The relationship between vascular inflammation and target organ damage in hypertensive crises

Abstract

ObjectiveHypertensive crises, divided depending on the presence of target organ damage (TOD), are associated with increased cardiovascular mortality and morbidity. Monocyte chemoattractant protein-1 (MCP-1) is responsible for the recruitment of monocytes to sites of vascular inflammation. The aim of this study was to evaluate the role of vascular inflammation in development of TOD. MethodThe patients were categorized according to the presence of TOD. Thirty-three patients (15 female; mean age, 68 ± 12 y) with TOD and 30 patients (14 female; mean age, 64 ± 12 y) without TOD were included to the study. In addition to routine laboratory parameters, neutrophil-lymphocyte ratio, uric acid, C-reactive protein (CRP), high sensitive CRP, and plasma MCP-1 levels were evaluated. ResultsNeutrophil counts, white blood cells, high sensitive CRP, and uric acid levels were higher in patients with hypertensive crises. More importantly, CRP (7.2 mg/dL [2-37.8 mg/dL] vs 4.6 mg/dL [1.5-14 mg/dL] vs 2.7 mg/dL [1-8.1 mg/dL], P < .01) and MCP-1 levels (546 pg/mL [236-1350 pg/mL] vs 407 pg/mL [78-942 pg/mL] vs 264 pg/mL [34-579 pg/mL], P < .01) were higher in the group with TOD compared with other groups. ConclusionIn conclusion, plasma MCP-1 levels were significantly higher in patients with TOD. According to our results, we suggest that increased vascular inflammation and MCP-1 levels might be associated with the development of TOD in hypertensive crisis.