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EFFECT OF THE DECREASE IN ACTIVITY OF RHEUMATOID ARTHRITIS IN PATIENTS WITH COMBINED PATHOLOGY ON THE STRUCTURAL AND FUNCTIONAL PARAMETERS OF THE HEART: RESISTANT HYPERTENSION AND RHEUMATOID ARTHRITIS
Stakhova A.,
PhD, assistant ofprofessor of the Department of Propaedeutics of Internal Medicine №2 of the National
Bogomolets Medical University, Kyiv, Ukraine
Kondratiuk V.
Professor, Head of the Department of Propaedeutics ofInternal Medicine №2 of the National Bogomolets
Medical University, Kyiv, Ukraine DOI: 10.5281/zenodo.7401732
Abstract
The aim of our study was to determine the effect of the decrease in the activity of rheumatoid arthritis (RA) in patients with combination of RA and resistant hypertension (RH) on structural and functional features of the heart after 12-month therapy, including angiotensin-converting enzyme inhibitor, calcium channel blocker, diuretic, spironolactone, statin, and immunosuppressant (methotrexate).
Materials and methods. We examined 60 patients (mean age, 67.0 ± 8.0 years; 52% of them were women) with RA in combination with RH after 12 month of treatment (angiotensin-converting enzyme inhibitor, calcium channel blocker, diuretic, spironolactone, statin, and methotrexate), who were divided into two groups: A - reached the target value of low laboratory activity of RA (C-reactive protein (CRP) <5.0 mmol/l) (n=27), B - did not reach (n=33). Office blood pressure (BP) measurements, 24-Hour Ambulatory Blood Pressure Monitoring (ABPM) and Doppler echocardiography with the measurement of myocardial mass index of the left ventricle (LVMMI), index of dilatation of LV (end-diastolic volume (EDV)\ body surface area (BSA)), left atrial volume index (LAVI) for the evaluation of the LV structure and maximum velocity of early (peak E, cm/sec) and late (peak A, cm/sec) diastolic filling, early diastolic myocardial velocity in the region of the lateral and mitral leaflets of the mitral annulus (e' lat and e' med respectively, cm/sec) using tissue Doppler for the assessment of LV diastolic dysfunction (DD) were performed before and after 12 months of therapy.
The results. After the decrease in RA activity, BP control was determined as more pronounced: in group A, the levels of office systolic (SBP), diastolic (DBP), and pulse (PBP) decreased by 15.0 mm Hg, 7.5 mm Hg and 10.0 mm Hg, respectively (all p<0.01) against a decreased only in SBP by 10.0 mm Hg (p<0.05) in group B. Similar results were obtained according to ABPM: in group A, average 24h, day and night SBP, DBP and PBP decreased (average 24h SBP by 13.7 mm Hg, DBP by 9.7 mm Hg, PBP at 7.7 mm Hg, average day SBP by 10.5 mm Hg, DBP by 5.8 mm Hg, PBP at 6.6 mm Hg, average night SBP by 19.2 mm Hg, DBP by 7.0 mm Hg, PBP by 9.1 mm Hg (all p<0.05)) versus a less significant decrease in group B. After the analysis of the structural and functional state of the heart, it was determined that in group A the degree of left atrium and left ventricle dilatation decreased (LAVI decreased by 5.8 ml/m2, and EDV/BSA decreased by 4.7 ml/m2, both p<0.05) and LV hypertrophy (LVH) (decreased of LVMMI by 15.1 g/m2, p<0.05) in the absence of positive dynamics in group B. After 12 months of treatment in group A, an improvement in diastolic dysfunction (DD) was also determined (E/A increased by 0.17, E' by 1.9 cm/sec and E/E' decreased by 0.69 (all p<0.05)).
Conclusions. To improve the effectiveness of antihypertensive therapy and more pronounced regression of hypertensive changes of the heart, patients with RH in combination with RA should seek the reduction of the clinical and laboratory activity of RA or reach the target DAS 28-CRP <3.2.
