Abstract
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.
Highlights
Isolated systolic hypertension (ISH) defined as elevated systolic blood pressure (SBP) ≥140 mmHg and diastolic blood pressure (DBP) ≤90 mmHg, is a reflection of increasing arterial stiffness and loss in arterial compliance with age [1]
All patients were known stable cases of isolated systolic hypertension (ISH) and their BP was controlled with medications at the time of recruitment
Patients were taking anti-hypertensive drug therapies according to European Society of Hypertension (ESH), 2014 guidelines for ISH [13]
Summary
Isolated systolic hypertension (ISH) defined as elevated systolic blood pressure (SBP) ≥140 mmHg and diastolic blood pressure (DBP) ≤90 mmHg, is a reflection of increasing arterial stiffness and loss in arterial compliance with age [1]. The well-established, standard, and accurate marker of systemic low-grade inflammation for clinical importance is high sensitivity C-reactive protein (hsCRP). 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 study aimed to measure the serum levels of inflammatory marker ChE in comparison to high sensitivity Creactive protein (hsCRP) to predict the presence of low-grade systemic inflammation and their correlation with blood pressure in ISH patients. Results: hsCRP and ChE levels were found significantly high in hypertensive patients than in healthy subjects (p
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