CNIC cohort study of 3471 adults links white blood cell count to early arterial plaque burden
In the PESA cohort, systemic inflammation was associated with subclinical plaque volume at 6 years independently of LDL cholesterol and systolic blood pressure.
Researchers at the Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC) reported in the European Heart Journal that systemic inflammation is linked to the burden of subclinical atherosclerosis independently of LDL cholesterol (LDLc) and systolic blood pressure (SBP). The work used data from the PESA study (Progression of Early Subclinical Atherosclerosis) in 3471 middle-aged participants without known cardiovascular disease, with a median age of 45 years. oup.com
European Heart Journaloup.comOpen source ↗
Participants were screened at baseline, at 3 years and at 6 years. Each visit included blood tests (white blood cell count, fibrinogen, oxidized LDLc, high-sensitivity C-reactive protein), a physical examination, three-dimensional vascular ultrasound of peripheral arteries and coronary artery calcium quantification. The primary outcome was global plaque volume (GPV, mm³), the bilateral carotid plus femoral plaque burden, at 6-year follow-up.
Inflammatory markers and plaque volume
At 6 years, 58% of participants had subclinical atherosclerosis (GPV above 0 mm³). After adjustment for age, sex, baseline LDLc and mean SBP, white blood cell (WBC) count had the strongest statistical association among the inflammatory markers: GPV was 32.6% higher per one standard deviation (SD) of WBC. For fibrinogen the increase was 16.8% per SD. High-sensitivity C-reactive protein did not predict greater GPV. For WBC, the marked trend in risk appeared only above its median.
Comparison with LDL cholesterol and blood pressure
GPV at 6 years rose 40.9% per SD of baseline LDLc (SD 29.4 mg/dL) and 42.7% per SD of mean SBP (SD 11.5 mmHg). Similar patterns were observed for carotid and femoral plaque volumes analysed separately and for coronary artery calcium. Higher WBC and fibrinogen were also associated with a greater anatomical spread of disease. oup.com
European Heart Journaloup.comOpen source ↗
The authors conclude that inflammation, captured with systemic markers, contributes to plaque burden beyond the effects of LDLc and SBP, with an impact comparable to theirs. Co-lead author Borja Ibáñez said the next step is to determine whether reducing inflammation can halt the atherosclerotic process; earlier clinical trials in this area were conducted in more advanced atherosclerosis. The study is observational and did not test any treatment.
