Current Cardiology Reviews最新文献

Background: From 1931 to 2025, spanning 94 years, cardiac cancer has remained a rare and sporadic tumor that poses both an investigative dilemma and a therapeutic challenge. Autopsy findings indicate that the incidence of primary cardiac malignancies is approximately 0.02 percent. Surgical resection is considered a viable and often successful treatment option.

Aims: The present study aims to provide an overall assessment of cardiac cancer in Isfahan Province, Iran.

Objectives: To provide detailed information on specific aspects, such as frequency and demographic characteristics of cardiac cancer.

Methods: The representative data of this study were drawn from the general population of Isfahan Province. SEER (Surveillance, Epidemiology, and End Results) data were obtained from the Deputy of Health, Division of Registry of Cancer (between 2011 and 2015). With attention to subject selection (the authors followed the Sex and Gender Equity in Research (SAGER) Guidelines), and according to the ICDO topography code, C38 was considered for further investigation as heart cancer or cardiac tumors.

Results: During the study period, a total of 30,465 cancer patients were recorded, comprising 14,638 females and 15,827 males. Among these, 122 cases (0.4 percent) were identified as cardiac cancer, including 42 females and 80 males. The patients' ages ranged from 3 to 95 years, with a mean age of 46.8 ± 21.5 years. The annual distribution of reported cardiac tumors during the study period was as follows: 34, 37, 18, and 33 cases, respectively. Based on available data from the monographic code M, which does not specify subtypes, the following conditions were recorded: mesothelioma (n = 25), neoplasm (n = 11), Hodgkin lymphoma, nodular sclerosis, NOS (n = 14), and other unspecified conditions. A total of three deaths were reported.

Conclusion: In the population studied, the frequency of cardiac cancer in men was significantly higher than in women. Age related to cardiac cancer in 51% was between 40-70 years old. For the patient satisfaction and financial aspects of the Iranian health system, further consideration is suggested regarding referral systems, evidence-based pharmacotherapy, and post-surgery outcome inquiries.

Background: Traumatic tricuspid regurgitation resulting from blunt chest trauma is a rare complication, and the surgical options remain unclear Case Presentation: We describe the case of a 19-year-old male who sustained polytrauma in a scooter accident. Concomitant medical findings included massive right hemothorax, splenic burst with active bleeding, hemoperitoneum, L1-L3 spinous apophysis fracture, and 2 rib arches. Despite 6 hours of medical treatment, including high doses of noradrenaline and dobutamine, complete stabilization was not achieved. A transesophageal echocardiogram was performed, which revealed tricuspid valve damage, with one leaflet flaring due to rupture of the papillary muscle (impression of the anterior leaflet). An emergent surgery was performed, and the valve was repaired with excellent outcomes. Additionally, hemodynamic stability was achieved postsurgery, and the repair proved to be effective and durable in the medium term.

Conclusion: Severe traumatic acute tricuspid regurgitation in polytrauma patients can lead to cardiogenic shock and may require emergent correction of the valvopathy, as demonstrated in this case. In instances of traumatic acute tricuspid regurgitation caused by papillary muscle rupture, valve repair is a feasible approach and has shown favorable outcomes at midterm followup. Given the complex medical conditions associated with polytrauma and the typically young age of these patients, particular emphasis was placed on preserving the native valve.

Introduction: Cardiac hypertrophy and fibrotic scarring are fundamental contributors to the progression of heart failure and are associated with poor clinical outcomes. Recent advancements in cardiovascular research have emphasized the central role of epigenetic mechanisms, including DNA methylation, histone modifications, chromatin remodeling, and non-coding RNAs, in regulating the gene expression changes underlying these pathological processes.

Method: A comprehensive literature review was conducted using databases, including PubMed, Scopus, and Web of Science. Predefined keywords and inclusion/exclusion criteria were applied to select relevant studies focusing on epigenetic regulation in cardiac hypertrophy and fibrosis. Particular attention was given to studies involving DNA methyltransferases, TET enzymes, histone deacetylases, demethylases, chromatin remodeling complexes, and non-coding RNAs. Methodological transparency was ensured through a structured screening and data extraction process.

Results: The review highlights the dynamic regulation of cardiac gene expression by epigenetic factors. DNA methylation and demethylation influence fibroblast activation and extracellular matrix deposition. Histone-modifying enzymes reshape chromatin architecture, altering transcriptional accessibility. Chromatin remodeling complexes regulate nucleosome positioning during stress responses. Emerging insights into epigenetic memory and transgenerational epigenetic inheritance further reveal the heritable nature of disease susceptibility.

Discussion: These epigenetic perturbations collectively orchestrate the maladaptive gene expression patterns seen in cardiac hypertrophy and fibrosis. Understanding their roles provides a mechanistic basis for identifying biomarkers and therapeutic targets. The review also discusses recent omics-based technologies that aid in the characterization of epigenetic alterations, thereby expanding diagnostic and therapeutic horizons.