Keywords: resistant hypertension, rheumatoid arthritis, DAS28-CRP.
Introduction. The impact of arterial hypertension (H) on the state of health in the general population remains significant and was studied insufficiently. The contribution of concomitant pathology into the development and progression of H still attracts the attention of many researchers all over the world. Autoimmune diseases, in particular rheumatoid arthritis (RA), play an important role in the progression of many extra-articular manifestations, that include cardiovascular (CV) events. Even in the absence of concomitant CV pathology, RA patients have a significant increase in CV risk
that could reach 51%. Additionally, the risk of the development of ischemic heart events among them is comparable to that in diabetes [5]. Treatment of patients with H remains a difficult issue in cardiology. Furthermore, patients with RA are twice as likely to have H (in 49.4% of people, before the study H was not diagnosed among them), characterized by poorer control and frequent combination with resistant hypertension (RH) [24]. According to recent data, only half of patients with H in the general population could reach the target blood pressure (BP) levels [13]. However, only 42% of
patients with RA achieved the target BP level [24]. There are no data on the dynamics of lowering BP and regression of left ventricular (LV) hypertrophy (LVH) along with the reverse development of diastolic dysfunction (DD) depending on the improvement of clinical and laboratory activity of RA in patients with combined pathology.
In patients with H, changes in the geometry of the LV, such as eccentric or concentric hypertrophy, are closely related to the risk of developing negative CV events [17]. In patients with RA, LV remodeling and negative CV events develop earlier, even with normal levels of BP and lipids [9]. It was determined that the presence of RA could be an independent factor for increasing the risk of developing LVH, primarily severe LVH, and high levels of CRP and anti-CCP determine the development of adverse CV events in the future (hazard ratio (HR) for LVH 3.28, 95% CI 1.03-9 .20, p = 0.03) [9].
LV DD includes mechanical and structural abnormalities, such as hypertrophy or interstitial fibrosis, impaired myocyte relaxation due to ischemia, reduced dis-tensibility, and weakened LV diastolic filling [22]. LV DD could be precursors to heart failure (HF). In patients with RA, compared to those who do not suffer from either RA or any CV disease, LV DD can be determined without the manifests of HF [14, 19]. The prevalence of LV DD varies from 31 to 37%, which was determined according to the 2009 American Society of Echocardiography and European Association of Cardiovascular Imaging (ASE/EACVI) criteria in patients with RA [12, 16]. It another study, among 319 patients (average age 58 years, 78 % of women, low activity, without known CV diseases) the frequency of LV DD was 24% [20]. It should be noted that the 2016 ASE/EACVI criteria are not widely used so far and the assessment of LV DD was carried out using E/A [11, 21]. It should be noted, that people with RA are more prone to the development of LV dilatation and increased systolic pressure in the pulmonary artery [4, 23]. Moreover, not all of the investigators agree on the high prevalence of LV DD among patients with RA. In the study that included 60 patients with RA (average age 50 ±10.2, 91.7% women, average DAS28-CRP 2.9 ± 0.9) LV DD was not determined. Thus, the modern analysis of tissue Doppler echocardiography data of a wide sample of patients with RA with high activity and the presence of concomitant pathologies is relevant and may allow obtaining new data.
Materials and methods. We analyzed 570 medical documents such as ambulatory patient cards and medical history). We selected patients who were available according to the inclusion criteria and were able to give their informed consent; possible causes of secondary H were excluded in our study. Firstly, 101 patients with RA and H were chosen to the study. All of them underwent at the screening visit dose correction of their disease-modifying drug for RA (15 mg/week of methotrexate) as well as dose adjustment and, if it was necessary, the inclusion of additional antihypertensive drug for H (all patients with H took angiotensin-con-verting enzyme inhibitor, calcium channel blocker, di-
uretics, and statin). In 1 month period, basic assessments were made in patients who, on the triple antihy-pertensive therapy with drugs in maximal and submaximal doses, did not reach the target BP levels and met the criteria of RH (25 mg of spironolactone was added), 60 patients were selected (mean age, 67.0 ± 8.0 years; 52% of them were women).
