Dysregulation of sympathoadrenal system activity in patients with microvascular angina

Abstract

Abstract Introduction Recent studies have highlighted that a significant proportion of patients (up to 47%) undergoing coronary angiography due to clinical indications do not exhibit significant stenosis in epicardial vessels. Among these patients, up to 50% may suffer from microvascular angina (MVA). Despite the absence of intramural coronary artery lesions typically associated with atherosclerosis, the occurrence of transient myocardial ischemia and cardiac pain syndrome raises interest due to the incomplete understanding of their underlying mechanisms. Objective This study aims to comprehensively investigate sympathoadrenal system activity in patients with microvascular angina. Materials and Methods A total of 40 patients diagnosed with MVA, aged 35-76 years, including 11 (27.5%) men and 29 (72.5%) women, were enrolled, along with 20 healthy individuals. Assessment of sympathoadrenal system (SAS) activity involved determining daily urinary excretion levels of free and conjugated catecholamine fractions (CA) using solid-phase enzyme immunoassay: adrenaline (A), noradrenaline (NA), dopamine (DA), and DOFA. Additionally, catecholamine deamination enzyme activity—monoamine oxidase (MAO)—was determined using solid-phase EIA. Results Patients with MVA exhibited a significant increase in the excretion of all CA fractions. Specifically, adrenaline (A) excretion increased by 56.7%, surpassing the control by 1.7 times (p<0.001). Noradrenaline (NA) levels were elevated by 59.5% in MVA patients, which was 1.6 times higher than the control group (p<0.001). Dopamine (DA) levels in MVA patients increased by 31.0%, surpassing control values by 1.36 times (p<0.001). Moderate elevation in DOFA levels by 19.7% was observed, which was 1.23 times higher than the control (p<0.01). Ratios of CA sulfocatecholamine formation processes indicated pronounced deviations from normal. Gender differences revealed marked changes in sympathoadrenal activity, particularly in women (p<0.001). Studies of MAO activity on the first day identified a moderate decrease in its activity in MVA patients—0.03±0.002 units/ext. (p<0.01), while healthy individuals exhibited an activity level of 0.07±0.001 units/ext. Conclusion The findings underscore the crucial pathogenetic role of SAS in the development of MVA. The study demonstrates that the severity of ischemia correlates with disruptions in SAS components. Notably, these disruptions are pronounced in MVA, indicating an overload of the sympathoadrenal system—a critical component of organismal homeostasis. Under conditions of SAS overload, the pivotal enzyme in biogenic amine oxidation, MAO, undergoes significant transformation, leading to reduced activity towards monoamines. These findings were consistent with our clinical investigation.