Cardiovascular Medicine
The Link between Arterial Atherosclerotic and Venous Thromboembolic Disease
Traditionally arterial atherosclerotic (AA) and venous thromboembolic (VTE) diseases have been separated into two independent entities. However a body of evidence suggests the link between arterial and venous disease. In this narrative review the relationship between these two vascular diseases is discussed. Different risk factors are common in both diseases such as dyslipidaemia metabolic syndrome and thrombophilia. Etiopathogenetic mechanisms of both diseases are similar. Inflammation as a basic pathogenetic mechanism of atherosclerotic disease is also involved in the pathogenesis of VTE. Inflammation as a response to vessel wall injury promotes coagulation and inhibits endogenic fibrinolytic activity which results in thromboembolic events in the arterial as well as in the venous system. A relationship has also been observed between preclinical or clinical atherosclerotic disease and VTE. These findings indicate that atherosclerosis may induce VTE or that common risk factors simultaneously stimulate the development of both diseases. The relationship between arterial and venous disease is also supported by the efficacy of some drugs (antiplatelets anticoagulants statins) in the prevention of both diseases.
In conclusion arterial and venous diseases share similar pathophysiological mechanisms often driven by common risk factors. This overlap suggests that a unified approach to prevention and treatment may be beneficial for both conditions potentially improving patient outcomes by addressing the underlying shared pathways.
Evaluation of the Effect of Virgin Rice Bran Oil (VRBO) on Doxorubicin-Induced Cardiotoxicity in Wistar Rats
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.
VRBO and DOX injections were administered to thirty male Wistar rats for 42 days after being randomly assigned to five groups.
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-to-body 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.
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.
Roles of Empagliflozin in Diabetic Cardiomyopathy: A Review
Empagliflozin (EMPA) a sodium-glucose cotransporter 2 inhibitor (SGLT2i) represents a novel therapeutic agent for diabetes management. Over the past decade studies have consistently demonstrated that EMPA not only effectively lowers blood glucose levels but also confers substantial cardiovascular benefits without inducing hypoglycemia. This holds for individuals with or without diabetes highlighting EMPA’s potential in mitigating the risk of adverse cardiovascular events and cardiovascular mortality. The underlying mechanisms driving these advantageous effects remain incompletely understood with presently elucidated pathways encompassing blood pressure reduction oxidative stress attenuation anti-inflammatory properties metabolic regulation uric acid level modulation inhibition of Na+/H+ exchangers preservation of mitochondrial function vascular protection and regulation of myocardial autophagy. In this review we considered the effects and mechanisms of EMPA in combating diabetic cardiomyopathy (DCM) underscoring its therapeutic relevance in addressing cardiovascular complications associated with diabetes.
Nose-to-Brain Targeting of Resveratrol Nanoformulations
Resveratrol [RES] is a polyphenolic stilbene with therapeutic potential owing to its antioxidant anti-inflammatory neuroprotective and cardioprotective properties. However the very poor oral bioavailability fast metabolism and extremely low stability under physiological conditions pose a severe detriment to the clinical use of RES. This newly developed field of nanotechnology has led to the formulation of RES into nanoformulations with the goal of overcoming metabolic-pharmacokinetic limitations and enhancing the targeted transport of RES to the central nervous system [CNS]. Among the various routes of administration the combination of nose-to-brain [N2B] delivery via the intranasal [IN] route has recently garnered attention as a straightforward non-invasive route for transport to the blood-brain barrier [BBB] for greater effects and less harmful systemic side effects by transporting nano-encapsulated RES into the neural tissues. This review critically summarizes the mechanisms and benefits of the N2B route for the delivery of RES nanoformulations collating in vivo data demonstrating increased CNS bioavailability and stability and consequently improved therapeutic efficacy in animal models of neurodegenerative diseases. Compared with the more 'traditional' routes of administration IN administration of RES nanoformulations is less toxic cost-effective and efficient in crossing the BBB. Therefore this route represents a promising approach to the management of CNS disorders. Further optimization of nanoformulation design and clinical protocols is required to translate these promising findings into therapeutic strategies aimed at neuroprotection and disease modification in human CNS pathologies.
