Acute pulmonary embolism in conjunction with intramural right ventricular thrombus in a SARS-CoV-2-positive patient

Sulemane, Samir; Baltabaeva, Aigul; Barron, Anthony; Chester, Ruth; Rahman-Haley, Shelley

doi:10.1093/ehjci/jeaa115

Cited by 22 publications

(18 citation statements)

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“…5). Many COVID-19 patients were reported to have pulmonary embolism and thrombosis 74 , which could be the effect of altered hypoxic responses. www.nature.com/scientificreports/ www.nature.com/scientificreports/ Similarly, several lung development and respiratory process genes/proteins were found to be dysregulated in the COVID-19 patient's lung (Fig.…”

Section: Discussionmentioning

confidence: 99%

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Lung transcriptome of a COVID-19 patient and systems biology predictions suggest impaired surfactant production which may be druggable by surfactant therapy

Islam

Khan

2020

Sci Rep

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An incomplete understanding of the molecular mechanisms behind impairment of lung pathobiology by COVID-19 complicates its clinical management. In this study, we analyzed the gene expression pattern of cells obtained from biopsies of COVID-19-affected patient and compared to the effects observed in typical SARS-CoV-2 and SARS-CoV-infected cell-lines. We then compared gene expression patterns of COVID-19-affected lung tissues and SARS-CoV-2-infected cell-lines and mapped those to known lung-related molecular networks, including hypoxia induced responses, lung development, respiratory processes, cholesterol biosynthesis and surfactant metabolism; all of which are suspected to be downregulated following SARS-CoV-2 infection based on the observed symptomatic impairments. Network analyses suggest that SARS-CoV-2 infection might lead to acute lung injury in COVID-19 by affecting surfactant proteins and their regulators SPD, SPC, and TTF1 through NSP5 and NSP12; thrombosis regulators PLAT, and EGR1 by ORF8 and NSP12; and mitochondrial NDUFA10, NDUFAF5, and SAMM50 through NSP12. Furthermore, hypoxia response through HIF-1 signaling might also be targeted by SARS-CoV-2 proteins. Drug enrichment analysis of dysregulated genes has allowed us to propose novel therapies, including lung surfactants, respiratory stimulants, sargramostim, and oseltamivir. Our study presents a distinct mechanism of probable virus induced lung damage apart from cytokine storm.

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Section: Discussionmentioning

confidence: 99%

“…5 ). Many COVID-19 patients were reported to have pulmonary embolism and thrombosis 74 , which could be the effect of altered hypoxic responses.…”

Section: Discussionmentioning

confidence: 99%

Lung transcriptome of a COVID-19 patient and systems biology predictions suggest impaired surfactant production which may be druggable by surfactant therapy

Islam

Khan

2020

Sci Rep

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“…Many COVID-19 patients are reported to have pulmonary embolism and thrombosis [91], this hypoxic responses could suggest the probable routes of this.…”

Section: Discussionmentioning

confidence: 92%

Lung biopsy cells transcriptional landscape from COVID-19 patient stratified lung injury in SARS-CoV-2 infection through impaired pulmonary surfactant metabolism

Islam

Khan

2020

Preprint

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Clinical management of COVID-19 is still complicated due to the lack of therapeutic interventions to reduce the breathing problems, respiratory complications and acute lung injury -which are the major complications of most of the mild to critically affected patients and the molecular mechanisms behind these clinical features are still largely unknown. In this study, we have used the RNA-seq gene expression pattern in the COVID-19 affected lung biopsy cells and compared it with the effects observed in typical cell lines infected with SARS-CoV-2 and SARS-CoV. We performed functional overrepresentation analyses using these differentially expressed genes to signify the processes/pathways which could be deregulated during SARS-CoV-2 infection resulting in the symptomatic impairments observed in COVID-19. Our results showed that the significantly altered processes include inflammatory responses, antiviral cytokine signaling, interferon responses, and interleukin signaling etc. along with downmodulated processes related to lung's functionality likeresponses to hypoxia, lung development, respiratory processes, cholesterol biosynthesis and surfactant metabolism. We also found that the viral protein interacting host's proteins involved in similar pathways like: respiratory failure, lung diseases, asthma, and hypoxia responses etc., suggesting viral proteins might be deregulating the processes related to acute lung injury/breathing complications in COVID-19 patients. Protein-protein interaction networks of these processes and map of gene expression of deregulated genes revealed that several viral proteins can directly or indirectly modulate the host genes/proteins of those lung related processes along with several host transcription factors and miRNAs. Surfactant proteins and their regulators SPD, SPC, TTF1 etc. which maintains the stability of the pulmonary tissue are found to be downregulated through viral NSP5, NSP12 that could lead to deficient gaseous exchange by the surface films. Mitochondrial dysfunction owing to the aberration of NDUFA10, NDUFAF5, SAMM50 etc. by NSP12; abnormal thrombosis in lungs through atypical PLAT, EGR1 functions by viral ORF8, NSP12; dulled hypoxia responses due to unusual shift in HIF-1 downstream signaling might be the causative elements behind the acute lung injury in COVID-19 patients. Our study put forward a distinct mechanism of probable virus induced lung damage apart from cytokine storm and advocate the need of further research for alternate therapy in this direction.

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“…In addition, the new investigational therapies may carry serious drug-drug interactions with antiplatelet agents and anticoagulants [ 8 ]. To our knowledge, there has been only one case of a SARS-CoV-2-positive patient with acute pulmonary embolism in conjunction with intramural RVT [ 9 ]. Similar to our patient, the patient from the Sulemane et al study was found to have McConnell’s sign on echo as well as right ventricular pressure overload.…”

Section: Discussionmentioning

confidence: 99%

A Case Report of Polymerase Chain Reaction-Confirmed COVID-19 in a Patient With Right Ventricular Thrombus and Bilateral Deep Vein Thrombosis

Elkattawy

Younes

Noori³

2020

Cureus

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The new coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), that causes the highly contagious coronavirus disease 2019 (COVID-19) has led to an unprecedented global health crisis. Infected patients have been shown to trigger a heightened inflammatory response, increasing thrombotic risk. We report the case of a polymerase chain reaction (PCR)-confirmed COVID-19 in a Hispanic male with no past medical history who presented to the ED with upper respiratory tract symptoms including shortness of breath and cough, requiring continuous positive airway pressure (CPAP) therapy. He was found to have a right ventricular thrombus (RVT) and bilateral deep vein thrombosis (DVT) on the day of admission, which were detected on transthoracic echocardiogram and duplex venous ultrasound, respectively. The patient was started on therapeutic enoxaparin sodium, which led to an improvement in oxygenation, and he was eventually downgraded to the medical floors for further management.

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Acute pulmonary embolism in conjunction with intramural right ventricular thrombus in a SARS-CoV-2-positive patient

Cited by 22 publications

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Lung transcriptome of a COVID-19 patient and systems biology predictions suggest impaired surfactant production which may be druggable by surfactant therapy

Lung transcriptome of a COVID-19 patient and systems biology predictions suggest impaired surfactant production which may be druggable by surfactant therapy

Lung biopsy cells transcriptional landscape from COVID-19 patient stratified lung injury in SARS-CoV-2 infection through impaired pulmonary surfactant metabolism

A Case Report of Polymerase Chain Reaction-Confirmed COVID-19 in a Patient With Right Ventricular Thrombus and Bilateral Deep Vein Thrombosis

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