Changes in the structural and functional status of the left ventricle in patients with arterial hypertension who have undergone myocardial infarction, taking into account the angiotensin II type 1 receptor gene polymorphism during long-term dynamic observ
The need for daily monitoring of pressure in patients with arterial hypertension who have suffered a myocardial infarction to establish the level and all fluctuations of blood pressure during the day with determination of the effectiveness of treatment.
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Changes in the structural and functional status of the left ventricle in patients with arterial hypertension who have undergone myocardial infarction, taking into account the angiotensin II type 1 receptor gene polymorphism during long-term dynamic observation
Kolesnyk T.V., Fursa O.V. Dnipro State Medical University
The study is devoted to changes in the structural and functional state of the left ventricle in patients with arterial hypertension who suffered a myocardial infarction, taking into account the A1166C polymorphism of the angiotensin II type 1 receptor gene during long-term dynamic observation. The study included 36 men with arterial hypertension of the 1st to 3rd degree who had suffered a myocardial infarction. The average age was 57.0 (52.0; 64.0) years, the experience of arterial hypertension was 6.3 (4.0; 15.0) years, the period after the myocardial infarction was 48.0 (12.0; 144.0) months. The A1166C polymorphism of the angiotensin II type 1 receptor gene was determined, according to which the patients were divided into 3 groups: group 1 consisted of 18 (50%) patients with the AA genotype, group 2 included 12 (33.3%) patients with the AC genotype, and in 3 - 6 (16.7%) patients with CC genotype of angiotensin II type 1 receptor gene. Daily blood pressure monitoring and echocardiography were performed at the beginning of the study and after 38 months.
Determination of the AA11SS polymorphism of the angiotensin II type 1 receptor gene in patients with arterial hypertension after a myocardial infarction made it possible to establish the features of the course of the disease. Patients with the AA genotype of the angiotensin II type 1 receptor gene had progression of left ventricular hypertrophy despite reaching the target blood pressure level. In patients with AS, the angiotensin II receptor gene genotype showed a tendency to regression of left ventricular hypertrophy when reaching the target average blood pressure level in all periods of the day. At a comparable level of office blood pressure, patients with the CC genotype of the angiotensin II type 1 receptor gene demonstrated the highest average nighttime blood pressure level associated with the highest parameters of pathological remodeling of the left ventricle.
Key words: arterial hypertension and previous myocardial infarction, left ventricular hypertrophy, A1166C polymorphism of the angiotensin II type 1 receptor gene.
Introduction
Adverse consequences and cardiovascular complications of arterial hypertension (AH) are largely due to progressive morpho-functional changes of the heart.
The development of left ventricular hypertrophy (LVH) is associated with a higher risk of morbidity and cardiovascular mortality [1]. Today, LVH is an independent marker of cardiovascular complications, a special target for the treatment of hypertension. But in patients who have already suffered a myocardial infarction (MI), regression or progression of LVH is not used to assess the prognosis. In general, the influence of previous arterial hypertension on post-infarction LV remodeling has not been sufficiently studied.
Since blood pressure (BP) is the leading modifiable risk factor for morbidity and mortality worldwide, its correct measurement and assessment are essential factors in the diagnosis and, especially, in the treatment of hypertension [2]. Recently, against the background of the use of standardized treatment regimens for hypertension, more and more scientists are searching for personalised treatment approaches. And this role is confidently occupied by genetic testing of gene poly- morphisms related to blood pressure regulation [3], especially in patients with very high cardiovascular risk [4].
