Risk factors and surrogate indicators for cardiovascular disease are prevalent in Common Variable Immunodeficiency and associate with inflammatory phenotype.

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.