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1.
Circulation: Cardiovascular Quality and Outcomes ; 15, 2022.
Article in English | EMBASE | ID: covidwho-1938114

ABSTRACT

Background: Patients hospitalized with COVID-19 who develop cardiopulmonary arrest often have poor prognosis, prompting discussions with families about goals of care. The relationship between clinical and social determinants of code status change is poorly understood. Methods: This retrospective study included adult COVID-19 positive patients admitted to the intensive care unit with cardiac arrest in a multihospital center over the first 9 months of the pandemic (3/1/2020-12/1/2020). Data on medical and social factors was collected and adjudicated. Results: We identified 208 patients over the study timeline. The mean age was 63.7 ± 14.5 years and 54.3% (n=113) were male. The majority of patients with cardiopulmonary arrest had pulseless electrical activity (PEA) as their initial rhythm (91.3%, n=190). Code status was changed in 56.3% (n=117) of patients. The majority of COVID-19 patients with cardiac arrest were Hispanic (53.4%, n=111), followed by African American (27.9%, n=58), and White patients (13.5%, n=28). Race/ethnicity did not affect the rate of code status change. COVID-19 patients who had a code status change were statistically more likely to have a lower salary ($54,838 vs $62,374), have a history of stroke/transient ischemic attack (15.4 vs 4.4%, 18:4), or heart failure (28.2 vs 15.6%, 33:14), all with P<0.05. Patients with code status change had shorter courses of cardiopulmonary resuscitation (11.9 vs 16.9 minutes, P<0.05). Both groups had similar levels of aggressive care received including continuous renal replacement therapy, vasopressor and broad-spectrum antibiotics requirements. Insurance status, ethnicity, religion, and education did not lead to statistically significant changes in code status in COVID patients. Conclusion: Patients hospitalized with cardiopulmonary arrest and positive for COVID-19 are more likely to have a change in code status. This code status change is affected by cardiovascular comorbidities such as stroke and heart failure, along with lower income but not by insurance status, ethnicity, religion, and educational level.

2.
Annals of the Rheumatic Diseases ; 80(SUPPL 1):198-199, 2021.
Article in English | EMBASE | ID: covidwho-1358911

ABSTRACT

Background: Granulocyte/macrophage-colony stimulating factor (GM-CSF) is a cytokine both vital to lung homeostasis and important in regulating inflammation and autoimmunity1,2,3 that has been implicated in the pathogenesis of respiratory failure and death in patients with severe COVID-19 pneumonia and systemic hyperinflammation. 4-6 Mavrilimumab is a human anti GM-CSF receptor α monoclonal antibody capable of blocking GM-CSF signaling and downregulating the inflammatory process. Objectives: To evaluate the effect of mavrilimumab on clinical outcomes in patients hospitalized with severe COVID-19 pneumonia and systemic hyperinflammation. Methods: This on-going, global, randomized, double-blind, placebo-controlled seamless transition Phase 2/3 trial was designed to evaluate the efficacy and safety of mavrilimumab in adults hospitalized with severe COVID-19 pneumonia and hyperinflammation. The Phase 2 portion comprised two groups: Cohort 1 patients requiring supplemental oxygen therapy without mechanical ventilation (to maintain SpO2 ≥92%) and Cohort 2 patients requiring mechanical ventilation, initiated ≤48 hours before randomization. Here, we report results for Phase 2, Cohort 1: 116 patients with severe COVID-19 pneumonia and hyperinflammation from USA, Brazil, Chile, Peru, and South Africa;randomized 1:1:1 to receive a single intravenous administration of mavrilimumab (10 or 6 mg/kg) or placebo. The primary efficacy endpoint was proportion of patients alive and free of mechanical ventilation at Day 29. Secondary endpoints included [1] time to 2-point clinical improvement (National Institute of Allergy and Infectious Diseases COVID-19 ordinal scale), [2] time to return to room air, and [3] mortality, all measured through Day 29. The prespecified evidentiary standard was a 2-sided α of 0.2 (not adjusted for multiplicity). Results: Baseline demographics were balanced among the intervention groups;patients were racially diverse (43% non-white), had a mean age of 57 years, and 49% were obese (BMI ≥ 30). All patients received the local standard of care: 96% received corticosteroids (including dexamethasone) and 29% received remdesivir. No differences in outcomes were observed between the 10 mg/kg and 6 mg/ kg mavrilimumab arms. Results for these groups are presented together. Mavrilimumab recipients had a reduced requirement for mechanical ventilation and improved survival: at day 29, the proportion of patients alive and free of mechanical ventilation was 12.3 percentage points higher with mavrilimumab (86.7% of patients) than placebo (74.4% of patients) (Primary endpoint;p=0.1224). Mavrilimumab recipients experienced a 65% reduction in the risk of mechanical ventilation or death through Day 29 (Hazard Ratio (HR) = 0.35;p=0.0175). Day 29 mortality was 12.5 percentage points lower in mavrilimumab recipients (8%) compared to placebo (20.5%) (p=0.0718). Mavrilimumab recipients had a 61% reduction in the risk of death through Day 29 (HR= 0.39;p=0.0726). Adverse events occurred less frequently in mavrilimumab recipients compared to placebo, including secondary infections and thrombotic events (known complications of COVID-19). Thrombotic events occurred only in the placebo arm (5/40 [12.5%]). Conclusion: In a global, diverse population of patients with severe COVID-19 pneumonia and hyperinflammation receiving supplemental oxygen therapy, corticosteroids, and remdesivir, a single infusion of mavrilimumab reduced progression to mechanical ventilation and improved survival. Results indicate mavrilimumab, a potent inhibitor of GM-CSF signaling, may have added clinical benefit on top of the current standard therapy for COVID-19. Of potential importance is that this treatment strategy is mechanistically independent of the specific virus or viral variant.

