25 March 2021

Connection between COVID-19 and pulmonary vascular disease

Watch the replay


  • Albert Osterhaus // SARS-1, MERS, SARS-2 and more: are coronavirus infections an ubiquitous part of our lives?
  • Danny Jonigk // Endothelitis and aberrant angiogenesis – mechanisms of COVID-19 induced vascular injury
  • Stavros Konstantinides // Venous thromboembolism in COVID-19: Prevalence and clinical picture
  • Anna Hemnes // ACE-II receptors – Modulation of PVD in COVID-19?
  • Claes Frostell // Tricuspid regurgitation, as proxy for acute pulmonary hypertension, and its association with short-term outcome in severe Covid-19
  • Vicky Mai // Venous and arterial thromboembolism in COVID-19: a systematic review with meta-analysis


Here are the answers to some of the questions which we were unable to answer during the webinar. Please contact us if you have any further questions. 

  • Q: Is pulmonary embolism dominant in the COVID 19 severe pneumonia? Is thrombolysis had role to diminish the embolism?
  • A: What we found in all of our COVID-19 patients at the site of symptom, so to speak, was micro (!) thrombi. >80% had been given some form of anticoagulation, so larger thrombosis was mixed. Micro thrombi were not.


  • Q: There are some papers suggesting the resistance of SARS-CoV2 infection in primary pulmonary endothelial cells in culture, why do we see this discrepancy in tissue vs cell culture?
  • A: Very good question; we see the same in our culture experiments. The actual blood flow and dynamic interface at the blood / endothelial barrier likely account for this. Also, while the virus definitrely is present in pulmonary endothelial cells and damages these, the damage due to the host response is much more dominant.


  • Q: Would the current PH drugs be effective to treat the subset Covid patients who develops PH?
  • A: According to the predicted molecular regulation: yes; we all will be forced to look for efficient drugs very soon


  • Q: To what extent is abberant angiogeneis within the lung thought to be co-located with the alveolar damage (GGO) visible on conventional CT? Is there endotholial damage in parts of the lung where the airspaces remain relatively unaffected?
  • A: We looked at more than 100 lungs of COVID-19 patients and always found I Angiogenesis where the vascular (lymphocytic) inflammation was present. This (and hyaline membranes) correlates to the GGO.


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