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Cardiac hypotrophy in young women with low blood pressure.

Introduction

Nowadays low systolic blood pressure (LSBP) is considered to be a risk factor for cardiovascular complications and impairs quality of life. However LSBP still remains a largely unexplored problem [1]. In young women LSBP occurs in 7.2% of cases [2]. Up to 70% of women with LSBP complain of any health disorder, while 43% of women complain of pain in the heart, and 30% have low physical activity tolerance [3,4]. However, the results of echocardiographic studies of the heart in patients with LSBP are contradictory and don't give a true picture about an organic or functional nature of cardiovascular complaints in women with LSBP. They also hinder an effective patient care.

The purpose of the research is to evaluate the cardiac structure and function in young women with LSBP.

Materials and Methods

The object of the research is young women with LSBP, the subject of the research is structural and functional cardiac parameters, and the type of the study is cross-sectional. LSBP is defined as systolic blood pressure (SBP) equal to 99 mmHg or less [5-7]. Normal SBP was defined as SBP in the range of 120-129 mmHg [1]. The study didn't enroll women with the presence of anemia, dysplasia of connective tissue, cancer, diabetes, hypothyroidism, adrenal insufficiency, collagenoses, congenital heart and blood vessels diseases, cardiac surgery in past, any term of pregnancy, drug abuse, and acute infectious diseases at the moment of the study. Exclusions from the study were carried out on the basis of analysis of medical records and interviews. The study was conducted during an examination of university students before admission to sporting activities. Site of the medical examination is outpatient department with a time of the examination from 15 to 19 hours. We examined 1,264 women aged from 18 to 35 years, divided into 2 groups: a test group with LSBP (N = 69) and control one with normal systolic blood pressure (N = 35 subjects) (Table 1).

The blood pressure was measured after 5 min rest, twice, on the right shoulder in the sitting position, with the forearm on the table and an interval of 3 minutes. A&D UA-777 tonometer was used (AGD Company Ltd., Japan, 2012). Based on the obtained results, the mean value of the two measurements was calculated. Echocardiography was performed at rest using En Vizor CHD device (Philips, 2009). The following parameters were monitored in order to assess cardiac hemodynamics: morphometry of anatomical structures of the heart, Doppler ultrasound to measure the blood flow and functional parameters of the heart.

Ethical issues

The protocol of the study on volunteers conformed to the Helsinki Declaration of 1975 as revised (59th WMA General Assembly, Seoul, Republic of Korea, October 2008). Plan and design of the study were approved by the Ethics Committee of the Academy (protocol number 74). Persons admitted to the survey, gave a written informed consent to participate in this study. Statistical analysis was performed using the software "Statistica 6.1" (serial number AXXR912E53722FA, StatSoft-Russia, 2009). Distribution of variation rows wasn't symmetrical (H. Lilliefors criterion, at p < 0.05). Comparing of the two groups was performed using Mann-Whitney U-test [8].

Results

There was an increase in the size of aorta (Ao), and reduction in dimensions of right ventricle (RV) and left ventricle end-diastolic dimension (LVEDD) in the test group. It was also observed an increase in thickness of the interventricular septum (TIVS), thickness of the left ventricular posterior wall (TLVPW) in systole and diastole in the test group (Table 2).

Analysis of the functional echocardiographic parameters revealed some increased parameters in test group than that in the control group: fractional shortening (FS), ejection fraction (EF), left ventricular myocardial mass (LVMM), left ventricle diastolic function--maximum early peak velocity (peak E) (LVDF-[V.sub.e]), maximum early peak velocity (peak E)/maximum later peak velocity (peak A) ([V.sub.e]/[V.sub.a]), maximum blood flow velocity-mitral valve ([V.sub.max]-MV) (Table 3). The following parameters were below the level in the control group: left ventricle end-systolic volume (LVESV), left ventricle end-diastolic volume (LVEDV), stroke volume (SV), cardiac output (Q), stroke volume index (SVI), left ventricle end-diastolic volume/left ventricular myocardial mass (LVEDV/LVMM), stroke index (SI), left ventricle diastolic function--maximum later peak velocity (peak A) (LVDF-[V.sub.a]), maximum blood flow velocity--aortic valve ([V.sub.max]-AoV), gradient (difference) of blood pressure--mitral valve ([Pg.sub.max]-MV), gradient (difference) of blood pressure--aortic valve ([Pg.sub.max]--AoV), and gradient (difference) of blood pressure - pulmonary valve ([Pg.sub.max]-PuV).