3.
Jurnal Ketahanan Nasional ; 26(2):132-154, 2020.
Article in Indonesian | Indonesian Research | ID: covidwho-1235459

ABSTRACT

Tersebarnya Corona Virus Disease 2019 (COVID-19) telah memberikan pengaruh pada kondisi keamanan dan ketertiban masyarakat di Indonesia dan ketahanan nasional. Hal ini sudah ditanggapi oleh World Health Organization (WHO) dengan menetapkan status pandemi global pada COVID-19 mengingat dampak negatif yang menyerang banyak negara di dunia.Metode penelitian kualitatif digunakan guna mendapatkan informasi dari narasumber terkait bahwa, dengan kebijakan yang ada, pemerintah Indonesia telah menjalankan berbagai upaya dalam rangka deteksi, pencegahan dan penanggulangan COVID-19 ini. Beberapa di antaranya adalah adanya Keppres No. 9 tahun 2020 tentang Perubahan atas Keppres No. 7 Tahun 2020 tentang Gugus Tugas Percepatan Penanganan COVID-19, Peraturan Pemerintah Republik Indonesia No. 21 tahun 2020 tentang Pembatasan Sosial Bersakala Besar (PSBB) dalam rangka Percepatan Penanganan COVID-19 dan Keppres No. 12 tahun 2020 tentang Penetapan Bencana Non-alam penyebaran COVID-19 sebagai Bencana Nasional.Model analisis kebijakan kelompok menemukan bahwa dalam kondisi masyarakat yang tidak stabil di tengah pandemi ini, kebijakan PSBB didukung dengan adanya Gugus Tugas tersebut merupakan langkah yang tepat dalam rangka penanganan COVID-19 di Indonesia dibandingkan opsi lockdown yang bisa memberikan efek domino pada kondisi bangsa. Selain itu, tulisan ini juga mensimulasikan opsi kebijakan pemerintah dengan menerapkan pola kebijakan pelaksanaan rapid test, karantina maupun operasional RS untuk penanganan COVID-19 (Opsi C) dan kebijakan physical distancing / social distancing dengan pola bekerja dari rumah (Opsi D) yang dapat memberikan hasil penurunan jumlah kasus COVID-19 di Indonesia.

4.
Cardiovascular Pathology ; 48, 2020.
Article | WHO COVID | ID: covidwho-325621

ABSTRACT

This paper collates the pathological findings from initial published autopsy reports on 23 patients with coronavirus disease 2019 (COVID-19) from 5 centers in the United States of America, including 3 cases from Houston, Texas. Findings confirm that COVID-19 is a systemic disease with major involvement of the lungs and heart. Acute COVID-19 pneumonia has features of a distinctive acute interstitial pneumonia with a diffuse alveolar damage component, coupled with microvascular involvement with intra- and extravascular fibrin deposition and intravascular trapping of neutrophils, and, frequently, with formation of microthombi in arterioles. Major pulmonary thromboemboli with pulmonary infarcts and/or hemorrhage occurred in 5 of the 23 patients. Two of the Houston cases had interstitial pneumonia with diffuse alveolar damage pattern. One of the Houston cases had multiple bilateral segmental pulmonary thromboemboli with infarcts and hemorrhages coupled with, in nonhemorrhagic areas, a distinctive interstitial lymphocytic pneumonitis with intra-alveolar fibrin deposits and no hyaline membranes, possibly representing a transition form to acute fibrinous and organizing pneumonia. Multifocal acute injury of cardiac myocytes was frequently observed. Lymphocytic myocarditis was reported in 1 case. In addition to major pulmonary pathology, the 3 Houston cases had evidence of lymphocytic pericarditis, multifocal acute injury of cardiomyocytes without inflammatory cellular infiltrates, depletion of splenic white pulp, focal hepatocellular degeneration and rare glomerular capillary thrombosis. Each had evidence of chronic cardiac disease: hypertensive left ventricular hypertrophy (420 g heart), dilated cardiomyopathy (1070 g heart), and hypertrophic cardiomyopathy (670 g heart). All 3 subjects were obese (BMIs of 33.8, 51.65, and 35.2 Kg/m2). Overall, the autopsy findings support the concept that the pathogenesis of severe COVID-19 disease involves direct viral-induced injury of multiple organs, including heart and lungs, coupled with the consequences of a procoagulant state with coagulopathy.

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