The plan of diagnosis and treatment of RA was determined in concordance with the latest updates of EULAR 2019 [8]. The diagnosis of H was distinguished according to the 2018 ESC/ESH recommendations on H. Patients were evaluated according to their attainment of the target office BP levels within the level of SBP less than 140 mm Hg and/or DBP less than 90 mm Hg. The target value of ambulatory blood pressure monitoring (ABPM) SBP less than 130 mm Hg and/or DBP less than 80 mm Hg were included [10, 12]. RH was recognized as uncontrolled when patients did not reach the target values despite optimal doses of 3 classes of antihypertensive drugs, including a thiazide diuretic, or when 4 or more antihypertensive drugs of different classes were needed for adequate BP control [3, 15].
Research design. A parallel-group, prospective, randomized study including 60 patients with RA and RH and the left ventricular ejection fraction 40% or greater.
Inclusion criteria: age 45-74 years, patients with stage II RH and RA, receiving disease-modifying therapy - methotrexate, chronic kidney disease (CKD) not higher than stage II (GFR not less than 60 ml/min/1.73 m2), K + serum level from 3.0 to 5.0 mmol/l, informed consent to participate in the study.
All patients were assessed by clinical, laboratory, and instrumental methods of examination. Complete blood count, blood glucose, lipid profile, K+, Na+, Cl, creatinine, AST, bilirubin, total protein, C-reactive protein (CRP), urinalysis, and electrocardiography (ECG) were performed.
Office BP measurement were performed for all patients. 24-hour ABPM was performed using ABPM50 (Heaco, Great Britain) to assess BP levels. SBP, DBP, and PBP were determined. Doppler echocardiography was fulfilled on Arietta S60 (Aloka-Hitachi) with the help of 2.5 - 3.5 MHz transducer. The next parameters of the heart geometry were determined: left atrial volume (LAV), left atrial volume index (LAVI) using the formula: LAVI= LAV /BSA (where BSA is the body surface area and is calculated with help of the modified Dubois-Dubois formula (BSA = 0,007184 * Weight (kg) 0,425 * Height (cm) 0,725), the thickness of an interventricular septum of LV (IVS), a posterior wall of LV (PW), LV end-diastolic dimension (LVEDD), LV end-systolic dimension (LVESD), LV end-diastolic volume (LVEDV), LV end-systolic volume (LVESV), and LV stroke volume (LVSV). LV mass (LVM) was calculated with the help of R. Devereux modified formula: LVM = 0.8 * (1.04 * (LVEDD + IVS + PW)3-LVEDD3))) + 0.6, LVM index (LVMI) in accordance with the formula: LVMI = LVM/ BSA, relative wall thickness (RWT) in accordance with the formula: RWT= 2 * PW / LVEDD, LV fractional shortening
(FS), LV midwall fractional shortening (mFS), and LV chamber dilatation (LVEDV/BSA).
The types of LV geometry were evaluated based on the next parameters of RWT, LVMI and LVEDV/ BSA: concentric LV hypertrophy (LVH) with dilatation (LVMI >115 g/m2 in men and >95 g/m2 in women, RWT>0.42, LVEDV /BSA >74 ml/m2 in men, LVEDV /BSA > 68 ml/m2 in women); concentric LVH without dilatation (LVMI >115 g/m2 in men and >95 g/m2 in women, LVEDV /BSA <74 ml/m2 in men, RWT >0.42, LVEDV /BSA <68 ml/m2 in women); eccentric LVH with dilatation (LVMI >115 g/m2 in men and >95 g/m2 in women, RWT <0.42, LVEDV /BSA >74 ml/m2 in men, LVEDV /BSA >68 ml/m2 in women); eccentric LVH without dilatation (LVMI >115 g/m2 in men and >95 g/m2 in women, RWT<0.42, LVEDV /BSA <74 ml/m2 in men, LVEDV /BSA <68 ml/m2 in women); normal LV geometry (LVMI <115 g/m2 in men and <95 g/m2 in women, RWT <0.42, LVEDV /BSA <74 ml/m2 in men, LVEDV /BSA <68 ml/m2 in women) [6].
