A growing body of evidence suggests that low grade inflammation contributes to the development of cardiovascular disease and, specifically, coronary artery disease (CAD). WBC-derived macrophages and other phagocytes are believed to contribute to vascular injury and atherosclerotic progression. Multiple markers of inflammation have been tested as potential risk factors for the development of CAD such as IL-6, E-selectin and CRP.
Elevated white blood cell count (WBC) that is well within the normal range was associated with an increased risk for developing CAD in multiple studies.
A large-scale study demonstrated that a single measurement of WBC in healthy young men may predict CAD incidence independently from other risk factors for CAD such as elevated lipids, and a positive family history. WBC level above 6,900 cells/mm3 was associated with a 2-fold increase in the risk for CAD with a significant 17.4% increase in CAD incidence observed for every increment of 1,000 WBC/mm3: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0047183
An elevated WBC count may enhance atherogenesis. Granulocytes and monocytes are believed to be involved in the pathogenesis of atherosclerosis. Monocyte-derived macrophages produce oxidants that can induce endothelial cell injury and subsequent thrombus formation. Activated WBCs also reflect the inflammatory activity of atherosclerosis that perpetuates vascular injury and tissue ischemia.
WBC count is associated with several cardiovascular disease risk factors:
- positive associations with body weight, systolic blood pressure, cigarette smoking, fasting glucose level, and fasting insulin level
- negative associations with high density lipoprotein cholesterol level, family income, alcohol consumption, and physical activity or physical fitness
High-normal WBC count is an independent and reliable risk factor for CAD.
The joint effect of WBC count, a readily available measurement, with other known risk factors for CAD may help to better identify people at either high or low cardiovascular risk.
References:
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0047183
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