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.     

Mitochondrial compromise in 3‐year old patas monkeys exposed in utero to human‐equivalent antiretroviral therapies

Antiretroviral (ARV) drug therapy, given during pregnancy for prevention of mother‐to‐child transmission of human immunodeficiency virus 1 (HIV‐1), induces fetal mitochondrial dysfunction in some children. However, the persistence/reversibility of that dysfunction is unclear. Here we have followed Erythrocebus patas (patas) monkey offspring for up to 3 years of age (similar in development to a 15‐year old human) after exposure of the dams to human‐equivalent in utero ARV exposure protocols. Pregnant patas dams (3–5/exposure group) were given ARV drug combinations that included zidovudine (AZT)/lamivudine (3TC)/abacavir (ABC), or AZT/3TC/nevirapine (NVP), for the last 10 weeks (50%) of gestation. Infants kept for 1 and 3 years also received drug for the first 6 weeks of life. In offpsring at birth, 1 and 3 years of age mitochondrial morphology, examined by electron microscopy (EM), was compromised compared to the unexposed controls. Mitochondrial DNA (mtDNA), measured by hybrid capture chemiluminescence assay (HCCA) was depleted in hearts of patas exposed to AZT/3TC/NVP at all ages (P < 0.05), but not in those exposed to AZT/3TC/ABC at any age. Compared to unexposed controls, mitochondrial reserve capacity oxygen consumption rate (OCR by Seahorse) in cultured bone marrow mesenchymal fibroblasts from 3‐year‐old patas offspring was ～50% reduced in AZT/3TC/ABC‐exposed patas (P < 0.01), but not in AZT/3TC/NVP‐exposed patas. Overall the data show that 3‐year‐old patas sustain persistent mitochondrial dysfunction as a result of perinatal ARV drug exposure. Environ. Mol. Mutagen. 57:526–534, 2016. © 2016 Wiley Periodicals, Inc.     

Erratum: Correction of Nomenclature of Mutations

[This corrects the article on p. 1111 in vol. 26, PMID: 21860566.].