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Letter to the Editor
DOI: 10.1016/j.rec.2020.08.021
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Available online 15 October 2020
A new inflammatory-microthrombotic syndrome as an explanation for thrombotic complications in patients with COVID-19
Un nuevo síndrome inflamatorio-microtrombótico como explicación para las complicaciones trombóticas en pacientes con COVID-19
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Francisco Valgaa,
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fvalga@hotmail.com

Corresponding author:
, Nicanor Vega-Díaza, Manuel Macíab, José Carlos Rodríguez-Péreza
a Servicio de Nefrología, Hospital Universitario de Gran Canaria Doctor Negrín, Las Palmas de Gran Canaria, Las Palmas, Spain
b Servicio de Nefrología, Hospital Universitario Nuestra Señora de la Candelaria, Santa Cruz de Tenerife, Spain
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Rev Esp Cardiol. 2020;73:769-7110.1016/j.rec.2020.05.008
Juan R. Rey, Juan Caro-Codón, Dolores Poveda Pineda, José Luis Merino, Ángel M. Iniesta, José Luis López-Sendón
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To the Editor,

We have read with great interest the article by King et al.1 recently published in Revista Española de Cardiología. In this article, the authors discuss the higher incidence of thrombotic events in multiple territories and a higher International Society on Thrombosis and Haemostasis (ISTH) disseminated intravascular coagulation (DIC) score in hospitalized patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Although the authors mention that they have not ruled out a pre-existing prothrombotic state, our group, consistent with what the authors described,2 has proposed a possible role of endothelial injury, complement, and coagulation in the pathogenesis of coronavirus disease 2019 (COVID-19).3

Our pathogenic scheme is based on the similarity of certain clinical and histopathologic findings of various entities that have thrombotic microangiopathy in common with COVID-19, and it postulates that the damage induced by this disease has an endothelial origin with 2 pathogenic routes: an inflammatory route, with predominance of the “cytokine storm” component, and a microangiopathic route involving the complement system.3

Furthermore, endothelial involvement could lead to platelet activation, thus altering coagulation and causing DIC, as described by the authors of the article. This fact per se could increase thrombin and prothrombin and trigger complement activation through C5.4 For instance, thrombotic microangiopathy has been reported in a patient with severe COVID-19, indicating a pathogenic relationship between these conditions.5 The potential role of ADAMTS13 deficiency in serious forms of the disease is another possible factor, as described by Huisman et al.6 in a recent article.

Additionally, the inflammatory route itself could activate complement through certain neutrophil serine proteases and macrophages.7 Consequently, we believe that there is a strong relationship between inflammation, complement, thrombotic microangiopathy, and coagulation in the pathogenesis of COVID-19. This may represent a new COVID-19–related inflammatory-microthrombotic syndrome which could explain the authors’ interesting findings.2–4

References
[1]
J.R. Rey, J. Caro-Codón, D. Poveda, J.L. Merino, A.M. Iniesta, J.L. López-Sendón.
Complicaciones arteriales trombóticas en pacientes hospitalizados con COVID-19.
Rev Esp Cardiol., 73 (2020), pp. 769-771
[2]
M. Noris, A. Benigni, G. Remuzzi.
The case of complement activation in COVID-19 multiorgan impact.
Kidney Int., 98 (2020), pp. 314-322
[3]
F. Valga, N. Vega-Díaz, M. Macia, T. Monzón, J.C. Rodriguez-Perez.
Targeting complement in severe coronavirus disease 2019 to address microthrombosis.
Clin Kidney J., 13 (2020), pp. 477-479
[4]
M. Huber-Lang, J.V. Sarma, F.S. Zetoune, et al.
Generation of C5a in the absence of C3: a new complement activation pathway.
Nat Med., 12 (2006), pp. 682-687
[5]
K.D. Jhaveri, L.R. Meir, B.S. Flores Chang, et al.
Thrombotic microangiopathy in a patient with COVID-19.
Kidney Int., 98 (2020), pp. 509-512
[6]
A. Huisman, R. Beun, M. Sikma, J. Westerink, N. Kusadasi.
Involvement of ADAMTS13 and von Willebrand factor in thromboembolic events in patients infected with SARS-CoV-2.
Int J Lab Hematol., (2020),
[7]
M. Huber-Lang, E.M. Younkin, J.V. Sarma, et al.
Generation of C5a by phagocytic cells.
Am J Pathol., 161 (2002), pp. 1849-1859
Copyright © 2020. Sociedad Española de Cardiología
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