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10.1097/RTI.0000000000000530 http://scihub22266oqcxt.onion/10.1097/RTI.0000000000000530 32349055!7253049!32349055     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=32349055&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       J+Thorac+Imaging 2020 ; 35 (6): 344-345 Nephropedia Template TP {{tp|p=32349055|t=2020. Is COVID Evolution Due to Occurrence of Pulmonary Vascular Thrombosis?|pdf=|usr=}}{{32349055}} gab.com Text Is COVID Evolution Due to Occurrence of Pulmonary Vascular Thrombosis JO: J Thorac Imaging http://www.kidney.de/pget.php?&tw=1&pmid=32349055 #FOAvip In this hypothesis paper, we suggest that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may induce intravascular pulmonary thrombosis, which may result in the rapid worsening of clinical conditions and, eventually, exitus. Previously published papers have demonstrated that increased levels of D-dimer at hospital admission correlate with a more severe disease (0.5 mg/L) or occurrence of death (1 mg/L). The potential prothrombotic action of the SARS-CoV-2 is supported by the topographical involvement of the lung regions with a predilection for the lower lobe with peripheral involvement. If this hypothesis is demonstrated, this could suggest the benefit of using antithrombotic/coagulation regimens for SARS-CoV-2 and, at the same time, the urgency to identify drugs that could alter the inflammatory storm, thus protecting the vessel wall. Twit Text FOAVip Is COVID Evolution Due to Occurrence of Pulmonary Vascular Thrombosis ????J Thorac Imaging http://www.kidney.de/pget.php?&tw=1&pmid=32349055 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32349055 #FOAvip English Wikipedia <ref>{{Cite pmid|32349055}}</ref> Is COVID Evolution Due to Occurrence of Pulmonary Vascular Thrombosis? #MMPMID32349055 Saba L; Sverzellati N J Thorac Imaging 2020[Nov]; 35 (6): 344-345 PMID32349055show ga In this hypothesis paper, we suggest that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may induce intravascular pulmonary thrombosis, which may result in the rapid worsening of clinical conditions and, eventually, exitus. Previously published papers have demonstrated that increased levels of D-dimer at hospital admission correlate with a more severe disease (0.5 mg/L) or occurrence of death (1 mg/L). The potential prothrombotic action of the SARS-CoV-2 is supported by the topographical involvement of the lung regions with a predilection for the lower lobe with peripheral involvement. If this hypothesis is demonstrated, this could suggest the benefit of using antithrombotic/coagulation regimens for SARS-CoV-2 and, at the same time, the urgency to identify drugs that could alter the inflammatory storm, thus protecting the vessel wall. |COVID-19/blood/*complications/*physiopathology[MESH] |Fibrin Fibrinogen Degradation Products/metabolism[MESH] |Humans[MESH] |Lung Diseases/blood/etiology/physiopathology[MESH] |Lung/physiopathology[MESH] |SARS-CoV-2[MESH]Is COVID Evolution Due to Occurrence of Pulmonary Vascular Thrombosis?(epmc).pdf DeepDyve Pubget Overpricing