Minerva cardiology and angiology最新文献

Percutaneous coronary intervention (PCI) of coronary chronic total occlusion (CTO PCI) is one of the most challenging but rewarding procedures in the portfolio of interventional cardiologists. Several challenges, however, still must be overcome and many questions need to be answered. After coronary artery bypass graft (CABG), disease of the conduits and concomitant progression of atherosclerotic disease to CTO of the subtended native coronary vessels are common and associated with onset of new anginal symptoms and worsening of the prognosis. Which is the best strategy for these post-CABG CTOs? Furthermore, what is the role of physiology in the setting of CTO PCI? In the last decades, many researchers tried to demystify the complex maze but technical limitations and the demanding procedure itself, for both the patient and the operator, do not allow extensive investigation of its impact on clinical practice. Can we enhance periprocedural planning of CTO PCI with a more tailored and multidimensional evaluation? Analysis of coronary computed tomography angiography (CCTA) scans is getting more and more incorporated into the clinical routine and training of interventional cardiologists but mainly focuses on structural valvular disease. Nevertheless, with the appropriate expertise, a lot of information can be derived for coronary intervention to improve procedural planning and potentially outcomes. Finally, in the era of drug-eluting stent, is there a place for strategies that minimize metal implantation in the coronaries to further reduce late-onset adverse events in CTO PCI? This approach could be attractive in CTOs due to the higher risk of target vessel failure and revascularization shown in literature but, at the same time, more challenging due to the histological and anatomical complexity of the disease. In this review, we aim to tackle these questions and concomitantly provide a vision of potential future application of new techniques and technology in CTO PCI that could allow further advancement in this field.

Acute coronary syndrome is one of the leading causes of death worldwide. Up to 60% of patients present with additional significant non-culprit lesions. Complete revascularization (CR) of all (culprit and non-culprit) lesions is recommended and recent randomized trials showed the benefit of performing complete multivessel percutaneous coronary intervention in a single setting. Immediate CR is associated with a reduced risk of repeat myocardial infarction and unplanned ischemia driven revascularization. Furthermore, immediate CR resulted in less implanted stents, total contrast use and a shorter duration of hospitalization while maintaining a similar success rate of complete revascularization. Further studies need to evaluate the role of coronary physiology and intravascular imaging for enhanced understanding of the pathophysiology of early events in non-culprit lesions.

Background: The aim of this study is to investigate the association between inflammation-related markers in COVID-19 infection and ST-segment elevation myocardial infarction (STEMI).

Methods: We conducted an observational, single-center, retrospective study between January 2020 and November 2022. A total of 149 patients aged between 34 and 90 years, 28.2% (N.=42) female and 71.8% (N.=107) male, were included in the study. Systemic immune-inflammation index (SII), systemic inflammation-response indexes (SIRI), platelet-to-lymphocyte ratio (PLR) and neutrophil-to-lymphocyte ratio (NLR) were calculated for each patient. The patients were divided into two groups based on their presence or absence of a confirmed SARS-CoV-2 infection.

Results: During the in-hospital follow-up, mortality occurred in 12% (N.=20) of patients. Among the COVID-19 (+) and STEMI group, the mortality rate was 24.3% (N.=10), while it was 5.6% (N.=6) in the COVID-19 (-) and STEMI group (P=0.001). In multivariate logistic regression analysis, SII ([HR] = 7.198 [1.423-36.411], P=0.017) and PLR ([HR] = 5.762 [1.783-18.619], P=0.003) remained significant risk factor for mortality.

Conclusions: The SII, SIRI, NLR, and PLR are relatively new, simple, and effective inflammation-related markers that determine mortality risk in STEMI patients.

Background: Complications of arrhythmia often occur in patients with acute myocardial infarction (AMI). This study mainly explored the expression and diagnostic significance of long non-coding RNA CYTOR (lncRNA CYTOR) in patients with AMI with arrhythmia, and analyzed the effects of CYTOR on inflammation and oxidative stress responses of cardiomyocytes.

Methods: CYTOR expression in serum samples from 119 cases of AMI with arrhythmia and 119 healthy subjects was determined by qRT-PCR. Receiver operating characteristic (ROC) curve was drawn to evaluate the diagnostic function of serum CYTOR in AMI with arrhythmia. AMI cell models were constructed by hypoxia/reoxygenation treatment. The pathological function of CYTOR in AMI was determined by the detection of inflammatory factors and oxidative stress indicators.

