key: cord-0700708-l51cun19
authors: Carbillon, Lionel; Fermaut, Marion; Benbara, Amelie; Boujenah, Jeremy
title: COVID‐19, Virchow's triad and thromboembolic risk in obese pregnant women
date: 2021-03-24
journal: Clin Cardiol
DOI: 10.1002/clc.23602
sha: 84150d86ca5df18202d7811797a92bdc834dd654
doc_id: 700708
cord_uid: l51cun19

nan

boprophylaxis, as soon as the diagnosis of Coronavirus-Infectious-Disease-2019 (COVID-19) has been made in these patients.

Indeed, from their recent reviews analyzing the three pivotal factors described by Virchow in the genesis of thromboembolism (TE), Ahmed et al 2 as well as Mehta et al, 3 showed that all components of this classic triad contributed together to an increased thromboembolic risk during the course of COVID-19. Thus, angiotensin-converting enzyme 2 (ACE2) protein, which constitutes the functional receptor for SARS coronavirus, is present in endothelial cells, thus allowing the virus to enter and to induce endothelial dysfunction. 2, 3 In addition, hypercoagulability occurs early in the disease due to an overwhelming inflammatory state. Lastly, blood flow is altered by the elevated fibrinogen which is a major determinant of blood viscosity, and of course by blood stasis when the patient is hospitalized and immobilized.

Importantly, a similar analysis of the questions related to the pathophysiology of thromboembolism during pregnancy and the peripartum period, thanks to these three categories of contributing factors characterized by Virchow, has also been applied to the high risk of TE as pregnancy progresses. 4 Indeed, firstly, the gravid uterus mechanically compresses veins as its volume increases, while the action of progesterone induces a loss of tone of the vein wall, 4 and these factors combine their effect to slow blood flow.

Secondly, a state of hypercoagulability culminates in late gestation and is partly explained by, and well reflected in the highly significant rise in D-dimer levels from the first to the third trimester. 5 In this context, any factor shifting the "hemostasis imbalance" is associated with an increased risk of maternal TE. Lastly, during pregnancy circulating cytokines and growth factors may contribute to the breakdown of the endothelial monolayer. 4 In this regard, obese pregnancy is associated with chronic preexisting impairment of endothelial function secondary to even increased production of inflammatory T-helper cells-2 cytokines. 6 57% and 5% of the cases received prophylactic and therapeutic heparin/ low-molecular-weight heparin (LMWH), respectively. Even more importantly, these authors indicated that the need for therapeutic heparin/LMWH was significantly associated with critical condition (p < .001).

Both the International Subcommittee for Women's Health Issues in Thrombosis and Haemostasis (ISTH) and the American Society of Hematology recommended that all hospitalized COVID-19 patients receive thromboprophylaxis. 12 Moreover, the ISTH recommended that prophylaxis with LMWH should be considered "in the presence of immobility, high fever, dehydration, or additional maternal risk factors for venous TE". 12 However, as the available data show that overweight/obesity in pregnant women is a strong risk factor for both thromboembolism and severe COVID-19, the benefit-risk assessment is in favor of anticoagulant prophylaxis, as soon as the diagnosis of COVID-19 has been made in these patients, and it appears sound to recommend this practice. Unfractionated heparin and LMWH do not cross the

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