Impact of transducer frequency setting on speckle tracking measures

Speckle tracking echocardiography is an emerging technique, which is currently being included in clinical guidelines. We sought to investigate the impact of transducer frequency settings on speckle tracking derived measures. The study comprised of 22 subjects prospectively enrolled for a randomized controlled trial (LOOP-study, Clinicaltrials.gov:NCT02036450). Patients were above 70 years of age with increased risk of stroke, and had an echocardiogram performed, which included focused images of the left ventricle. Focused images were obtained with the transducer frequency set at both 1.7/3.3 and 1.5/3.0 MHz. The images were obtained immediately after each other at the exact same position for the two settings. Speckle tracking was performed in three apical projections, allowing for acquisition of layered global longitudinal strain (GLS) and strain rate measures. Concordance between the frequency settings was tested for endo-, mid-, and epicardial GLS and strain rates by coefficients of variation, bias coefficients and visually displayed by Bland–Altman plots. Bland–Altman plots did not reveal any significant over- or underestimation of any speckle tracking measure. Bias coefficients showed that none of the measurements differed significantly between the two settings (bias for GLS_endo?=???0.07?±?2.94, p?=?0.91; GLS_mid?=?0.02?±?2.70, p?=?0.98, GLS_epi?=?0.07?±?2.53, p?=?0.90). Coefficients of variation were as follows: GLS_endo?=?15.11%, GLS_mid?=?15.28%, GLS_epi?=?17.26%, systolic strain rate?=?15.66%, early diastolic strain rate?=?38.46%, late diastolic strain rate?=?11%. Changing between transducer frequency settings does not systematically derange speckle tracking measures. One can safely reduce the transducer frequency without compromising the validity of speckle tracking derived measures.     

The long‐term influence of repetitive cellular cardiac rejections on left ventricular longitudinal myocardial deformation in heart transplant recipients

The aim of the study was to evaluate the long‐term influence of repeated acute cellular rejections on left ventricular longitudinal deformation in heart transplantation (HTX) patients. One hundred and seventy‐eight HTX patients were included in the study. Rejections were classified according to the International Society of Heart and Lung Transplantation (ISHLT) classification (0R–3R). Patients were divided into three groups according to rejection scores (RSs). Group 1: <50% of biopsies with 1R rejection and no ≥2R rejections; Group 2: ≥50% of biopsies with 1R rejection or one biopsy with ≥2R rejection; Group 3: ≥Two biopsies with ≥2R rejections. All patients had a comprehensive echocardiographic examination and coronary angiography. We found significantly decreasing global longitudinal strain (GLS) comparing to rejection groups (GLS group 1: ?16.8 ± 2.4 (%); GLS group 2: ?15.9 ± 3.3 (%); GLS group 3: ?14.5 ± 2.9 (%), P = 0.0003). After excluding patients with LVEF < 50% or vasculopathy, GLS was still significantly reduced according to RS groups (P = 0.0096). Total number of 1R and 2R rejections correlated significant to GLS in a linear regression model. In contrast, we found fractional shortening and LVEF to be unaffected by repeated rejections. In conclusion, repeated cardiac rejections lead to impaired graft function as detected by decreasing magnitude of GLS. In contrast, traditional systolic graft function surveillance by LVEF did not correlate to rejection burden.     

Identification of hepoxilin A3 in inflammatory events: a required role in neutrophil migration across intestinal epithelia

The mechanism by which neutrophils [polymorphonuclear leukocyte (PMNs)] are stimulated to move across epithelial barriers at mucosal surfaces has been basically unknown in biology. IL-8 has been shown to stimulate PMNs to leave the bloodstream at a local site of mucosal inflammation, but the chemical gradient used by PMNs to move between adjacent epithelial cells and traverse the tight junction at the apical neck of these mucosal barriers has eluded identification. Our studies not only identify this factor, previously termed pathogen-elicited epithelial chemoattractant, as the eicosanoid hepoxilin A(3) (hepA(3)) but also demonstrate that it is a key factor promoting the final step in PMN recruitment to sites of mucosal inflammation. We show that hepA(3) is synthesized by epithelial cells and secreted from their apical surface in response to conditions that stimulate inflammatory events. Our data further establish that hepA(3) acts to draw PMNs, via the establishment of a gradient across the epithelial tight junction complex. The functional significance of hepA(3) to target PMNs to the lumen of the gut at sites of inflammation was demonstrated by the finding that disruption of the 12-lipoxygenase pathway (required for hepA(3) production) could dramatically reduce PMN-mediated tissue trauma, demonstrating that hepA(3) is a key regulator of mucosal inflammation.