Safety and Efficacy of Transendocardial Stem Cells Therapy in Chronic Ischemic Heart Failure: A Systematic Review and Meta-analysis of Randomized Controlled Trials
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.
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.
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.
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.
Exploring the Involvement of New Members of the Interleukin Family in Cardiovascular Disease
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.
Introducing the Concept of Hypertensive Heart Disease to Improve Hypertensive Left Ventricular Hypertrophy
Among the organ damage mediated by hypertension cardiac lesions hold significant importance. Numerous authors focus on hypertensive heart disease (HHD) rather than exclusively on left ventricular hypertrophy (LVH).
This narrative review aims to assess the incorporation of the concept of 'hypertensive heart disease' (HHD) in hypertension (HTN) guidelines. Furthermore if HHD is not addressed the review will evaluate the potential benefits of including this concept in future studies.
The following databases were searched: Scopus Medline Springer Science Direct Wiley SAGE Cambridge Oxford Journals and Google Scholar. Attention was given to the guidelines related to hypertension(HTN); the search items were “guidelines” and “hypertension.” Within these guidelines we specifically sought references to ‘hypertensive heart disease.’.
The concept of “HHD” is clearly advantageous compared to “HTN LVH” as it not only addresses LVH but also considers other structures of the heart that may be severely affected which can significantly influence treatment. The concept of “hypertensive heart disease” is mentioned in only 8 out of 36 guidelines on HTN. The therapeutic implications and recommendations are absent in the guidelines.
The concept of HHD is reasonable and evidence-based and there is no reason to focus only on LVH when considering HTN-induced damage to the heart. It is time to update our recommendations for heart treatment by using the phrase “Treatment of hypertensive heart disease” instead of “Treatment of hypertensive LVH.” This update can enhance our awareness of the need to improve not only HTN LVH but the other parts of the heart as well.
The Early Pharmacological Strategy with Inodilator, bEta-blockers, Mineralocorticoid Receptor Antagonists, Sodium-glucose coTransporter-2 Inhibitors and Angiotensin Receptor-neprylisin Inhibitors in Acute Heart Failure (PENTA-HF)
The management of acute heart failure (AHF) is crucial and challenging. Regarding the use of inotropes correct patient selection and time of administration are of the essence. We hypothesize that the early use of Levosimendan favouring hemodynamic stabilization and enables rapid optimization of guideline-directed medical treatment (GDMT) in patients with HF eventually impacting the patient’s prognosis during the vulnerable phase.
This prospective observational study enrolled consecutive patients admitted due to AHF. Propensity score matching (PSM) analysis has been used to homogenize differences between groups. In group 1 (G1) patients were treated with early 24-h Levosimendan infusion followed by in-hospital introduction/up-titration of GDMT. In group 2 (G2) patients were treated with alternative inotropes/vasopressors followed by in-hospital introduction/up-titration of GDMT. The comparison between the two groups has been performed at the 6-month follow-up in terms of cardiovascular (CV) mortality and HF hospitalizations (HFH).
233 patients were included in the present study and after propensity match adjustments 176 patients were analysed 88 patients for each group. No differences in the baseline characteristics have been reported between the groups. At 6 months follow-up no statistically significant differences were shown in terms of the composite endpoint of CV death and HFH (p= 0.445) and CV death (p=0.62). Statistically significant differences between the two groups were reported in terms of HFH (p= 0.02). The Kaplan-Meier survival analysis showed that patients in G1 were significantly less hospitalized compared to G2 during the 6 months after the index hospitalization (log-rank p= 0.03).
Early 24-hour infusion of Levosimendan followed by rapid optimization of HF disease-modifying therapies results in a significant reduction of HFH in the vulnerable post-discharge phase.
A New Mechanism of Supraventricular Tachycardia: Gene Mutation
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.
Through analysis of epidemiology familial clustering and gene mutations of the relevant literaturethe review elucidates the genetic properties and potential pathophysiology of SVT.
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.
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.
Unlocking Platelet Mechanisms through Multi-Omics Integration: A Brief Review
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.
