Current Cardiology Reviews最新文献

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.

Background: 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).

Case report: 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.

Conclusions: In cases of unsatisfactory lipid control under conventional therapy, PCSK9i may offer a viable option for managing HTG-AP.

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.

Background: 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 hyperlipidemia, 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.

Methodology: 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.

Result: 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).

Conclusion: 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 proteinencoded 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.

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.

Cardiovascular Disease [CVD], the leading cause of death globally, poses a significant burden on the healthcare sector. Its association with stress and Cushing's Syndrome has driven cortisol, the 'stress hormone,' to be a potential candidate in determining CVD risk. Cortisol synthesis and release through the hypothalamic-pituitary-adrenal [HPA] axis are regulated by several hormones and receptors involved in the pathological cascade towards CVD. Evidence suggests that metabolic syndrome plays a major role in cortisol-mediated CVD risk. On the other hand, non-metabolic features are also implicated when the association between cortisol and CVD risk remains significant upon normalisation of metabolic parameters. Correspondingly, the treatment for hypercortisolism is often found effective in lowering CVD risk. Despite available evidence, several factors continue to hinder the clinical use of cortisol as a risk biomarker for CVD. This review provides an insight into the role of serum cortisol in CVD progression and risk, with emphasis on the mechanistic features and parameters.

Introduction: Peripheral arterial disease (PAD) is a marker of significant atherosclerotic cardiovascular disease and is associated with greater healthcare burden and worse prognosis in individuals with chronic inflammatory disease (CID). We aimed to investigate temporal trends and disparities of PAD-related mortality in populations with CID from 1999-2020 across six common CIDs (i.e., chronic viral hepatitis, human immunodeficiency virus, inflammatory bowel disease, psoriasis, rheumatoid arthritis, and systemic lupus erythematosus).

Methods: United States (US) PAD and CID-related mortality and demographic data from 1999- 2020 were extracted from the CDC database through the multiple-cause-of-death files. Ageadjusted mortality rates (AAMR) per 1,000,000 and 95% confidence intervals were standardized to the 2000 US population. The mortality trends were analyzed using Joinpoint Regression.

Results: A total of 22,175 PAD-related deaths were recorded in the population with CID between 1999 and 2020. Mortality remained stable during the 22-year period (AAPC -0.04%, p=0.95) with a cumulative AAMR of 4.64. Mortality was highest in rural counties (AAMR 5.27), and among non-Hispanic Black populations (AAMR 7.06). Among the CID subtypes, PAD mortality was highest in populations with RA (AAMR 2.48) and lowest in populations with psoriasis (AAMR 0.11).

Conclusion: Our findings highlight the disparities of PAD mortality in patients with CID, with the Black population and rural communities disproportionately affected. Further investigation with individual- level data is warranted to identify the contributing factors for the observed disparities.

Introduction: Long-term heart failure hospitalization (HFH) after radiofrequency catheter ablation (RFCA) in atrial fibrillation (AF) patients with heart failure and preserved ejection fraction (HFpEF) and its risk factors remain to be investigated.

Methods: AF patients with HFpEF who underwent RFCA from January, 2014 to December, 2018 from three centers were retrospectively included. Patients were assigned to the training and testing cohorts, respectively. In the training cohort, logistic regression analyses were performed to discriminate those with and without HFH. A scoring system was developed accordingly and validated.

Results: A total of 417 AF patients with HFpEF receiving RFCA were enrolled. About 35 patients (8.4%) had HFH for 6 years. In the training cohort, the use of diuretics, atrial tachycardia (AT)/AF recurrence, prior HFH, and female sex were independent predictors of HFH in the multivariable analysis. A DAPF score (ranging from 0 to 9.0) was developed. The area under the receiver operating characteristic curve (AUC) of the DAPF score was 0.880 (95% CI, 0.830- 0.929). A DAPF score ≥3.5 could predict HFH with a sensitivity of 81.8% and a specificity of 74.6%. The performance in the testing cohort remained robust (AUC, 0.858; 95% CI, 0.749- 0.967).

Conclusion: HFH in patients with AF and HFpEF after RFCA is not rare. The DAPF score could predict the risk of HFH in AF patients with HFpEF after RFCA and guide our treatment strategy.