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Objective: Right ventricular (RV) function is a major determinant of survival in patients with pulmonary arterial hypertension (PAH). Metabolic alterations may precede haemodynamic and clinical deterioration. Increased RV fluorodeoxyglucose (FDG) uptake in positron emission tomography (PET) was recently associated with progressive RV dysfunction in MRI, but the prognostic value of their combination has not been established.Methods: Twenty-six clinically stable patients with PAH (49.9±15.2 years) and 12 healthy subjects (control group, 44.7±13.5 years) had simultaneous PET/MRI scans. FDG uptake was quantified as mean standardised uptake value (SUV) for both left ventricle (LV) and RV. Mean follow-up time of this study was 14.2±7.3 months and the clinical end point was defined as death or clinical deterioration.Results: Median SUVRV/SUVLV ratio was 1.02 (IQR 0.42-1.21) in PAH group and 0.16 (0.13-0.25) in controls, p<0.001. In PAH group, SUVRV/SUVLV significantly correlated with RV haemodynamic deterioration. In comparison to the stable ones, 12 patients who experienced clinical end point had significantly higher baseline SUVRV/SUVLV ratio (1.21 (IQR 0.87-1.95) vs 0.53 (0.24-1.08), p=0.01) and lower RV ejection fraction (RVEF) (37.9±5.2 vs 46.8±5.7, p=0.03). Cox regression revealed that SUVRV/SUVLV ratio was significantly associated with the time to clinical end point. Kaplan-Meier analysis showed that combination of RVEF from MRI and SUVRV/SUVLV assessment may help to predict prognosis.Conclusions: Increased RV glucose uptake in PET and decreased RVEF identify patients with PAH with worse prognosis. Combining parameters from PET and MRI may help to identify patients at higher risk who potentially benefit from therapy escalation, but this hypothesis requires prospective validation. [ABSTRACT FROM AUTHOR]

Inflammatory processes and platelet activity play an important role in the pathophysiology of pulmonary arterial hypertension (PAH). Enhanced IL-6 signaling and higher concentration of stromal-derived factor alpha (SDF-1) have been previously shown to be linked with prognosis in PAH. We hypothesized that platelets of PAH patients have higher content of IL-6 and SDF-1 and thus are involved in disease progression. We enrolled into study 22 PAH patients and 18 healthy controls. Patients with PAH presented significantly higher plasma concentrations and platelet contents of IL-6, sIL-6R, and SDF-1 than healthy subjects (platelet content normalized to protein concentration: IL-6 (0.85*10–10 [0.29 – 1.37] vs. 0.45*10–10 [0.19–0.65], sIL-6R 1.54*10–7 [1.32–2.21] vs. 1.14*10–7 [1.01–1.28] and SDF-1 (2.72*10–7 [1.85–3.23] vs. 1.70*10–7 [1.43–2.60], all p < 0.05). Patients with disease progression (death, WHO class worsening, or therapy escalation, n = 10) had a significantly higher platelet SDF-1/total platelet protein ratio (3.68*10–7 [2.45–4.62] vs. 1.69*10–7 [1.04–2.28], p = 0.001), with no significant differences between plasma levels. Kaplan–Meier analysis revealed that patients with higher platelet SDF-1/total platelet protein ratio had more frequently deterioration of PAH in the follow-up (15.24 ± 4.26 months, log-rank test, p = 0.01). Concentrations of IL-6, sIL-6 receptor and SDF-1 in plasma and platelets are elevated in PAH patients. Higher content of SDF-1 in platelets is associated with poorer prognosis. Our study, despite of limitation due to small number of enrolled patients, suggests that activated platelets may be an important source of cytokines at the site of endothelial injury, but their exact role in the pathogenesis of PAH requires further investigation. [ABSTRACT FROM AUTHOR]