Currently, despite numerous molecular genetic studies, literature data on the influence of the A1166C polymorphism of the angiotensin II receptor type 1 gene (AGTR1) on blood pressure and the development of LVH are ambiguous, and studies devoted to long-term follow-up in this cohort of patients are few and far between [5]. One of the first ECTIM studies (Bonnardeaux, 1994) demonstrated the association of this polymorphism with myocardial infarction. The work of Osterop AP (1998) shows a significantly large mass of the LV myocardium, the thickness of the interventricular septum in patients with the C-allele of AGTR1. In 1998, the association of myocardial infarction with SS genotype was confirmed for the first time in Japanese (Tetsuya Fusazaki) and Chinese (Xiang K) populations, citing Zaitseva [6]. In the 2000s, many studies demonstrated the effect of the C-allele of AGTR1 on the development of LVH [7]. The results of a study by Deepak N Parchwani et al. (2018) demonstrated that the distribution of the genotype and alleles of the A1166C variant was significantly different in hypertensive and normotensive subjects, and the presence of the SS genotype increased the risk of essential hypertension by 1.74 times [8]. According to the results of the latest (2019) meta-analysis, the A allele and the AA genotype of the AT1R A1166C gene polymorphism are associated with a protective effect against essential hypertension, while the C allele and the AC AT1R A1166C genotype are correlated with an increased risk of essential hypertension [9].
Genetic testing today makes it possible to identify candidate genes for increased blood pressure and the risk of developing LVH, which are the main triggers of cardiac remodeling and determine the type of response of cardiomyocytes to hemodynamic overload. Therefore, the search for the interaction of hemodynamic and structural indicators, taking into account the genotype, to assess the stages of the development of heart remodeling, as part of the progression of a single pathological process that leads to the formation of heart failure (HF) is relevant and necessary.
The aim of the study.
To determine the features of changes in the structural and functional state of the left ventricle in patients with arterial hypertension who suffered a myocardial infarction, taking into account the polymorphism of the angiotensin II type 1 receptor gene A1166C during longterm dynamic observation.
Object and research methods
The study included 36 men with stage III hypertension (HBP), grade 1-3 hypertension who underwent MI. The average age in the study group was 57.0 (52.0; 64.0) years, HBP experience was 6.3 (4.0; 15.0) years. The average period after the MI was 48.0 (12.0; 144.0) months. According to the localization of type 1 MI, the most frequent were front - 11 (30.6%), lower - 7 (19.4%) and rear - 3 (8.3%). Posterior-lateral MI was registered in only 1 (2.8%) patient. 14 (38.9%) patients underwent type 2 MI. The median office BP was 140.0 (130.0; 160.0 mm Hg for systolic BP (sBP) and 90.0 (80.0; 100.0) mm Hg for diastolic BP (dBP).
14 (38.9%) patients had the status of an active smoker, 9 (25%) patients had previously smoked and quit after a heart attack, 13 (36.1%) patients had never smoked. Aggravated heredity for hypertension was found in 14 (38.9%) patients and for coronary artery disease - in 5 (13.9%) patients. 13 (36.1%) patients had atherosclerosis of the main vessels of the head and 12 (33.3%) of the lower limb arteries. HF I stage 2 FC was established in 7 (19.4%) patients, IIA 2 FC - in 11 (30.6%), IIA 3 FC - in 18 (50.0%) patients.
The diagnosis of HBP, coronary heart disease (CHD) and HF was established according to national and international recommendations [10, 11, 12]. At the time of inclusion in the study, all patients were recommended to adhere to treatment per Ukrainian and international protocols for treating HBP, coronary heart disease and HF [11, 12, 13, 14, 15].
Standardized antihypertensive therapy (AHT) was prescribed to all patients. The basis of combined AHT was angiotensin-converting enzyme (ACE) inhibitors in 29 (80.5%) patients and sartans in 7 (19.5%) patients. 8 (22.2%) patients took ACE in combination with a diuretic, 5 (13.9%) patients in combination with a calcium channel antagonist. Sartans combined with a diuretic were taken by 2 (5.6%) patients and with calcium channel blocker by 2 (5.6%). The study did not conduct a comparative analysis of the effectiveness of various antihypertensive drugs and their combinations.
To achieve the anti-anginal effect and maintain the target heart rate (HR) level, 32 (88.9%) patients received beta-blockers. Two (5.6%) patients received ivabradine. The recommended HR range is 55 - 70 bpm per minute reached 22 (61.1%) patients.
