Diagnostic Performance of Serum MicroRNAs for ST-Segment Elevation Myocardial Infarction in the Emergency Department.

Prompt diagnosis of ST-segment elevation myocardial infarction (STEMI) is essential for initiating timely treatment. MicroRNAs have recently emerged as biomarkers in cardiovascular diseases. This study aimed to evaluate the discriminatory capacity of serum microRNAs in identifying an ischemic origin in patients presenting with chest discomfort to the Emergency Department. The study included 98 participants (78 with STEMI and 20 with nonischemic chest discomfort). Significant differences in the expression levels of miR-133b, miR-126, and miR-155 (but not miR-1, miR-208, and miR-208b) were observed between groups. miR-133b and miR-155 exhibited 97% and 93% sensitivity in identifying STEMI patients, respectively. miR-126 demonstrated a specificity of 90% in identifying STEMI patients. No significant associations were found between microRNAs and occurrence of major adverse cardiovascular events (MACE). However, patients with MACE had higher levels of interleukin (IL)-15, IL-21, IFN-γ-induced protein-10, and N-terminal pro B-type natriuretic peptide compared to non-MACE patients. Overall, there were significant associations among the expression levels of microRNAs. However, microRNAs did not demonstrate associations with either inflammatory markers or cardiovascular risk scores. This study highlights the potential of microRNAs, particularly miR-133b and miR-126, as diagnostic biomarkers for distinguishing patients with STEMI from those presenting with nonischemic chest discomfort to the Emergency Department.

Should a recent SARS-CoV-2 infection be considered a risk or prognostic factor for ST-segment elevation myocardial infarction?

Objective: The aim of the study was to assess whether a recent SARS-CoV-2 infection could by itself be a risk or prognostic factor for ST-segment elevation myocardial infarction (STEMI). Method: An observational study in unvaccinated patients with STEMI confirmed by cardiac catheterization was conducted. A recent or concurrent SARS-CoV-2 infection was identified by the presence of serum IgG against the nucleocapsid protein, or a positive polymerase chain reaction test on nasopharyngeal swabs. Baseline cardiovascular risk factors, clinical STEMI severity, main catheterization findings, and occurrence of major adverse cardiovascular events (MACE) during hospitalization were compared between study subgroups. Results: Of a total of 89 patients recruited, 14 (16%) had a recent SARS-CoV-2 infection. Patients with STEMI and recent SARS-CoV-2 infection had a markedly lower frequency of high blood pressure (20% versus 55%; P = 0.03) as well as a tendency to have fewer comorbidities. Regarding the clinical presentation, there were no differences in the severity of the STEMI. Furthermore, the main findings during cardiac catheterization including the atherosclerotic burden and the number of vessels affected, as well as the occurrence of MACE during follow-up, were not significantly different between the groups. Conclusions: A recent SARS-CoV-2 infection appears to facilitate the triggering of STEMI, as these patients have fewer traditional cardiovascular risk factors than their uninfected counterparts. However, this does not seem to affect the clinical presentation or the in-hospital course of STEMI patients.

Levels of Vascular Endothelial Growth Factor and Its Association with Pulmonary Embolism in COVID-19.

Coronavirus disease 2019 (COVID-19) is associated with pulmonary embolism, a condition mechanistically related to vascular endothelial growth factor (VEGF). Our objective was to identify whether VEGF levels, measured at hospital admission, may predict the occurrence of pulmonary embolism (and other thrombosis) during hospitalization. Of a total of 139 patients included in the study, a pulmonary embolism occurred in 4%, other thrombosis in 16%, and 80% remained thrombus free. Clinical and laboratory data at admission were similar among groups. VEGF levels were elevated in COVID-19 patients compared with 38 healthy controls (50.7 versus 15.0 pg/mL; P < 0.001), with an area under the receiver operating characteristic curve of 0.776. At a cutoff point >15.7 pg/mL, VEGF showed 64.7% sensitivity, 92.1% specificity, and a positive likelihood ratio of 8.2 to discriminate COVID-19. In COVID-19, VEGF levels were not different in patients with pulmonary embolism, other thrombosis, and thrombus-free patients (15.0 versus 84.0 versus 48.5 pg/mL, respectively; P = 0.19). VEGF correlated with C-reactive protein (ρ = 0.25), fibrinogen (ρ = 0.28), ferritin (ρ = 0.18), and the neutrophil-to-lymphocyte ratio (ρ = 0.20). Our study showed that VEGF is elevated in sera from patients with COVID-19 on arrival at the hospital and its levels correlate with inflammatory markers, although they are unable to predict the appearance of pulmonary embolism during hospitalization.

Activation Status of NLRP3 Inflammasome in Peripheral Blood Mononuclear Cells From Patients With Gout Flare.