Conclusion

Previously performed studies have shown that LSBP is accompanied by changes in the structure and function of the heart. Poznyakova revealed increased sizes of the aorta base in 10.6% of cases among 81 patients with blood pressure below 100/65 mmHg aged from 16 to 35 years [9]. The study performed by Atayan showed reduced values of left atrium (LA), left ventricle (LV), LVEDV, and LVESV at the level of blood pressure below 105-100/65-60 mmHg. The last study involved 65 men and women of middle age-about 42 years [10]. There was an increase of SVI caused by an increase in the LVEF and the heart rate. Tyurina also shows the reduced size of heart and myocardial mass, the diameter of the aorta and its branches in patients with LSB based on the study of 240 people with primary arterial hypotension with a mean age of 53 years. The author relates an intensity of the structural changes to the minimum level of blood pressure [11]. Belova revealed the presence of diastolic dysfunction, later filling of the left ventricle and increased isovolumic relaxation period revealed in 120 young persons with LSBP [12].

In our study we revealed that women with LSBP had a lower body weight compared with women of the same age and normal blood pressure. Low body weight by itself is associated with hemodynamic changes and signs of cardiac hypotrophy. Romano et al. showed that the weight loss can cause cardiac hypotrophy accompanied by a decrease in hemodynamics parameters. Echocardiographic parameters of 91 women with an average age of 20 years and the body mass index of 15.6 kg/[m.sup.2] were compared with such parameters of 62 women with an average age of 22 years and the body mass index of 22.5 kg/[m.sup.2] [13]. The following findings were revealed in women with low body weight:

1. Lower left ventricular myocardial mass with systolic dysfunction.

2. Smaller dimensions of the left ventricle.

3. Thinner walls of the left ventricle.

4. Considerable decrease in ejection fraction, heart rate, stroke volume and cardiac output.

5. Increase in peripheral resistance.

The results of our study showed some differences from the previously received echocardiography data in patients with LSBP:

a) Besides the already known structural features (Ao dilatation and reduced dimensions of RV, LVEDD), we showed an increase in TIVS and TLVPW in systole and diastole, as well as an increase in the left ventricular myocardial mass;

b) As well as in the previous studies it was shown that LVEF value was increased, however the values of SVI, SI, Q, and LVSV were reduced while LVSF was increased;

c) Slower rate of a blood flow at the level of the mitral and aortic valves;

d) There was a smaller pressure gradient during the passage of blood through the mitral, aortic, and pulmonic valves;

e) Diastolic dysfunction of the left ventricle in the form of growth of [V.sub.e]/[V.sub.a] index is the subject of special attention. In our study this index is significantly higher than that in patients with normal blood pressure, and is close to 2.0.

Luo relates an increase in [V.sub.e]/[V.sub.a] index to the most severe manifestations of isolated diastolic dysfunction in the absence of a compensatory increase in total body fluid due to an increased passive stiffness (restrictive or R-type) [14]. This R-type is manifested by three features, two of which were identified in our study:

1) Increase in the velocity of peak E of the diastolic flow;

2) Decrease in the velocity of peak A of the diastolic flow;

3) An increase in E/A ratio greater than 2.

We assume that structural and functional changes of the heart in young women with LSBP are associated with the signs of cardiac hypotrophy. It is possible that cardiac hypotrophy is a primary nosology, while LSBP develops as a complication of cardiac hypotrophy. Cardiac hypotrophy and atrophy were described previously in induced starvation and malnutrition, including young women [15-18]. A group of scientists from Ireland led by Owens performed 24-hour blood pressure monitoring in 254 bank employees and their families and found that the low weight is the most important independent predictor of low blood pressure. This is especially true for women [19]. The relationship between LSBP and reduced weight is also shown in other studies [7,19-21]. Cardiac hypotrophy is described after a long-term (more than 6 weeks) bed rest in a horizontal position, or after a brief space flight, i.e., in the absence of an adequate physical exercises. Perhonen and colleagues used magnetic resonance imaging (MRI) to measure the mass of the left and right ventricular myocardial mass, end diastolic volume of the left ventricle in 3 healthy men before and after 2-, 6-, and 12-weeks of bed rest in a horizontal position, and in 8 astronauts before and after 10-day space flight. During a bed rest LVMM decreased by 8%, an average TLVPW decreased by 4%, and LVEDV decreased by 14%. After the space flight LVMM decreased by 12% [22]. Dorfman revealed cardiac atrophy in women after 60 days of a bed rest [23]. MRI in 24 healthy women aged 32 years revealed a significant decrease in the volume of the LV (from 96 to 77 ml) before and after 60 days of a bed rest and a decrease in the volume of the RV (from 104 to 86 ml).