33 (91.2%) patients received antithrombotic therapy 22 (61.1%) patients received hypolipidemic treatment.
Exclusion criteria from the study were the presence of HF IIB FK 4 and III stage diabetes in patients.
The study was conducted in accordance with the principles of bioethics outlined in the Helsinki Declaration "Ethical Principles of Medical Research Involving Humans", the "General Declaration on Bioethics and Human Rights (UNESCO)" and the Order of the Ministry of Health of Ukraine "On Approval of the Procedure for Conducting Clinical Trials of Medicines and Examination of Clinical Materials" tests and standard regulations on ethics commissions" No. 690 dated 09/23/2009, also approved by the biomedical ethics commission of the Dnipro State Medical University. All patients gave informed consent for the necessary research methods.
The study of A1166C polymorphism of the AGTR1 gene using the "DNA-sorb-B" test system was carried out by the polymerase chain reaction method with restriction endonuclease products [16].
The structural and functional state of the heart was determined by echocardiography (EchoCG), which was performed at the beginning of the study and after 38 months. We measured the thickness of the posterior wall (TPW), the interventricular septum (TIVS) in diastole, the end-diastolic size (EDS) of the LV with subsequent calculation of the end-diastolic volume (EDV) and the values of these parameters adjusted to the body surface area: DDI indices (iEDS) and KDO (iEDV). The LV's ejection fraction (EF) was calculated according to the Teichholz formula. The weight of the left ventricular myocardium (LVMI) was calculated according to the formula of the American Society of Echocardiography (ASE), adjusted to the body surface of the LVMI (g/m2) and to the height of the LVMI2-7 (g/m2-7) [17].
To determine changes in blood pressure level within 24 hours. patients underwent daily blood pressure monitoring (APDM) (AVRM-04, Hungary) according to the standard method at the beginning of the study and after 38 months. Average values of systolic and diastolic blood pressure during the day (sBPd and dBPd) and at night (sBPn and dBPn) were evaluated. According to the ESC recommendations on APDM [18], the target blood pressure levels for the daytime were considered to be <135/85 mm Hg. Art., for the night - <120/70 mm Hg (corresponding to sBP/dBP).
Statistical processing was carried out using the computer program packages "STATISTICA 6.1 (StatSoftInc., serial number AGAR909E415822FA), "Microsoft Excel (Office Home Business 2KB4Y-6H9DB-BM47K-749PVPG- 3KT). Values are given as median and interquartile data distribution (Me (25.0%; 75.0%)). Comparative analysis of independent groups was performed using the Mann- Whitney test, and the Wilcoxon test was used to compare data in dynamics. The difference was considered probable at a significance level of p<0.05 [19].
Research results and their discussion
According to the set goal, the patients were divided into 3 groups based on the results of molecular genetic research: group 1 consisted of 18 (50%) patients with the AA genotype of the AGTR1 gene, group 2 included 12 (33.3%) patients with the AC genotype, and 3 - 6 (16.7%) patients with CC genotype of the AGTR1 gene.
According to the results of the examination of patients with hypertension who underwent MI, at the beginning of the study, it was established that all patients in the group had a threshold level of target sBPof and dBPof, which remained unchanged after 38 months (table 1).
According to the APDM results, in the group as a whole, all patients had normal sBP and dBP levels at the initial examination, and these levels remained unchanged at the 38-month follow-up (table 1). Thus, the obtained data demonstrate the need for APDM, since office AP does not always reflect real AP levels during the day, which is important in patients with hypertension and very high cardiovascular risk.
