key: cord-1011555-2ut2anpg
authors: Manenti, Antonio; Roncati, Luca; Manco, Gianrocco
title: COVID-19 Disease and Cardiac Surgery: Reciprocal Interrelations
date: 2021-01-11
journal: Ann Thorac Surg
DOI: 10.1016/j.athoracsur.2020.12.007
sha: 09fd113a3fdef2b206984381ef82ecdc07580aab
doc_id: 1011555
cord_uid: 2ut2anpg

nan

To the Editor:

The interesting paper by Fukuhara and colleagues 1 merits some patho-physiologic observations. After surgery, the innate immune system weakens in its cell and humoral components for an increased release of cortisol, and catecholamines, and anestheticanalgesic medications. This more involves cardiac surgery, mainly if performed with cardiopulmonary bypass and hypothermia, as a consequence of the ischemia-reperfusion injury, that, followed by a great release of reactive oxygen species and proinflammatory cytokines, electively damages the pulmonary capillaries and increases their permeability. 2 In COVID-19 infection these structures are subjected to an "endotheliitis", consisting in infiltration by neutrophils and mononuclear cells and a consequent thrombosis. 3, 4 It explains the great incidence of pulmonary complications, until a severe pneumonia, in the course of this viral infection, preexisting or occurring in the early postoperative period. 1 COVID-19 disease can evolve toward a "hypersensitive vasculitis", where a dysregulated adaptive immunity causes an abnormal production of immunoglobulins and antibodies, that, infiltrating the arterial walls of small/medium sized vessels, trigger an "immunothrombosis", with the subsequent danger of organ malperfusion or acute ischemia. 4 This dangerous condition affects cardiac surgery more often, especially in cases of postoperative low cardiac output syndrome. Moreover, in severe COVID-18 disease, platelets, activated to repair endothelia, perform a "covercytosis" against virions, in agreement with their myeloid lineage and direct origin from megakaryocytes modified in their genome with mRNA fragments derived from the SARS-CoV-2ZN1 gene. They demonstrate also a greater power of aggregation and adhesion to fibrin filaments, and favor production of microcomplexes with neutrophils, monocytes and T lymphocytes. 5 This pathology affects not only the pulmonary microvessels, but also, in the COVID-19 hypercoagulative milieu, causes thromboembolic complications in medium/large sized vessels, differently expressing, according to their hemodynamics, from mural thrombi, occasionally discovered, to a complete thrombosis. In surgery, all this increases the risk of thrombo-embolic events, and after a cardiopulmonary bypass specifically affects the pulmonary vessels and further deranges the hemostatic system. In perspective, we have to consider another complication of COVID-19 infection, consisting of an intramural hematoma, caused by endothelial ulceration and necrotic-inflammatory lesions of the medial tunica, evolving in an acute dissection, if not protectively restrained and converted into a mural thrombus by activated platelets and thanks to a hypercoagulative state .  1  2  3  4  5  6  7  8  9  10  11  12  13  14  15  16  17  18  19  20  21  22  23  24  25  26  27  28  29  30  31  32  33  34  35  36  37  38  39  40  41  42  43  44  45  46  47  48  49  50  51  52  53  54  55  56  57  58  59  60  61  62  63  64  65  66  67  68  69  70  71  72  73 

Acute type A aortic dissection during the COVID-19 outbreak

Inflammatory response and endothelial dysfunction following cardiopulmonary bypass: pathophysiology and pharmacological targets

Endothelial cell infection and endotheliitis in COVID-19

Type 3 hypersensitivity in COVID-19 vasculitis

A proof of evidence supporting abnormal immunothrombosis in severe COVID-19: naked megakaryocyte nuclei increase in the bone marrow and lungs of critically ill patients

5:16 am ce Ó 2021 by The Society of Thoracic Surgeons