Minerva cardiology and angiology最新文献

Obesity is a major risk factor for chronic non-communicable diseases (NCDs) and it has increased to epidemic proportions. Unhealthy diet represents a modifiable risk factor for both obesity and NCDs, however, there is no universal dietary intervention to improve obesity-related NCDs and particularly to reduce the risk for major adverse cardiovascular events. Energy restriction (ER) and diet quality changes, with and without ER, have been widely investigated in preclinical and clinical studies, however, the potential underlying mechanisms driving the benefits of those dietary interventions remain largely unclear. ER affects multiple metabolic, physiological, genetic, and cellular adaptation pathways associated with prolonged lifespan, particularly in preclinical models, while these benefits remain to be established in humans. Moreover, the sustainability of ER and its implementation across the different diseases remains challenging. On the other hand, diet quality with improvements, with or without ER, has been associated with more favorable long-term metabolic and cardiovascular outcomes. This narrative review will describe the role of ER and/or diet quality improvements on the risk for NCDs. It will also discuss the potential mechanisms of action underlying the potential beneficial effects of those dietary approaches.

Coronary physiological assessment has garnered extensive application in managing patients with coronary artery disease, encompassing both acute and chronic scenarios. Beyond the historical purpose as tool to define the hemodynamic significance of a given artery lesion, coronary artery physiology allows for a complete investigation of epicardial and microvascular circulation. The longitudinal assessment of the distribution pattern of coronary disease based on pressure wire technology provides crucial information to define the best management and procedural planning. Moreover, post-percutaneous coronary intervention physiology reassessment showed a strong association with clinical outcomes and, more importantly, it can spot residual pressure gradients potentially amenable to further intervention and optimization. Growing evidence about the non-invasive angiography-based indices helps to overcome the limitations of the use of intracoronary physiology. This review aims to provide an overview of different utilizations of coronary physiology offering a historical perspective with a particular focus on current challenges and future potential applications.

Residual shunt (RS) after percutaneous patent foramen ovale (PFO) closure has classically been a question of debate for controversial results about its association with increased risk of recurrent ischemic events. Different underlying processes of neural tissue injury have to be taken into account evaluating clinical impact of residual shunt after PFO closure: clotting mechanisms and non-clotting, vasoactive or oxidative mechanisms. Some biochemical studies demonstrated the importance of effective PFO closure aimed to obtain significant reduction of several molecules involved in PFO related strokes. Blood levels of serotonin and homocysteine seem to significantly decrease after percutaneous procedures. A recent study on a pro-thrombotic phenotype of migraineurs with aura and PFO demonstrated that PFO closure reduce activated platelets and thrombin at the value of healthy subjects, underlining the importance of the correct sealing of the defect. The aim of this review is to examine currently available literature studies. Different and discordant results have been obtained due to heterogeneity of study population, instrumental assessment of RS and follow-up methods and length. In the 2021 American Guidelines for the prevention of stroke, RS was definitely considered a predictor of recurrence of ischemic events. Management of this subset of patients is still an unresolved issue and more studies are encouraged.

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.