Frontiers in immunology · 2026
Risk factors and surrogate indicators for cardiovascular disease are prevalent in Common Variable Immunodeficiency and associate with inflammatory phenotype.
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Yu Aidan Jia Sheng, Moreira Fernando, Symes Andrew, Curlewis Keegan, O'Sullivan Mary, Jayasundera Joseph, El Rhermoul Fatema-Zahra, Lever Charley, Stoenchev Kostadin, Chow Ke Li, Uysal Omer Faruk, Alharbi Ahmad M, Workman Sarita, Halliday Neil, Laurence Arian, Verma Nisha, Tadros Susan, Kiani-Alikhan Sorena, Barnett Joseph, Burns Siobhan O, Hurst John R, Lowe David M
Аннотация
BACKGROUND: Common variable immunodeficiency (CVID) is traditionally characterised by recurrent infections and immune dysregulation, but growing evidence suggests an increased risk of endothelial dysfunction and premature atherosclerosis in this population.
OBJECTIVE: To evaluate cardiovascular risk in patients with CVID through integration of clinical risk factors, biomarkers of endothelial dysfunction, and radiographic surrogates of subclinical atherosclerosis.
METHODS: A total of 101 CVID patients and 56 matched household controls were recruited. Data collected included cardiovascular risk factors, blood biomarkers (D-dimer, von Willebrand factor [vWF], fibrinogen, ESR, CRP), and immunological profiles. Existing imaging was reviewed, including thoracic CT for assessment of coronary artery calcification (CAC) and FibroScan for controlled attenuation parameter (CAP) scores; aortic pulse wave velocity (aPWV) was measured in a subset of participants. Subgroup analysis compared infection-only versus inflammatory/complex phenotypes of CVID.
RESULTS: CVID patients demonstrated high rates of hyperlipidaemia (38.6%), hypertension (23.8%), and diabetes/prediabetes (14.9%). CAC was present in 37%, with 82.4% having no known prior cardiovascular disease. Hepatic steatosis and elevated aPWV were observed in 30% and 6.5%, respectively. Patients with CAC were older and had higher rates of hypertension, diabetes, hyperlipidaemia, chronic kidney disease, elevated median vWF (227.5 vs 167 IU/dL, p=0.001), D-dimer (370.5 vs 271 ng/mL, p=0.011), and aPWV (8.2 vs 6.0 m/s, p=0.006). Patients with an inflammatory phenotype had higher vWF (224 vs 163 IU/dL, p<0.001) and D-dimer (314 vs 205 ng/mL, p=0.043) levels than those with infection-only CVID.
CONCLUSION: CVID is associated with a substantial burden of cardiovascular risk factors and subclinical atherosclerosis, especially in the inflammatory phenotype.
OBJECTIVE: To evaluate cardiovascular risk in patients with CVID through integration of clinical risk factors, biomarkers of endothelial dysfunction, and radiographic surrogates of subclinical atherosclerosis.
METHODS: A total of 101 CVID patients and 56 matched household controls were recruited. Data collected included cardiovascular risk factors, blood biomarkers (D-dimer, von Willebrand factor [vWF], fibrinogen, ESR, CRP), and immunological profiles. Existing imaging was reviewed, including thoracic CT for assessment of coronary artery calcification (CAC) and FibroScan for controlled attenuation parameter (CAP) scores; aortic pulse wave velocity (aPWV) was measured in a subset of participants. Subgroup analysis compared infection-only versus inflammatory/complex phenotypes of CVID.
RESULTS: CVID patients demonstrated high rates of hyperlipidaemia (38.6%), hypertension (23.8%), and diabetes/prediabetes (14.9%). CAC was present in 37%, with 82.4% having no known prior cardiovascular disease. Hepatic steatosis and elevated aPWV were observed in 30% and 6.5%, respectively. Patients with CAC were older and had higher rates of hypertension, diabetes, hyperlipidaemia, chronic kidney disease, elevated median vWF (227.5 vs 167 IU/dL, p=0.001), D-dimer (370.5 vs 271 ng/mL, p=0.011), and aPWV (8.2 vs 6.0 m/s, p=0.006). Patients with an inflammatory phenotype had higher vWF (224 vs 163 IU/dL, p<0.001) and D-dimer (314 vs 205 ng/mL, p=0.043) levels than those with infection-only CVID.
CONCLUSION: CVID is associated with a substantial burden of cardiovascular risk factors and subclinical atherosclerosis, especially in the inflammatory phenotype.