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Sazonova et al. Vessel Plus 2019;3:8 I http://dx.doi.org/10.20517/2574-1209.2019.01 Page 5 of 7

Table 3. Age characteristics of the study participants
Age
Investigated individuals Minimum, Mean, Maximum, Standard deviation
(years) (years) (years)
Conventionally healthy study participants 51 62 73 8.3
Patients with cardiac angina 52 64 76 8.1

Table 4. Demographic characteristics of the study participants
Parameter Conventionally healthy study participants Patients with cardiac angina Significance of differences
Sex, M/F 91:101 103:98 0.146
Age, years 62 (8.3) 64 (8.1) 0.111
Body mass index, kg/m 2 24.8 (5.9) 26.5 (6.3) 0.152
Systolic blood pressure, mmHg 123 (16) 147 (26) 0.214
Diastolic blood pressure, mmHg 82 (18) 91 (23) 0.319
Smoking, % 29 38 0.167

expansion of the sample, positive correlation m.5178C>A with cardiac angina will become significant. For
mutation m.15059G>A a significant negative correlation with this disease was found (P ≤ 0.05).

DISCUSSION
From the data obtained in this study, it can be concluded that mitochondrial genome mutations m.14459G>A
and m.5178C>A are risk factors for the occurrence and development of cardiac angina. Meanwhile, the
mutation m.15059G>A had a protective effect in this disease.

The detected mutations were localised in the coding region of mtDNA. Single nucleotide replacements
m.14459G>A and m.5178C>A were localised in the genes of the second and sixth subunits of NADH
dehydrogenase. We assume that the defects of this mitochondrial respiratory chain enzyme is a trigger of
pathological mechanisms in the human body, as a result of which ATP deficiency occurs. Energy deficit, in
turn, leads to the emergence and development of cardiac angina.

At the same time, mtDNA mutation m.15059G>A is localised in the cytochrome B gene. Perhaps this
mutation is involved in molecular cell processes which protect a person from the occurrence of cardiac
angina.

Mitochondrial genome mutations m.14459G>A and m.5178C>A may be candidates for the creation of
molecular cell models in the development of drug therapy for patients with cardiac angina. Mutation
m.15059G>A can be used for creating gene therapy approaches to this disease.

Molecular genetic markers for cardiac angina could help the identification of predisposition to the disease
much earlier than clinical methods for examining patients. At the present time, such studies are mainly
devoted to polymorphisms of nuclear genome genes. Studies of mitochondrial genome mutations in cardiac
angina are practically absent. Therefore, analysis of the association of mtDNA mutations with cardiac
angina, conducted by our research group, is very relevant.

In conclusion, according to the obtained data, three mitochondrial mutations of human genome correlated
with cardiac angina. A positive correlation was observed for mutation m.14459G>A (P ≤ 0.05). One single
nucleotide substitution m.5178C>A (P ≤ 0.1) had a trend for positive correlation. A negative correlation for
mutation m.15059G>A with cardiac angina (P ≤ 0.05) was found.