Table 1 - Dynamics of office, day and night blood pressure levels in patients with stage III AH, taking into account the A1166C polymorphism of the AGTR1 gene
|
Parameters |
Examination |
All patients (n=36) |
Groups of patients by AGTR1 genotype |
|||
|
1 gr., АА (n=18) |
2 gr., АС (n=12) |
3 gr., СС (n=6) |
||||
|
sBP of* mm Hg. |
primary |
140,0 (130,0; 160,0) |
140,0 (125,0; 160,0) |
145,0 (130,0; 160,0) |
142,0 (135,0; 160,0) |
|
|
after 38 months |
140,0 (130,0; 160,0) |
140,0 (130,0; 157,5) |
140,0 (130,0; 160,0) |
130,0 (110,0; 160,0) |
||
|
sBP„ d, mm Hg. |
primary |
133,69 (125,14; 143,06) |
134,67 (125,84; 140,53) |
131,31 (124,28; 140,71) |
140,51 (131,13; 156,00) |
|
|
after 38 months |
130,14 (122,97; 140,84) |
126,31 (122,89; 137,00) |
131,29 (126,22; 140,84) |
134,94 (131,69; 136,13) |
||
|
sBP mm Hg. |
primary |
118,42 (110,49; 129,74) |
115,28 (107,47; 124,37) |
119,51 (108,78; 124,58) |
137,68 (118,50; 153,33) * |
|
|
after 38 months |
118,00 (110,92; 125,86) |
113,86 (105,00; 122,75) |
120,36 (112,10; 129,00) |
124,56 (118,15; 125,86) § |
||
|
dBP, of, mm Hg. |
primary |
90,0 (80,0; 100,0) |
90,0 (80,0; 100,0) |
85,0 (80,0; 100,0) |
85,0 (82,5; 105,0) |
|
|
after 38 months |
90,0 (80,0; 100,0) |
85,0 (80,0; 100,0) |
90,0 (80,0; 90,0) |
80,0 (60,0; 100,0) |
||
|
dBPd, mm Hg. |
primary |
80,14 (75,07; 85,31) |
78,79 (75,56; 82,21) |
82,00 (74,19; 86,29) |
83,22 (79,62; 99,63) |
|
|
after 38 months |
77,11 (72,19; 84,72) |
75,20 (72,19; 82,98) § |
77,05 (72,81; 81,71) |
82,49 (81,81; 84,72) |
||
|
dBPn mm Hg. |
primary |
66,53 (60,97; 75,06) |
63,57 (59,00; 74,05) |
65,46 (62,29; 73,56) |
77,09 (73,81; 82,00)* |
|
|
after 38 months |
67,16 (61,80; 72,11) |
64,92 (61,00; 69,75) |
67,81 (64,85; 73,00) |
67,43 (66,40; 69,00) |
Notes: * probability of differences p<0.05 between AA and CC genotypes, § - probability of differences p<0.05 at initial examination and after 38 months.
When analyzing the office level of AP depending on the A1166C polymorphism of the AGTR1 gene, it was found that patients of group 1 had a threshold level of sAPof and dAPof at the initial examination.
After 38 months, the level of sAPof did not change, and the level of dAPof decreased by 5 mm Hg according to the median (p>0.05). Patients of 2 groups at the beginning of the study had a median elevated level of sAPof and a normal level of dAPof, after 38 months of observation, the median level of sAPof decreased by 5 mmHg, and the median level of dAPof, on the contrary, increased by 5 mmHg (p> 0.05). Patients of group 3 at the initial examination had a slightly increased level of sAPof and a normal level of dAPof, during the re-examination in patients of this group, a decrease in the level of sAPof by 12 mm Hg was noted and dAPof by 5 mmHg with reaching the target levels of office AP, although this dynamic was not reliable.