Results: Serum CYTOR was upregulated in patients with AMI with arrhythmia, which has a certain ability to distinguish patients from healthy individuals (P<0.001, AUC=0.8963). The levels of interleukin-1beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and malondialdehyde (MDA) were increased in the AMI cell model, while superoxide dismutase (SOD) levels were decreased (P<0.001), which was alleviated by silencing CYTOR.

Conclusions: Overexpression of CYTOR may aggravate the condition of AMI patients with arrhythmia, which promotes oxidative stress injury and inflammatory response of cardiomyocytes. CYTOR can be a reference factor for diagnostic biomarkers of AMI with arrhythmia.

Background: The clinical role of long non-coding RNA (MBNL1-AS1) in diagnosing atherosclerosis (AS) risks of hypertensive patients and the effects of MBNL1-AS1 on vascular smooth muscle cells (VSMCs) triggered by angiotensin II (Ang II) were investigated.

Methods: The hypertensive patients were recruited to assess MBNL1-AS1 expression. The ROC curve and Spearman analysis was performed for the significance of MBNL1-AS1. Human VSMCs were treated with Ang II (10^-5 mol/L) to establish a hypertensive cell model. MTT and Transwell chamber were used in proliferative and migratory detection of cell models. Targets of MBNL1-AS1 were verified by luciferase activity. Functional enrichment of shared targets of miR-424-5p was researched by GO and KEGG analysis.

Results: An increase of MBNL1-AS1 was observed in patients with increased carotid intima-media thickness (cIMT). MBNL1-AS1 could predict the risk of AS and related to cIMT levels. The knockdown of MBNL1-AS1 mitigated the influence of Ang II on cellular proliferation and migration by inhibiting miR-424-5p. Enrichment analysis corroborated that targets of miR-424-5p were mainly involved in serine/threonine kinase activity, MAPK signaling pathway, and PI3K-Akt signaling pathway.

Conclusions: MBNL1-AS1/miR-424-5p axis was connected with the progression of AS induced by hypertension.

Background: Jianxin (JX) granules is a traditional Chinese medicine widely used in the treatment of heart failure (HF), but the mechanism is unclear. This study aimed to investigate the mechanism of JX granules in the treatment of HF based on network pharmacology analysis and in-vivo experiments.

Methods: A series of network pharmacology methods was employed to ascertain potential targets and critical pathways implicated in the therapeutic action of JX granules against HF. Subsequently, molecular docking was utilized to investigate the binding affinity of key active constituents within JX granules to these targets. In-vivo experiments, echocardiography, hematoxylin and eosin, Masson's trichrome assay, and western blot analysis were conducted to validate the efficacy and mechanism of JX granules in treating rats with HF.

Results: A total of 122 active components, 896 drug targets, 1216 HF-related targets, and 136 targets pertinent to drug-disease interactions were identified. 151 key targets and 725 core clusters were detected through protein-protein interaction network analysis. Among these, interleukin 6 (IL-6), vascular endothelial growth factor a (VEGFA), and serine/threonine kinase 1 (AKT1) were core hub genes. Kyoto encyclopedia of genes and genomes (KEGG) enrichment analysis revealed the critical pathways, including epidermal growth factor receptor (EGFR), advanced glycation end products (AGEs) and their receptors (RAGE) pathway, along with hypoxia-inducible factor 1 (HIF-1) signaling pathway. Molecular docking studies demonstrated high binding affinities between key targets and the pivotal active ingredients of Danshenol A, salvianolic acid B, and arachidonic acid. Furthermore, animal studies corroborated that JX granules improve cardiac function and reduce myocardial fibrosis, potentially by modulating the expression of IL-6, VEGFA, and p-AKT1.

Conclusions: The bioactive components within JX granules, such as Danshenol A, salvianolic acid B, and arachidonic acid may exert therapeutic effects on HF through modulation of IL-6, VEGFA, and AKT1 gene expression. This study provides a scientific basis for subsequent clinical application of JX granules and an in-depth investigation of their mechanisms of action.