Clinical characteristics of patients
LV diastolic dysfunction (LV DD) was estimated from the apical 4-chamber position after the assessment of transmitral blood flow on the mitral and tricuspid valves, respectively with the help of pulsed-wave Doppler and Continuous-Wave Doppler. Mitral peak early diastolic filling velocity (peak E, cm sec) and mitral peak late diastolic filling velocity (peak A, cm/sec), the ratio of early to late diastolic filling velocity (E/A) were measured. Early diastolic mitral annular velocity at the lateral and medial parts (e 'lat and e' med, respectively, cm/sec) were obtained via tissue Doppler-imaging to fully assess DD.
The groups of patients were comparable in age, sex, duration of RA and H, RA activity by CRP level and DAS28-CRP scale (high disease activity in both cases), Steinbrocker radiological stage, stage of functional impairment (FI), smoking status, the usage of nonsteroidal anti-inflammatory drugs (NSAIDs) and glucocorticosteroids (GCs) at the beginning of the study. See tablel for more details.
Table 1
with RH in combination with RA
Group A (n=27) Group B (n=33)
Mean Age, years, M ± c 62.8 ± 7.3 61.4 ± 8.2
Gender (female), n (%) 20 (74.1) 24 (72.7)
Seropositive RA, n (%) 24 (88.8) 26 (78.8)
DAS28-CRP, M ± c 5.7 ± 1.5 5.6 ± 1.4
X-ray stage II, n (%) 8 (29.6) 7 (21.2)
X-ray stage III, n (%) 13 (48.1) 15 (45.5)
X-ray stage IV, n (%) 6 (22.2) 11 (33.3)
FI stage I, n (%) 7 (25.9) 7 (21.2)
FI stage II, n (%) 17 (63.0) 18 (54.5)
FI stage III, n (%) 30 (11.1) 5 (15.2)
NSAIDs, n (%) 23 (85.2) 25 (75.8)
GCs, n (%) 9 (33.3) 10 (30.3)
RA duration, years, M ± c 9.2 ±5.2 8.9 ± 6.4
H duration, years, M ± c 10.3 ± 7.4 11.0 ± 7.1
I stage of H, n (%) 24 (88.9) 27 (81.8)
II stage of H, n (%) 3 (11.1) 6 (18.2)
Smoking status, n (%) 6 (22.2) 8 (24.2)
Statistical processing of the obtained results was performed via Statistics SPSS 22. WE used the Shapiro-Wilk test for the assessement of the distributions normality. Parametric statistical methods were used in cases of normal distribution of the samples. For descriptive statistics we used the mean value (M), standard deviation (c), standard error (SE), and 95% confidence interval for the mean (95% CI). The median (Me), 25 and 75 quartiles (Q25 - Q75) were chosen for the descriptive part of the study. For categorical part variables were expressed as a percentage (%). To compare two independent groups the Mann-Whitney U-test was used. Pearson's chi-squared (x2) test (corrected by Yates) and Fisher's exact test were used for a comparison of groups on qualitative binary data.
Results. Prior to inclusion in the study, the groups were comparable in terms of BP. The target level of office BP was achieved in 24 (88.9%) patients versus 15 (45.5%) patients (x2 = 11.3, p <0.001) in the group of
12-month antihypertensive therapy and CRP decline to the level of <5.0 mmol/l compared with the CRP >5.0 mmol/l After the decrease in RA activity, the improvement in BP control is more pronounced: in group A, the levels of office SBP, DBP, and PBP decrease by 15.0 mm Hg, 7.5 mm Hg, and by 10.0 mm Hg (all p<0.01) respectively, in comparison to a decrease in SBP by 10.0 mm Hg (p<0.05) in group B (Table 2). According to the results of ABPM, identical results were obtained: in group A, average 24h, day and night SBP, SBP and PBP decreased (average 24h SBP by 13.7 mm Hg, DBP by 9.7 mm Hg, PBP by 7.7 mm Hg; average day SBP by 10.5 mm Hg, DBP by 5.8 mm Hg, PBP by 6.6 mm Hg; average night SBP by 19.2 mm Hg, DBP by 7.0 mm Hg, PBP by 9.1 mm Hg (all p<0.05)) against a less significant decrease in group B. Under conditions of CRP level <5.0 mmol/l after 12 months, nocturnal BP fall for SBP and DBP increase by 8.2% and 8.8%, respectively (Table 2).