Comparative analysis of sBP levels according to APDM data considering the A1166C polymorphism of the AGTR1 gene shows that the median sBPd level in groups 1 and 2 corresponded to the normal range and was increased in patients of group 3 (p>0.05). When examining patients after 38 months, the level of sBPd in patients of group 1 significantly decreased by 8.36 mm Hg. Art., remained unchanged in patients of group 2 and decreased, although not significantly, in patients of group 3 by 5.57 mm Hg. The median level of sBPn in group 1 patients was within normal values and remained almost unchanged after 38 months. The median level of sBPn in patients of group 2 at the initial examination was at the upper limit of the normal value, and at the examination after 38 months, it had a tendency to increase (p>0.05) and slightly exceeded the target value. In patients of group 3, at the initial examination, the median level of sBPn was higher than the norm by 17.68 mm Hg and was significantly different from the level of sBPn of patients of group 1. At re-examination in patients of group 3, the median sBPn level significantly decreased by 13.12 mm Hg, but did not reach the target value and was the highest among all patient groups.
When conducting a comparative analysis of dBP levels according to APDM data, taking into account the A1166C polymorphism of the AGTR1 gene, it was established that dBPd levels in patients of all 3 groups corresponded to the target values at the initial examination and insignificantly decreased at the examination after 3 months (p>0.05). The median dBPn level was within the normal range in groups 1 and 2 and exceeded the target value in all patients of group 3, significantly different from the dBPn level of patients in group 1. At the 38-month follow-up, dBPn levels in patients of groups 1 and 2 remained unchanged, and patients in group 3 decreased to the target value (table 1).
The obtained data are confirmed in the literature. So, according to Deepak N. Parchwani et al. The CC polymorphism of the AGTR1 gene created a 1.7886-fold increased risk of hypertension compared to the AC and AA genotypes, and statistically significant intergenotypic variations in mean sBP and dBP were also found, with patients with the CC genotype having the highest BP values than patients with AC and AA genotypes [8]. According to the research of Semyaniv (2020), carriers of the C-allele of the AGTR1 gene have levels of sBP and dBP higher than those of owners of the AA genotype by 5.38% and 5.15%. The presence of the C-allele of the AGTR1 gene (A1166C) increases the risk of a severe course of essential arterial hypertension almost twice [20].
According to the results of Echocardiography (table 2) during the initial examination of patients with AH who underwent MI, it was established that all patients had LVH due to the thickening of the walls with normal dimensions of the LV cavity according to the levels of EDS, EDV and their indices. After 38 months, in the group as a whole, a tendency to an increase in EDV by almost 5 ml (p>0.05) with a reliable increase in EDS by 0,78 cm and a tendency to a decrease in TPW by 0.02 cm (p>0.05) was noted in the group reliable thickening of the TIVS by 0.05 cm. At the same time, the indexed indicators of the LV remained almost unchanged. The LV ejection fraction was within the normal range at the initial examination, and after 38 months, the median EF of the LV had a tendency to decrease by more than 2% (p>0.05) and remained normal (table 2).
