Serum Cholinesterase Level as a Marker of Systemic Low-Grade Inflammation in Isolated Systolic Hypertension: A Cross-Sectional Study

Background: Autonomic regulation of local and systemic inflammation through the ‘cholinergic anti-inflammatory pathway’ may have role in persistence of low-grade systemic inflammation in isolated systolic hypertension (ISH). The augmented activity of the enzyme cholinesterase (ChE) leads to degradation of the main anti-inflammatory neurotransmitter ‘acetylcholine’ of this pathway. Despite the role of inflammation in hypertension, serum level of cholinesterase enzyme has not been determined till now in ISH. The study aimed to measure the serum levels of inflammatory marker ChE in comparison to high sensitivity C-reactive protein (hsCRP) to predict the presence of low-grade systemic inflammation and their correlation with blood pressure in ISH patients. Methods: A cross-sectional study was conducted in ISH patients (n=30; mean age, 51.00±1.24 years; male/female (M/F) number=18/12). Age and sex matched healthy subjects (n=30, mean age, 51.86±1.40 years; M/F=16/14) were taken as control. Subjects were divided into three groups based on hsCRP levels; group I (healthy: hsCRP≤1.0mg/L), group IIa (patients with mild inflammation: hsCRP≤1.0mg/L), group IIb (patients with moderate to severe inflammation: hsCRP 1.0-10.0mg/L). Overnight fasting blood samples were collected and ChE and hsCRP were assessed using Cholinesterase Liqui-Check and hsCRP turbi-latex diagnostic kits, respectively. Results: hsCRP and ChE levels were found significantly high in hypertensive patients than in healthy subjects (p<0.05). In patients at mild stage of inflammation, there was an increase in both ChE and hsCRP, but not linearly as they had no significant correlation with each other. But at moderate to severe inflammation stage, there was a linear rise in both hsCRP and ChE levels. SBP, DBP and PP were significantly correlated with both ChE and hsCRP in patients (p<0.01). Moreover, as the SBP was increased from grade I to II, both hsCRP and ChE levels were also increased. Conclusion: Many factors interplay in propagating inflammatory cascade in ISH and all biomarkers of inflammation may not elevate at same point in time and in linear manner. ChE may act as a marker of low-grade systemic inflammation but its comparison must be tested against a standard marker such as hsCRP in large scale studies for finding its true significance in predicting cardiovascular disease risk.