Minerva cardiology and angiology最新文献

Background: Coronary chronic total occlusions (CTO) are associated with an increased chance of untreatable symptoms and worse prognosis. However, limited data are available about the interaction between treatment strategy, potential ischemia burden reduction and quality of life (QoL) improvement.

Methods: Our prospective registry aims to assess the potentially different impacts of treatment strategies (coronary artery bypass grafting vs.. percutaneous coronary intervention vs. optimal medical therapy) on clinical outcomes and QoL domains. This article specifically focuses on describing the registry's rationale, design, and baseline characteristics of the enrolled patients.

Results: A total of 157 patients were enrolled. Every patient was evaluated for baseline symptoms, ischemic burden and QoL and allocated to a treatment arm. In 112 patients (71.3%) ischemia baseline assessment was performed and for 116 (73.9%) Seattle Angina Questionnaire (SAQ) was available. At baseline, a significant functional limitation was evident, especially in terms of angina stability (mean score 69±31%) and disease perception (mean score 69±27%). In 49.1% of patients, ischemia testing was positive. Patients with documented ischemia were generally more symptomatic (CCS class 1 36.4% vs.. 57.9%, P=0.023) and a significant inverse correlation between CCS class and SAQ domains was found. No association between ischemia burden and self-reported QoL scores was found.

Conclusions: The PETS-CTO registry is the first prospective registry investigating the impact of different treatment strategies on QoL and ischemia burden in patients with CTOs. At baseline, the severity of symptoms was directly associated with ischemia burden and inversely associated with self-reported QoL evaluation.

Background: To investigate the protective effect of carvedilol against atherosclerosis by inhibiting the NLRP3 inflammasome.

Methods: In-vitro experiments, human umbilical vein endothelial cells (HUVEC) were divided into the control group, ox-LDL group, carvedilol 5 μM group, carvedilol 10 μM group, and carvedilol 20 μM group. The optimal concentration of carvedilol was determined using the CCK-8 method to assess cell proliferation levels and oil red O staining to observe intracellular lipid droplet formation. Subsequently, the cells were further divided into the control group, ox-LDL group, carvedilol 5 μM (optimal concentration) group, and MCC950 (inhibitor of NLRP3 Inflammasome) group. The expression levels of intracellular proteins NLRP3, pro-Caspase-1, Caspase1, pro-IL-1β, IL-1β, p65, GSDMD, and N-GSDMD were detected by ELISA, or Western Blotting.

Results: Compared to the control group, the ox-LDL group exhibited a significant reduction in cell proliferation level (P<0.05), accompanied by an increase in lipid droplet formation upon induction. In contrast, pretreatment with carvedilol at concentrations of 5 μM, 10 μM, and 20 μM effectively promoted cell proliferation (P<0.05) and inhibited intracellular lipid droplet formation. Notably, the most pronounced effect was observed with carvedilol pretreatment at a concentration of 5μM. Furthermore, compared to the control group, HUVEC cells in the ox-LDL group demonstrated substantial upregulation of NLRP3, pro-Caspase-1, Caspase1, pro-IL-1β, IL-1β, p65 GSDMD and N-GSDMD; however, these markers were downregulated following treatment with carvedilol and MCC950 administration-particularly evident in the carvedilol group.

Conclusions: Carvedilol effectively inhibits the progression of atherosclerosis by targeting the NLRP3 inflammasome, thereby providing valuable mechanistic insights into its beneficial effects on atherosclerotic cardiovascular disease.

At the end of 2019, the novel coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) became prevalent worldwide, which brought a heavy medical burden and tremendous economic losses to the world population. In addition to the common clinical respiratory symptoms such as fever, cough and headache, patients with COVID-19 often have hematological diseases, especially platelet dysfunction. Platelet dysfunction usually leads to multiple organ dysfunction, which is closely related to patient severity or mortality. In addition, studies have confirmed significant changes in the gene expression profile of circulating platelets under SARS-CoV-2 infection, which will further lead to changes in platelet function. At the same time, studies have shown that platelets may absorb SARS-COV-2 mRNA independently of ACE2, which further emphasizes the importance of the stability of platelet function in defense against SARS-CoV-2 infection. This study reviewed the relationship between COVID-19 and platelet and SARS-CoV-2 damage to the circulatory system, and further analyzed the significantly differentially expressed mRNA in platelets after infection with SARS-CoV-2 on the basis of previous studies. The top eight hub genes were identified as NLRP3, MT-CO1, CD86, ICAM1, MT-CYB, CASP8, CXCL8 and CXCR4. Subsequently, the effects of SARS-CoV-2 infection on platelet transcript abnormalities and platelet dysfunction were further explored on the basis of 8 hub genes. Finally, the treatment measures of complications caused by platelet dysfunction in patients with COVID-19 were discussed in detail, so as to provide reference for the prevention, diagnosis and treatment of COVID-19.