Aims: The aim of this study was to determine the value of the Acute Physiology and Chronic Health Evaluation II (APACHE II), Sequential Organ Failure Assessment (SOFA) and CardShock scoring systems in predicting the risk of in-hospital, 30 day and 3 year mortality in patients with cardiogenic shock (CS)., Methods: This was a single-centre observational study conducted between May 2016 and December 2017. Data from consecutive patients with CS admitted to the intensive cardiac care unit (ICCU) were included in the analysis., Results: The study group comprised 63 patients with CS {median age 71.0 [interquartile range (IQR), 59-82]; 42 men}: 32 patients with ischaemic and 31 with non-ischaemic aetiology. The median APACHE II, SOFA and CardShock scores were 13 (IQR, 9.9-19.0) points, 8.0 (IQR, 6.0-10.0) points and 3.0 (IQR, 2.0-5.0) points, respectively. The in-hospital, 30 day and 3 year mortality rates were 39.7%, 41.3% and 77.8%, respectively. APACHE II and SOFA scores were significantly higher in the group of patients who died at 30 days (P = 0.043 and P = 0.045, respectively). The CardShock score was higher in patients with CS who died in hospital (P = 0.007) and within 30 days (P = 0.004). No score was statistically significant for 3 year mortality. Area under the curve (AUC) analysis showed that the CardShock score had the highest value in predicting in-hospital and 30 day mortality relative to APACHE II and SOFA, with a cut-off score of 5 points [AUC: 0.70; 95% confidence interval (CI): 0.59-0.81; P = 0.001] and 4 points (AUC: 0.71; 95% CI: 0.60-0.82; P < 0.001), respectively. The Bayesian Weibull model demonstrated the utility of all scales in estimating short-term risk in patients with CS, with the impact of APACHE II and SOFA on patient life expectancy decreasing to a non-significant level at approximately 32 days and CardShock at 33 days. The forest plots derived from the Bayesian logistic regression analysis show significant estimated coefficients with 94% highest density interval (HDI) for in-hospital and 30 day mortality. The use of invasive or non-invasive ventilation, a higher heart rate and a less negative fluid balance showed an unfavourable prognosis. Survival was associated with being in the pre-CS class, with a higher glomerular filtration rate and a higher platelet count., Conclusions: APACHE II and SOFA could be used for the risk stratification of patients with CS admitted to the ICCU. CardShock proved to be a more appropriate tool for assessing short-term prognosis in patients with CS of all aetiologies, suggesting that there is potential for its promotion for use in daily clinical practice., (© 2024 The Author(s). ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.)

Introduction: In the course of acute myocardial infarction (AMI) cardiomyocyte injury, activation and destruction of endothelial cells together with inflammation lead to miRNA expression alterations., Aim: To assess levels of circulating cardiac-specific (miR-1) and endothelial-specific (miR-126) miRNAs in the acute phase of AMI and after a follow-up period., Material and Methods: Seventeen AMI patients (mean age: 64.24 ±13.83 years, mean left ventricle ejection fraction (LVEF): 42.6 ±9.65%), treated with primary percutaneous coronary intervention within the first 12 h, had plasma miRNAs isolated (quantitative real-time PCR, Exiqon) on admission and after 19.2 ±5.9 weeks. Measurements were also performed in a control group of healthy volunteers matched for age and sex., Results: Concentrations of both miRNAs were significantly higher in AMI patients as compared to healthy controls: miR-1: 5.93 (3.15-14.92) vs. 1.46 (0.06-2.96), p = 0.04; miR-126: 4.5 (3.11-7.64) vs. 0.54 (0.36-0.99), p = 0.00003, respectively. Levels of both miRNAs significantly decreased after the follow-up period: miR-1: 5.93 (3.15-14.92) vs. 1.34 (0.04-2.34), p = 0.002; miR-126: 4.5 (3.11-7.64) vs. 1.18 (0.49-1.68), p = 0.0005). Moreover, miR-1 correlated positively with maximal troponin I concentration ( r = 0.59, p = 0.02) and negatively with LVEF ( r = -0.76, p = 0.0004)., Conclusions: In our study, miR-1 emerged as a marker of cardiomyocyte injury and loss of myocardial contractility, whereas dynamics of miR-126 concentration may reflect endothelial activation and damage in the most extreme stage of atherosclerosis, followed by angiogenesis in ischemic myocardium. However, to fully elucidate the role of miR-1 and miR-126 as biomarkers of AMI and future therapeutic targets, further research is required., Competing Interests: The authors declare no conflict of interest., (Copyright © 2020 Termedia Sp. z o. o.)

Introduction: MicroRNAs (miRNAs) are small RNAs that play an important role in the regulation of gene expression. miRNA dysregulation has been associated with phenotypic changes, including cardiovascular diseases (CVDs)., Objectives: The aim of the study was to obtain a list of single nucleotide polymorphisms (SNPs) related to CVDs, with computationally predicted effect on miRNA binding sites, which would verify the hypothesis that miRNA dysregulation can lead to the development of CVDs., Materials and Methods: SNPs, CVDs, and miRNAs were the 3 factors subjected to analysis. Based on the publicly available databases, we created a set of SNPs associated with the phenotype of interest and of SNPs located in known miRNA binding sites. We then merged the records assigned by the same SNP, which allowed us to indicate miRNA target sites, whose variants may be associated with CVDs. The results were supplemented with the additional data such as miRNA and mRNA coexpression, differences in the expression between various tissues, and Expression Quantitative Trait Locus analysis. Only in-silico methods, on the basis of publically available information tools and databases, were used., Results: We obtained a list of 47 entries, constituting unique miRNA-SNP allele-phenotype linkages., Conclusions: Computational approach supports the hypothesis of the linkage between alterations in miRNA function and numerous CVDs. Given the high frequency of SNP incidence, this pathomechanism may be common in the population. Although the obtained results need to be further experimentally validated, limiting the number of interactions to the most probable ones will facilitate the identification of clinically significant associations.