Table 2 - Dynamics of LV morpho-functional parameters in patients with AH III stage depending on the A1166C polymorphism of the AGTR1 gene
|
Parameters |
Examination |
All patients (n=36) |
Groups of patients by AGTR1 genotype |
|||
|
1 gr., АА (n=18) |
2 gr., АС (n=12) |
3 gr., СС (n=6) |
||||
|
EDS, sm |
primary |
5,22 (4,80; 5,57) |
5,28 (4,62; 5,54) |
5,16 (4,89; 5,50) |
4,98 (4,63; 5,97) |
|
|
after 38 months |
5,30 (5,05; 5,70) § |
5,35 (5,12; 5,60) § |
5,10 (5,00; 5,40) |
5,80 (5,10; 6,07) |
||
|
iEDS |
primary |
2,56 (2,33; 2,76) |
2,56 (2,33; 2,75) |
2,57 (2,42; 2,72) |
2,42 (2,28; 2,82) |
|
|
after 38 months |
2,57 (2,44; 2,78) |
2,65 (2,49; 2,83) § |
2,46 (2,43; 2,66) |
2,52 (2,49; 2,95) |
||
|
EDV, ml |
primary |
130,66 (107,26; 151,47) |
133,88 (98,33; 149,90) |
127,24 (112,28; 147,42) |
116,88 (99,09; 178,57) |
|
|
after 38 months |
135,34 (118,24; 156,85) |
138,33 (124,94; 153,66) § |
123,87 (118,24; 141,31) |
166,56 (123,81; 184,83) |
||
|
iEDV |
primary |
63,99 (52,81; 74,83) |
67,16 (49,68; 74,74) |
60,60 (56,78; 74,68) |
56,83 (48,30; 83,95) |
|
|
after 38 months |
66,45 (58,01; 77,40) |
68,92 (60,90; 78,19)§ |
62,90 (57,10; 69,00) |
76,59 (59,00; 84,80) |
||
|
EF, % |
primary |
64,26 (57,72; 68,67) |
64,26 (57,95; 68,22) |
62,54 (57,05; 68,69) |
67,60 (55,35; 71,26) |
|
|
after 38 months |
61,95 (55,24; 65,24) |
63,53 (54,45; 65,69) |
61,29 (58,45; 64,35) |
46,50 (45,38; 66,92) |
||
|
TIVS, sm |
primary |
1,32 (1,20; 1,59) |
1,26 (1,20; 1,49) |
1,37 (1,26; 1,55) |
1,69 (1,29; 1,83) * |
|
|
after 38 months |
1,37 (1,25; 1,54) § |
1,33 (1,20; 1,50) § |
1,38 (1,26; 1,56) § |
1,70 (1,41; 1,75) * |
||
|
TPW, sm |
primary |
1,12 (1,01; 1,30) |
1,10 (1,00; 1,20) |
1,15 (1,10; 1,30) |
1,25 (1,06; 1,42) |
|
|
after 38 months |
1,10 (1,05; 1,20) |
1,10 (1,05; 1,20) |
1,10 (1,05; 1,20) |
1,14 (1,10; 1,20) |
||
|
LVMI, g |
primary |
258,19 (216,87; 313,22) |
241,60 (206,71; 280,35) |
273,50 (228,28; 299,54) |
318,47 (258,11; 431,27) |
|
|
after 38 months |
263,55 (223,53; 321,45) |
268,67 (225,15; 304,70) |
257,44 (224,17; 311,63) |
331,28 (327,38; 404,90) # |
||
|
iLVMI, g/m2 |
primary |
129,55 (109,55; 153.006) |
118,46 (106,09; 144,43) |
142,47 (114,51; 151,47) |
154,86 (131,69; 196,65)* |
|
|
after 38 months |
129,70 (112,30; 321,45) |
135,58 (113,17; 156,71) § |
124,63 (106,42; 138,72) |
167,77 (161,00; 168,66) # |
||
|
iLVMI 2,7, g/ m2,7 |
primary |
58,65 (49,27; 68,57) |
55,30 (47,77; 63,98) |
61,42 (49,75; 67,93) |
72,65 (58,74; 90,91) |
|
|
after 38 months |
58,17 (47,71; 71,61) |
61,16 (51,26; 72,36) |
56,82 (49,23; 70,94) |
76,96 (72,00; 82,82) # |
Notes: * probability of differences p < 0.05 between genotypes AA and CC, # probability of differences p < 0.05 between genotypes AA and CC and AC and CC, § - probability of differences p < 0.05 at initial examination and after 38 months .