Percutaneous coronary intervention (PCI) with drug-eluting stents (DES) represents the treatment of choice for the majority of patients with coronary artery disease. While currently available DES, in addition to physiological support, has failed to show the non-inferiority to coronary artery bypass grafting (CABG) in terms of cumulative incidence of clinical events over the short-term follow-up. Studies have also shown that DES is associated with an increased risk of target vessel revascularization compared to CABG after long-term follow-up. Drug-coated balloons (DCB) have been shown to provide clinically significant benefits in the management of in-stent restenosis and diffuse coronary artery disease, as well as small coronary artery lesions. The aim of this review was to describe the inherent technical limitations of DES and highlight the potential advantages of PCI with DCB for long-term outcomes and potentially demonstrate its non-inferiority to CABG. Currently, ongoing studies will provide more information and help to understand if a blended therapy of DCB+DES can match the performance of CABG in the need for revascularization in more complex patients.

Background: Aortic valve stenosis (AS) is a common valvular heart disease, especially in the elderly, and is associated with a high prevalence of atrial fibrillation. Although the risk of atrial fibrillation is expected to decrease after the intervention, atrial fibrillation develops in many patients undergoing surgical or percutaneous transaortic valve implantation. We aimed to evaluate atrial refractoriness since it may play a key role in the occurrence of atrial fibrillation after transaortic valve implantation.

Methods: Seventy-nine consecutive patients who underwent TAVI between October 2021 and May 2023 were enrolled in this trial. Sixty-seven patients underwent electrophysiology study before and after TAVI. We evaluated the changes in PA and AH intervals, as well as atrial effective refractory periods.

Results: Besides the hemodynamic changes, atrial effective refractory periods increased, and atrial effective refractory period dispersion (39.8±21.6 vs. 31.1±18.0) decreased significantly after TAVI. The change in atrial effective refractory period dispersion after TAVI was correlated only with the changes in left ventricular end-diastolic pressure (r=0.77, P=0.001) and the changes in aortic gradient (r=0.4, P=0.001). The independent variables affecting the changes in atrial effective refractory period dispersion were basal pro-BNP levels, besides the changes in left ventricular end-diastolic pressure and aortic gradient after transaortic valve implantation.

Conclusions: Our results show an acute improvement in atrial refractoriness after TAVI, though high atrial fibrillation rates are reported in the literature. The timing of aortic valve replacement is important, as irreversible maladaptive changes might have already developed by the time of intervention.

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.

Background: Conduction disorders and arrhythmias frequently accompany cardiac amyloidosis (CA), with atrial fibrillation (AF) being the most prevalent manifestation. The prevalence of AF varies across different types of CA, with transthyretin (TTR) type showing the highest prevalence upon diagnosis.

Methods: A retrospective, observational analysis was conducted to evaluate the prevalence of AF and to identify echocardiographic predictors related to the development of AF in our population of patients with transthyretin cardiac amyloidosis (TTR-CA).

Results: A total of 99 patients with TTR-CA were identified, with a median age of 82 (75-85) years, a median ejection fraction of 50% (43-60) and 97 of them wild type. At the time of cardiomyopathy diagnosis, 55% had AF, and during follow-up, 43% developed new AF. Among the latter group, there was a non-significant tendency to have a smaller diastolic diameter, lower left ventricular ejection fraction, increased septal thickness, higher pulmonary pressure, and lower tissue velocities, with statistical significance only found in the right ventricular S wave velocity: 8.5 cm/s (7.7-9) vs. 9.7 cm/s (8.4-10) (P=0.046).

Conclusions: The high prevalence and incidence of AF in TTR-CA is demonstrated in our series. Doppler echocardiography might help to identify patients with signs of more advanced cardiomyopathy, such as lower right ventricle tissue velocity, who might be at higher risk of developing AF and gain the benefit of prompt diagnosis and treatment.