Lundgreen Aaen (matchoxygen28)

Hospitalizations for COVID-19 dramatically increase with age. This is likely because of increases in fragility across biological repair systems and a weakened immune system, including loss of the cardiorenal protective arm of the renin--angiotensin system (RAS), composed of angiotensin-converting enzyme-2 (ACE2)/angiotensin-(1--7) [Ang-(1--7)] and its actions through the Mas receptor. The purpose of this review is to explore how cardiac ACE2 changes with age, cardiac diseases, comorbid conditions and pharmaceutical regimens in order to shed light on a potential hormonal unbalance facilitating SARs-CoV-2 vulnerabilities in older adults. Increased ACE2 gene expression has been reported in human hearts with myocardial infarction, cardiac remodeling and heart failure. We also found ACE2 mRNA in atrial appendage tissue from cardiac surgical patients to be positively associated with age, elevated by certain comorbid conditions (e.g. COPD and previous stroke) and increased in conjunction with patients' chronic us.We performed a multicenter retrospective cohort study of children with 14 days to 18 years of age in the United States from 2011 to 2016 with cancer or hematopoietic cell transplant (HCT) who were supported with veno-venous extracorporeal membrane oxygenation (V-V ECMO). We compared the outcomes of children with oncological diagnoses or HCT supported with V-V ECMO to other children who have received V-V ECMO support. In this cohort of 204 patients supported with V-V ECMO, 30 (15%) had a diagnosis of cancer or a history of HCT. There were 21 patients who had oncological diagnoses without HCT and 9 children were post-HCT. The oncology/HCT group had a higher overall ICU mortality (67% vs. 28%, P less then 0.001), mortality on ECMO (43% vs. 21%, P less then 0.01), and ICU mortality among ECMO survivors (35% vs. 8%, P less then 0.01). The oncology/HCT group had a higher rate of conversion to veno-arterial (V-A) ECMO (23% vs. 9%, P = 0.02) (RR, 2.5; 95% CI, 1.1-5.6). Children with cancer or HCT were older (6.6 vs. 2.9 years, P = 0.02) and had higher creatinine levels (0.65 vs. 0.4 mg/dL, P = 0.04) but were similar to the rest of the cohort for other pre-ECMO variables. For post-HCT patients, survival was significantly worse for those whose indication for HCT was cancer or immunodeficiency (0/6) as compared to other nonmalignant indications (3/3) (P = 0.01).Tissue factor pathway inhibitor (TFPI) has multiple anticoagulant properties. To our knowledge, no studies have measured TFPI levels in adult veno-arterial (VA) extracorporeal membrane oxygenation patients. We hypothesized that adult VA ECMO patients would have increased TFPI levels and slowed tissue factor triggered thrombin generation. Twenty VA ECMO patients had TFPI levels and thrombin generation lag time measured on ECMO day 1 or 2, day 3, and day 5. TFPI levels and thrombin generation lag time were compared against healthy control plasma samples. Mean TFPI levels were significantly higher in ECMO patients on ECMO day 1 or 2 = 81,877 ± 19,481 pg/mL, day 3 = 73,907 ± 26,690 pg/mL, and day 5 = 77,812 ± 23,484 pg/mL compared with control plasma = 38,958 ± 9,225 pg/mL (P less then 0.001 for all comparisons). Median thrombin generation lag time was significantly longer in ECMO patients on ECMO day 1 or 2 = 10.0 minutes [7.5, 13.8], day 3 = 9.0 minutes [6.8, 12.1], and day 5 = 10.7 minutes [8.3, 15.2] compared with control plasma = 3.6 minutes [2.9, 4.2] (P less then 0.001 for all comparisons). TFPI is increased in VA ECMO patients and tissue factor triggered thrombin generation is slowed. Increased TFPI levels could contribute to the multifactorial coagulopathy that occurs during ECMO.Extracorporeal membrane oxygenation (ECMO) can be lifesaving but suffers from high rates of bleeding and repeated transfusions. Current monitoring of blood cell damage during ECMO is limited to platelet counts, hematocrit, and plasma hemoglobin levels. Extracelluar vesicles (EV) are s