Conclusion: Epigenetic mechanisms are pivotal in the development and progression of cardiac hypertrophy and fibrosis. Advances in epigenomic profiling are facilitating the development of precise and targeted interventions. This review underscores the potential of epigenetic therapies and calls for intensified research efforts to translate these findings into clinical applications.

In clinical practice, mortality risk assessment in patients with myocardial infarction often relies on scales such as GRACE and TIMI. However, these scales were developed based on cohorts assembled many years ago. Since then, numerous changes have occurred, ranging from shifts in MI patient profiles to the introduction of new antiplatelet medications and the adoption of more restrictive lipid therapy targets. To address this issue, researchers are working to develop new stratification tools. Artificial intelligence (AI), which finds applications in nearly every area of medicine, also presents solutions to this problem. This review includes sixteen papers that contain machine learning and deep learning models used to prognosticate mortality risk at different points. Machine learning (ML) models, such as random forest, gradient boosting, and support vector machines, have demonstrated good to excellent performance. However, no single algorithm appears to be top-performing. Although artificial neural networks are considered one of the most promising algorithms, they do not invariably outperform other ML methods. The adaptability of AI models to various scenarios and their ability to handle complex datasets reassures us of their potential in cardiology. Concerning variables that influence the risk of mortality, most are well-established factors, such as age, left-ventricular ejection fraction, lipid parameters, and B-type natriuretic peptide. Additionally, less apparent indicators include platelet parameters, neutrophil count, and blood urea nitrogen. In conclusion, utilizing AI-based models in myocardial infarction risk stratification presents a significant opportunity to develop effective and tailored tools.

Introduction: This study aims to investigate the impact of different double-stent methods on the structure and mechanics of coronary bifurcation lesions, providing reference indicators for clinicians in selecting an appropriate interventional procedure.

Methods: Three-dimensional reconstruction of coronary Computed Tomography Angiography (CTA) image data of a patient with coronary bifurcation disease was performed. Two types of double-stent (Cullotte and Crush) procedures were simulated, and their effects were evaluated using Finite element analysis. Intravascular Ultrasound (IVUS) validation and retrospective clinical analysis were performed to support computational findings.

Results: The stress distribution following the Cullotte stent was concentrated in the SB, whereas the stress after the Crush procedure was localized at the overlap with the proximal main vessel three-layer stent. Compared with the Crush procedure, the Culotte approach resulted in a lower percentage of double-stent malapposition, better dilation of vascular stenosis, and less narrowing of the SB stent, suggesting a more favorable clinical outcome. IVUS validation and retrospective clinical analysis were performed to support computational findings.

Discussion: Culotte stenting resulted in better stent-vessel conformity and more favorable stress distribution. The findings support FEA as a valuable tool in procedural planning.

Conclusions: The findings suggest that the Culotte technique may offer mechanical advantages over the Crush technique, potentially improving long-term clinical outcomes. These results emphasize the role of computational modeling in optimizing interventional strategies.

Introduction: Amyloidosis complicated by heart failure (HF) poses significant mortality. We sought to identify trends in comorbid amyloidosis and HF mortality in the recent 22- year period.

Methods: Mortality due to amyloid and HF as contributors of death were queried from death certificates using the CDC database from 1999 to 2020. Mortality rates and their 95% confidence intervals were adjusted for age (AAMR) through the Direct method and compared by demographic subpopulations. The Monte-Carlo permutation test was used to estimate the annual percentage change (APC). Log-linear regression models were utilized to assess temporal variation in mortality.

Results: Age-adjusted mortality rates (AAMR) increased from 0.09 [0.08-0.10] in 1999 to 0.27 [0.25-0.29] in 2020. Mortality increased from 1999 to 2013 (APC +1.4, p=0.048) with an accelerating inflection point in 2013 to 2020 (APC +13.3, p<0.001). AAMR was higher among male populations (AAMR 0.20 [0.20-0.21]) compared to female populations (AAMR 0.07 [0.07- 0.07]). A significant inflection point in uprising mortality rates was observed for both male and female populations in 2013 (p<0.001). Mortality was highest among Black populations (AAMR 0.33), followed by White (AAMR 0.10), Asian/Pacific Islander (AAMR 0.06), and American Indian/Alaska Native populations (AAMR 0.04). Among Black populations, mortality remained consistent from 1999 to 2012 (APC +1.1, p=0.184), followed by an increase from 2012 to 2020 (APC +14.0, p<0.001). Among White populations, mortality remained stagnant from 1999 to 2013 (APC +0.7, p=0.302), followed by an increase starting in 2013 to 2020 (APC +13.5, p<0.001).

Discussion: Our findings of a marked rise in HF-related mortality in patients with amyloidosis since 2013 highlighted the profound impact of enhanced diagnostic awareness, novel imaging techniques, and emerging therapeutics. Our analysis also showed mortality disparities between sexes, and geographic locations, races, and ethnicity that warrant targeted public health interventions.