We hypothesize that the LSBP is associated with cardiac hypotrophy and hypofunction of the heart on the background of low body weight of a young woman. However the main feature of cardiac hypotrophy (myocardial mass reduction) wasn't found. It's likely that myocardial mass reduction didn't occur due to an increase in TLVPW and TIVS. Additional sign indicating left ventricular remodeling is its isolated diastolic dysfunction. We can also explain an absence of reduction in myocardial mass in our study by an involuntary physical and social activity in a young age, indicating an adequacy of the adaptation period allowing cardiovascular system to adapt to the lower weight and lower blood pressure.

Summary

LSBP in young women is associated not only with the lower body weight, but also with cardiac hypotrophy--reduced sized of the heart chambers, left ventricular remodeling, isolated diastolic dysfunction, and decreased intracardiac hemodynamics.

Abbreviations: Ao: Aorta; AoV: Aortic Valve; DF: Diastolic Function; EDV: End-diastolic Volume; EDD: End-diastolic Dimension; ESV: End-systolic Volume; ESD: End-systolic Dimension; LV: Left Ventricle; LA: Left Atrium; MV: Mitral Valve; LVMM: Left Ventricular Myocardial Mass; Q: Cardiac Output; MRI: Magnetic Resonance Imaging Device; LSBP: Low Systolic Blood Pressure; RV: Right Ventricle; PuV: Pulmonary Valve; SBP: Systolic Blood Pressure; SVI: Stroke Volume Index; TLVPW: Thickness of the Left Ventricular Posterior Wall; TIVS: Thickness of the Interventricular Septum; TrV: Tricuspid Valve; SI: Stroke Index; SV: Stroke Volume; EF: Ejection Fraction; FS: Fractional Shortening; ECHO-CG: Echocardiography; [Pg.sub.max]: Gradient (difference) of Blood Pressure; [V.sub.max]: Maximum Blood Flow Velocity; [V.sub.a]: Maximum Later Peak Velocity (peak A); [V.sub.c]: Maximum Early Peak Velocity (peak E).

References

[1.] Mancia G, De Backer G, Dominiczak A, Cifkova R, Fagard R, et al. (2007) Guidelines for the management of arterial hypertension: the task force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). European Heart Journal 28(12): 1462-1536.

[2.] Kudryavtseva EN (2013) Parameters of the blood pressure in female students. In collection of scientific works of young scientists. Perm, E. A. Vagner Perm State Medical Academy of Health Ministry, p. 59.

[3.] Baev VM, Koryukina IP, Kudryavtseva EN, Koltyrina EN, Kozlov DB (2013) Self-rating of mental status and depression; autonomic nervous system disbalance in young women with low blood pressure. World Journal of Medical Sciences 8(4): 382-386.

[4.] Miwa K, Fujita M (2009) Cardiovascular dysfunction with low cardiac output due to a small heart in patients with chronic fatigue syndrome. Internal Medicine 48(21): 1849-1854.

[5.] Maasova D (1997) Systemic arterial hypotension. In: Pathophysiology, Hulin, Bratislava I (Eds.), 6th Edition, Slovak Academic Press, pp. 169-171.

[6.] Owens PE, O'Brien ET (1996) Hypotension: a forgotten illness? Blood Pressure Monitoring 2(1): 3-14.

[7.] Bengtsson C, Edstrom K, Furunes B, Sigurdsson JA, Tibblin G (1987) Prevalence of subjectively experienced symptoms in a population sample of women with special reference to women with arterial hypertension. Scandinavian Journal of Primary Health Care 5(3): 155-162.

[8.] Glantz SA (1994) Sample of biostatistics. McGraw-Hill Inc., p. 459.

[9.] Poznyakova AV (2009) System analysis of basic hemodynamic and anthropometric parameters in primary arterial hypotension and changes of their relationship under the impact of gutron, author's abstract from thesis of Candidate of Medical Sciences, Orel State University, Orel, p. 21.

[10.] Atayan AS (2011) Idiopathic hypotension: neurological disorders, central cerebral hemodynamics, author's abstract from Ph.D. thesis, Russian Academy of Medical Sciences Research Center of Neurology, Moscow, p. 18.

