"Mosaic Perfusion Pattern" on Dual-Energy CT in COVID-19 Pneumonia: Pulmonary Vasoplegia or Vasoconstriction?

Abstract

HomeRadiology: Cardiothoracic ImagingVol. 2, No. 5 PreviousNext Letters to the EditorFree Access“Mosaic Perfusion Pattern” on Dual-Energy CT in COVID-19 Pneumonia: Pulmonary Vasoplegia or Vasoconstriction?Amit Jain* , D. John Doyle*, Ramesh Mangal†Amit Jain* , D. John Doyle*, Ramesh Mangal†Author AffiliationsAnesthesiology Institute, Cleveland Clinic Abu Dhabi, Al Maryah Island, Abu Dhabi, United Arab Emirates*Radiology Institute, Mednext, Ahmedabad, India†e-mail: [email protected]Amit Jain* D. John Doyle*Ramesh Mangal†Published Online:Sep 10 2020https://doi.org/10.1148/ryct.2020200433MoreSectionsPDF ToolsImage ViewerAdd to favoritesCiteTrack Citations ShareShare onFacebookTwitterLinked In Editor:Finding dilated subsegmental vessels at dual-energy CT (DECT), Dr Lang and colleagues (1) proposed inflammatory-mediated impaired hypoxic pulmonary vasoconstriction (HPV) with overactive regional vasodilation to explain coronavirus disease 2019 (COVID-19) hypoxemia in their article in the June issue of Radiology: Cardiothoracic Imaging. However, this was not associated with increased pulmonary blood volume (PBV) in consolidated areas; instead, most (96%) patients had decreased peripheral perfusion corresponding to peripheral lung opacities, and only one-third demonstrated a halo of increased perfusion surrounding peripheral opacities. If HPV loss occurs in consolidated regions, PBV should have increased, producing hyperemia rather than oligemia. We instead propose an angiotensin II–mediated, nonimmune, noninflammatory mechanism to explain the mosaic perfusion pattern.Severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) infection of alveolar epithelium results in downregulation of angiotensin-converting enzyme 2 (ACE-2) and ACE-angiotensin II-angiotensin II type 1 receptor pathway overactivity, producing heterogeneous small vessel vasoconstriction (2) and recruitment of segmental/subsegmental vessels with relatively less vasoconstriction, causing regional overperfusion, reduced diffusion capacity, increased shunt and hypoxia, even in the absence of radiologically evident lesions. Where precapillary constriction is intense (due to high local concentration of angiotensin II), PBV would decrease, reducing perfusion even in normal lung or may produce wedge-shaped areas of pulmonary deficit on DECT (3). In areas of ineffective constriction due to lower concentrations of angiotensin II, capillary filtration pressure would increase, resulting in capillary stress failure and hydrostatic interstitial edema with patchy ground-glass opacities (GGOs) on CT. Disruption of the alveolocapillary membrane develops, with SARS-CoV-2 directly infecting endothelial cells. Endothelialitis with intracapillary fibrin-microthrombi blocks alveolar capillaries and further decreases perfusion within the areas of GGOs and consolidation but, with dilatation of proximal subsegmental arterioles, along with a halo of increased perfusion surrounding regions of consolidation. Thus, in COVID-19 pneumonia as the GGOs worsens to consolidation, oligemia or hyperemia in the area of consolidation is largely determined by the balance between the endothelialitis-mediated capillary obstruction (in consolidation regions) versus angiotensin II-mediated regional vasoconstriction (in healthy lung regions) (3,4).Our theory is supported by high incidence of raised PVR and right ventricular dysfunction in early COVID-19 disease (5) and reports of lung perfusion deficits that do not overlap with GGOs or consolidation and are not associated with major vessel occlusion (3). We believe determining the predominant pathophysiology—heterogeneous pulmonary vasoconstriction versus pulmonary vasoplegia—has treatment implications: pulmonary vasoconstrictors versus vasodilators.Disclosures of Conflicts of Interest: A.J. disclosed no relevant relationships. D.J.D. disclosed no relevant relationships. R.M. disclosed no relevant relationships.