PATTERNS OF ACETYLCHOLINESTERASE AND BUTYRYLCHOLINESTERASE ACTIVITY IN COMMON CARDIOVASCULAR PHENOTYPES.

BACKGROUND: Cardiovascular disease (CVD) is characterized by autonomic nervous system imbalance and chronic low-grade inflammation, processes reflected by the activity of blood cholinesterase enzymes-acetylcholinesterase (AChE) and butyrylcholinesterase (BChE). Given this link, the study set out to determine whether blood AChE and BChE activities differ among patients with common cardiovascular conditions (hypertension, ischemic heart disease, heart failure, and isolated dyslipidemia) compared to healthy individuals, and whether these enzymes levels correlate with disease severity or control status.

METHODS: Plasma BChE and erythrocyte AChE activities were measured in 298 adults (age 30-55 years) between December 2024 and May 2025. The patients were divided to group with either hypertension (HTN), or with ischemic heart disease (IHD), or with heart failure (HF), or with isolated dyslipidemia (DLIP), alongside with 30 healthy controls. Each patient was further classified as controlled or uncontrolled (based on achieving guideline blood pressure or disease targets) and as uncomplicated or complicated (depending on the presence of co-morbid conditions). Cholinesterase activity was quantified using an electrometric assay. Group comparisons were performed with Student's t-tests, using a significance threshold of α=0.05.

RESULTS: Patients with poorly controlled hypertension and co-morbid complications showed the greatest reductions in cholinesterase activity: their mean BChE was 1.05±0.17 and AChE 0.92±0.12, significantly lower than in healthy controls (1.16±0.14 and 0.98±0.01, respectively; p<0.05). Heart failure cases had uniformly low enzyme levels regardless of disease control status, with BChE ranging 0.93-0.98 and AChE 0.83-0.86. In IHD, cholinesterase patterns were heterogeneous: only the extreme subgroups (those who were controlled without complications and those uncontrolled with complications) had activities significantly different from controls, indicating intermediate values in other IHD patients. In contrast, individuals with isolated dyslipidemia exhibited elevated cholinesterase levels (BChE 1.22±0.11; AChE 1.08±0.07) relative to controls. Notably, neither the class of medications used, polypharmacy (multiple concurrent drugs), nor the presence of additional co-morbidities had any independent effect on AChE or BChE levels.

CONCLUSION: Declining blood cholinesterase activity correlates with worsening cardiovascular status: it progressively decreases with poorer control of hypertension and reaches the lowest levels in heart failure, whereas isolated dyslipidemia is associated with higher cholinesterase activity, with IHD patients showing intermediate changes. Routine measurement of plasma and erythrocyte cholinesterase could thus serve as a simple, inexpensive indicator of autonomic/inflammatory stress in CVD and help refine risk stratification if interpreted in the context of the patient's lipid profile. Larger prospective multicenter studies are warranted to validate these findings and to establish prognostic cutoff values for cholinesterase activity in cardiovascular risk assessment.