Background: Pulmonary embolism (PE) treatment is based on risk stratification according to European Society of Cardiology (ESC) guidelines. However, emerging therapies in acute PE may require a more granular risk classification. Therefore, the objective of the present study was to propose a new RIsk claSsification Adapting the SCAI shock stages to right ventricular failure due to acute PE (RISA-PE).

Methods: This registry included consecutive intermediate-high risk (IHR) or high-risk (HR)-PE patients selected for catheter-directed interventions (CDI) from 2018 to 2023 in 15 Spanish centers (NCT06348459). Patients were grouped according to RISA-PE classification as A (right ventricular dysfunction and troponin elevation); B (A + serum lactate >2 mmol/L OR shock index ≥1); C (persistent hypotension); D (obstructive shock); and E (cardiac arrest). In-hospital adverse events were assessed to evaluate RISA-PE performance.

Results: A total of 334 patients were included (age 62.1±15.2 years, 55.7% males). The incidence of in-hospital all-cause death was progressively higher with increasing RISA-PE stage (1.2%, 6.4%, 19.0%, 25.6%, and 57.7% for stages A, B, C, D, and E, respectively, P value for linear trend<0.001). However, using the ESC classification, there was an abrupt difference between IHR- and HR-PE patients regarding mortality (4.3% vs. 29.3%, P<0.001). The incidence of in-hospital major bleeding and acute kidney injury followed a similar pattern.

Conclusions: The user-friendly RISA-PE classification may improve the granularity in stratifying PE patients' risk and warrants evaluation in larger studies with different therapeutic approaches in order to detect its utility as a decision-making scale.

Background: The aging population in the USA has led to a concomitant rise in the prevalence of vascular dementia (VaD), yet there remains a paucity of investigation into mortality trends associated with VaD among adults.

Methods: This cross-sectional analysis utilized death certificate data from the Centers for Disease Control and Prevention's WONDER database. VaD-associated mortality was identified using the International Statistical Classification of Diseases and Related Health Problems-10th revision (ICD-10) code F01. Crude, and age-adjusted VaD-associated mortality rates per 100,000 and their corresponding 95% confidence intervals (CI) were computed. Age-adjusted mortality rates (AAMRs) were standardized to the 2000 US census population.

Results: From 2005 to 2020, there were 375,575 deaths attributed to VaD among older adults. We observed a gradual increase in AAMR (APC: 3.70, 95% CI [-4.14, 5.21]) from 2005 to 2015, succeeded by a pronounced escalation (APC: 9.07, 95% CI [6.09, 17.62]) until 2020. The highest AAMR was noted in the West (17.65, 95% CI [17.55, 17.76]), followed by the Midwest (AAMR: 12.66, 95% CI [12.58, 12.75]), the South (AAMR: 12.60, 95% CI [12.54, 12.67]), and the Northeast (AAMR: 8.60, 95% CI [8.53, 8.68]). Metropolitan areas exhibited higher AAMRs (10.9, 95% CI [10.8, 11.0]) compared to non-metropolitan areas (8.1, 95% CI [8.00, 8.3]). Among age groups, individuals aged 75-85 and older showed the highest overall AAMR (99.80, 95% CI [99.47, 100.14]). In addition, non-Hispanic Black or African-American subset of the population showed the highest overall AAMR (8.12, [95% CI: 8.03, 8.20]).

Conclusions: Our findings underscore the imperative for targeted public health interventions aimed at addressing regional disparities and age-specific vulnerabilities to mitigate the mounting burden of VaD-related mortality.

Right heart function is essential for overall heart health and plays a crucial role in the prognosis of patients with heart failure. A comprehensive assessment of the right ventricle (RV) that includes various clinical and hemodynamic parameters, as well as imaging techniques, provides important insights into the structure and function of the right heart. Advanced imaging methods, such as cardiac MRI, offer further clarity regarding the morphology and performance of the right heart. Interventional therapies have transformed treatment options and the prognosis for patients with advanced RV failure, and these therapies should be integrated into a comprehensive care plan. Ongoing research into the molecular and genetic factors contributing to right heart dysfunction is expected to reveal new therapeutic targets. Continued advancements in imaging and treatment options are vital for enhancing patient outcomes. In this review, we provide a detailed analysis of RV function, diagnosis, and therapy for RV failure.