Connection between COVID-19 and pulmonary vascular disease (CME credits available)

24 March 2021

  • days
  • Hours
  • Minutes

Chair and moderators

Marion Delcroix, University Hospitals of Leuven, Belgium
Sylvia Cohen-Kaminsky, Université Paris Saclay, France 


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A deeper look

A year ago, WHO declared COVID 19 a global pandemic. The causative agent was identified as Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) and since then, the international scientific community focused on the fight against this disease.  The infection from the virus displays clinical and pathophysiological features that have not been described before in an infectious pneumonia; therefore the third webinar of the PVRI2021 Digital: Complete Webinar series, entitled “Connection between COVID-19 and pulmonary vascular disease” will provide us new insights. Since emerging coronaviruses have created global health concerns in the last two decades, the first presentation will focus on the impact of coronavirus infections on our lives. Τhe next two presentations will investigate the mechanisms behind endothelitis and angiogenesis, as well as the venous thromboembolism seen in such patients and its prevalence. Pulmonary vascular disease (PVD) appears to be a major component of COVID-19 infection; therefore the forth presentation will examine the role of ACE-II receptor on PVD modulation in this disease. Last but not least, the two best abstracts will (1) focus on the usefulness of tricuspid regurgitation assessment in COVID-19-related acute pulmonary hypertension, and (2) present a systematic review and meta- analysis on venous and arterial thromboembolism in COVID-19.


SARS-1, MERS, SARS-2 and more: are coronavirus infections an ubiquitous part of our lives?

15:00-15:22 GMT

Presenter: // Albert Osterhaus, University of Veterinary Medicine Hannover, Germany

Awaiting further information.


Endothelitis and aberrant angiogenesis – mechanisms of COVID-19 induced vascular injury

15:22-15:45 GMT

Presenter: // Danny Jonigk, Hannover Medical School, Germany

Progressive respiratory failure is the primary cause of death in the coronavirus disease 2019 (Covid-19) pandemic. Despite widespread interest in the pathophysiology of the disease, relatively little is known about the associated morphologic and molecular changes in the peripheral lung of patients who die from Covid-19.


Venous thromboembolism in COVID-19: Prevalence and clinical picture

15:45-16:08 GMT

Presenter: // Stavros Konstantinides , University Medical Center of Mainz, Germany

The clinical spectrum of COVID-19 is broad. Many patients will experience no, or only minor non-specific symptoms, but in some cases severe disease may develop, progressing from pneumonia to the acute respiratory distress syndrome and shock with multi-organ failure. The cytokine storm following the viral infection elicits an acute systemic inflammatory response and severe endothelial damage; these changes may result in potentially life-threatening thrombosis. Haemostatic laboratory abnormalities, including marked elevations of D-dimer and fibrinogen levels, are frequently observed in patients with COVID-19, and they have been associated with an unfavourable in-hospital outcomes (1). In parallel, the clinically reported prevalence rate of venous thromboembolism among hospitalized patients with COVID-19 was in the range of 20-36% (2-5), or even higher (6), depending on the overall severity of COVID-19. Arterial thrombosis or thromboembolism are less frequent (3, 4). Importantly, thrombotic events contribute to COVID-19-associated morbidity and mortality (7). It is therefore recommended to adhere to the standards for the prevention, diagnosis and management of thrombosis associated with COVID-19 in clinical practice:

1)    Thromboprophylaxis. Recommendations on prophylactic anticoagulation should be followed in all hospitalized patients with COVID-19. Prophylactic anticoagulation in selected ambulatory patients is currently undergoing testing in randomized trials. As for the dose, standard prophylactic doses of low molecular weight heparin should generally be used. Administration of higher, intermediate or even therapeutic doses of heparin is empirically considered for severely ill patients and currently under evaluation in ongoing trials.

2)    Awareness and suspicion of thrombosis. Unexpected respiratory worsening, new or unexplained tachycardia, a fall in blood pressure not attributable to tachyarrhythmia, hypovolaemia or sepsis, new-onset ECG changes suggestive of pulmonary embolism, and signs of deep vein thrombosis of the extremities, all should trigger a suspicion of pulmonary embolism (8).

3)    Diagnosis and treatment of pulmonary embolism. Current guideline recommendations on the diagnosis and treatment of acute pulmonary embolism must be followed (9). The need to rationalize the available resources during a pandemic, and the adherence to isolation precautions when considering diagnostic (computed tomography pulmonary angiography, bedside echocardiography) or therapeutic procedures (catheter-directed interventions) should be taken into account in institutional clinical protocols.


ACE-II receptors – Modulation of PVD in COVID-19?

16:08-16:30 GMT

Presenter: // Anna Hemnes, Vanderbilt University, USA

There has been longstanding interest in the role of ACE2 in the pulmonary vasculature. ACE2 catalyzes the degradation of Angiotensin II to Angiotensin (1-7), which in turn stimulates the Mas receptor and may meliorate pulmonary vascular disease through this receptor. More recently, ACE2 has been recognized as the functional receptor for COVID-19 and shown to have high level expression in the lung, including the epithelium. Clinically, COVID-19 is a disease that affects the lungs including the pulmonary vasculature with increased rates of pulmonary embolism compared with other, similar populations. This talk will review recent literature understanding how ACE2 may mediate pulmonary vascular disease in COVID-19 infection and whether this may be an impactful therapeutic target in COVID-19.  


