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In the last decade a strong and definitive link has been established between inflammation and cardiovascular disease. Inflammation occurs in the vasculature as a response to several types of injury. Various risk factors, including hypertension, diabetes, and smoking, together with oxidized low-density lipoprotein cholesterol, trigger a chronic inflammatory reaction, the result of which is a vulnerable plaque, prone to rupture and thrombosis. Epidemiological and clinical studies have consistently shown links between markers of inflammation and risk of future cardiovascular events. Activation of macrophages, T lymphocytes, and smooth muscle cells leads to the release of additional mediators, including adhesion molecules, cytokines, chemokines, and growth factors, all of which play important roles in atherogenesis. Inflammation plays a role in all stages of atherothrombosis, the underlying cause of approximately 80% of all sudden cardiac deaths. The study by Çimen et al. published in this issue of the Journal examines the relationship between 24-hour ambulatory blood pressure (BP) and a systemic inflammation marker, the neutrophil-to-lymphocyte ratio (NLR). The

Neutrophil-to-lymphocyte ratio and ambulatory blood pressure: Exploring the link between inflammation and hypertension