Minerva cardiology and angiology最新文献

Angiotensin receptor neprilysin inhibitor (ARNI) decreases renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous systems (SNS) activity promoting vasodilation, decreasing myocardial hypertrophy and fibrosis. Beyond the SNS, RAAS and natriuretic peptide systems, ARNI results in increased circulatory and myocardial nitric oxide levels activating cGMP and protein kinase G, which reduces oxidative stress, myocyte hypertrophy, cell death and has anti-thrombotic effects. ARNIs have a class I indication by heart failure (HF) guidelines in HFrEF patients with NYHA class II to III symptoms. Beyond HFrEF, the use of ARNIs has also been expanded to other clinical settings including HF with preserved ejection fraction (EF, HFpEF), acute HF, advanced HF, hypertension, arrhythmias and chronic kidney disease. This paper reviews the clinical benefits of ARNIs in both HF and the aforementioned cardiovascular conditions. We also discuss the combined use of ARNI with SGLT2i and their potential synergistic benefits on cardiovascular outcomes.

Background: The no-reflow phenomenon (NRP) is associated with increased mortality and morbidity in patients with ST-segment elevation myocardial infarction (STEMI). Despite the lack of a definitive treatment for NRP, predicting procedural success remains a challenge. This study aims to evaluate the potential of intracoronary electrocardiography (ic-ECG) in predicting the success of the primary percutaneous coronary intervention (pPCI) in STEMI patients who develop NRP.

Methods: Patients with acute anterior STEMI who underwent pPCI between November 2021 and May 2022 were included in this prospective study. Patients were categorized into two groups based on the thrombolysis in myocardial infarction (TIMI) flow grade, with those having a grade less than 3 defined as NRP. The NRP group was further analyzed to explore the relationship between the percentage of ST-segment resolution (STR) in ic-ECG records taken during pPCI and the recovery of left ventricular ejection fraction (LVEF).

Results: Seventy-one patients with acute anterior STEMI were included in the study, 26 of whom (36.6%) developed the NRP. Baseline characteristics such as peak troponin levels (6267.8±2488.4 vs. 3244.6±3183 ng/mL, P=0.013), low-density lipoprotein cholesterol (LDL-C) levels (104.5±40 vs. 138.8±29.9 mg/dL, P=0.021), and total cholesterol levels (167.5±44.5 vs. 222.7±69.2 mg/dL, P=0.024) were significantly different between patients with and without LVEF recovery in the NRP group. Importantly, the change in ic-ECG STR was significantly higher in the recovery group (65.5±17% vs. 21±22.3%, P<0.001). Multivariate regression analysis confirmed that the percentage change in ic-ECG STR was an independent predictor of LVEF recovery (P=0.035). A cut-off ic-ECG STR change greater than 42% was identified through ROC analysis as a predictor of LVEF recovery with a sensitivity of 100% and specificity of 84.6% (AUC=0.938, P<0.001).

Conclusions: The percentage change in ST-segment resolution measured by ic-ECG is an independent predictor of LVEF recovery in STEMI patients who develop NRP. A greater than 42% change in ic-ECG STR during the procedure is independently associated with improved LVEF, highlighting its value in guiding clinical decision-making and improving patient outcomes.

Eosinophilic myocarditis (EM) is characterized by acute myocardial inflammation due to eosinophilic tissue infiltration. It is a rare and underdiagnosed condition, which may be either idiopathic or secondary to vasculitides, hypereosinophilic syndromes, drugs, or infections. Diagnosis is based on laboratory findings, echocardiography, cardiac magnetic resonance imaging and may sometimes need endomyocardial biopsy. Treatment depends on the underlying cause and often consists of immunosuppressive agents and anticoagulation therapy. This case series includes nine patients with EM, specifically seven cases secondary to eosinophilic granulomatosis with polyangiitis, one case secondary to acute lymphocytic leukemia, and one case of idiopathic EM, and aims to describe and review the diagnostic work-up and tailored treatment of this heterogeneous disease.

Background: The association between epicardial adipose tissue (EAT) and heart failure has garnered significant attention. The objective of this study is to investigate the relationship between EAT and cardiac function across various heart failure phenotypes.

Methods: The study cohort included 33 cases in the control group and 121 cases in the heart failure group, stratified into subgroups: 40 with heart failure with reduced ejection fraction (HFrEF), 38 with heart failure with mid-range ejection fraction (HFmrEF), and 43 with heart failure with preserved ejection fraction (HFpEF). Researchers collected epicardial adipose tissue thickness, clinical data, and echocardiographic parameters from all participants. Left ventricular (LV) systolic function was assessed using global longitudinal strain (GLS), and left atrial (LA) function was evaluated using LA strain during reservoir, conduit, and contraction phases. Fitted curves illustrating the relationship between EAT and LV ejection fraction (LVEF), as well as GLS and LA strain, were constructed. Multivariable linear regression was employed to analyze the correlation between EAT and GLS, LASr, LAScd, and LASct after adjusting for confounding factors.

