# Integrated Analysis of Parenchymal and Vascular HRCT Patterns with Circulating Biomarkers in Severe COVID-19 Pneumonia

**Authors:** Aldo Carnevale, Luca Morandi, Gaetano Scaramuzzo, Savino Spadaro, Gianluca Calogero Campo, Melchiore Giganti, Alberto Papi, Marco Contoli

PMC · DOI: 10.3390/diagnostics16040587 · 2026-02-15

## TL;DR

This study links lung CT scan patterns with blood biomarkers in severe COVID-19, suggesting imaging and blood tests together could help predict disease severity and guide treatment.

## Contribution

The study is the first to integrate HRCT imaging patterns with specific circulating biomarkers in severe COVID-19 pneumonia for clinical stratification.

## Key findings

- Higher parenchymal HRCT scores correlated with longer hospital stays, ICU admissions, and elevated inflammatory biomarkers.
- Vascular HRCT patterns were linked to increased Angiopoietin-2 levels but not directly to ICU admission or mortality.
- Parenchymal and vascular HRCT scores showed a significant positive correlation.

## Abstract

Purpose: To explore the correlation between radiologic patterns on high-resolution computed tomography (HRCT) and circulating biomarkers of inflammation and endothelial activation in patients with COVID-19 pneumonia, with the aim of identifying imaging-biomarker phenotypes that may offer insights for clinical stratification. Materials and Methods: This prospective single-center study included 84 consecutive patients hospitalized with PCR-confirmed SARS-CoV-2 infection and respiratory failure. All underwent baseline HRCT, along with parallel biohumoral profiling, including inflammatory (IL-1Ra, IL-6, IL-10) and endothelial (Angiopoietin-2, sVCAM-1, sE-Selectin) biomarkers. HRCT scans were reviewed for parenchymal and vascular abnormalities (vascular tree-in-bud [TIB], vascular enlargement pattern [VEP]). Semi-quantitative scores were assigned for parenchymal (PS) and vascular (VS) involvement. Results: Patients with higher PS had significantly prolonged hospital stay (35 vs. 17 days; p = 0.014), increased ICU admission rates (68.8% vs. 21.4%; p = 0.003), and elevated serum levels of IL-1Ra, IL-6, and IL-10 (p < 0.05). At multivariable analysis, PS remained independently associated with ICU admission after adjustment for age, inflammatory burden, and comorbidities (p = 0.014). A high VS was associated with significantly increased Angiopoietin-2 levels (p = 0.036), although it did not directly correlate with ICU admission or mortality. A significant positive correlation was observed between PS and VS (r =0.392; p < 0.001). Conclusions: in this study, HRCT-based parenchymal and vascular patterns appear significantly correlated with biological processes occurring in severe COVID-19 pneumonia. These observations, although preliminary, may offer a conceptual basis for future studies exploring radiologic and biomarker-based stratification in severe respiratory infections.

## Linked entities

- **Proteins:** IL1R1 (interleukin 1 receptor type 1), IL6 (interleukin 6), IL10 (interleukin 10), ANGPT2 (angiopoietin 2)

## Full-text entities

- **Genes:** ICAM1 (intercellular adhesion molecule 1) [NCBI Gene 3383] {aka BB2, CD54, P3.58}, ANGPT2 (angiopoietin 2) [NCBI Gene 285] {aka AGPT2, ANG2, LMPHM10}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, IL1A (interleukin 1 alpha) [NCBI Gene 3552] {aka IL-1 alpha, IL-1A, IL1, IL1-ALPHA, IL1F1}, IFNG (interferon gamma) [NCBI Gene 3458] {aka IFG, IFI, IMD69}, IFNA2 (interferon alpha 2) [NCBI Gene 3440] {aka IFN-alpha-2, IFN-alphaA, IFNA, IFNA2B, leIF A}, IL13 (interleukin 13) [NCBI Gene 3596] {aka IL-13, P600}, SELE (selectin E) [NCBI Gene 6401] {aka CD62E, ELAM, ELAM1, ESEL, LECAM2, selectin-e}, VCAM1 (vascular cell adhesion molecule 1) [NCBI Gene 7412] {aka CD106, INCAM-100}, IL1RN (interleukin 1 receptor antagonist) [NCBI Gene 3557] {aka CRMO2, DIRA, ICIL-1RA, IL-1RN, IL-1ra, IL-1ra3}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}
- **Diseases:** alveolar (MESH:D002282), hypoxemia (MESH:D000860), ARDS (MESH:D012128), pulmonary thromboembolism (MESH:D011655), COPD (MESH:D029424), Pneumonia (MESH:D011014), immune-mediated organ damage (MESH:C567355), Respiratory failure (MESH:D012131), hypoxic (MESH:D002534), asthma (MESH:D001249), alveolar damage (MESH:D055370), dyspnea (MESH:D004417), lung damage (MESH:D008171), endothelial dysfunction (MESH:D014652), cancer (MESH:D009369), TIB (MESH:D021184), cryptogenic organizing pneumonia (MESH:D018549), disease (MESH:D004194), injury to (MESH:D014947), infectious respiratory diseases (MESH:D012141), Inflammation (MESH:D007249), critical illness (MESH:D016638), endothelialitis (MESH:D005642), immune dysregulation (OMIM:614878), vascular anomalies (MESH:D020785), diffuse alveolar damage (MESH:D000070625), pulmonary tumor thrombotic microangiopathy (MESH:D057049), VEP (MESH:D006332), ILD (MESH:D017563), systemic hyperinflammation (MESH:D015619), heart failure (MESH:D006333), organizing pneumonia (MESH:D000092124), VS (MESH:D057772), infected (MESH:D007239), coagulopathy (MESH:D001778), COVID (MESH:D000086382), acute respiratory syndrome (MESH:D012120), deaths (MESH:D003643), viral infection (MESH:D014777), PS (MESH:D002543), anemia (MESH:D000740), GGO (MESH:C000721427), atelectasis (MESH:D001261), microvascular abnormalities (MESH:D017566), thrombosis (MESH:D013927)
- **Chemicals:** oxygen (MESH:D010100)
- **Species:** Severe acute respiratory syndrome coronavirus 2 (no rank) [taxon 2697049], Homo sapiens (human, species) [taxon 9606]

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12939422/full.md

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Source: https://tomesphere.com/paper/PMC12939422