Minerva cardiology and angiology最新文献

Cardiac contractility modulation (CCM) signals are non-excitatory signals that are applied during the myocyte's absolute refractory period. These signals have been demonstrated to have an inotropic effect without increasing myocardial oxygen consumption. This has been observed in both preclinical animal studies and randomized clinical trials. CCM influences the expression of various genes that are abnormally expressed in heart failure: it reverses fetal myocyte gene programming associated with heart failure and regulates the expression of genes associated with calcium cycling and myocardial contractile machinery. Clinical investigations have primarily focused on patients with heart failure and normal QRS duration where CCM has demonstrated its safety and effectiveness in reducing heart failure-related hospitalizations, as well as improving symptoms, functional capacity, and overall quality of life. Currently, for individuals experiencing symptomatic heart failure with an ejection fraction ranging from 25% to 45% and a QRS duration of less than 130 ms, who are not suitable candidates for cardiac resynchronization therapy, CCM offers a viable treatment option. Even though promising results in specific HF subgroups have been published, further studies are needed to understand the role of CCM in tailored treatment for heart failure. Moreover, the role of multimodality imaging in lead placement and prognostic stratification in CCM patients should be further investigated. This review aims to summarize the main pathophysiological evidence related to the use of CCM and to highlight its role as a possible additional weapon in tailored treatment for specific subgroups of patients with heart failure.

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: Atrial fibrillation (AF) is the most common atrial arrhythmia after transcatheter aortic valve implantation (TAVI) and is associated with high mortality. Although some clinical and echocardiographic variables have been defined to predict new-onset atrial fibrillation (NOAF), electrophysiologic (EP) parameters have not been identified yet. We aimed to investigate the impact of atrial refractoriness on NOAF after TAVI.

Methods: Seventy-nine consecutive patients who underwent TAVI were enrolled in this trial. All patients undergoing TAVI were screened for AF.

Results: Fifteen (19%) had AF during the follow-up period. Patients with NOAF were older and had a higher BMI and STS. Left atrial diameter (LAD) was higher, left ventricular ejection fraction (LVEF) was lower, and preprocedural LVEDP was higher in patients with NOAF. As electrophysiologic (EP) parameters, atrial effective refractory periods (AERP) (in high right atrium [AERPHRA], in right posterolateral atrium [AERPRPL], and in distal coronary sinus [AERPDCS]) were lower, difference between atrial effective refractory periods (AERPDISP) and PA intervals were higher in patients with AF than those without AF. The only independent parameter that influenced the development of AF after TAVI was AERPDISP. The Receiver Operating Characteristic (ROC) analysis showed that an AERPDISP>46 msec significantly separated those with AF and those without AF with a sensitivity of 85% and a specificity of 97%.

Conclusions: The current study demonstrates that the only independent variable predicting NOAF is AERPDISP. Therefore, increased AERPDISP values may help predict patients with high risk for NOAF and needing specific therapies.

Background: Acute myocardial infarction (AMI) is a major cause of death in cardiovascular patients. SOCS3's protective role in cardiac I/R-I is being explored, and miRNAs, particularly miRNA-148a-3p, are suspected to target SOCS3. To elucidate the role of miRNA-148a-3p targeting lipid metabolism gene SOCS3 in cardiac ischemia-reperfusion injury (I/R-I) in rats.

Methods: Derived mRNA expression data GSE59867 from GEO, identified 558 lipid metabolism genes from KEGG and GSEA, and screened for differentially expressed genes in acute myocardial infarction (AMI). Predicted miRNA-148a-3p targeting SOCS3 using TargetScanHuman, validated binding via luciferase assay and 3'UTR mutation. Established a rat I/R-I model to assess miRNA-148a-3p and SOCS3 expression, and investigated SOCS3 regulation by miRNA-148a-3p overexpression. Analyzed expression of NF-κB p65, IL-1β, and TNF-α-related proteins, and evaluated cardiac hemodynamics post-SOCS3 regulation by miRNA-148a-3p.

Results: In GSE59867, TSPO, SOCS3, LRP1, PLB1, CYP1B1, PPARG, ACSL1, and CYP27A1 were identified as differentially expressed lipid metabolism genes in AMI. The results of immune infiltration showed a close relationship between the differential lipid metabolism genes and the infiltration of immune cells such as macrophages and monocytes. The random forest algorithm identified SOCS3 as the key gene. The luciferase reporter gene demonstrated the participation of miRNA-148a-3p in the regulation of SOCS3 by binding to its 3'UTR. In vivo experiments revealed low expression of miRNA-148a-3p in myocardial I/R, while SOCS3 was highly expressed. Elevated miRNA-148a-3p expression led to a decrease in SOCS3, NF-κB p65, IL-1β, and TNF-α levels during cardiac I/R-I. Overexpression of miRNA-148a-3p enhanced the cardiac performance in rats experiencing cardiac I/R-I.

