The non-linear association between ascending aorta diameter and risk of 12-month mortality in Chinese patients with heart failure: A retrospective cohort study.

Background: There is no conclusive proven link between ascending aorta diameter (AoD) and the risk of death from heart failure (HF). As a result, a retrospective cohort analysis was carried out to determine whether AoD is associated with 12-month mortality in Chinese HF patients. Methods: From January 2017 to March 2020, we collected data on 575 Chinese patients with HF. The exposure and outcome variables were baseline AoD and 12-month risk of mortality (all-cause + cardiac origin), respectively. Data on demographics, drug usage, clinical characteristics, recognized indicators of HF, and comorbidities were included as covariates. To investigate the independent relationships of AoD with the risk of 12-month death, binary logistic regression and two-piecewise linear models were utilized. Results: Our findings imply that there was a non-linear relationship between AoD and the risk of 12-month mortality. For the AoD range of 23 to 37, there was no association with the risk of cardiac mortality [odds ratio (OR) 0.78, 95% confidence interval (CI), 0.62-1.04]. In the AoD range of 37-49, however, the risk of 12-month cardiac death increased by approximately 70% for every 1 mm increase in AoD (OR 1.70, 95% CI, 1.13-2.55). When all-cause death was chosen as the outcome, the same outcome was shown. Conclusion: An AoD larger than 37 mm is a hazardous threshold for Chinese HF patients. Beyond this limit increased the risk of cardiac death by 70% for every 1 mm increase in AoD.

Endothelial cell-specific deficiency of the adenosine deaminase ADAR1 aggravates LPS-induced lung injury in mice via an MDA5-independent pathway.

Adenosine deaminase acting on RNA 1 (ADAR1) has been shown to participate in the regulation of endothelial cells (ECs), as well as local and systemic inflammatory responses. Here, we find that bacterial lipopolysaccharide (LPS)-induced upregulation of ADAR1 in lung ECs is impaired in aged mice, an animal model with high rates of sepsis and mortality. Endothelial cell-specific ADAR1 knockout (ADAR1ECKO ) mice suffer from higher mortality rates, aggravated lung injury, and increased vascular permeability under LPS challenge. In primary ADAR1 knockout ECs, expression of the melanoma differentiation-associated gene 5 (MDA5), a downstream effector of ADAR1, is significantly elevated. MDA5 knockout completely rescues the postnatal offspring death of ADAR1ECKO mice. However, there is no reduction in mortality or apoptosis in lung cells of ADAR1ECKO /MDA5-/- mice challenged with LPS, indicating the involvement of an MDA5-independent mechanism in this process.