Editorial
Leucocyte Count: Inflammatory and ROS Biomarkers of ASCVD
2024 Volume 31 Issue 6 Pages 861-863
Details
2024 Volume 31 Issue 6 Pages 861-863
See article vol. 31: 864-875
Personalized risk stratification of ASCVD is critical for developing effective prevention measures, which currently focus on lifestyle interventions and the optimal control of traditional risk factors1, 2). The routine assessment of inflammatory and reactive oxidative burdens is also recommended for better cardiovascular risk stratification3-5). The concept of “residual inflammatory risk” has been invented to describe patients who, despite achieving an optimal control of risk factors, remain at a high risk for future cardiovascular events due to vascular and/or systemic inflammation/ROS3-5). Several clinical and experimental studies have focused on the inflammatory and ROS biomarkers of ASCVD3-5). The Japan Atherosclerosis Society (JAS) guidelines for the prevention of atherosclerotic cardiovascular disease 2022), high-sensitivity C-reactive protein (hs-CRP), pentraxin 3 (PTX3), and interleukin (IL)-6 have been described as promising inflammatory biomarkers for comprehensive risk assessment to prevent ASCVD1). However, numerous other biomarkers may also be useful for the stratification of ASCVD risk.
The leukocyte count has been reported to be associated with various cardiovascular diseases, including coronary artery disease, and it has been considered a marker of inflammation and ROS for several decades6). Recent evidence has clarified the pathways that increase the systemic myeloid cell number, leukocyte trafficking via the modulation of hematopoiesis, and the modulation of immune cell phenotypes in the cardiovascular system6) (Fig.1). Interestingly, the modulation of hematopoiesis begins with modifiable lifestyle factors, such sedentary lifestyle, unideal diet, mental stress, poor sleep, and, smoking, leading to leukocyte migration and a deterioration of the immune system in the context of cardiovascular health6, 7). The neuroendocrine system, including the hypothalamic–pituitary–adrenal (HPA) axis (corticotrophin-releasing hormone (CRH)- adrenocorticotropic hormone (ACTH)-cortisol) and the autonomic nervous system (catecholamines), is also strongly linked to leukocytosis in both homeostatic and inflammatory conditions in people with ASCVD risks8) (Fig.1).
See text in detail. ACTH: adrenocorticotropic hormone
Takeshita et al. reported that 24 months of treatment with febuxostat, a xanthine oxidase inhibitor, modestly but significantly decreased the total leukocyte count in patients with asymptomatic hyperuricemia9). The change in the total leukocyte count was associated with the change in the hs-CRP level, but it was not significantly associated with the mean common carotid artery intima-media thickness (CCA-IMT). It is interesting to note that treatment with hyperuricemia decreased the leukocyte count, as well as several medications, including statins and inhibitors of the renin-angiotensin-aldosterone system (RAAS)7), for the optimal control of traditional risk factors1, 2). These findings may reflect a beneficial anti-inflammatory action in the treatment of hyperuricemia10). Further studies are needed to assess the true impact of leukocytosis on ASCVD, compare it with other inflammatory markers, and determine the utility of ASCVD prediction6-8).
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