When analyzing the structural and functional parameters of Echocardiography, taking into account the A1166C polymorphism of the AGTR1 gene, it was established that patients of all groups at the initial examination had normal median EDS, iEDS, EDV, iEDV, EF, LV dimensions and did not reliably differ depending on the genotype. Patients of group 1 had the largest EDV and iEDV during the initial examination, and group 3 had the smallest (p>0.05). All patients differed unreliably in terms of TPW, namely patients of group 2 had a median TPW greater than patients of group 1 by 0.05 cm, patients of group 3 had a median TPW of 0.15 cm and 0.10 cm more than patients of 1 and 2 groups, respectively. Patients of group 1 had the smallest TIVS, patients of group 2 had a TIVS greater than that of patients of group 1 by 0.11 cm, patients of group 3 had a TIVS greater than that of patients of group 1 by 0.43 cm (p<0.05) and greater than in patients of group 2 by 0.32 cm (p>0.05). Patients of all groups differed in LVMI, so the difference between patients of groups 1 and 2 was 31.90 g, between patients of groups 1 and 3 - 76.87 g, between patients of groups 2 and 3 - 44.97 g (p>0.05) . Patients of all groups differed in iLVMI: the difference between patients of groups 1 and 2 was 25.01 g/m2 (p>0.05), between patients of groups 1 and 3 - 36.40 g/m2 (p<0.05), between patients of groups 2 and 3 - 12.39 g/m2 (p>0.05). But they did not reliably differ according to iLVMI adjusted for height: the difference between patients of groups 1 and 2 was 6.12 g/m2'7, between patients of groups 1 and 3 - 17.35 g/m2'7, between patients of groups 2 and 3 - 11.23 g/m2'7 (p>0.05). Patients in group 3 had the largest wall thickness and LVMI.
The obtained data are comparable to the literature data, which demonstrated the connection of the C-allele and the development of LVH due to the thickening of the LV walls and the thickening of the TIVS [6, 7]. In our study, significant LVH in patients of group 3 also attracts attention.
During the examination after 38 months, a significant increase in EDS, EDV and their indices was registered in patients of group 1, although these parameters remained in the normal range. LV EF did not change significantly. Also of note is the significant thickening of TIVS by 0.07 cm at the median with unchanged TPW and the significant increase in iLVMI by 17.12 g/m2, despite achieving target BP levels. In patients of group 2, a decrease in LV hemodynamic parameters (EDS, iEDS and EDV), as well as a decrease in TPW by 0.05 cm and a decrease in iLVMI by 17.84 g/m on the median, with unchanged LV EF, were registered. Although these changes were implausible, they illustrate the tendency for LVH to regress when BP targets are reached and the expected response to long-term AHT. In patients of group 3, a tendency towards negative changes in LV hemodynamic parameters according to the median was registered, namely an increase in EDS by 0.82 cm, iEDS by 0.10, EDV by 49.68 ml and iEDV by 19.76, a decrease in LV EF by 21.10% (p > 0.05). Due to LV dilatation in patients of 3 groups, LVMI increased by 12.81 g, iLVMI by 12.91 g/m2, and iLVMI2.7 by 4.31 g/m, despite the tendency to regression of LVH by wall thickness (unreliable decrease in TPW by 0.11 cm). But when examined after 38 months, patients of groups 1 and 2 differed significantly from patients of group 3 in terms of LVMI, iLVMI and iLVMI2,7.
Data from the literature demonstrate the effect of the A1166C polymorphism of the AGTR1 gene on the regulation of blood volume and the stimulation of the growth and reproduction of cardiac cells, and therefore the development of LVH, but are contradictory regarding the development of HF [8]. Also, in patients who have undergone MI, LV volumes are the most stringent prognostic criteria [1]. In our study, we obtained data on the progression of LVH due to an increase in the LV cavity in patients with homozygous genotypes of the AGTR1 gene polymorphism and over time, the development of HF with a decrease in LV EF in patients with CC of the AGTR1 gene polymorphism, despite reaching target BP levels.
To assess the influence of blood pressure levels at different times of the day on the structural and functional parameters of the LV, taking into account the A1166C polymorphism of the AGTR1 gene, a correlation analysis was performed (table 3).
Correlation analysis showed that in patients with the AA genotype of the AGTR1 gene, only the average nocturnal sBP level was associated with TIVS, LVMI, and iLVMI, and in patients with the AS genotype of the AGTR1 gene, there was no association between the BP level in any period of the day and parameters of LSH. In contrast to patients of groups 1 and 2, high-strength correlations were established in patients with the CC genotype of the AGTR1 gene. The level of nocturnal sBP and dBP was directly associated with EDS and EDV (r=0.89, p<0.05). The increase in the degree of LVH was associated first of all with the level of DBP mainly during the day, the night level of sBP and dBP also had an effect, but smaller in value, on the increase of TPW, LVMI, iLVMI. The obtained data confirm the modern concept of the most prognostic value of the nocturnal blood pressure level as a predictor of adverse cardiovascular events, including fatal ones [10].
