Vol 7, No 2 (2013)

Atherosclerotic lesion of lower extremity arteries frequently complicates the long-term course of hypertension and it is generally associated with coronary heart disease. Our study has attempted to evaluate the impact of combination antihypertensive therapy involving amlodipine, bisoprolol, and lisinopril on quality of life in this category of patients.

The paper considers the main causes of cardiac embolic events. It is emphasized that atrial fibrillation is a major risk factor for systemic embolism. Main approaches to assessing the risk of stroke/systemic embolisms and their prevention using the currently available anticoagulants are given.

The paper considers the basic mechanisms for the occurrence of asthenic syndrome in chronic neurological diseases. It shows the significance of
this problem in nosological entities, such as stroke sequels, multiple sclerosis, and Parkinson’s disease. The main asthenia diagnostic scales are
described. Possible therapeutic strategies aimed at reducing the degree of asthenia in neurological patients are also presented.

Ischemic stroke (IS) is a severe disease associated with high mortality and persistent disability. Prior IS is related to the drastically increased risk of repeat IS. Antiplatelet therapy is an efficient way to prevent repeat IS. Acetylsalicylic acid, the administration of its enteric-coated formulation
can reduce the risk of gastric mucosal lesion, has a special efficacy. The possibilities of using other antiaggregants and indirect anticoagulants
are considered.

Acute and chronic brain ischemia is accompanied by complex metabolic rearrangements in the neurons. The ability of the cells to survive is largely determined by the presence of energy substrates and oxygen, the synthesis of neurotransmitters, and some other factors. The increased
persistence of nerve tissue in ischemia and chances of recovering the impaired function can be achieved by the use of neuroprotective and neurotrophic agents. The efficiency of neurometabolic therapy is considered using Ceraxon and Actovegin as an example. It is emphasized that the
efficiency of their administration can be achieved by the mandatory concurrent use of a wide range of nondrug treatments.

Objective: to analyze the distribution of components of insulin resistance (IR) syndrome and to study the frequency of their combinations in relation to the genotypes and allelic variants of the angiotensin-converting enzyme (ACE) gene.

Subjects and methods. A group of clinically healthy patients (50 women and 42 men) with different genotypes of the ACE gene was examined.
The distribution of IR syndrome components and the frequency of their combinations were analyzed in relation to the genotypes and allelic
variants of the ACE gene.

Results. A group of D allele carriers compared to A allele ones showed a pronounced tendency for the frequency of IR to reduce due to the
higher proportion of patients with complete IR syndrome. This observation becomes statistically significant in the assessment of homozygous variants of the ACE gene. At the same time dyslipidemia and hypertension in the presence of IR significantly more frequently occurred in patients with the DD genotype than in those with genotype II.

Conclusion. There was a marked predominance of the manifestations of IR syndrome with a complete set of components in the DD genotypic
group, which confirms the significant strong association between ACE gene polymorphism and IR syndrome.

Mitochondria are not only the major producers of adenosine triphosphate, but also an endogenous source of reactive oxygen species. Mitochondrial
dysfunction plays a key role in the trigger and progression of atherosclerotic lesion. Impaired function in the mitochondria due to their elevated level of oxidized oxygen species, the accumulation of mitochondrial DNA damages, and the exhaustion of respiratory chains induces dysfunction and apoptosis in the endothelial cells; activation of matrix metalloproteinases; growth of vascular smooth muscle cells and their migration into the intima; expression of adhesion molecules, and oxidation of low-density lipoproteins. Mitochondrial dysfunction may be an important unifying mechanism that accounts for the atherogenic effect of major cardiovascular risk factors. Small clinical pilot studies have shown an association of different mitochondrial genome mutations with atherosclerotic lesion in the artery. Taking into account the available data on the possible role of mitochondria in atherogenesis, novel drugs are now being designed to affect mitochondrial function.