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Hamostaseologie 2022; 42(04): 230-238
DOI: 10.1055/a-1661-0240
Review Article

Pulmonary Hypertension and COVID-19

Laura Castiglione
1   Department of Cardiology and Angiology, University Hospital Tübingen, Tübingen, Germany
,
Michal Droppa
1   Department of Cardiology and Angiology, University Hospital Tübingen, Tübingen, Germany
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Abstract

Coronavirus disease 2019 (COVID-19) is a primary respiratory infectious disease, which can result in pulmonary and cardiovascular complications. From its first appearance in the city of Wuhan (China), the infection spread worldwide, leading to its declaration as a pandemic on March 11, 2020. Clinical research on SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) suggests that the virus may determine changes in the pulmonary hemodynamics through mechanisms of endothelial dysfunction, vascular leak, thrombotic microangiopathy, and venous thromboembolism that are similar to those leading to pulmonary hypertension (PH). Current available studies report echocardiographic signs of PH in approximately 12 to 13% of hospitalized patients with COVID-19. Those with chronic pulmonary obstructive disease, congestive heart failure, pulmonary embolism, and prior PH are at increased risk to develop or worsen PH. Evidence of PH seems to be associated with increased disease severity and poor outcome. Because of the importance of the pulmonary hemodynamics in the pathophysiology of COVID-19, there is growing interest in exploring the potential therapeutical benefits of inhaled vasodilators in patients with COVID-19. Treatment with inhaled nitric oxide and prostacyclin has shown encouraging results through improvement of systemic oxygenation, reduction of systolic pulmonary arterial pressure, and prevention of right ventricular failure; however, data from randomized control trials are still required.

Zusammenfassung

COVID-19 ist eine respiratorische Infektionskrankheit, die zu pulmologischen und kardiologischen Komplikationen führen kann. Seit dem ersten Auftreten in Wuhan (China), breitete sich die Virusinfektion weltweit aus, bis zur Einstufung als Pandemie am 11. März 2020. SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) beeinträchtigt die Lungenhämodynamik durch verschiedene Mechanismen, wie endotheliale Dysfunktion, vaskuläres Leck, thrombotische Mikroangiopathie und Lungenarterienembolie. Diese sind pathophysiologisch ähnlich zu denen, die zur pulmonalen Hypertonie (PH) führen. In den aktuellen Studien finden sich Hinweise auf eine PH in 12-13% von hospitalisierten Patienten mit COVID-19. Vorbestehende chronische obstruktive Lungenerkrankungen, Herzinsuffizienz, Lungenarterienembolie und pulmonale Hypertonie sind relevante Risikofaktoren für die Entwicklung oder Verschlechterung einer PH im Rahmen der viralen Infektion. Anderseits korreliert die PH mit einem schwereren Krankheitsbild und einer schlechteren Prognose. In Hinblick auf die Beteiligung des pulmonalen Kreislaufs in der Pathophysiologie von COVID-19, besteht ein wachsendes Interesse an einem potentiellen therapeutischen Nutzen von inhalativen Vasodilatatoren. Obwohl die Therapien mit inhalativem Stickstoffmonoxid und Prostacyclin ermutigenden Ergebnisse gezeigt hatten (Verbesserung der systemischen Oxygenierung, Senkung des systolischen pulmonalen Drucks und Vorbeugung der Rechtsherzinsuffizienz), ist eine stärkere Evidenz von randomisierten kontrollierten Studien erforderlich.

Keywords

COVID-19 - pulmonary hypertension - right heart failure

Schlüsselwörter

COVID-19 - pulmonale Hypertonie - Rechtsherzinsuffizienz


Publication History

Received: 25 June 2021

Accepted: 05 October 2021

Article published online:
21 December 2021

© 2021. Thieme. All rights reserved.

Georg Thieme Verlag KG
Rüdigerstraße 14, 70469 Stuttgart, Germany

 

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