Table 3 - Relationship of LVH parameters with average levels of sBP and dBP in different periods of the day according to APDM data Correlation coefficient, r
|
EDS |
EDV |
TIVS |
TPW |
LVMI |
iLVMI |
iLVMI , |
||
|
1 gr., АА (n=18) |
||||||||
|
sBPd |
-0,04 |
-0,04 |
0,26 |
0,15 |
0,20 |
0,24 |
0,17 |
|
|
sBP n |
0,15 |
0,15 |
0,47* |
0,06 |
0,36* |
0,35* |
0,38 |
|
|
dBPd |
0,21 |
0,21 |
0,13 |
0,15 |
0,25 |
0,25 |
0,16 |
|
|
dBP n |
0,16 |
0,16 |
0,29 |
-0,02 |
0,23 |
0,18 |
0,11 |
|
|
2 gr., АС (n=12) |
||||||||
|
sBP d |
0,16 |
0,16 |
0,28 |
-0,13 |
0,29 |
0,45 |
0,31 |
|
|
sBP n |
-0,12 |
-0,12 |
0,35 |
-0,22 |
0,09 |
0,27 |
0,25 |
|
|
dBP d |
-0,05 |
-0,05 |
0,01 |
-0,25 |
0,03 |
0,06 |
-0,15 |
|
|
dBP n |
-0,02 |
-0,02 |
0,36 |
0,36 |
-0,04 |
0,07 |
0,00 |
|
|
3 gr., СС (n=6) |
||||||||
|
sBP d |
0,43 |
0,43 |
-0,31 |
0,83* |
0,60 |
0,60 |
0,54 |
|
|
sBP n |
0,89* |
0,89* |
0,09 |
0,89* |
0,89* |
0,89* |
0,77 |
|
|
dBP„ |
0,77 |
0,77 |
-0,09 |
0,94* |
0,94* |
0,94* |
0,83* |
|
|
dBP n |
0,89* |
0,89* |
0,09 |
0,68 |
0,83* |
0,83* |
0,77 |
Notes: r - correlation coefficient; * - p<0.05.
The study demonstrates a different type of hypertension in patients who have undergone MI, taking into account the AA11SS polymorphism of the AGTR1 gene. The obtained data on the adverse course of hypertension in patients with homozygous genotypes and the tendency to develop HF in patients with the CC genotype of the AGTR1 gene are confirmed in the literature. Although, in general, the literature data regarding the study of AA11CC polymorphism of the AGTR1 gene are heterogeneous, which is probably related to the design of studies, heterogeneity of groups, environmental factors, or, more importantly, may be related to the special genetic structure of the studied population [8]. Nevertheless, we believe that determining AA11CC polymorphism of the AGTR1 gene may help predict clinical outcomes and find personalized treatment regimens.
arterial hypertension infarction patient
Conclusions
The results of the study demonstrate the need for daily monitoring of blood pressure in patients with arterial hypertension who have suffered a myocardial infarction and are patients with a very high cardiovascular risk to establish the actual level and all fluctuations of blood pressure during the day with the determination of the effectiveness of treatment.
During dynamic observation repeated echocardiography in patients who have suffered a myocardial infarction is mandatory to establish the degree of left ventricular hypertrophy and its reversal against the background of antihypertensive therapy.
Determination of the AA11SS polymorphism of the angiotensin II type 1 receptor gene in patients with arterial hypertension after a myocardial infarction made it possible to establish the features of the course of the disease. At a comparable level of office blood pres-sure, patients with the CC genotype of the angiotensin II receptor type 1 gene showed the highest mean nocturnal blood pressure level, which was associated with the highest values of left ventricular remodeling parameters.
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