Table 2
Blood pressure in patients depending on the laboratory activity of RA, Me (25% - 75%)_
Group A (n=27) Group B (n=33)
Start of research After 12 months Start of research After 12 months
Office SBP, mm Hg 140.0 (140.0-150.0) 125.0 (120.0-135.0)**# 140.0 (140.0-146.3) 130.0 (125.0-135.0)*
Office DBP, mm Hg 80.0 (80.0-90.0) 72.5 (70.0-80.0)**# 80.0 (70.0-90.0) 80.0 (70.0-80.0)
Office PBP, mm Hg 60.0 (50.0-60.0) 50.0 (48.8-55.0)**# 57.5 (50.0-61.3) 52.0 (50.0-56.3)
24h SBP by ABPM, mm Hg 140.4 (134.4-143.1) 126.7 (120.8-130.4)**# 141.4 (138.6-145.9) 131.6 (125.4-135.4)*
24h DBP by ABPM, mm Hg 83.9 (77.6-85.3) 74.2(70.6-76.7)**# 84.4 (80.7-89.6) 78.8 (70.7-82.6)
24h PBP by ABPM, mm Hg 56.1 (47.8-61.2) 48.4 (46.2-59.7)**# 55.7 (49.2-59.5) 55.5 (48.1-61.6)
Day SBP by ABPM, mm Hg 138.3 (131.9-145.0) 127.8 (124.5-134.0)**# 139.0 (131.4-146.2) 130.4 (125.7-139.8)*
Day DBP by ABPM, mm Hg 77.3 (73.9-86.6) 71.5 (70.5-84.5)*# 78.4 (67.1-87.7) 76.4 (64.9-85.4)
Day PBP by ABPM, mm Hg 57.0 (48.7-61.4) 50.4 (46.8-57.8)**# 55.5 (48.1-59.4) 53.8 (47.8-62.1)
Night SBP by ABPM, mm Hg 143.8 (133.7-154.6) 124.6 (114.8-132.1)**# 145.8 (125.7-157.8) 132.5 (130.1-148.7)*
Night DBP by ABPM, mm Hg 85.4 (71.5-89.7) 78.4 (75.4-80.2)**# 86.7 (72.5-91.2) 80.4 (70.4-87.4)
Night PBP by ABPM, mm Hg 55.5 (46.2-64.1) 46.4 (44.5-60.7)**# 55.7 (47.6-68.0) 53.1 (46.5-68.7)
Nocturnal SBP fall, % 4.5(-2.8-13.8) 12.7 (7.4-25.4)**# 5.2(-3.2-12.8) 11.4 (6.4-19.8)
Nocturnal DBP fall, % 9.9 (4.2-18.7) 18.7(10.4-25.4)**# 9.8 (3.2-17.4) 13.4 (9.8-18.7)
Notes: ** - P < 0.01, compared to the values of indicators before treatment, # - P < 0.05, in group A compared to the values of group B.
