COVID-19 Disease and Cardiac Surgery: Reciprocal Interrelations

Abstract

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.