Acta cardiologica最新文献

Objective: We aimed to examine the correlation between the platelet-to-lymphocyte ratio (PLR) and coronary artery lesions (CALs) in individuals diagnosed with Kawasaki disease (KD) and to evaluate its prognostic significance.

Methods: Our study entailed a detailed retrospective examination and analysis of clinical records for patients diagnosed with KD at the First Affiliated Hospital of Anhui Medical University from January 2017 to January 2023. In our methodological approach, we applied various statistical techniques - including univariate analyses, binary logistic regression, and receiver operating characteristic (ROC) curve analysis - to meticulously assess the relationship between the PLR and the incidence of CALs in this patient cohort. Our objective was to elucidate potential predictive markers for CALs development in KD patients, thereby contributing valuable insights into the prognosis and management of this condition.

Results: In the conducted research, a total of 364 patients were analysed, among which 63 individuals (17.3%) exhibited CALs upon admission. Through the application of binary logistic regression analysis, our findings underscored PLR as a statistically significant predictor for the presence of CALs. Furthermore, the ROC curve analysis demonstrated an AUC (area under the curve) value of 0.707 (95%CI 0.641-0.772, p < .001) for the prognostic capacity of PLR concerning CALs.

Conclusions: The outcomes of our investigation indicate that PLR acts as a significant risk indicator for CALs. Such insights pave the way for improved risk stratification and potentially guide therapeutic decision-making in patients with KD.

Aim: The aim of this study was to determine whether the office white-coat effect tail (OWCET), defined as decreasing of SBP ≥10 mmHg in multiple office systolic blood pressure measures, predicts major long-term fatal events in the nearly extinct European cohorts of the Seven Country Study (ECSCS).

Material and methods: In the present analysis, 4,937 men (49 ± 5 years) were included. All-cause mortality and specific mortalities [cardiovascular mortality (CVD) including stroke, coronary heart disease (CHD) death as well as heart disease of uncertain aetiology (HDUE)] were considered using Cox models. Also non-CVD deaths were studied by Fine-Gray competing risk analysis.

Results: At inclusion, subjects with OWCET were significantly more hypertensive. After 60-year follow-up, OWCET was not associated with risk of both CVD [aHR: 0.95 (95% CI: 0.82-1.03), p = 0.5] and all-cause death [aHR: 0.92 (95% CI: 0.82-1.03), p = 0.16] independently of traditional risk factors (age, SBP, BMI, total cholesterol and cigarettes) in ECSCS. Same results were found for Northern and Southern Europe cohorts of ECSCS concerning CVD death [aHR: 0.98 (95% CI: 0.76-1.26), p = 0.85 and aHR: 0.95 (95% CI: 0.74-1.20), p = 0.66] and all-cause death, respectively [aHR: 0.90 (95% CI: 0.75-1.07), p = 0.23 and aHR: 0.93 (95% CI: 0.79-1.09), p = 0.38].

Conclusions: In a general population of men, OWCET is not associated to CVD or non-CVD and all-cause mortality and consequently cannot improve stratification of long-term CVD risks in ECSCS.

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.