It was found out, that high RA activity determines the development of LV dilatation (r=0.32, p<0.05), which corresponds to previously obtained data [18], and Night-peackers have a higher risk of developing severe LVH (r=0.38, p<0.05) [1]. At the time of inclusion in the study in groups A and B, LVH was detected in 25 (92.6%) and 28 (87.9%) patients, respectively. Severe LVH was dominated in the structure of LVH in both groups (Table 3). The frequency of LVH detection declined by 11.2% (x2 = 4.5, p = 0.037) in patients of
Table 3
Distribution in patients depending on the laboratory activity of RA, according to the stage of LVH and the
group A due to a 1.5-fold reduction in the frequency of detection of severe LVH. The most common was eccentric LVH with LV dilatation in group A before the treatment, which indicated a worse prognosis for patients with the development of HF [2, 7]. The frequency of it reduced by 1.5 times after 12 months of therapy. A number of patients with concentric LVH with LV dilatation diminished by 1.5 times. Statistically non-reliable changes were observed in group B (Table 3).
Group A (n=27) Group B (n=33)
Start of research After 12 months Start of research After treatment
Mild LVH, n (%) 1 (3.7%) 2 (7.4%) 1 (3.0%) 2 (6.1%)
Moderate LVH, n (%) 2 (7.4%) 5 (18.5%)*** 4 (12.1%) 3 (9.1%)
Severe LVH, n (%) 22 (81.5%) 15 (55.5%)*** 24 (72,7%) 25 (75.8%)
No LVH, n (%) 2 (7.4%) 5 (18.6%)** 4 (12.1%) 3 (9.1%)
Eccentric LVH with dilatation, n (%) 12 (44.4%) 8 (29.6%)** 10 (30.3%) 9 (27.3%)
Concentric LVH without dilatation, n (%) 7 (26.0 %) 6 (22.2%) 9 (27.3%) 11 (33.3%)
Concentric LVH with dilatation, n (%) 3 (11.1 %) 2 (7.4%)** 5 (15.2%) 4 (12.1%)
Eccentric LVH without dilatation, n (%) 3 (11.1%) 5 (18.6%) 5 (15.2%) 5 (15.2%)
Notes: * - P <0,05, ** - P <0,01, *** - P <0,001 in comparison with values of data before treatment.
When analyzing the structural state of the myocardium, we determined that in group A, the degrees of LA and LV dilatation decrease (LAVI decreases by 5.8 ml/m2, and EDV/BSA by 4.7 ml/m2, both p<0.05) and LVH (decrease of LVMM and LVMI by 58 g and 15.1 g/m2 by reducing IVS by 0.5 mm, all p<0.05) with no changes of LV PW in the absence of positive dynamics
Table 4
Indicators of the structural state of the heart in patients of experimental groups depending on the labora-
in group B. The values of the LV contractile were within the reference range in patients of both groups. However, the data that reflects the regional contractility (FS and mFS) were likely to increase by 10.4% and 10.2%, respectively, and the global LV contractility (EF) - by 9.9 % (all p <0, 01) (Table 4).
Group A (n=27) Group B (n=33)
Start of research After 12 months Start of research After 12 months
LAVI, ml/m2 35.6 29.8 35.1 38.5
(28.8-42.7) (24.2-35.3)**## (33.2-50.7) (29.5-53.7)
IVS, mm 11.0 10.5 11.0 11.5
(10.0-12.0) (9.8-12.0)*# (10.6-13.0) (10.0-12.0)
LV PW, mm 10.0 10.0 11.0 11.0
(9.0-11.0) (9.0-11.0)# (10.0-12.0) (10.0-12.0)
LV MM, g 263.0 205.0 262.5 252.5
(191.0-306.0) (175,0-265.0)*## (207.7-178.5) (227.5-281.5)*
LV MI, g/m2 124.1 (105.5-147.9) 109.1 (100.0-138.5)*# 124.9 (113.1-161.8) 134.0 (120.1-157.7)*
LVEDV/BSA, 66.7 62.0 68.7 69.6
ml / m2 (55.0-76.1) (51.5-71.0)*# (59.2-77.4) (60.4-84.7)
FS, % 28.8 39.2 30.5 33.5
(27.5-35.2) (32.8-40.1)** (27.9-35.4) (28.7-35.4)
mFS, % 15.2 25.4 16.7 18.4
(14.2-21.7) (18.9-28.2)** (12.7-21.5) (13.1-21.9)
LV EF, % 57.5 67.4 60.3 61.5
(56.1-63.8) (61.5-69.9)** (54.9-65.4) (55.8-66.9)
Notes: * - P < 0.05, ** - P < 0.01, compared to the values of indicators before treatment, # - P < 0.05, ## - P < 0.01 in group A compared to the values of group B.