Conclusions: Overexpression of miRNA-148a-3p regulates NF-κB signaling pathway by targeting lipid metabolism gene SOCS3, reduces inflammatory response, and then reduces cardiac I/R-I in rats.

The chest X-ray (CXR) has a wide range of clinical indications in the field of cardiology, from the assessment of acute pathology to disease surveillance and screening. Despite many technological advancements, CXR interpretation error rates have remained constant for decades. The application of machine learning has the potential to substantially improve clinical workflow efficiency, pathology detection accuracy, error rates and clinical decision making in cardiology. To date, machine learning has been developed to improve image processing, facilitate pathology detection, optimize the clinical workflow, and facilitate risk stratification. This review explores the current and potential future applications of machine learning for chest radiography to facilitate clinical decision making in cardiology. It maps the current state of the science and considers additional potential use cases from the perspective of clinicians and technologists actively engaged in the development and deployment of deep learning driven clinical decision support systems.

Background: We explored the link between sST2 and NT-proBNP levels and postoperative atrial fibrillation (POAF) incidence in non-cardiac surgery patients in this study.

Methods: The research involved 302 participants over 40 years old who underwent medium and/or high-risk non-cardiac surgeries. These patients were divided into two groups: those who developed POAF and those who did not.

Results: The study cohort consisted of a total of 302 patients, with 14 (4.6%) experiencing POAF. POAF was more common in patients with previous heart failure, a high Left Atrial Volume Index (LAVI), and elevated ASA and RCRI scores (all P<0.05). LAVI, sST2, NT-proBNP, and RCRI scores were found to be independent predictors of POAF in patients undergoing non-cardiac surgeries (all P<0.05). The area under the curve (AUC) for sST2 and NT-proBNP in predicting POAF was 0.707 (95% CI 0.544-0.869; P=0.009) and 0.727 (95% CI 0.598-0.857; P=0.004), respectively. Combined elevation of sST2 and NT-proBNP increased the likelihood of developing POAF by approximately 8.5 times (OR: 8.65, CI 95% 1.06-35.3, P=0.044).

Conclusions: sST2 and NT-proBNP are valuable predictors of POAF in patients undergoing non-cardiac surgery. Identifying these predictors can help in recognizing high-risk patient groups for POAF.

Background: Postoperative atrial fibrillation (POAF) is common after aortic valve replacement (AVR). However, the long-term risk of cerebrovascular ischemic events (CVA) associated with POAF in this scenario is not known. The study objective was to look at the long-term risk of stroke in patients undergoing AVR with POAF compared to those with no POAF, particularly in patients having a bioprosthetic valve and not discharged on anticoagulation. We also looked at the risk of peri-operative stroke and long-term mortality.

Methods: A retrospective study of 831 patients undergoing AVR were followed up for a median of 6.5 years. The primary outcome was the occurrence of CVA after discharge, comparing those with to those without POAF, after excluding patients with a past history of atrial fibrillation (AF). They were divided into two cohorts, those having bioprosthetic valves (without oral anticoagulation), and those with a mechanical valve (with oral anticoagulation). Other outcomes studied were the incidence of early perioperative CVA comparing patients with a history of AF to those with no history, and long-term mortality in the different cohorts.

Results: There was no increased risk of long-term stroke in patients with POAF when compared to those without POAF, neither in bioprosthetic valves (adjusted HR 1.14; CI 95% 0.46-2.83, P=0.78)-nor in mechanical valves (adjusted HR 1.41; CI 95% 0.55-3.65, P=0.48). Patients with a history of AF had an increased risk of perioperative stroke (OR 1.5; CI 95% 1.3-13.8, P=0.01).

Conclusions: Patients undergoing bioprosthetic AVR who develop POAF are not at an increased risk of stroke despite not being on any oral anticoagulation.

Background: Acute myocardial infarction (AMI) remains one of the leading causes of mortality and morbidity worldwide.

Methods: GSE61144 and GSE66360 were the sources of microarray gene expression profiles for acute myocardial infarction patients and were acquired from the Gene Expression Omnibus (GEO) database (https://www.ncbi.nlm.nih.gov/geo/). After merging the datasets, genes that were differentially expressed were chosen.

