highlighting the profound impact of hypoxia on heart development. Understanding these dynamics is crucial for managing risks and improving health outcomes in high-altitude environments.

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 CVD, 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 CVD 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.

Thirty percent of deaths worldwide are caused by cardiovascular disorders (CVDs). As per the WHO data, the number of fatalities due to CVDs is 17.9 million years, and it is projected to cause 22.2 million deaths by 2030. In terms of gender, women die from CVD at a rate of 51% compared to 42% for males. Most people use phytochemicals, a type of traditional medicine derived from plants, either in addition to or instead of commercially available medications to treat and prevent CVD. Phytochemicals are useful in lowering cardiovascular risks, especially for lowering blood cholesterol, lowering obesity-related factors, controlling blood sugar and the consequences of type 2 diabetes, controlling oxidative stress factors and inflammation, and preventing platelet aggregation. Medicinal plants that are widely known for treating CVD include ginseng, Ginkgo biloba, ganoderma lucidum, gynostemma pentaphyllum, viridis amaranthus, etc. Plant sterol, flavonoids, polyphenols, sulphur compound and terpenoid are the active phytochemicals present in these plants. The aim of this article is to cover more and more drugs that are used for cardiovascular diseases. In this article, we will learn about the use of different herbal drugs, mechanism of action, phytochemical compounds, side effects, etc. However, more research is required to comprehend the process and particular phytochemicals found in plants that treat CVD.

Introduction: Infective Endocarditis (IE) has emerged to be one of the most impactful adverse complications post-transcatheter procedures, especially Transcatheter Pulmonary Valve Replacement (TPVR). We conducted a systematic review and meta-analysis with the aim of identifying the incidence of IE post-TPVR with the MELODY valve in the pediatric population.

Methods: A comprehensive literature search was performed across several prominent databases, including PubMed/MEDLINE, SCOPUS, and Science Direct. Studies compared the clinical outcomes of pediatric patients who received TPVR using the MELODY valve. Data extraction was done for variables like the total pediatric patient population that underwent TPVR with MELODY valve, mean age, the sex of the patients, the incidence rate of IE following the procedure, and the duration between the procedure and the occurrence of IE. Inverse Variance was used to estimate the incidence of IE in patients who underwent TPVR with respective 95% confidence interval (CI).

Results: In total, 4 studies with 414 pediatric patients who underwent TPVR using the MELODY valve were included in the study. The mean age of the study population was 12.7 ± 3.11 years. The pooled incidence of IE following TPVR with MELODY valve in the pediatric population was 17.70% (95% Cl 3.84-31.55; p<0.00001). Additionally, the mean length of duration to develop IE following TPVR with MELODY valve in the pediatric population was 2.18 years (95% Cl 0.35-4.01; p<0.00001).

Conclusion: Our meta-analysis reveals that IE post-TPVR with MELODY valve in pediatric patients is a significant complication, clinically and statistically. Further research needs to be done to understand the risk factors and develop better management strategies.

Background: Sodium-glucose co-transporter 2 inhibitors (SGLT2i) and angiotensin receptor neprilysin inhibitors (ARNi) are new classes of medications with an evolving role in heart failure (HF) patients. However, the effect of combining these drugs with cardiac resynchronization therapy (CRT) remains less certain.

Objective: This study aimed to investigate the impact of combined treatment with ARNi and SGLT2i on clinical and echocardiographic outcomes in CRT patients during 12-month followup.

Methods: HF patients with CRT implantation indications were enrolled in the non-randomized and retrospective study and were grouped in no ARNi and SGLT2i (1st group) and combined treatment with ARNi and SGLT2i (2nd group) cohorts. The CRT response criteria were as follows: improvement of NYHA class ≥1 and left ventricular end-systolic volume reduction ≥15% or left ventricular ejection fraction improvement ≥5% from the baseline during the 12-month follow- up.

Results: A total of 52 patients were included. At the 12-month follow-up, 18 of 35 (51.4%) patients in the 1st group and 16 of 17 patients (94.1%) in the 2nd cohort met CRT responder criteria (p=0.002). In multivariable logistic regression, combined treatment with ARNi and SGLT2i [odds ratio (OR): 20.09; 95% confidence interval (CI): 2.10-192.15; p=0.009] and non-ischemic HF (OR 5.51; 95% CI 1.21-24.91; p=0.026) were associated with CRT response.

Conclusion: The combined treatment with SGLT2i and ARNi in patients with CRT improved the echocardiographic and clinical outcomes during the 12-month follow-up. In our study cohort, the CRT response was associated with non-ischemic HF and combined treatment with ARNi and SGLT2i.

Recent advancements have emerged in understanding the epidemiology and optimal therapeutic options for left ventricular thrombi (LVT). With early percutaneous interventions in acute myocardial infarction, the prevalence of LVT has decreased. However, the best strategies for prevention, risk stratification, and management remain unclear, especially among nonischemic cardiomyopathy disorders. This review outlines these advancements and provides an overview of the diagnostic and therapeutic implications of LVT in ischemic and non-ischemic cardiomyopathies. Significant gaps in the current evidence persist, particularly regarding the optimal timing for LVT screening and the need for prophylactic anticoagulation, highlighting opportunities for prospective cohort studies. Furthermore, a better understanding of the unique risk factors that contribute to increased LVT risk would lead to more comprehensive algorithms that may quantify the risk of LVT development, aiding in developing preventive strategies targeted at reducing rates of LVT. Until more definitive evidence is available, clinicians should custom LVT screening, preventive measures, and management strategies based on individual patient risk factors.

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.

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.