Citation: Olga Visternichan (2017), Evaluation of Purine Metabolism in Patients with Ischemic Heart Disease. Int J Car & Hear Heal. 1:2, 16-17. DOI:
10.25141/2575-8160-2017-2.0020
Introduction:
Ischemic heart disease (IHD) continuous to take the leading position
in the world as the cause of death and early disablement of
persons able to work, in spite of active introduction of modern
methods of diagnostics and treatment. Stents introduction with
drug covering allows to show the priority of endovascular surgery
in the chose of the methods of the coronary artery passage restoration.
In spite of the endovascular surgery progress high percents
of complications stays after percutaneous coronary angioplasty.
Therefore, the determination of new biochemical markers of early
diagnosis, progression and complication of IHD it is the actual
question of modern cardiology.
One of the directions of modern biochemistry is the determination
of the role of extracellular purines in the development of various
pathological conditions. The main purines are adenine and guanine.
Xanthine and hypoxanthine are intermediates in the adenine
and guanine metabolism. The final product of purines catabolism
is uric acid. Activity of purines connected with activation of different
specific receptors in the heart mussel, vessels and other organs
and tissues.
According to the literature data, different types of P2Y receptors
are found in the healthy heart and some of them take place in the
development of heart failure. In addition, according to results of
some scientific investigations, hyperuricemia is the initiator of
aseptic inflammation [6,7]. The ability of hyperuricemia to have an
adverse effect to the vascular wall and to the system of hemostasis
has been noted [5]. Therefore, the involvement of other intermediates
of purine catabolism in the mechanism of ischemic heart
disease development can be possible .
The aim of the research is to evaluate the diagnostic significance
of the purine catabolites in blood plasma in patients with coronary
heart disease.
Materials and Methods:
35 patients in age from 40 to 75 years old with IHD were examined.
Concentration of guanine, hypoxanthine, adenine, xanthine
and uric acid were determined. The control group consisted of 30
healthy individuals of the similar age. Venous blood in amount of
5 ml was used as a research material. The blood was stabilized by
heparin. Metabolites of purine metabolism were determined by the
method of Oreshnikov E.V. and co-authors (2008) [8].The patients
with such comorbidities as diabetes melitus, chronic obstructive
pulmonary diseases, chronic rheumatic fever, cancer, gout and renal
failure was excluded from the scientific investigation.
Statistical analysis of the data was performed using the software
package STATISTICA Version 8.0.
Results and Discussion:
In the group of patients with IHD, there was a tendency to increase
the content of guanine (p-0.000008), adenine (p-0.000001), xanthine
(p-0.000002) and uric acid (p-0.000001) in contrast to the
group of control (Figure 1).
Figure 1. Analysis of plasma purine concentration in patients
with ischemic heart disease and in control group.
Another reason may be desturbance of the reverse transport of
purine nucleotides and intermediates of their catabolism into the
cells, which is caused by disturbance of their capture by specific
receptors on the cell membranes.
Uric acid and xanthine are inducers of vascular endothelial damage,
which in turn contributes to the progression of atherosclerosis
and aggravates the course of IHD.
Conclusion:
The increase of purine catabolites concentration is prognostically
unfavorable factor, because of purine bases take part in progression
of atherothrombosis and angiogenesis.
In this regard, changes of xanthine oxidase activity and concentration
of intermediates of purine metabolism can be used as a
markers of progression of the atherosclerotic process and development
of complications of IHD.
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