Promising Adventitia in Atherosclerosis
The adventitia the artery's most intricate layer has received little attention.. During atherosclerosis adventitia components undergo significant changes such as angiogenesis lymphangiogenesis Artery Tertiary Lymphoid Organ (ATLO) formation axon density increase fibroblast activation and stem cell differentiation. The reasons behind these changes and their contribution to atherosclerosis are beginning to be understood. In this review we summarize the adventitia components and their role in normal arteries and then discuss the changes pathogenesis and potential clinical application of the adventitia in atherosclerosis.
Neutrophil Elastase as A Potential Target in Ischemia-Reperfusion Injury
Neutrophil elastase (NE) a major protease in neutrophils is important in promoting inflammation and multiple pathological processes. While NE is released abundantly in ischemia-reperfusion (I/R) injury the intricate relationship between NE and I/R injury remains unclear. We examine several aspects of how NE is involved in I/R injury. We also discuss the possibility of NE inhibitors used for abbreviating various types of I/R injury such as myocardial infarction based on preclinical research and clinical trials. Furthermore we highlight the key question the balance of NE and NE inhibitors and propose new research directions. This review is useful for understanding the intrinsic interplay between NE and I/R injury-related diseases and expects to facilitate the development of effective NE inhibitors applied for I/R injury.
The Immune System: An Arrow to the Heart and Principles of Cardioimmunology as an Emerging Branch of Medicine
Cardioimmunology is an emerging branch of medicine whose development has been facilitated by more sophisticated diagnostic procedures. Recent studies have mainly focused on the immune response during myocardial infarction (MI) and there is evidence that both resident and external immune cells participate in acute inflammatory disease as well as tissue remodeling.
Following MI macrophages dendritic cells (DCs) and mast cells (MCs) are the main players in the heart. Under steady-state conditions cardiac resident macrophages (CRMs) protect the heart against stress and infectious events being involved in cell and matrix turnover as well as phagocytosis of apoptotic cells. Moreover CRMs contribute to the resolution of inflammation via release of interleukin (IL)-10 and efferocytosis of dying cells. Conversely CCR2+ monocyte-derived macrophages promote inflammation in the acute phase of myocardial damage with the release of pro-inflammatory cytokines. Conventional (c) DCs possess enhanced capacity to present antigens to T lymphocytes. In MI patient autopsies massive infiltration of T helper (Th) cells and CDs has been detected in the myocardium. Cardiac MCs play a dual role during MI with the production of cytokines for early inflammatory response and the release of anti-inflammatory cytokines IL10 and IL-13 during the resolution phase.
In experimental coronary artery ligation the myocardium is infiltrated with Th1 Th2 Th17 and T regulatory (TREG) cells which participate in the acute inflammation. In cardiac repair T cell reparative response is mediated by TREG cells with improved ventricular remodeling and function post-ischemia.
In this review emphasis will be placed on the innate and adaptive immune response during and post-MI. At the same time immunotherapy-based cardiac failure following chimeric antigen receptor T-cell and immune checkpoint inhibitory therapy will be pointed out.
Sodium Glucose Cotransporter-2 Inhibitors Improve Endothelial Function and Arterial Stiffness in Diabetic Individuals: A Systematic Review and Network Meta-Analysis
Sodium Glucose cotransporter-2 inhibitors (SGLT2is) possess pleiotropic effects such as antioxidant antifibrotic anti-inflammatory and vascular remodeling activities. Considering the lack of literature a network meta-analysis was conducted to explore the impact of SGLT2is on endothelial dysfunction and arterial stiffness in the diabetic population.
Electronic databases were searched to identify randomized clinical trials evaluating the effects of SGLT2is on outcomes such as Flow-mediated Vasodilation (FMV) Pulse Wave Velocity (PWV) and Augmentation Index (AIx). Direct indirect and mixed treatment comparisons generated pooled estimates using random-effects modeling. Effect sizes were reported as Hedges' g with 95% Confidence Interval (95% CI). Bootstrap and permutation meta-analyses were performed using ranking plots. The certainty of evidence was graded.
