Effect of impaired myocardial contractility on coronary flow reserve and inflammatory processes in chronic coronary syndrome
DOI:
https://doi.org/10.14739/2310-1210.2024.4.305572Keywords:
ischemic heart disease, inflammation, chronic coronary syndrome, stable angina, inflammation biomarkers, endothelial dysfunction, leukocyte inflammation markers, left ventricular ejection fraction, heart failure, obesityAbstract
Aim. To study the relationship between myocardial contractility impairment in chronic coronary syndrome and the state of coronary flow reserve, the degree of systemic inflammation and endothelial dysfunction.
Materials and methods. We examined 120 patients with stable angina pectoris (SAP) of functional class (FC) II–III, who were assigned into two groups: group 1 comprised 65 patients with left ventricular ejection fraction (LVEF) ≥55 %, and group 2 was composed of 55 patients with LVEF <55 %. Diagnostic methods included clinical and instrumental examination data, analyses of lipid profile, inflammation biomarkers, endothelial functional state, hemogram data, leukocyte inflammation markers, and questionnaires.
Results. Compared to group 1, group 2 patients showed an increase in the left atrium (p < 0.001) and right ventricle (p = 0.027) sizes; significantly lower LVEF (50.16 ± 0.42 % vs 58.77 ± 0.41 %; p < 0.001); thickening of the intima-media complex in the right (p = 0.003) and left (p = 0.017) common carotid arteries; significantly lower load threshold values (p = 0.008), exercise tolerance (p = 0.004) and heart rate variability indicators – SDNN (standard deviation of normal-to-normal intervals over 24 hours; p = 0.046).
Group 2 patients were characterized by more active low-grade chronic inflammation, as indicated by increased levels of leukocytes (p = 0.024), neutrophils (p < 0.001), and decreased lymphocyte levels (p = 0.021); significantly higher levels of leukocyte inflammation markers, in particular, the neutrophil-to-lymphocyte ratio (p < 0.001), platelet-to-lymphocyte ratio (p = 0.004), systemic immune-inflammation index (p < 0.001), systemic inflammation response index (p < 0.001), and aggregate index of systemic inflammation (p < 0.001) as compared to group 1 individuals. Patients with LVEF <55 % had higher levels of fibrinogen (p < 0.001), uric acid (p = 0.002), high-sensitivity C-reactive protein (p = 0.007), and endothelin-1 (p < 0.001) compared to those with LVEF ≥55 %.
Conclusions. Group 2 patients need a more thorough monitoring and a more intensive treatment aimed at reducing the inflammatory process.
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