The aim at this study was to assess the influence of the tricuspid regurgitation volume (TRvol) in right atrium (RA) reservoir phase myocardial mechanics. We included 55 heart failure (HF) patients referred for transthoracic echocardiography during a 2-month period. 18 Had HF with a reduced ejection fraction (HFREF) and 37 HF with a preserved ejection fraction (HFPEF). TR was chronic and functional. TRvol was calculated according to the PISA method. This study of RA used 2D-speckle tracking echocardiography to measure strain (rεR) and strain rate (rSR(R)). The reference frame coincided with the onset of the QRS. RA stiffness was assessed as the ratio: (rE/e')/rε(R). The median age of the sample was 78 (64-84) years, with female gender predominance (63.6%). The median value of rε(R) was 16% (range, 12.7-24.0) and of rSR(R) was 1.57 s(-1) (range, 1.09-2.05). We observed a significant negative correlation between rε(R) (r = -0.68, p < 0.01) and rSR(R) (r = -0.58, p < 0.01) and TRvol. RA mechanics decreased significantly with an increase in the TR grade. We created two multivariate linear regression models for rε(R) and rSR(R), separately for the patients with sinus rhythm or atrial fibrillation. The TRvol was independently associated with rε(R) after adjusting to the RA area, right ventricular longitudinal systolic function and the estimated pulmonary vascular resistance. We demonstrated an increase in RA stiffness with an increase in TR severity, and an association for functional status (NYHA class) and RA compliance. The HFREF group had a significantly lower rε(R) and rSR(R) that the HFPEF patients. According to our study, in HF patients, a chronic volume overload state significantly reduced the RA reservoir phase mechanics.
Evaluation of vascular mechanics through twodimensional speckle-tracking (2D-ST) echocardiography is a feasible and accurate approach for assessing vascular stiffening. Degenerative aortic stenosis (AS) is currently considered a systemic vascular disease where rigidity of arterial walls increases. To assess the circumferential ascending aorta strain rate (CAASR) in thoracic aortas of patients with AS, applying 2D-ST technology. 45 patients with indexed aortic valve areas (iAVA) B0.85 cm 2 /m 2 were studied. Global CAASR served to assess vascular deformation. Clinical, echocardiographic, and non-invasive hemodynamic data were collected. A follow up (955 days) was also performed. Average age of the cohort was 76. ± 10.3 years, with gender balance. Mean iAVA was 0.43 ± 0.15 cm 2 /m 2 . Waveforms adequate for determining CAASR were found in 246 (91 %) of the 270 aortic segments evaluated, for a mean global CAASR of 0.74 ± 0.26 s -1 . Both intra-and inter-observer variability of global CAASR were deemed appropriate. CAASR correlated significantly with age (r = -0.49, p \ 0.01), the stiffness index (r = -0.59, p \ 0.01), systemic arterial compliance and total vascular resistance. There was a significant positive correlation between CAASR, body surface area (BSA), iAVA, and a negative relationship with valvulo-arterial impedance and E/e' ratio (r = -0.37, p = 0.01). The stiffness index was (b = -0.41, p \ 0.01) independently associated with CAASR, in a model adjusted for age, BSA, iAVA and E/e'. Patients with a baseline CAASR B0.66 s -1 had a worse long-term outcome (survival 52.4 vs. 83.3 %, Log Rank p = 0.04). CAASR is a promising echocardiographic tool for studying the vascular loading component of patients with AS.
A proper description of the immune response to SARS-CoV-2 will be critical for the assessment of protection elicited after both infection and vaccination. Uncoupled T and B cell responses have been described in acute and convalescent patients and exposed individuals. We assessed the potential usefulness of whole blood stimulation assays to identify functional cellular immune responses to SARS-CoV-2. Blood from COVID-19 recovered individuals (5 months after infection) and negative subjects was stimulated for 24 hours with HLA predicted peptide “megapools” of the Spike and Nucleoprotein, or the mixture of them. After stimulation, cytokines were quantified using a beads-based multiplex assay. Interleukin-2 and IFN-γ were found to be specific biomarkers of SARS-CoV-2 cellular response. Using the Spike and Nucleoprotein mixture, 91.3% of COVID-19 recovered individuals presented an IL-2 stimulation index over the cut-off, while 82.6% showed IFN-γ. All the negative individuals presented an IL-2 response under the cut-off, while 5.3% of these subjects presented positive IFN-γ stimulation indexes. Moreover, IL-2 production correlated with IgG levels for Spike 1, RBD, and Nucleocapsid. In conclusion, we demonstrate the potential of whole blood stimulation assays and the quantification of IL-2 and IFN-γ for the analysis of SARS-CoV-2 functional cellular responses.
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