Twelve low risk of bias articles (706 participants) were included. SGLT2is were associated with significant improvements in FMV (g: 0.48; 95% CI: 0.08 0.88) confirmed by bootstrap meta-analysis (g: 0.48; 95% CI: 0.1 0.85) and permutation meta-analysis of FMD (g: 0.48; 95% CI: 0.05 0.9). Within SGLT2is dapagliflozin (g: 0.39; 95% CI: 0.14 0.65) and empagliflozin (g: 0.66; 95% CI: -0.65 1.97) significantly improved FMV and dapagliflozin (g: -0.61 95% CI: -0.98 -0.24) and tofogliflozin (g: -3.51; 95% CI: -4.05 -2.98) significantly improved PWV. A low risk of publication bias was observed and the ranking plots revealed dapagliflozin to have the best probability (0.99) of being the most effective for improving FMV. Low certainty of evidence was observed for all outcomes.
SGLT2 inhibitors improve endothelial function and arterial stiffness in the diabetic population. Clinical studies evaluating the association between improvements in endothelial function with SGLT2is and reduced adverse cardiovascular and cardiorenal events and mortality are urgently needed.
Successful Use of Proprotein Convertase Subtilisin/Kexin Type 9 Inhibitors in Hypertriglyceridemia-induced Acute Pancreatitis: A Case Report
Managing hypertriglyceridemia-induced acute pancreatitis (HTG-AP) can be challenging particularly due to the need for rapid triglyceride reduction to below 500mg/dL (5.645mmol/L).
This is a case describing a 39-year-old female patient who presented to the Emergency Department with acute abdominal pain resulting from severe HTG-AP. However under conventional therapy with oral lipid-lowering drugs the triglyceride levels remained uncontrolled. Oral moderate-intensity statins could not only reduce low-density lipoprotein cholesterol (LDLc) by 25%-50%. However increasing the dose could not further reduce blood lipids while increasing the risk of liver damage. After the administration of proprotein convertase subtilisin/kexin type 9 inhibitor (PCSK9i) the triglyceride levels were well controlled with no additional side effects and the symptoms of the patients were completely relieved.
In cases of unsatisfactory lipid control under conventional therapy PCSK9i may offer a viable option for managing HTG-AP.
Identifying Biomarkers for Atherosclerosis via Gene Expression and Biological Networking
Atherosclerosis is a chronic disease caused by the accumulation of lipids inflammatory cells and fibrous elements in arterial walls leading to plaque formation and cardiovascular conditions like coronary artery disease stroke and peripheral arterial disease. Factors like hyperlipide
mia hypertension smoking and diabetes contribute to its development. Diagnosis relies on imaging and biomarkers while management includes lifestyle modifications pharmacotherapy and surgical interventions. Computational biology is transforming biological knowledge into clinical practice by identifying biomarkers that can predict clinical outcomes. This involves omics data predictive modeling and data integration. Statistical analysis-based methods are also being developed to develop and integrate methods for screening diagnosing and prognosing atherosclerosis.
The present work aimed to uncover critical genes and pathways to enhance the understanding of the mechanism of atherosclerosis. GSE23746 was analyzed to find differentially expressed genes (DEGs) using 19 control samples and 76 atherosclerotic samples.
A total of 76 DEGs were identified. Analysed DEGs using Gene Ontology (GO) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) to generate enrichment datasets. A Protein-Protein Interaction (PPI) network of DEGs was created utilizing the Search Tool for the Retrieval of Interacting Genes (STRING).
Ten hub genes namely EGR1 PTGS2 TNF NFKBIA CXCL8 TNFAIP3 CCL3 IL1B PTPRC and CD83 were found to be significantly linked to atherosclerosis. Furthermore the metabolic pathway analysis through KEGG and STRING provides potential targets for therapeutic interventions through HUB genes to diagnose the illness at an early stage which aids in the reduction of cardiovascular risk. From risk factor profiling to the discovery of novel biomarkers several components such as phospholipids ANGPTL3 LCAT and the protein-encoded OCT-1 gene play a vital role in crucial processes. These compounds are potential therapeutic targets for early diagnosis of atherosclerotic lesions and future novel biomarkers.
