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Introduction: Obesity is an important risk factor associated with poor cardiovascular outcomes. Lifestyle modification, pharmaceutical, and intragastric balloons weight loss therapy are often unsuccessful, unsustainable, or accompanied by risks. Transcatheter bariatric embolotherapy (TBE) is a promising therapy in which the left gastric artery is embolized to reduce the expression of “hunger” hormones from the gastric fundus. Despite several early clinical trials, long-term safety or efficacy has yet to be studied. We originally studied TBE in a double-blind, sham procedure, first in human RCT of 40 obese patients (pts) (NCT03185949). Complete details regarding the initial RCT were previously published, briefly the study demonstrated up to 9.3% TBWL at 1-year post-TBE. Following completion of the initial study at 1 year follow-up, we asked subjects to return for long-term evaluation. Methods: Subjects who previously completed the RCT with no major protocol deviations were asked to return for SOC follow-up visits at 2-, 2.5-, and 3-years post-embolization for further evaluation on weight loss, blood pressure, pre-diabetic clinical status, satiety, and Quality of Life (QoL). Given the evolving situation of the COVID-19 pandemic, the study site was unable to complete all planned study visits. Results: Between 2-3 years post-TBE subjects (n=11) demonstrated a mean 9% TBWL and 25% EBWL. This cohort of patients demonstrated a long-term weight loss maintenance, with previously reported weight loss of 8% TBWL at 1-year post-embolization. Overall QoL at 2 years post-TBE increased by approximately 22%. The volume to achieve satiety was reduced by 33% in long-term follow-up. Oral Disposition Index increased from 1.89 mM -1 at 6 months post-TBE to 4.41 mM -1 2 years post-TBE. 1-hr Oral Glucose Tolerance Test (OGTT) C-Peptide levels decreased from 3.22 nmol/L at 6 months to 2.53 nmol/L at 2 years post-TBE. 2-hr OGTT C-Peptide levels also showed a decrease from 2.95 nmol/L at 6 months to 1.78 nmol/L at 2 years post-TBE, possibly indicating an improvement in pre-diabetic status. Conclusions: Bariatric embolization is safe and when used along with lifestyle therapy, results in clinically significant and sustained weight loss up to 2-3 years post-TBE.

Introduction: Acute respiratory distress syndrome (ARDS) is one of the main causes of mortality in patients with COVID-19. Despite numerous studies, therapies for ARDS in COVID-19 remain significantly limited. Currently, there have been reports of the efficient use of mesenchymal stem cell (MSC) for the treatment of ARDS. Several studies have reported that MSC produces anti-inflammatory cytokines, promotes the maturation of dendritic cells, and modulates NK cells. The safety of MSC therapy has been demonstrated in early-stage clinical studies with a relatively small number of patients. We investigated the influence of freeze-dried human placental mesenchymal stem cells (HPMSC) in a preclinical rodent model of ARDS. Methods: Sixty rats were randomly divided into three groups of 20: the first group was the control, the second group received dexamethasone, and the third group received HPMSC. Results: Survival was highest in the HPMSC group (75%, 95%CI: 50, 88) when compared to the control group. In a cox regression model, mortality of HPMSC group (HR: 11.30 [95% CI: 4.05, 31.50]) when compared to control was statistically significant (p < 0.001). Mortality in the dexamethasone (HR: 64.25 [95% CI: 32.71, 126.19]) was not statistically significant (p = 0.199). Plasma serum TNF-α levels were statistically significant in the HMPSC group when compared to the control (p < 0.001) and dexamethasone group (p < 0.001). Single factor ANOVA comparing TNF-α levels between all groups was also significant (p < 0.0001). Trends (Table 1) indicated that plasma serum cytokine levels for TNF-α, IL-1β, and Il-6 were less in the HPMSC group than the control and dexamethasone groups. Conclusions: These experiments demonstrated that HPMSC significantly decreased mortality, endogenous intoxication, and a reduction in the release of pro-inflammatory cytokines. The freeze-dried placental stem cell is a promising biomaterial that can be used nebulized for the treatment of coronavirus disease.

