key: cord-0944898-qd3qkh42
authors: Chau, Yves; Orban, Jean-Christophe; Sédat, Jacques; Arnoffi, Paolo; Jamjoom, Modhar; Mondot, Lydiane; Flory, Violaine
title: Could bronchial artery embolization be a modality for treating Severe Acute Respiratory Syndrome coronavirus 2?
date: 2020-08-26
journal: J Vasc Interv Radiol
DOI: 10.1016/j.jvir.2020.08.022
sha: cabef75e6660afe222c8039c019a76a4a5093616
doc_id: 944898
cord_uid: qd3qkh42

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This study was not supported by any funding.

The authors declare that they have no conflict of interest.

All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.

For this type of study formal consent is not required.

The Institutional Review Board (IRB) has given its approval of this study.

For this type of study informed consent is not required.

For this type of study consent for publication is not required.

Bronchial artery circulation has not been carefully studied in human severe acute respiratory syndrome (SARS).

However, bronchial artery circulation has been studied in detail in animal models of smoke inhalation-induced lung injury (1, 2) . These models recapitulate the classical features of SARS, which is characterized histologically by diffuse alveolar damage and by new vessel growth; biologically, by an intense inflammatory reaction with a cytokine storm (1), by coagulation disorders, by increased angiotensin-converting enzyme (ACE) and ACE2 expression in the lungs; and radiologically by CT scan bilateral diffuse ground-glass opacity (2,3). All of these findings have been described in COVID-19 patients. In a smoke inhalation ovine model, bronchial artery flow (normally 1% of cardiac output) was increased, 15-fold in the left main bronchus, 20-fold in the right main bronchus, and ~ 4-and 6-fold in the right and left lungs, respectively (2) . Sclerosis of the bronchial artery after smoke inhalation has been reported to greatly improve lung function and to drastically reduce animal mortality (2, 4) . Thus, bronchial artery sclerosis resulted in a statistically significant improvement of the PaO 2 /FiO 2 ratio, and led to attenuation of the increase of pulmonary pressure, of elevation of pulmonary artery vascular resistance; suppression of the formation of bronchial casts; and reduction of the myeloperoxidase activity compared with an animal smoke inhalation control group (4).

The mechanism by which the bronchial circulation contributes to the pathogenesis in lung parenchyma has not been fully elucidated. Cellular and humoral mediators of inflammation produced in response to local pulmonary injury may enter into the bronchial circulation and could be delivered to the whole pulmonary parenchyma, as the bronchial arterial circulation mainly drains into the pulmonary arterial circulation by precapillary anastomoses. Thus, the increase in bronchial circulation could spread inflammatory mediators and cells throughout the whole pulmonary Table 1 . There were 40 CTAs (37 patients) in the CT+PCR+ group and 30 CTAs (30 patients) in the CT-PCR-group. The median age in the CT+PCR+ group was 65 years (IQR 57-76) versus 68 years (IQR 53-80) in the CT-PCR-group (p = 0.64). The median diameter of the bronchial artery at the origin was drastically increased in the CT+PCR+ group (Fig 1 and 2) compared to the CT-PCR-group (Fig 3 and 4) : 2.00 mm (IQR 1.50-3.00) vs. 0.40 mm (IQR 0.00-1.50) (p < 0.01).

Similarly, a much larger median diameter of the bronchial artery in the hilum was observed in the CT+PCR+ compared to the CT-PCR-patients: 1.50 mm (IQR 1.00-2.05) vs. 0.35 mm (IQR 0.00-1.00); (p < 0.01). Patients in the CT+PCR+ group displayed different levels of damage: less than 10% damage (n = 1), 10 to 25% (n = 16), 25 to 50% (n = 8), 50 to 75% (n = 9), and more than 75% (n = 6). The median diameter of the bronchial artery at the origin was found to increase in parallel with the percentage of damage, from 0.70 mm (IQR 0.70-0.70) in the 10% class to 3.60 mm (IQR 2.55-3.75) in the > 75% class (p < 0.01). Those observations seem to show that bronchial artery dilatation could be either a pre-existing factor spreading the disease to the whole lung parenchyma or a consequence of Covid-19 infection. Bronchial artery occlusion, before or after smoke inhalation, significantly improves clinical parameters and animal survival. Bronchial arteries embolization studies may be mandated to evaluate its efficacy, its safety and its role among the different therapeutic options for SARS-Cov-2 treatment. 

Effects of different corticosteroid doses and durations on smoke inhalationinduced acute lung injury and pulmonary fibrosis in the rat

research challenges, and clinical management of smoke inhalation injury. The Lancet

Assessment of severity of ovine smoke inhalation injury by analysis of computed tomographic scans

Sclerosis therapy of bronchial artery attenuates acute lung injury induced by burn and smoke inhalation injury in ovine model