The Intersection of Heart Failure and Iron Deficiency Anemia: Diagnostic and Therapeutic Approaches
Iron deficiency anemia (IDA) is highly prevalent among individuals with heart failure (HF) impacting 40-70% of patients and serving as a significant prognostic indicator. Linked with oxidative metabolism and myocardial cell damage IDA exacerbates HF symptoms including reduced exercise capacity diminished quality of life and heightened cardiovascular morbidity. This review explores the diagnosis treatment clinical outcomes prognostic indicators and forthcoming challenges associated with IDA in HF patients. Crucially addressing IDA in HF is critical for enhancing prognosis including clinical outcomes quality of life hospitalizations and survival rates. While oral iron therapy shows efficacy in reducing mortality and hospitalizations it falls short in improving exercise capacity and quality of life often deterring patients due to side effects. In contrast intravenous (IV) iron therapy is highly effective in enhancing hematological parameters functional capacity and reducing HF hospitalizations. Optimizing IV iron dosing based on individual patient characteristics is essential for balancing treatment efficacy and adverse effects. Emphasizing individualized approaches with IV iron emerging as a superior option underscores the necessity for ongoing research to refine dosing strategies and explore novel therapies. Compliance remains paramount for positive outcomes with IDA treatment with oral supplementation being cost-effective and easily accessible. However parenteral supplementation proves beneficial for patients intolerant to oral therapy. Addressing IDA through tailored interventions including oral or parenteral supplementation is pivotal in averting complications and improving outcomes in HF patients. This paper consolidates insights into the diagnosis treatment impact pathophysiology clinical outcomes research gaps and future directions concerning IDA in HF patients drawing on extensive literature to offer a comprehensive understanding of this critical issue.
Unlocking the Potential: Phytoestrogens and Cardiovascular Health
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.
Delineating the NOX-Mediated Promising Therapeutic Strategies for the Management of Various Cardiovascular Disorders: A Comprehensive Review
Cardiovascular disorders (CVDs) are reported to occur with very high rates of incidence and exhibit high morbidity and mortality rates across the globe. Therefore research is focused on searching for novel therapeutic targets involving multiple pathophysiological mechanisms. Oxidative stress plays a critical role in the development and progression of various CVDs such as hypertension pulmonary hypertension heart failure arrhythmia atherosclerosis ischemia-reperfusion injury and myocardial infarction. Among multiple pathways generating reactive oxygen species (ROS) Nicotinamide adenine dinucleotide phosphate (NADPH) oxidases of the NOX family as the major source of ROS generation and plays an intricate role in the development and progression of CVDs. Therefore exploring the role of different NADPH oxidase isoforms in various cardiovascular pathologies has attracted attention to current cardiovascular research. Focusing on NADPH oxidases to reduce oxidative stress in managing diverse CVDs may offer unique therapeutic approaches to prevent and treat various heart conditions. The current review article highlights the role of different NADPH oxidase isoforms in the pathophysiology of various CVDs. Moreover the focus is also to emphasize different experimental studies that utilized various NADPH oxidase isoform modulators to manage other disorders. The present review article considers new avenues for researchers/scientists working in the field of cardiovascular pharmacology utilizing NADPH oxidase isoform modulators.
Current Strategies for Atrial Fibrillation Prevention and Management: Taming the Commonest Cardiac Arrhythmia
Atrial fibrillation (AF) is the commonest cardiac arrhythmia constituting a major cause of morbidity and mortality with an age-dependent incidence and prevalence ranging from 1-2% in the general population to ~10% in persons aged >60 years. The global prevalence of AF is rapidly increasing mostly due to the aging population. If not properly and timely managed this arrhythmia adversely affects left ventricular function increases the risk of stroke five-fold impairs quality of life and shortens longevity. There is a genetic hence non-modifiable predisposition to the arrhythmia while several life-style and cardiometabolic inciting factors such as hypertension heart failure coronary disease metabolic syndrome alcohol use and thyroid disorders can be addressed attesting to the importance of a holistic approach to its management. Thromboembolism is a serious consequence of AF which could lead to a disabling stroke or have a lethal outcome. The risk of a thromboembolic complication can be estimated as based on a scoring system that takes into consideration the patient’s age previous thromboembolic events and clinical comorbidities. In addition rapid AF could affect cardiac performance leading to an elusive type of arrhythmia-induced cardiomyopathy and heart failure with grave consequences if undetected and untreated. Furthermore AF may cause silent brain infarcts and/or its hemodynamic perturbations can account for a type of dementia that needs to be taken into account emphasizing the need for AF screening and prevention strategies. All these issues are herein detailed the causes of the arrhythmia are tabulated and an algorithm illustrates our current approach to its management.