Best abstract


Presenter: // Claes Frostell

Abstract topic: // Tricuspid regurgitation, as proxy for acute pulmonary hypertension, and its association with short-term outcome in severe Covid-19


Best abstract


Presenter: // Vicky Mai

Abstract topic: // Venous and arterial thromboembolism in COVID-19: a systematic review with meta-analysis





  1. Valerio L, Ferrazzi P, Sacco C, Ruf W, Kucher N, Konstantinides SV, et al. Course of D-Dimer and C-Reactive Protein Levels in Survivors and Nonsurvivors with COVID-19 Pneumonia: A Retrospective Analysis of 577 Patients. Thromb Haemost. 2020.
  2. Poissy J, Goutay J, Caplan M, Parmentier E, Duburcq T, Lassalle F, et al. Pulmonary Embolism in Patients With COVID-19: Awareness of an Increased Prevalence. Circulation. 2020;142(2):184-6.
  3. Lodigiani C, Iapichino G, Carenzo L, Cecconi M, Ferrazzi P, Sebastian T, et al. Venous and arterial thromboembolic complications in COVID-19 patients admitted to an academic hospital in Milan, Italy. Thromb Res. 2020;191:9-14.
  4. Klok FA, Kruip M, van der Meer NJM, Arbous MS, Gommers D, Kant KM, et al. Incidence of thrombotic complications in critically ill ICU patients with COVID-19. Thromb Res. 2020;191:145-7.
  5. Cui S, Chen S, Li X, Liu S, Wang F. Prevalence of venous thromboembolism in patients with severe novel coronavirus pneumonia. J Thromb Haemost. 2020;18(6):1421-4.
  6. Llitjos JF, Leclerc M, Chochois C, Monsallier JM, Ramakers M, Auvray M, et al. High incidence of venous thromboembolic events in anticoagulated severe COVID-19 patients. J Thromb Haemost. 2020;18(7):1743-6.
  7. Bikdeli B, Madhavan MV, Jimenez D, Chuich T, Dreyfus I, Driggin E, et al. COVID-19 and Thrombotic or Thromboembolic Disease: Implications for Prevention, Antithrombotic Therapy, and Follow-Up: JACC State-of-the-Art Review. J Am Coll Cardiol. 2020;75(23):2950-73.
  8. ESC Guidance for the Diagnosis and Management of CV Disease during the COVID-19 Pandemic2020 May 25, 2020, Available from:
  9. Konstantinides SV, Meyer G, Becattini C, Bueno H, Geersing GJ, Harjola VP, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS). Eur Heart J. 2020;41(4):543-603.
  10. Shahin Y, Rajaram S, Parkash V, Wild JM, Kiely DG, Swift AJ. Patterns of thromboembolic pulmonary vascular disease in COVID-19. Pulm Circ. 2021 Jan 21;11(1):2045894020979198. doi: 10.1177/2045894020979198. PMID: 33532054; PMCID: PMC7829513.
  11. John Wort S, Arachchillage DJ, McCabe C, Price LC. Covid-19 pneumonia and pulmonary vascular disease: A UK Centre perspective. Respir Med Res. 2020 Nov; 78:100781. doi: 10.1016/j.resmer.2020.100781. Epub 2020 Aug 3. PMID: 32889497; PMCID: PMC7398050.
  12. Ackermann M, Verleden SE, Kuehnel M, Haverich A, Welte T, Laenger F, Vanstapel A, Werlein C, Stark H, Tzankov A, Li WW, Li VW, Mentzer SJ, Jonigk D. Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19. N Engl J Med. 2020 Jul 9;383(2):120-128. doi: 10.1056/NEJMoa2015432. Epub 2020 May 21. PMID: 32437596; PMCID: PMC7412750.
  13. Pine AB, Meizlish ML, Goshua G, Chang CH, Zhang H, Bishai J, Bahel P, Patel A, Gbyli R, Kwan JM, Won CH, Price C, Dela Cruz CS, Halene S, van Dijk D, Hwa J, Lee AI, Chun HJ. Circulating markers of angiogenesis and endotheliopathy in COVID-19. Pulm Circ. 2020 Nov 25;10(4):2045894020966547. doi: 10.1177/2045894020966547. PMID: 33282193; PMCID: PMC7691906.
  14. Provencher S, Potus F, Bonnet S. COVID-19 and the pulmonary vasculature. Pulm Circ. 2020 Jun 10;10(3):2045894020933088. doi: 10.1177/2045894020933088. PMID: 32577218; PMCID: PMC7288817.

CME Credits

Attendees are able to claim up to 2 EACCME credits for this webinar. Please contact in order to claim. 


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