A sporadic COVID-19 pneumonia treated with extracorporeal membrane oxygenation in Tokyo, Japan: A case report.

INTRODUCTION: An ongoing outbreak of a novel coronavirus disease (coronavirus disease 2019, COVID-19) has become a global threat. While clinical reports from China to date demonstrate that the majority of cases remain relatively mild and recover with supportive care, it is also crucial to be well prepared for severe cases warranting intensive care. Initiating appropriate infection control measures may not always be achievable in primary care or in acute-care settings. CASE: A 45-year-old man was admitted to the intensive care unit due to severe pneumonia, later confirmed as COVID-19. His initial evaluation in the resuscitation room and treatments in the intensive care unit was performed under droplet and contact precaution with additional airborne protection using the N95 respirator mask. He was successfully treated in the intensive care unit with mechanical ventilation and extracorporeal membrane oxygenation for respiratory support; and antiretroviral treatment with lopinavir/ritonavir. His total intensive care unit stay was 15 days and was discharged on hospital day 24. CONCLUSIONS: Strict infection control precautions are not always an easy task, especially under urgent care in an intensive care unit. However, severe cases of COVID-19 pneumonia, or another novel infectious disease, could present at any moment and would be a continuing challenge to pursue appropriate measures. We need to be well prepared to secure healthcare workers from exposure to infectious diseases and nosocomial spread, as well as to provide necessary intensive care.

Afadin Facilitates Vascular Endothelial Growth Factor-Induced Network Formation and Migration of Vascular Endothelial Cells by Inactivating Rho-Associated Kinase Through ArhGAP29.

OBJECTIVE: We previously reported that afadin, an actin filament-binding protein, regulated vascular endothelial growth factor-induced angiogenesis. However, the underlying molecular mechanisms are poorly understood. Here, we investigated the mechanisms of how Rho-associated kinase is activated in afadin-knockdown human umbilical vein endothelial cells (HUVECs) and how its activation is involved in defects of vascular endothelial growth factor-induced network formation and migration of the cells. APPROACH AND RESULTS: Knockdown of afadin or ArhGAP29, a GTPase-activating protein for RhoA, increased Rho-associated kinase activity and reduced the vascular endothelial growth factor-induced network formation and migration of cultured HUVECs, accompanied by the defective formation of membrane protrusions, such as lamellipodia and peripheral ruffles. Treatment of the afadin- or ArhGAP29-knockdown HUVECs with Rho-associated kinase inhibitors, Y-27632 or fasudil, partially restored the reduced network formation and migration as well as the defective formation of membrane protrusions. ArhGAP29 bound to afadin and was colocalized with afadin at the leading edge of migrating HUVECs. The defective formation of membrane protrusions in ArhGAP29-knockdown HUVECs was restored by expression of mutant ArhGAP29 that bound to afadin and contained a RhoGAP domain but not mutant ArhGAP29 that could bind to afadin and lacked the RhoGAP domain or mutant ArhGAP29 that could not bind to afadin and contained the RhoGAP domain. This suggested the requirement of both the interaction of afadin with ArhGAP29 and RhoGAP activity of ArhGAP29 for migration of HUVECs. CONCLUSIONS: Our results highlight a critical role of the afadin-ArhGAP29 axis for the regulation of Rho-associated kinase activity during vascular endothelial growth factor-induced network formation and migration of HUVECs.

Chest compression-related fatal internal mammary artery injuries manifesting after venoarterial extracorporeal membrane oxygenation: a case series.

BACKGROUND: Cardiopulmonary resuscitation-related bleeding, especially internal mammary artery injuries, can become life-threatening complications after initiating venoarterial extracorporeal membrane oxygenation owing to the frequent involvement of concomitant anticoagulant treatment, antiplatelet treatment, targeted temperature management, and bleeding coagulopathy. We report the cases of five patients who experienced this complication and discuss their management. CASE PRESENTATION: We retrospectively evaluated five patients with cardiopulmonary resuscitation-related internal mammary artery injuries who were treated between February 2011 and February 2016 at our institution. All five patients were Asian men, aged 56 to 68-years old, who had received concomitant intravenously administered unfractionated heparin (3000 units) with antiplatelet therapy. Four patients received targeted temperature management. The injuries and hematomas were detected using contrast-enhanced computed tomography in all cases. Three patients were treated using transcatheter arterial embolization within 6 hours following cardiopulmonary arrest, and two were resuscitated and received appropriate treatment following early recognition of their injuries. Two patients died of hemorrhagic shock with delayed intervention. Four of the five patients had excessively prolonged activated partial thromboplastin times before their interventions. CONCLUSIONS: Computed tomography should be performed as soon as possible after the return of spontaneous circulation to identify injuries and consider appropriate treatments for patients who have experienced cardiac arrest. Delayed bleeding may develop after treating hypovolemic shock and relieving arterial spasms; therefore, transcatheter arterial embolization should be performed aggressively to prevent delayed bleeding even in the absence of extravasation. This approach may be superior to thoracotomy because it is less invasive, causes less bleeding, and can selectively stop arterial bleeding sooner. A 3000-unit intravenous bolus of unfractionated heparin may be redundant; heparin-free extracorporeal cardiopulmonary resuscitation may be a more appropriate alternative. Unfractionated heparin treatment can commence after the bleeding has stopped.

Embolic stroke during apixaban therapy for left atrial appendage thrombus.

Left atrial appendage (LAA) thrombus is associated with atrial fibrillation (AF) and is a powerful predictor of cardiogenic thromboembolism. Warfarin is an established anticoagulant therapy for patients with LAA thrombus to prevent thromboembolic complications. Apixaban is superior to warfarin in the prevention of thromboembolic complications in patients with AF, and there are case reports showing apixaban-associated resolution of LAA thrombus; however, the efficacy and safety of apixaban for the treatment of LAA thrombus remains unproven. Here we report a patient who experienced embolic stroke while taking apixaban for the treatment of LAA thrombus. Thrombolysis therapy was initiated at the onset of stroke and the patient recovered remarkably. Apixaban is known to make thrombi mobile and/or fragile by shifting the coagulation/fibrinolysis balance to a relative predominance of fibrinolytic activity; therefore, it is necessary to monitor for thromboembolic complications after the initiation of apixaban for the treatment of pre-existing LAA thrombus.