COVID-19 Disease and Cardiac Surgery: Reciprocal Interrelations

To the Editor:

The interesting paper by Fukuhara and colleagues¹ 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 for anesthetic-analgesic medications. This involves preferentially 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 case 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 not only affects 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 tunica media, evolving in an acute dissection, if not protectively restrained and converted into a mural thrombus by activated platelets and thanks to a hypercoagulative state.