Minerva cardiology and angiology最新文献

Background: The aim of this study was using bioinformatic tools to identify hub genes in the relationship between septic cardiomyopathy (SCM) and cuproptosis and predict potential Chinese herbal drug candidates.

Methods: SCM datasets were downloaded from the gene expression omnibus. Cuproptosis related genes were collected from a research published on Science in March, 2022. The expression profiles of genes related to cuproptosis in SCM were extracted. Differentially expressed genes (DEGs) were analyzed using R package limma. A single-sample gene set enrichment analysis was conducted to measure the correlation between DEGs and immune cell infiltration. Hub genes were screened out by random forest model. Finally, HERB database and COREMINE database were used to predict Chinese herbal drugs for hub genes and carry out molecular docking.

Results: A total of 9 DEGs were identified. Cuproptosis differential genes PDHB, DLAT, DLD, FDX1, GCSH, LIAS were significantly correlated with one or more cells and their functions in immune infiltration. The random forest model screened pyruvate dehydrogenase E1 beta subunit (PDHB) as the hub gene. PDHB was negatively correlated with Plasmacytoid dendritic cell infiltration. Pyruvic acid, rhodioloside and adenosine were predicted with PDHB as the target, and all three components are able to bind to PDHB.

Conclusions: Cuproptosis related gene PDHB is associated with the occurrence and immune infiltration of septic cardiomyopathy. Rhodioloside and other Chinese herbal drugs may play a role in the treatment of SCM by regulating the expression of PDHB.

Circulating lipoproteins may interact with platelets, increasing platelet sensitivity to aggregating agonists and their tendency towards activation and thrombus formation. In particular, patients with hypercholesterolemia exhibit a higher degree of platelet reactivity compared to normolipidemic. Moreover, accruing evidence report that lipid-lowering therapies can reduce thrombus formation, particularly in the absence of concomitant antiplatelet therapy. However, the underlying biological mechanism(s) explaining these clinical observations are not completely understood. Baseline platelet reactivity and high on-treatment platelet reactivity while on antiplatelet therapy (e.g., aspirin and clopidogrel) are associated with poor clinical outcomes. Therefore, strategies to reduce baseline platelet reactivity or improve the pharmacodynamic profile of antiplatelet therapies are an unmet clinical need. The potential use of lipid-lowering therapies for optimizing platelet reactivity provides several advantages as there is strong evidence that reducing circulating lipoproteins can improve clinical outcomes, and they may avoid the need for potent antiplatelet therapies that, although more effective, are associated with increased bleeding risk. This review will provide a systematic overview of the effects of lipid-lowering therapy on platelet reactivity in patients treated with and without antiplatelet therapy. We will focus on the potential biological mechanism(s) of action and the effect of statins, ezetimibe, proprotein convertase subtilisin/kexin 9 inhibitors, omega-3 fatty acids, and recombinant high-density lipoprotein on platelet reactivity. Ultimately, we will assess the current gaps in the literature and future perspective in the field.

Heart failure is a resource-intensive condition to manage and typically involves a multi-disciplinary and multi-modality approach leading to an expensive treatment paradigm. It is worth noting that hospital admissions constitute over 80% of heart failure management costs. In the past two decades, healthcare systems have developed new ways of following patients remotely to prevent them from being readmitted to the hospital. However, despite these efforts, hospital admissions have still increased. Many successful readmission reduction programs prioritize education and self-care to increase patients' awareness of their disease and promote lasting lifestyle changes. While socioeconomic factors impact success, interventions tend to be effective when medication adherence and guideline-directed medical therapy are emphasized. Monitoring intracardiac pressure can improve resource allocation efficiency and has demonstrated significant reductions in readmissions with improved quality of life in outpatient and remote settings. Data from several studies focused on remote monitoring devices strongly suggest that understanding congestion using physiological biomarkers is an effective management strategy. Since most cases of heart failure are first presented in acute hospitalization settings, immediate access to intracardiac pressure for treatment and decision-making purposes could result in substantial management improvements. However, a notable technology gap needs to be addressed to enable this at a low cost with less reliability on scarce specialist care resources. Contemporary evidence is conclusive that direct hemodynamic are the vital signs in heart failure with the highest clinical utility. Therefore, future ability to obtain these insights reliably using non-invasive methods will be a paradigm-changing technology.