Results: A nonlinear relationship was observed between EAT and LVEF, GLS, LASr, LAScd, and LASct. EAT thickness varied across groups: HFpEF (7.9±0.8 mm)>Control (5.1±0.6 mm)>HFmrEF (4.6±0.9 mm)>HFrEF (4.0±0.7 mm). After adjusting for age, gender, BMI, and relevant medical history, the correlation coefficients between EAT and GLS were 0.21, 0.17, and -0.12 in HFrEF, HFmrEF, and HFpEF groups, respectively. In the HFrEF group, EAT showed positive correlations with LASr and LAScd (0.1 and 0.1), and negative correlations with LASr, LAScd, and LASct in the HFpEF group (-0.03, -0.06, and -0.07).

Conclusions: EAT thickness follows the order: HFpEF>Control>HFmrEF>HFrEF. Thicker EAT in HFpEF is associated with poorer LV and LA function, while the opposite trend is observed in HFrEF and HFmrEF. LA function is more compromised in HFmrEF and HFrEF compared to HFpEF.

Introduction: The ideal antiplatelet therapy to maintain graft patency after coronary artery bypass graft surgery (CABG) remains controversial. This review of randomized controlled trials (RCTs) aims to compare aspirin monotherapy, ticagrelor monotherapy, dual antiplatelet therapy (DAPT) with aspirin and ticagrelor (Asp+Tica) or with aspirin and clopidogrel (Asp+Clopi) to evaluate differences in post-CABG saphenous vein graft (SVG) occlusion, internal mammary artery (IMA) occlusion, myocardial infarction (MI), bleeding, and all-cause mortality (ACM) rates.

Evidence acquisition: The literature review was conducted on several electronic databases, including Medline, Embase, and Cochrane Central, from inception to August 10, 2022. Data was extracted using a predefined proforma. A Bayesian random-effects model was used for calculating point effect estimates (odds ratio and standard deviation). Quality assessment was done using the Cochrane RoB-2 tool.

Evidence synthesis: Ten RCTs comprising 2139 patients taking anti-platelets post-CABG were included. For preventing SVG occlusion, Asp+Tica showed the lowest mean AR of 0.144±0.068. Asp+Tica also showed a trend toward lesser postoperative MI risk and lower ACM rates, with a mean AR of 0.040±0.053 and 0.018±0.029, respectively. For maintaining IMA graft patency, Asp+Clopi showed the lowest mean AR of 0.092±0.053. Ticagrelor had the lowest mean AR of 0.049±0.075, with Asp+Tica showing a similar mean AR of 0.049±0.045 for postoperative major bleeding risk.

Conclusions: Our analysis demonstrates that Asp+Tica can be the ideal therapy for patients undergoing CABG using SVG as it decreases the risk of post-CABG SVG occlusion and is not associated with a significantly higher risk for major bleeding.

Background: Circular RNAs (circRNAs) are implicated in the pathogenesis of acute myocardial infarction (AMI). Current research aims to evaluate the diagnostic and functional value of circFOXP1 in AMI patients.

Methods: The expression of circFOXP1 was assessed using RT-qPCR, and its diagnostic potential was determined through receiver operating characteristic (ROC) curve. The target gene of circFOXP1 was identified using a luciferase reporter assay. An in vitro hypoxia/reoxygenation (H/R) model was established in AC16 cells, while an AMI model was constructed in C57BL/6 mice. The proliferation and apoptosis of AC16 cells were evaluated using CCK8 and flow cytometry (FCM). The impact of circFOXP1 on inflammation was measured by assessing levels of TNF-α, IL-1β, and IL-6, while the effects of circFOXP1 on oxidative stress were evaluated through measurements of reactive oxygen species (ROS), glutathione (GSH), and lactate dehydrogenase (LDH) levels.

Results: circFOXP1 expression was found to be downregulated in AMI patients compared to controls. The ROC curve indicated an area under the curve (AUC) was 0.881 (95%CI=0.847-0.915), with a sensitivity of 0.930 and a specificity of 0.785. Additionally, miR-9-3p was identified as a direct target gene of circFOXP1. High levels of circFOXP1 did not significantly affect f the proliferation of H/R stimulated AC16 cells; however, increased circFOXP1 resulted in significant reduction in cell apoptosis (P<0.001). TNF-α, IL-1β, and IL-6 levels were significantly lower in pcDNA3.1-circFOXP1-transfected cells (P<0.001). ROS concentration and LDH level were markedly reduced in these cells (P<0.01), while GSH level (P<0.001) was significantly elevated. miR-9-3p, as a direct target gene of circFOXP1, was found to reverse the effects of circFOXP1 on H/R AC16 cells and AMI model.

Conclusions: circFOXP1 was decreased in AMI patients and may serve as a diagnostic marker for AMI. Overexpression of circFOXP1 was shown to suppress apoptosis, inflammation, and oxidative stress via miR-9-3p in AC16 cells and the AMI model.