When analyzing the functional state of the heart under conditions of achieving a CRP level of <5.0 mmol/l after 12 months of treatment, there was an increase in peak E and the ratio of E / A by 12.2 cm / sec and 0.17, respectively (both p <0,01), a drop in peak A, the value of DT, and TR by 12.3 cm / sec, 30.7 msec, and 0.4 cm / sec respectively (all p <0.01). Significant
Table 5
The functional state of the heart in patients depending on the laboratory activity of RA, Me (25% - 75%)
positive changes in LV relaxation function after the decrease of RA activity in group A were confirmed and characterized by an increasing in e' med, e' lat and E' by 2,4 cm/sec, 1.4 and 1.9 cm/sec, respectively (all p <0.05), and decreasing E / e' med, E / e' lat and E / E' by 0.6, 0.8 and 0.7, respectively (all p <0,05) (Table 4).
Group A (n=27) Group B (n=33)
Start of research After 12 months Start of research After 12 months
LV E, cm / sec 63.7 (52.8-77.2) 76.2 (64.7-87.4)** 65.4 (53.8-79.5) 68.2 (55.9-73.8)
LV A, cm / sec 79.8 (65.2-97.3) 67.5 (62.5-85.2)** 78.5 (64.8-83.7) 74.8 (65.4-87.4)
LV E/A 0.81 (0.71-1.08) 0.98 (0.82-1.15)* # 0.82 (0.71-1.19) 0.87 (0.67-1.16)
LV DT, msec 194.7 (160.0-240.0) 164.0 (136.0-180.0)** 186.4 (160.0-220.0) 183.6 (145.0-240.0)
LV IVRT, msec TR, cm / sec 92.6 (84.0-110.0) 90.7 (84.0-88.0) 89.8 (75.5-100.0) 88.0 (84.0-94.0)
TR, cm / sec 2,6 (2,4-3,2) 2,2 (2,0-2,6)** 2,4 (2,2-3,0) 2,5 (2,3-3,0)
e' med, cm / sec 9.1 (8.0-11.0) 11.5 (9.5-13.5)** 9.3 (7.5-10.9) 9.5 (7.8-10.0)
e' lat, cm / sec 9.5 (8.4-11.1) 10.9 (9.9-13.9)* 9.5 (7.6-10.7) 9.6 (8.3-10.8)
E', cm/sec 9.3 (8.5-10.3) 11.2 (8.2-12.1)* # 9.2 (8.3-10.7) 9.6 (8.8-12.5)
E/ e' med 7.2 (5.4-8.7) 6.6 (4.9-7.8)* 7.0 (6.3-8.5) 7.2 (5.2-8.5)
E/e' lat 7.6 (5.2-8.9) 7.0 (5.7-7.8)* 7.6 (6.0-8.7) 7.8 (5.1-9.4)
E/E' 7.0 (6.03-8.49) 6.3 (5.6-7.6)* # 6.8 (6.1-8.1) 6.8 (5.7-8.5)
Notes: * - P < 0.05, ** - P < 0.01, compared to the values of indicators before treatment, # - P < 0.05, in group A compared to the values of group B.
Conclusions. Thus, in patients with resistant hy- reaching laboratory remission of rheumatoid arthritis pertension in combination with rheumatoid arthritis, enhances the antihypertensive effect of the drugs,
which is manifested by more frequent achievement of target blood pressure levels according to data from both office measurement and daily monitoring of blood pressure. It also provides a powerful antihypertrophic and remodulating effect, which is combined with the improvement of both systolic and diastolic functions of the left ventricle.
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