Introduction: With the rapid spreading of the coronavirus (COVID-19) pandemic and the limited capacities of real-time reverse transcriptase-PCR (RT-PCR) at the laboratory level, there is an emerging need for rapid, point-of-care (POC), molecular testing in the Emergency Department (ED). Aims and objectives: To compare the diagnostic performance of ID NOW COVID-19 assay (Abbott, Chicago, Il, USA) performed by ED doctors with a gold standard reference RT-PCR test (GeneXpert assay developed by Cepheid). Methods: Paired nasopharyngeal swabs were collected from consecutive adult patients suspected of having COVID-19 in the ED of a tertiary hospital in Athens (Greece); the first swab was directly used for the ID NOW COVID-19 assay in POC by an emergency physician and the second was analyzed with reference RT-PCR by a central laboratory technician. Cohen’s kappa was run to determine if there was sufficient agreement between the two diagnostic methods. Results: Seventy one consecutive patients (36 female, mean age 64.6) were enrolled in the present study from 15th January to 21th February, 2022. The two tests agreed on 20 positive and 50 negative results. On the contrary, ID NOW COVID-19 assay was found positive in one patient with a negative reference RT-PCR test. There was very good agreement between the two diagnostic methods [κ = 0.966 (95% CI, 0.900 to 1.032), p < 0.0001]. Conclusions: Comparison of a POC and a standard laboratory RT-PCR test in an ED patient population yielded high positive (95%) and negative percent agreement (100%). ID NOW COVID-19 assay seems to be a highly reliable POC test for early screening and triage of suspected COVID-19 patients.

Background:Inflammation plays a major role in the development of acute coronary syndromes. However, the role of viral infections remains unclear. We examined the role of hepatitis A virous (HAV), cytomegalovirus (CMV), herpes simplex virus (HSV), helicobacter pylori (HP), C-reactive protein (CRP), on endothelial function and clinical stability in patients with coronary artery disease.

Conclusions: Hypergammaglobulinemia is characteristic of HIV infection and has also been noted in select autoimmune diseases. In our study, increased levels of serum IgG were noted in both HIV infected and to a lower extent in HIV non-infected PPCM patients. It is of interest that serum IgG levels either remain elevated (non-HIV infected) or increase (HIV infected) following 6 months of therapy despite significant improvement in cardiac function.

Soluble CD40-ligand plays a key role in immune response, while vascular cell adhesion molecule (VCAM-1) and intercellular adhesion molecuse-1 (sICAM-1) mediate the leukocytes adhesion to endothelium. We investigated whether the expression of CD40 and the soluble forms of VCAM-1 and ICAM-1 are affected during the acute phase of unstable angina (UA) and myocardial infarction (MI). This study enrolled 26 patients with stable angina (SA), 23 patients with UA, 19 patients with MI and 13 healthy controls. Blood sampling was performed by admission to the hospital for UA and MI, and after at least 3 months of stable condition in SA. Serum levels of sVCAM-1, sICAM-1 and CD40-L were determined with ELISA. Serum levels of CD40-L were significantly lower in healthy controls (4.8±1.0 ng/ml) compared to SA (7.9±0.95 ng/ml, p<0.05), UA (7.83±0.8 ng/ml, p<0.05) and MI (7.21±1.65 ng/ml, p<0.05), while no difference was observed between patients with SA, UA or MI. Similarly, serum levels of sVCAM-1 were also significantly lower in healthy controls (369±87 ng/ml) compared to SA (906±118 ng/ml, p<0.05), UA (735±97 ng/ml, p<0.05) and MI (752±89 ng/ml, p<0.05), while no difference was observed between patients with SA, UA or MI. However, no significant difference was observed in sICAM-1 levels between controls and patients with SA, UA or MI (306±31 ng/ml, 338±13 ng/ml, 331±19 ng/ml and 362±22.7 ng/ml respectively, p=ns for all versus controls). CD-40 and sVCAM-1 are elevated in both stable and unstable coronary syndromes. Thus, these molecules may not be involved in the pathogenesis of plaque instability or rupture observed during unstable coronary syndromes.

Background: Soluble CD40-ligand plays a key role in immune response, while vascular cell adhesion molecule (VCAM-1) and intercellular adhesion molecuse-1 (sICAM-1) mediate the leukocytes adhesion to endothelium. We investigated whether the expression of CD40 and the soluble forms of VCAM-1 and ICAM-1 are affected during the acute phase of unstable angina (UA) and myocardial infarction (MI). Methods: This study enrolled 26 patients with stable angina (SA), 23 patients with UA, 19 patients with MI and 13 healthy controls. Blood sampling was performed by admission to the hospital for UA and MI, and after at least 3 months of stable condition in SA. Serum levels of sVCAM-1, sICAM-1 and CD40-L were determined with ELISA. Results: Serum levels of CD40-L were significantly lower in healthy controls (4.8 1.0 ng/ml) compared to SA (7.9 0.95 ng/ml, p 0.05), UA (7.83 0.8 ng/ml, p 0.05) and MI (7.21 1.65 ng/ml, p 0.05), while no difference was observed between patients with SA, UA or MI. Similarly, serum levels of sVCAM-1 were also significantly lower in healthy controls (369 87 ng/ml) compared to SA (906 118 ng/ml, p 0.05), UA (735 97 ng/ml, p 0.05) and MI (752 89 ng/ml, p 0.05), while no difference was observed between patients with SA, UA or MI. However, no significant difference was observed in sICAM-1 levels between controls and patients with SA, UA or MI (306 31 ng/ml, 338 13 ng/ml, 331 19 ng/ml and 362 22.7 ng/ml respectively, p ns for all versus controls). Conclusions: CD-40 and sVCAM-1 are elevated in both stable and unstable coronary syndromes. Thus, these molecules may not be involved in the pathogenesis of plaque instability or rupture observed during unstable coronary syndromes.