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In DCD liver transplantation, recipient female gender and high BMI were associated with a higher incidence of EAR, while the use of CD25-Ab and/or MMF had a protective effect.

The reported hepatotoxicity of methotrexate underlines the need for a repeated non-invasive and reliable evaluation of liver fibrosis. We estimated, using a non-invasive strategy, the prevalence of significant liver fibrosis in patients treated by methotrexate and the predictors of significant fibrosis (fibrosis≥F2).

Fibrosis was prospectively evaluated using 9 non-invasive tests in consecutive patients with psoriasis, rheumatoid arthritis, or Crohn’s disease. Significant fibrosis was assessed without liver biopsy by defining a “specific method” (result given by the majority of the tests) and a “sensitive method” (at least one test indicating a stage≥F2).

One hundred and thirty-one patients (66 Psoriasis, 40 rheumatoid arthritis, and 25 Crohn’s disease) were enrolled, including 83 receiving methotrexate. Seven tests were performed on average per patient, with a complete concordance in 75% of cases. Fibroscan® was interpretable in only 61% of patients. The best performances (AUROC>0.9) for predicting significant fibrosis were obtained by tests dedicated to steatohepatitis (FibroMeter NAFLD, NFS and FPI). The prevalence of fibrosis≥F2 according to the “specific” or the “sensitive” assessment of fibrosis was 10% and 28%, respectively. Methotrexate exposure did not influence the fibrosis stage. Factors independently associated with significant fibrosis according our “sensitive method” were age, male gender, and metabolic syndrome.

We provided a non-invasive approach for identifying liver fibrosis≥F2 by using 8 biochemical tests and Fibroscan®. In this population, the risk of significant fibrosis was related to age, male gender, and presence of metabolic syndrome, but was not influenced by methotrexate.

We provided a non-invasive approach for identifying liver fibrosis≥F2 by using 8 biochemical tests and Fibroscan®. AMG 487 In this population, the risk of significant fibrosis was related to age, male gender, and presence of metabolic syndrome, but was not influenced by methotrexate.

The objective of this study was to determine if there is an impact of surgical delay on 5-year overall survival (OS) from early stage colon cancer, and if so, to define how long surgery can safely be postponed.

Using the NCDB, we compared early (14-30 days) and delayed surgery (31-90 days) in patients with Stage I/II colon cancer. Outcomes included OS at five years and odds of death.

Delayed resection conferred a decreased 5-year OS of 73.0% (95% CI, 72.6-73.4), compared to early resection 78.3% (95% CI, 77.9-78.8). When time to surgery was divided into one-week intervals, there was no difference in the odds of death with delay up to 35-41 days (6 weeks), but odds of death increased by 9% per week thereafter.

These data support that definitive resection for early stage colon cancer may be safely delayed up to 6 weeks.

These data support that definitive resection for early stage colon cancer may be safely delayed up to 6 weeks.Each week, I record audio summaries for every paper in JACC, as well as an issue summary. Although this process is quite time-consuming, I have become familiar with every paper that we publish. Thus, I have personally selected the top 100 papers (both Original Investigations and Review Articles) from the distinct specialties each year. In addition to my personal choices, I have included papers that have been the most accessed or downloaded on our websites, as well as those selected by the JACC Editorial Board members. In order to present the full breadth of this important research in a consumable fashion, we will present these abstracts in this issue of JACC, as well as their Central Illustrations. The highlights comprise the following sections Basic & Translational Research, Cardiac Failure & Myocarditis, Cardiomyopathies & Genetics, Cardio-Oncology, Congenital Heart Disease, Coronary Disease & Interventions, Coronavirus (as a NEW section), Hypertension, Imaging, Metabolic & Lipid Disorders, Neurovascular Disease & Dementia, Promoting Health & Prevention, Rhythm Disorders & Thromboembolism, Valvular Heart Disease, and Vascular Medicine (1-100).Fabry disease (FD) is a rare X-linked inherited lysosomal storage disorder caused by deficient α-galactosidase A activity that leads to an accumulation of globotriasylceramide (Gb3) in affected tissues, including the heart. Cardiovascular involvement usually manifests as left ventricular hypertrophy, myocardial fibrosis, heart failure, and arrhythmias, which limit quality of life and represent the most common causes of death. Following the introduction of enzyme replacement therapy, early diagnosis and treatment have become essential to slow disease progression and prevent major cardiac complications. Recent advances in the understanding of FD pathophysiology suggest that in addition to Gb3 accumulation, other mechanisms contribute to the development of Fabry cardiomyopathy. Progress in imaging techniques have improved diagnosis and staging of FD-related cardiac disease, suggesting a central role for myocardial inflammation and setting the stage for further research. In addition, with the recent approval of oral chaperone therapy and new treatment developments, the FD-specific treatment landscape is rapidly evolving.Takotsubo syndrome (TTS) has been a recognized clinical entity for 31 years, since its first description in 1990. TTS is now routinely diagnosed in patients who present with acute chest pain, electrocardiographic changes, troponin elevation, unobstructed coronary arteries, and a typical pattern of circumferential left ventricular wall motion abnormalities that usually involve the apical and midventricular myocardium. Increasing understanding of this intriguing syndrome stems from wider recognition, possible increasing frequency, and a rising number of publications focused on the pathophysiology in clinical and laboratory studies. A comprehensive understanding of TTS pathophysiology and evidence-based treatments are lacking, and specific and effective treatments are urgently required. This paper reviews the pathophysiology of this fascinating syndrome; what is known from both clinical and preclinical studies, including review of the evidence for microvascular dysfunction, myocardial beta-adrenergic signaling, inflammation, and electrophysiology; and where focused research needs to fill gaps in understanding TTS.