Acta cardiologica最新文献

Background: Prostaglandin G/H synthase 1 (PTGS1) is known to regulate platelet function and inflammation. However, its role in atrial fibrillation (AF)-related thrombosis is not well understood. This study investigates the role of PTGS1 in AF-associated thrombus formation and its underlying mechanisms.

Methods: Left atrial appendage (LAA) tissues were collected from 48 patients undergoing valve replacement surgery, divided into three groups: sinus rhythm (SR), AF with thrombus [AF (+) T (+)], and AF without thrombus [AF (+) T (-)]. PTGS1 expression, platelet activation markers (MPA, sCD40L, and d-dimer), macrophage phenotypes (M1 and M2), inflammatory cytokines (IL-1β, TNF-α, IL-6), and autophagy-related proteins (LC3II and p62) were assessed. Furthermore, the effect of PTGS1 manipulation on autophagy in endocardial endothelial cells (EECs) was examined using cell transfection experiments.

Results: PTGS1 expression was significantly higher in LAA tissues of AF (+) T (+) patients compared to AF (+) T (-) and SR groups. It was positively correlated with reduced LAA emptying velocity (LAAEV), higher CHA2DS2-VASc scores, and elevated platelet activation markers (MPA, sCD40L, and d-dimer). Data also showed increased M1 macrophage infiltration and higher pro-inflammatory cytokines (IL-1β, TNF-α, IL-6) in AF (+) T (+) patients, with PTGS1 expression strongly linked to these markers. Furthermore, PTGS1 overexpression inhibited autophagy in EECs by decreasing LC3II/LC3I ratio and increasing p62 levels, while PTGS1 knockdown promoted autophagy, protecting against endothelial dysfunction.

Conclusions: PTGS1 is overexpressed in AF patients with thrombosis and may play an important role in promoting thrombus formation through enhanced platelet activation, inflammation, and inhibition of autophagy.

Background: The cardiometabolic index (CMI) combines abdominal obesity and abnormal blood lipid indices, representing a good predictive indicator of risk in cardiovascular diseases (CVDs). However, the association between CMI and myocardial infarction (MI) is not clear.

Objective: The present project was designed to explore the linkage between CMI and MI.

Methods: Data from the National Health and Nutrition Examination Survey (NHANES) 2005-2018 were employed in this project, with CMI as the independent variable and MI as the dependent variable. Weighted logistic regression was applied in the association analysis between CMI and MI. Restricted cubic spline (RCS), subgroup analysis, and interaction tests were employed to elucidate the non-linear relationship and stability of CMI and MI's link. Moreover, to verify the robustness of the results, sensitivity analysis was conducted, with the MI status of subjects taking lipid-lowering drugs as the outcome variable.

Results: A total of 13,923 participants were gathered in this project, with 605 cases of MI, accounting for 3.5%. In the weighted logistic regression model, a positive linkage was observed between CMI and the risk of MI (OR: 1.41, 95% CI: 1.18-1.68, p < 0.001). The RCS curves indicated a linear relationship between CMI and MI (P-non-linear = 0.146). Subgroup analysis manifested that CMI was positively linked with MI risk in males, individuals with BMI > 30kg/m², and alcohol drinkers (p < 0.05). In addition, the interaction results demonstrated that there was no heterogeneity in the association between CMI and MI risk in the subgroups (p > 0.05). The sensitivity analysis showed that after adjusting for all confounding factors in the model, there was still a significant positive correlation (p < 0.01) between CMI and MI in the population taking lipid-lowering drugs.

Conclusion: There is a significant positive linkage of CMI with MI risk, which is particularly significant in males, those with a BMI greater than 30 kg/m², and those who have drinking habits. Even after considering the impact of lipid-lowering drug therapy, the positive correlation between CMI and MI remains robust, supporting CMI as a promising tool for assessing MI risk and guiding clinical prevention. Further research is required to probe into the application of CMI in different populations and its role in the prevention of CVDs.

Background: The Melody^™ TPV has been used as an alternative to surgical pulmonary valve replacement; limited medium-term follow-up data are available.

Aims: To report the follow-up data of all Melody^™ TPVs implanted locally over a 15-year period (2006-2021).

Methods: Single-centre non-randomised prospective observational study of all implanted Melody^™ valves in the pulmonary position.

Results: 234 Melody^™ valves were implanted at a mean age of 20.8 ± 24.6y. Indications for valve implantation included: pulmonary stenosis (47.2%,) regurgitation (30.9%), and mixed pathology (21.9%). The implant zone substrate consisted of homograft in 52.6%, patched right ventricular outflow tract in 33.8%, and bioprostheses in 13.6% of the cases. Valve survival at 10 years was 89% and 72% at 15 years follow-up. Pulmonary stenosis and pulmonary and tricuspid valve regurgitation demonstrated no significant evolution over the 15-year follow-up. Over the study period, there were 7 deaths at a mean age of 54.2 ± 21.1y; none was valve related. Valve failure was observed in 22 cases (9.4%), mainly due to endocarditis 13/22 (59.0%). The overall incidence of endocarditis was 1.5% per patient-year and occurred in 10.2% (n = 24) of patients 2.7 ± 1.6y after TPV, mostly in younger men (median 18.3, range 8.1 - 49.5 y). Balloon dilatation to accommodate for somatic growth was successful in all 17 (7.3%) attempted cases.

Conclusion: The Melody^™ valve had a low risk for valve failure with overall well-preserved valve function over up to 15 years of follow-up. Endocarditis remains a concern. The Melody^™ valve is competitive with other surgical and percutaneous conduits.

Background: Current guidelines suggest the use of loop diuretics as the preferred agent for decongestion in patients with heart failure. However, there is no clear evidence as to superiority of one loop diuretic over the other. The understanding of pharmacokinetic and pharmacodynamic superiority of torsemide over furosemide has generated the hypothesis that these features could result in better clinical outcomes.

Objectives: To determine whether the use of torsemide is associated with reduced risk for mortality and rehospitalizations in comparison to furosemide among patients with heart failure.

Methods: The study involves a comprehensive search of literature from PubMed, Cochrane CENTRAL, and ClinicalTrials.gov of clinical trials addressing the use of torsemide vs. furosemide in patients with heart failure. Pooled risk ratios (RR) were used to measure association for all outcomes with inverse-variance weighting and random effects model.

Results: The literature search included 188 studies that were screened individually. A total of 24 studies were identified out of which 12 were excluded. The pooled risk ratio (RR) revealed all-cause mortality of 0.98 [0.87 to 1.10] with 0% heterogeneity, all cause rehospitalization of 0.95 [0.88 to 1.02] with 5% heterogeneity, and heart failure rehospitalization of 0.85 [0.52 to 1.38] with 55% heterogeneity.

Conclusion: Considering the evidence from pooled randomised trials, the use of torsemide compared to furosemide did not result in statistically significant differences in all-cause mortality or rehospitalization rates.