BACKGROUND/OBJECTIVE: Although gout flares are featured by systemic signs of inflammation, cellular sources of inflammatory mediators are not yet properly characterized. Our objective was to evaluate serum levels and gene expression in peripheral blood mononuclear cells (PBMCs) of several molecules associated with the activation of NLRP3 inflammasome. METHODS: Fifteen patients with gout flare and 15 individuals with asymptomatic hyperuricemia were cross-sectionally studied. Serum levels of interleukin 1ß (IL-1ß), IL-18, monocyte chemoattractant protein 1/chemokine (C-C motif) ligand 2 (CCL2), and vascular cell adhesion molecule 1 were measured as a reflection of systemic inflammation, whereas the expression of NLRP3, CASP1, IL18, and CCL2 genes was measured to assess the inflammatory characteristics of PBMCs. RESULTS: Serum levels of IL-1ß (1.27 [0.07-1.99] pg/mL vs. 0 [0-0.82] pg/mL, p = 0.032) and vascular cell adhesion molecule 1 (606 [435-748] pg/mL vs. 349 [305-422] pg/mL, p = 0.014) were significantly higher in patients with gout flare than in individuals with asymptomatic hyperuricemia, whereas differences in IL-18 and monocyte chemoattractant protein 1/CCL2 were not found. Notably, no differences were observed in the expression of NLRP3, CASP1, IL18, or CCL2 in PBMCs from individuals of one or another group. CONCLUSIONS: Systemic inflammation during gout flares does not appear to be associated with NLRP3 inflammasome activation in PBMCs, suggesting that it may represent the systemic spread of local (synovial) inflammation to monosodium urate crystals, which provides a rationale for redirecting anti-inflammatory therapy from a systemic approach to one centered on the inflamed joint.

Is Takayasu arteritis the result of a Mycobacterium tuberculosis infection? The use of TNF inhibitors may be the proof-of-concept to demonstrate that this association is epiphenomenal.

Although the association between Takayasu arteritis (TA) and latent or active Mycobacterium tuberculosis infection has been suggested for a long time, studies conducted in recent years are challenging this notion. Until recently, the possibility of a pathogenic relationship between TA and tuberculosis (TB) was considered a medical curiosity, but the advent of tumor necrosis factor (TNF) inhibitors as therapy for recalcitrant TA cases, as well as the widespread use of Bacille Calmette-Guérin (BCG) for vaccination purposes, has relocated this association as a top priority issue. In an attempt to define whether both diseases are pathogenically linked or if their association is only epiphenomenal in nature, we conduct a thorough literature search on the development of TB in patients with TA receiving TNF inhibitors. From a total of 13 studies that included 214 patients, the occurrence of TB was observed only in two individuals exposed to infliximab. This frequency of 0.93% is similar to that encountered in patients with other rheumatic diseases exposed to TNF inhibitors. Finally, we propose a novel pathogenic model that could reconcile the epidemiological, clinical, and immunological evidence that links TA and TB, while providing rationality for the use of TNF inhibitors in patients with TA.

Plasma let-7i, miR-16, and miR-221 levels as candidate biomarkers for the assessment of ankylosing spondylitis in Mexican patients naïve to anti-TNF therapy.

Novel biomarkers are needed for the diagnosis and clinical assessment of ankylosing spondylitis (AS). Our objective was to investigate plasma microRNAs differentially expressed between AS patients and controls and to evaluate their potential as biomarkers in Mexican subjects. A cross-sectional study including 15 AS patients naïve to anti-TNF therapy and 13 controls was performed. Disease activity, physical function, and global well-being were evaluated by the AS Disease Activity Score (ASDAS-CRP), the Bath AS Disease Activity Index (BASDAI), the Bath AS Functional Index (BASFI), and the AS Quality of Life Questionnaire (ASQoL), respectively. Total RNA was isolated from plasma of participants and relative expression of let-7i, miR-16, and miR-221 was evaluated. Serum levels of C-reactive protein (CRP), matrix metalloproteinase-1 (MMP-1), MMP-9, and intercellular adhesion molecule-1 (ICAM-1) were also measured. Expression of let-7i was higher in patients than in controls (1.8, 0.9 to 3.4 versus 0.6, 0.4 to 1.2; P = 0.033) with an AUC/ROC of 0.74 (0.54 to 0.93; P = 0.032). Levels of miR-16 and miR-221 were unable to discriminate between patients and controls. Notably, plasma miR-16 levels were inversely correlated with the ASDAS-CRP score (rho - 64, - 0.87 to - 0.18; P = 0.011), the BASFI score (rho - 0.78, - 0.93 to - 0.43; P = 0.001), and serum MMP-1 levels (rho - 0.59, - 0.85 to - 0.09; P = 0.022). No other associations were found. Plasma let-7i levels may serve as a biomarker for the diagnosis of AS in Mexican individuals. Additionally, plasma miR-16 levels are associated with disease activity and physical functionality in patients naïve to anti-TNF therapy.