Background: In the morphology of coronary arteries, changes such as atherosclerosis and ectasia occur over time. The aim of this study is to identify the factors influencing changes in coronary artery morphology.

Methods: One hundred twenty-seven patients were evaluated of their baseline characteristics, echocardiography findings, laboratory values, and screening for systemical diseases. Patients were divided into three groups. Group N: the group with normal coronary arteries. Group A: the group with atherosclerosis. Group E: the group with ectasia and/or aneurysm. Mann-Whitney U Test and Kruskal Wallis Test were used in analysis of measurement data that did not conform to the normal distribution.

Results: Diabetes mellitus, hypertension, and chronic kidney disease were found to be statistically significantly higher in Group A. The mean TAPSE/sPAP ratio in Group A patients is lower than in Group E and normal individuals (P<0.001) Vasculitis is more frequently observed in Group E (13.3%) compared to Group A. The frequency of at least one musculoskeletal disease in rheumatologic screening in Group A (100.0%) and in Group E (100.0%) is higher than in the Group N (69.8%) (P<0.001).

Conclusions: No specific risk factor or disease was identified in this study that increases the frequency of coronary artery ectasia. However, diabetes mellitus, hypertension, chronic kidney disease, and low ejection fraction were found to be significantly associated with atherosclerosis.

Percutaneous left atrial appendage occlusion (LAAO), currently recognized as a procedure with relatively low risk, is increasingly being adopted in clinical practice. However, due to the preventive nature of the procedure and the necessity to compare it with newer and safer oral anticoagulants, further optimization is required to address remaining challenges. These latter include acquiring comprehensive data on safety and efficacy, establishing standardized pre-procedural planning, and simplifying procedural process. Consequently, we have provided an overview that encompasses future opportunities for enhancing procedural safety and efficacy, thereby establishing LAAO as the mainstream strategy for stroke and systemic embolism prevention in patients with atrial fibrillation and absolute contraindications to anticoagulant drugs.

Background: Hypertension is the most prevalent chronic disease globally and the treatment and control ratio of hypertension patients are still low. The function of lncRNA MIR210HG in hypertension has not yet been announced.

Methods: Eighty-three hypertension patients and 79 healthy individuals were enrolled. The Human Umbilical Vein Endothelial Cells (HUVECs) treated with Ang II were employed to imitate hypertension. The relative expression of MIR210HG and miR-125b-5p were evaluated by qRT-PCR while the ROC curve was applied to assess the diagnostic performance of MIR210HG. The CCK-8 assay was performed to detect the proliferation ability. The transwell assay and flow cytometry were used to analyze the migratory or apoptosis, respectively. The dual luciferase reporter system was used to confirm the targeted relationship between MIR210HG and miR-125b-5p.

Results: Up-regulated MIR210HG was found in hypertension patients (P<0.001) compared to healthy individuals and the upregulation was positively associated with the severity of hypertension (P<0.01). Up-regulated MIR210HG exhibited a promising diagnosability for hypertension patients. The area under the ROC curve was 0.8765 with high sensitivity (81.93%) and specificity (83.28%). In hypertension cell model, increased MIR210HG was observed along with declined cell proliferation, migration and enhanced apoptosis, which were reversed by MIR210HG knockdown. MIR210HG knockdown also inhibited inflammation levels including TNF-α, IL-1β and IL-6. The miR-125b-5p was a potential downstream target of MIR210HG and they were negatively correlated in expression.

Conclusions: Up-regulated MIR210HG was a promising diagnostic biomarker in identifying hypertension patients. MiR-125b-5p was a potential downstream target of MIR210HG in HUVECs.

Acute chest pain (ACP) is one of the most common symptoms in patients admitted to emergency departments (ED). It can be related to several life-threatening cardiovascular conditions such as acute coronary syndrome (ACS), aortic dissection, and pulmonary embolism. The optimal triage of patients with ACP is a clinical and healthcare necessity given the large number of patients daily admitted to ED with this symptom. The first contact with the patient in ED includes the clinical appraisal of the characteristics of ACP and coexisting symptoms, and the assessment of the patient's medical history. Risk scores may help stratify a patient's likelihood of having cardiac chest pain. The ECG examination allows the identification of patients with ST-segment elevation, depression, or T-wave changes, but may be normal in patients with non-ST-segment elevation ACS. Rapid protocols based on serial high-sensitivity cardiac troponin assays within one or two hours are recommended for identifying candidates for early discharge. Due to the bedside feasibility, non-invasiveness, and wide availability, transthoracic echocardiography represents the first-line imaging modality for evaluating patients with ACP. In selected cases, computed tomography angiography may also be performed. A practical approach to ACP in ED should improve patient outcomes and reduce healthcare system costs. This review aimed to provide an overview of the characteristics of patients with ACP of cardiac origin and to describe the state of the art about their management in the ED.