Conclusions: Amyloid and HF mortality increased in the recent 22-year period, primarily starting in 2013, emphasizing the urgent need for targeted intervention to address these disparities.

Introduction: Immunologic responses to cardiac allografts initiate before transplantation during brain-dead organ procurement and might persist for years after transplantation, culminating in chronic allograft dysfunction. Despite remarkable advances in post-transplant care and immunosuppressive agents, acute cellular and antibody-mediated rejections as well as chronic allograft vasculopathy significantly affect cardiac allograft and patient survival.

Methods: Herein, recent findings of the molecular mechanisms involved in the inflammatory responses before and after heart transplantation, including brain death donor inflammation, acute cellular rejection, antibody-mediated rejection, and chronic allograft dysfunction, have been summarized, along with novel therapeutic approaches for their treatment. Finally, recent developments in prognostic and diagnostic biomarkers for immunological complications have been provided, with an overview of the most promising biomarkers to date.

Results: Due to the recent developments in the description of molecular mechanisms involved in the immunopathogenesis of cardiac allograft rejection, some immune cells, proinflammatory cytokines, and adhesion molecules have been proposed as therapeutic targets for the prevention or treatment of alloimmune responses. In addition, several molecules derived from graft tissue or immune cells, e.g. natriuretic peptides, cardiac troponins, exosomal products, microRNAs, and donor-derived cell-free DNA, have been suggested as potential biomarkers for the prediction or diagnosis of cardiac transplant rejection.

Conclusion: Considering the need to design non-invasive, low-cost tests for early diagnosis of post-transplant complications and convenient follow-up of the cardiac transplant recipients, peripheral blood biomarkers could be appropriate candidates for this purpose.

Introduction: The P2X7 receptor (P2X7R), which mediates inflammation, is implicated in an extensive variety of diseases, including cardiovascular dysfunction. Recently, studies focusing on the role of P2X7R in cardiovascular disorders have garnered significant attention. However, a bibliometric evaluation within this area has yet to be carried out.

Methods: A bibliometric analysis was performed by searching for research related to P2X7R and cardiovascular diseases in the Web of Science Core Collection (WoSCC) database from 2005 to 2024. The tools CiteSpace and VOSviewer were utilized to analyze data and create visual representations of various elements, including countries, institutions, authors, journals, and keywords.

Results: Over the past two decades, 371 articles in English were obtained in the last 20 years. The People's Republic of China, Nanchang University, the journal 'Purinergic Signalling,' and author Shandong Liang had the highest productivity in their respective categories. The top 4 keywords were ''activation,'' ''p2x7 receptor,'' ''ATP,'' and ''inflammation''. Burst keyword analysis indicated that ''purinergic signaling'' and ''oxidative stress'' are emerging key areas worthy of further investigation. These topics, seeing a surge in interest, are predicted to remain prominent in research.

Discussion: This is the first bibliometric analysis of P2X7R in cardiovascular disorders, which reports the hot spots and emerging trends. The interaction between ''purinergic signaling,'' ''inflammation,'' and ''oxidative stress'' are considered to be the current research priorities, suggesting that these topics are likely to remain central in future research.

Conclusion: This study underscores the growing importance of P2X7R in cardiovascular research and offers valuable insights to guide future investigations.

Ferroptosis, an instance of iron-dependent programmable cell death that results from oxidative stress & lipid peroxidation, has garnered interest due to its associations with cardiovascular diseases, such as atherosclerosis, myocardial infarction, as well as heart failure. Unlike necrosis or apoptosis, ferroptosis involves unique metabolic pathways that disrupt cellular redox balance and lipid homeostasis, leading to substantial cell damage in cardiovascular tissues. It is becoming recognized that phytoconstituents-bioactive compounds derived from plants-can modify ferroptosis pathways and provide cardioprotective advantages. Compounds including curcumin, resveratrol, quercetin, tanshinone IIA, and epigallocatechin gallate (EGCG) have shown potential in preclinical studies by concentrating on significant ferroptotic processes. Finally, by controlling iron homeostasis, boosting antioxidant responses (such as Nrf2 pathway activation), and reducing lipid peroxidation, these phytochemicals may mitigate ferroptosisinduced cardiac cell death. In animal studies, these natural compounds have shown promise in reducing oxidative damage and improving heart function after injury. This article summarises the mechanisms via which a variety of phytoconstituents influence ferroptosis and discusses their potential as an adjuvant treatment for CVD. While these findings are encouraging, further research is needed to use them in clinical settings, with a focus on long-term safety in human populations, optimal dose, and absorption. The cardioprotective properties of phytoconstituents, which focus on ferroptosis, may provide a unique, plant-based therapeutic strategy for the treatment of CVDs.