Pre-clinical and clinical studies suggest a role for inflammation in the pathophysiology of cardiovascular (CV) diseases. The NLRP3 (NACHT, leucine-rich repeat, and pyrin domain-containing protein 3) inflammasome is activated during tissue injury and releases interleukin-1β (IL-1β). We describe three paradigms in which the NLRP3 inflammasome and IL-1β contribute to CV diseases. During acute myocardial infarction (AMI), necrotic cell debris, including IL-1α, induce NLRP3 inflammasome activation and further damage the myocardium contributing to heart failure (HF) (acute injury paradigm). In chronic HF, IL-1β is induced by persistent myocardial overload and injury, neurohumoral activation and systemic comorbidities favoring infiltration and activation of immune cells into the myocardium, microvascular inflammation, and a pro-fibrotic response (chronic inflammation paradigm). In recurrent pericarditis, an autoinflammatory response triggered by cell injury and maintained by the NLRP3 inflammasome/IL-1β axis is present (autoinflammatory disease paradigm). Anakinra, recombinant IL-1 receptor antagonist, inhibits the acute inflammatory response in patients with ST elevation myocardial infarction (STEMI) and acute HF. Canakinumab, IL-1β antibody, blunts systemic inflammation and prevents complications of atherosclerosis in stable patients with prior AMI. In chronic HF, anakinra reduces systemic inflammation and improves cardiorespiratory fitness. In recurrent pericarditis, anakinra and rilonacept, a soluble IL-1 receptor chimeric fusion protein blocking IL-1α and IL-1β, treat and prevent acute flares. In conclusion, the NLRP3 inflammasome and IL-1 contribute to the pathophysiology of CV diseases, and IL-1 blockade is beneficial with different roles in the acute injury, chronic inflammation and autoinflammatory disease paradigms. Further research is needed to guide the optimal use of IL-1 blockers in clinical practice.

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.

Introduction: During the last decade, a small number of studies have used feature tracking (FT) cardiovascular magnetic resonance imaging (CMR) and speckle tracking echocardiography (STE) to investigate the effect of pectus excavatum (PE) on biventricular mechanics. The present systematic review and meta-analysis has been primarily designed to summarize the main findings of these studies and to examine the overall influence of PE on both left ventricular (LV)- and right ventricular (RV)-global longitudinal strain (GLS).

Evidence acquisition: All imaging studies assessing conventional indices of biventricular size and function and myocardial strain parameters in PE individuals vs.. healthy controls, selected from PubMed and EMBASE databases, were included. The risk of bias was evaluated by using the National Institutes of Health (NIH) Quality Assessment of Case-Control Studies. Continuous data (LV-GLS and RV-GLS) were pooled as a standardized mean difference (SMD) comparing PE group with healthy controls. The overall SMDs of LV-GLS and RV-GLS were calculated using the random-effect model.

Evidence synthesis: The full-text of 7 studies with a total of 374 PE individuals and 141 healthy controls were analyzed. Both average LV-GLS (-17.1±3.5% vs. -18.9±3.0%, P<0.001) and RV-GLS (-17.9±5.2% vs. -20.9±3.7%, P<0.001) were significantly lower in PE patients than controls. Subtotal SMD was small and not statistically significant for CMR studies assessing LV-GLS (-0.23, 95%CI -0.92,0.47, P=0.52) and RV-GLS (-0.33, 95%CI -0.94,0.28, P=0.28), whereas subtotal SMD was large and statistically significant for echocardiographic studies measuring LV-GLS (-1.46, 95%CI -2.55,-0.38, P=0.008) and RV-GLS (-1.71, 95%CI -2.68,-0.74, P=0.001). The overall effect of PE was statistically significant on RV-GLS (SMD -0.72, 95%CI -1.24,-0.21, P=0.006), but not on LV-GLS (SMD -0.58, 95%CI -1.17,-0.00, P=0.05). Substantial heterogeneity was found for the studies assessing LV-GLS (I²=88.2%) and RV-GLS (I²=86.9%). Egger's test gave a P-value of 0.64 for LV-GLS and 0.47 for RV-GLS assessment, indicating no publication bias. On meta-regression analysis, none of the moderators was significantly associated with effect modification for both LV-GLS and RV-GLS (all P<0.05).

Conclusions: The influence of PE on RV mechanics is greater than on LV mechanics. STE and FT-CMR may detect subtle impairment in biventricular mechanics in PE individuals. The attenuation of myocardial strain indices revealed by STE may be enhanced by methodological issues.

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.