I. Horbachevsky Ternopil State Medical University
Introduction. The role of serum uric acid (SUA) in the process of atherosclerosis and atherotrombosis is controversial. Epidemiological studies have recently shown that SUA may be a risk factor for cardiovascular diseases and a negative prognostic marker for mortality in subjects with pre-existing heart failure.
Aim. To study out disturbances of cardiohaemodynamics, heart rhythm, lipid, purine metabolism and systemic inflammation and efficiency of their correction in patients with postinfarction cardiosclerosis, associated with hyperuricemia.
Materials and methods. 147 patients, (59.2 ± 0.8) years old, with postinfarction cardiosclerosis were included in this study. They were divided into 2 groups depending on presence of hyperuricemia. The I group included 106 patients with high SUA (0.59 ± 0.06) mmol/l and II group – 41 patients with normal level of SUA (0.32 ± 0.05) mmol/l. Comparable evaluation of cardiohaemodynamics, heart rhythm disturbances, lipid and purine metabolism’s violation and systemic inflammation were performed.
According to program of treatment patients with high SUA, were divided in 4 groups: I – 30 patients, whom standard treatment was prescribed, II – 25 patients, who received eprosartan 600 mg instead of ACE-inhibitor, III – 25 patients, whom fenofibrate 200 mg additionally was given, IV – 26 patients, who received combination of eprosartan and fenofibrate. Echo, Holter ECG monitoring, markers of systemic inflammation (C reactive protein (CRP), Interleukin 1 (IL1), tumor necrosis factor α (TNF α)), lipidiogram were assessed before treatment and after 6 months.
Results. Elevated SUA level was associated with progression of postinfarction heart remodeling: increasing of left ventricle mass index (LVMI (220.9 ± 6.9) g/m2)) and violation of its geometry, particularly, concentric hypertrophy (56.6 %), eccentric hypertrophy (40.6 %) with diastolic dysfunction. SUA levels correlated significantly with mitral A wave velocity (r = 0.61, p < 0.01), E wave deceleration time (r = 0.26, p < 0.01), E/A ratio (r = 0.21, p < 0.05). Heterogenity of ventricular repolarization, decrease of time indexes of heart rate variability, as well as high grade premature ventricular complexes were observed in these patients. The correlation between elevated levels of CRP and SUA (r = 0.7, p < 0.01), TNF α (r = 0.8, p < 0.01), IL-1 (r = 0.7, p < 0.01) were found, confirming the direct role of SUA in inflammation. Complex treatment with eprosartan provided significant regress of left ventricle hypertrophy (LVMI was decreased to 14.3 g/m2 and increasing of ejection fraction from (46.2 ± 1,2) to (52.4 ± 1,1) %, normalization of circadian index, heart rate, complete recovery from ventricular tachycardia, reduced quantity of ventricular premature beats on 64.0 %, reduced duration of Q-T and its dispersion on 21.1 % and increased heart rate variability. Target levels of blood pressure were achieved in 85.7 % patients. Usage of fenofibrate provided reduction of total cholesterol by 21.1%, triglycerides – 44.2 %, low density lipoprotein – 30.1 %, SUA – 37.5 %, CRP – 71.2 %, TNF α – 69.0 %, IL-1 – 47.1 % and an increase of high density lipoprotein – 30.7 %. Conclusions. The combined therapy with eprosartan and fenofibrate is an adequate means for hypertension control, correction of dislipidemia, hyperuricemia and inflammation, prevention of heart remodeling in patients with postinfarction cardiosclerosis, associated with hyperuricemia. It was associated with improvement of heart rate variability indexes as well as with decrease of incidence of life-threatening arrhythmias.
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