Results: A total of 234 genes were found to have different expression levels. Of these, 206 genes were upregulated, and 28 genes were downregulated. Five coexpression modules were identified by WGCNA, with the yellow module showing a high correlation with AMI (r=0.65, P=2.0e-15). Ninety-two hub genes were selected in the yellow module by setting a threshold of module membership (MM) greater than 0.8 and gene significance (GS) higher than 0.4. By overlapping these genes with the differentially expressed genes, 81 hub genes were obtained. Five key genes (C5AR1, CXCL1, CXCL2, FPR1, and P2RY13) were identified through PPI analysis. AMI patients exhibited elevated levels of immune cell infiltration, and immune scores in AMI samples were significantly positively correlated with all five key genes. Moreover, the expression levels of these five genes were higher in AMI patients. These five genes possessed area under the curve (AUC) values exceeding 0.8 for diagnosing AMI, thereby demonstrating their efficacy as diagnostic markers.

Conclusions: C5AR1, CXCL1, CXCL2, FPR1, and P2RY13 have the potential to be useful biomarkers in diagnosing AMI and are linked to immune cell infiltration in AMI, opening up new avenues for future research into the pathogenesis of AMI.

Background: Atherosclerosis (AS) is the pathological basis of many cardiovascular and cerebrovascular diseases. To further the investigation of treatments for AS, this research analyzed the role of lncRNA MBNL1-AS1.

Methods: MBNL1-AS1 expression in the serum of AS patients and healthy controls were detected by qPCR. Its diagnostic value in AS was assessed by receiver operating characteristic curve (ROC). Additionally, the link between MBNL1-AS1, carotid intima-media thickness (CIMT) and C-reactive protein (CRP) was examined using the Spearman correlation coefficient. The prognostic value of MBNL1-AS1 in AS was assessed using the Kaplan-Meier survival curve and univariate and multivariate Cox regression analysis.

Results: The present study consisted of 103 patients with AS and 92 healthy patients (HC) and comparison of baseline data between the two groups revealed no remarkable difference (P>0.05) except for CRP (P<0.0001). The serum of AS patients exhibited a considerably higher expression of MBNL1-AS1 in comparison to the HC group. Furthermore, MBNL1-AS1 was highly expressed in patients following higher CIMT and CRP values, which was positively linked with both, respectively (r>0.5, P<0.001). Meanwhile. MBNL1-AS1 has enhanced diagnostic accuracy in AS patients (AUC=0.893) and can be utilized as an independent prognostic factor for AS. Patients with high MBNL1-AS1 expression have a higher likelihood of cardiovascular events. (log rang P=0.0025).

Conclusions: Elevated MBNL1-AS1p can be used as a potential marker for the clinical diagnosis of AS and is linked to a poor prognosis of AS.

Background: The aim of this paper was to investigate the diagnostic significance and severity assessment of serum neuron-specific enolase (NSE) combined with homocysteine (Hcy) for patients with coronary atherosclerosis (coronary artery disease, CAD).

Methods: Two hundred sixty-three patients with coronary artery disease were selected as the research group, and 400 healthy individuals who underwent physical examination during the same period were taken as the control group. Electrochemiluminescence immunoassay and biochemical analyzer were employed to detect the serum NSE and Hcy levels of all subjects. The diagnostic value of combined and individual serum NSE and Hcy detection for the combined group was analyzed using the ROC curve.

Results: The serum NSE (19.91±9.98 vs. 11.17±2.35) and Hcy levels (15.76±5.37 vs. 10.17±3.71) in the research group were significantly higher than those in the control group, with a statistically significant difference (P<0.05). The serum NSE (16.67±4.02 vs. 18.63±5.49 vs. 20.29±5.87) and Hcy levels (13.28±2.49 vs. 15.56±2.67 vs. 16.66±3.94) gradually increased across groups A, B, and C, and inter-group comparisons showed statistically significant differences (P<0.05). The AUC value of combined serum NSE and Hcy detection for CAD patients was higher (0.879 vs. 0.724 vs. 0.827) than individual NSE and Hcy testing. The specificity of Hcy for the diagnosis of CAD was the highest, reaching 90.3%. The sensitivity of combined NSE and Hcy (82.9%) was higher than the individual testing sensitivity of the two groups.

Conclusions: The combined detection of serum NSE and Hcy has high diagnostic efficacy for CAD and provides reference value in assessing the severity of the disease.