Usefulness of Left Ventricular Vortex Flow Analysis for Predicting Clinical Outcomes in Patients with Chronic Heart Failure: A Quantitative Vorticity Imaging Study Using Contrast Echocardiography

The goal of the study described here was to evaluate whether left ventricular vortex flow parameters, as assessed by contrast echocardiography, enhance prediction of major adverse cardiac events (MACE) in patients with chronic heart failure and systolic dysfunction. A total of 75 patients with contrast echocardiography and systolic dysfunction (ejection fraction ≤45%) were prospectively enrolled and underwent vortex flow analysis with particle image velocimetry using contrast echocardiography. Vortex flow parameters, including kinetic energy fluctuation (KEF), were evaluated. Patients were followed up for a primary endpoint of MACE that comprised hospital admission for cardiovascular causes and cardiac deaths. Across a median 277-d follow-up, 29 patients (38.7%) experienced MACE. Among these, the incidence of diabetes and the E/e' ratio were significantly higher in patients with MACE than in those without, whereas the hemoglobin level and ejection fraction were significantly lower. KEF was significantly lower in patients with MACE. In the multivariate analysis, higher KEF was associated with a lower risk of MACE (hazard ratio?=?0.18, 95% confidence interval: 0.04–0.97, p?=?0.046). The addition of KEF to a model with conventional parameters (e.g., age, diabetes, ejection fraction and the E/e' ratio) significantly improved the model's discrimination. Elevations in the quantitative left ventricular vortex flow parameter, KEF, as determined by contrast echocardiography, are associated with a lower risk of MACE and improved functional status among patients with chronic heart failure.     

Echocardiography and Cardiac Magnetic Resonance‐Based Feature Tracking in the Assessment of Myocardial Mechanics in Tetralogy of Fallot: An Intermodality Comparison

We investigated intermodality agreements of strains from two‐dimensional echocardiography (2DE) and cardiac magnetic resonance (CMR) feature tracking (FT) in the assessment of right (RV) and left ventricular (LV) mechanics in tetralogy of Fallot (TOF). Patients were prospectively studied with 2DE and CMR performed contiguously. LV and RV strains were computed separately using 2DE and CMR‐FT. Segmental and global longitudinal strains (GLS) for the LV and RV were measured from four‐chamber views; LV radial (global radial strain [GRS]) and circumferential strains (GCS) measured from short‐axis views. Intermodality and interobserver agreements were examined. In 40 patients (20 TOF, mean age 23 years and 20 adult controls), LV, GCS showed narrowest intermodality limits of agreement (mean percentage error 9.5%), followed by GLS (16.4%). RV GLS had mean intermodality difference of 25.7%. GLS and GCS had acceptable interobserver agreement for the LV and RV with both 2DE and CMR‐FT, whereas GRS had high interobserver and intermodality variability. In conclusion, myocardial strains for the RV and LV derived using currently available 2DE and CMR‐FT software are subject to considerable intermodality variability. For both modalities, LV GCS, LV GLS, and RV GLS are reproducible enough to warrant further investigation of incremental clinical merit.     

γ-Catenin-Dependent Signals Maintain BCR-ABL1+ B Cell Acute Lymphoblastic Leukemia

1. Download high-res image (135KB)
2. Download full-size image

     

Intracardiac flow analysis in cardiac resynchronization therapy: A new challenge?

In the past years, assessment of cardiac function has become possible through the analysis of intracardiac flow dynamics, performed noninvasively using phase‐contrast cardiac magnetic resonance and contrast and noncontrast ultrasound techniques. From 2013 to 2019, 9 echocardiographic investigations have considered 215 patients with cardiac resynchronization therapy (CRT) as a model for assessing flow dynamics within the left ventricle. Preliminary results have been reported about the acute hemodynamic effects of CRT and programming of the CRT device, showing the potential of an approach based on analysis of intracardiac flows. At present, there are only scarce data on the capability of intracardiac flow dynamics to predict LV remodeling after CRT and no information on clinical outcome prediction. Future investigations should be aimed at clarifying the mechanisms and impact of maladaptive intracardiac vortex dynamics on progressive LV remodeling as well as the prognostic meaning of implanted CRT device based on cardiac flow analysis.     

The balance between pro‐ and anti‐inflammatory cytokines is crucial in human allergic contact dermatitis pathogenesis: the role of IL‐1 family members

The interleukin (IL)‐1 family includes 11 members that are important in inflammatory processes. It includes various agonists and two antagonists, IL‐1Ra and IL‐36Ra. Our aim was to investigate whether the IL‐1 family is involved in allergic contact dermatitis (ACD). The expression of IL‐1 family members was evaluated by PCR and immunohistochemistry in the positive patch test reaction site (involved skin) and in the uninvolved skin of ACD patients. We also examined these cytokines in an ex vivo model of ACD. The antagonistic activity of IL‐36Ra was evaluated by injecting recombinant IL‐36Ra in uninvolved skin biopsies of ACD patients. IL‐1Ra and IL‐36Ra expression was quantified in mononuclear cells of nickel‐sensitized patients challenged in vitro with nickel. IL‐33 involvement in ACD was investigated by intra‐dermal injection of anti‐IL‐33 in the uninvolved skin of patients ex vivo. Results showed that IL‐1β, IL‐1Ra, IL‐36α, IL‐36β, IL‐36γ and IL‐33 expression, but not IL‐36Ra expression, was enhanced in ACD‐involved skin. Immunohistochemical analysis and ex vivo skin cultures confirmed these results. Injection of anti‐IL‐33 in ACD‐uninvolved skin inhibited IL‐8 expression, whereas IL‐36Ra inhibited IL‐36α, IL‐36β, IL‐36γ and IL‐8 expression. Nickel induced IL‐1Ra expression in lymphocytes of nickel‐sensitized patients. Hence, various IL‐1 agonists and antagonists may be involved in ACD pathogenesis.