Depression is associated with poor prognosis for cardiovascular disease (CVD) including mortality. Among multiple mechanisms linking depression and CVD, changes in platelet reactivity are known to be one of the major confounders of such adverse association. However, there are very limited data in children. Thus, we evaluated some conventional hemostatic indices including whole blood platelet aggregation in patients with documented pediatric depression and compared these data with those obtained from healthy children. The pediatric patients fulfilled criteria for major depression with a minimum score of 19 on the 21-item Beck Depression Inventory Scale. Plasma fibrinogen, D-dimer, platelet count, mean platelet volume, and platelet aggregation induced by ADP and collagen were measured in 67 pediatric patients with depression and matched by age and sex with 78 healthy controls. As expected, the depressed children had significantly higher BECK scales (P = 0.001) compared with the normal subjects. Platelet aggregation induced by ADP and collagen (P = 0.0001 for both) was significantly higher in depressed children. BECK scale scores correlated significantly with platelet aggregation induced by ADP (r = 0.3, P = 0.001) and collagen (r = 0.4, P = 0.01). In contrast, platelet counts, fibrinogen, D-dimer, mean platelet volume, and antithrombin-III levels were almost identical between both groups. Children with depression exhibit mostly intact hemostatic parameters, with the exception of significantly higher platelet activity when compared with healthy controls. These data match well with prior evidence from depressed adults supporting the hypothesis that platelets participate in the pathogenesis of depression. However, beyond pure assessment of platelet activity, other elements including serotonin content and cell receptor changes in pediatric depression should be elucidated before randomized trial(s) can be justified.

Aggressive dual antiplatelet therapy is associated not only with more bleeding, impaired wound healing, and potentially more solid cancer rates but it also causes higher infection risks including sepsis, and systemic inflammatory response syndrome (SIRS). This may be especially true considering the alarming off-label use of prasugrel. A 65-year-old white male patient with a history of myocardial infarction treated with percutaneous coronary intervention and implantation of 2 bare metal stents, was treated with off-label clopidogrel for 4 years, including a double daily dose (150 mg) for the initial 13 months. Still on clopidogrel, the patient was hospitalized with suspected pneumonia. A diagnostic cardiac catheterization revealed a 60%-70% blockage of the mid left anterior descending, but there was no need for coronary intervention. At discharge, clopidogrel 75 mg/d was switched over to off-label prasugrel 10 mg/d on top of aspirin (81 mg/d). On day 3 after prasugrel was given, a football-sized bruise appeared on the patient's lower right abdomen, but computed tomography results were unremarkable. On day 6 after administration of prasugrel, the patient became dizzy, disoriented, confused, experienced difficulty breathing, severe headache, weakness, intensive petechial rash covering the entire body, and breathing difficulty requiring ventilation. Within 24 hours, the patient was unable to correctly identify his age; his eyes were pale in color to almost colorless and when hearing a sound he would turn his entire head toward the sound and he appeared to be blind. His lungs, liver, and kidneys began to show signs of failure over the next 5-9 days. Sixteen days after the administration of the first prasugrel dose, the patient died of sepsis complicated with SIRS. Aggressive off-label use of clopidogrel (double dose for 13 months, and >4 years overall duration), followed by off-label switchover to the highest daily dose (10 mg) prasugrel may trigger sepsis and fatal SIRS. The mechanism responsible for such harmful association is probably indirect, and involves the weakening of platelet-neutrophil-endothelial crosstalk necessary to combat infections, and/or keep inflammation from spreading.

Radiocontrast-induced nephropathy is a well known consequence of cardiologic interventions. Acute radiocontrast nephropathy is the third most common cause of acute renal failure in patients admitted to a hospital ([1][1]). Up to 7% of patients with this condition need temporary dialysis or progress