[11.] Tyurina TV (2003) Hypotensive states: risk factors, target organ lesions, diagnosis and correction techniques, author's abstract from Ph.D. thesis in Medicine, Research Institute of Cardiology named after I.A. Almazov, Ministry of Health of Russia, St. Petersburg, p. 26.

[12.] Belova VV (2005) Clinical and functional characteristics of the initial manifestations of cerebral circulation insufficiency in young adults with idiopathic hypotension, author's abstract from Ph.D. thesis of Candidate of Medical Sciences, Ivanovo State Medical Academy, Ivanovo, p. 23.

[13.] Romano C, Chinali M, Pasanisi F, Greco R, Celentano A, et al. (2003) Reduced hemodynamic load and cardiac hypotrophy in patients with anorexia nervosa. American Journal of Clinical Nutrition 77(2): 308-312.

[14.] Luo C, Ramachandran D, Ware DL, Ma TS, Clark JW Jr. (2011) Modeling left ventricular diastolic dysfunction: classification and key indicators. Theoretical Biology and Medical Modelling 8: 14.

[15.] Gottdiener JS, Gross HA, Henry WL, Borer JS, Ebert MH (1978) Effects of self-induced starvation on cardiac size and function in anorexia nervosa. Circulation 58(3 Pt 1): 425-433.

[16.] Webb JG, Kiess MC, Chan-Yan CC (1986) Malnutrition and the heart. Canadian Medical Association Journal 135(7): 753-758.

[17.] Bloom WL, Azar G, Smith EG Jr. (1966) Changes in heart size and plasma volume during fasting. Metabolism 15(5): 409-413.

[18.] De Simone G, Scalfi L, Galderisi M, Celentano A, Di Biase G, et al. (1994) Cardiac abnormalities in young women with anorexia nervosa. British Heart Journal 71(3): 287-292.

[19.] Owens PE, Lyons SP, O'Brien ET (2000) Arterial hypotension: prevalence of low blood pressure in the general population using ambulatory blood pressure monitoring. Journal of Human Hypertension 14(4): 243-247.

[20.] Pilgrim JA, Stansfield S, Marmot M (1992) Low K blood pressure, low mood? British Medical Journal 304: 75-78.

[21.] Melendez JC, Mayordomo T, Sancho P, Tomas JM (2012) Coping strategies: gender differences and development throughout life span. The Spanish Journal of Psychology, 15(3): 1089-1098.

[22.] Perhonen MA, Franco F, Lane LD, Buckey JC, Blomqvist CG, et al. (2001) Cardiac atrophy after bed rest and spaceflight. Journal of Applied Physiology 91(2): 645-653.

[23.] Dorfman TA, Levine BD, Tillery T, Peshock RM, Hastings JL, et al. (2007) Cardiac atrophy in women following bed rest. Journal of Applied Physiology 103(1): 8-16.

Valery Michaylovich Baev *, Irina Petrovna Koryukina, Elena Nikolaevna Kudryavtseva, Inna Leonidovna Gulyaeva, Dmitry Borisovich Kozlov

Vagner Perm State Medical Academy, Petropavlovskaya Street 26, Perm 614990, Russia.

* Corresponding author: Vagner Perm State Medical Academy, Petropavlovskaya Street 26, Perm 614990, Russia.

Published: 1st July 2014
Table 1: Characteristics of the test and control groups.

Parameters             Median (25-75%)                   P

                        Test group        Control
                         (N = 69)      group (N = 35)

Age (years)             19 (18-20)       19 (18-20)     0.46
Height (cm)            162 (158-165)   164 (158-168)    0.24
Weight (kg)             53 (49-57)       56 (53-61)     0.01
Heart rate              74 (70-81)       76 (72-83)     0.27
  (beats per minute)

Note: p is the significance level.

Table 2: Comparative analysis of structural echocardiographic
parameters in subjects of the test and control groups.

Parameters               Median (25-75%)                         P

                            Test group          Control
                             (N = 69)        group (N = 35)

Ao (mm)                  26.7 (26.0-26.7)   24.3 (24.3-26.0)   0.000
LA (mm)                  29.0 (28.0-30.0)   28.2 (27.0-30.0)   0.094
LVEDD (mm)               44.9 (43.5-45.5)   45.5 (45.0-46.8)   0.012
LVESD (mm)               26.4 (26.0-27.0)   26.9 (25.0-27.9)   0.212
TIVS (diastolic) (mm)     7.6 (7.1-7.6)      7.4 (7.1-10.3)    0.297
TIVS (systolic) (mm)      9.5 (8.7-9.5)      8.7 (8.5-8.7)     0.000
RV (mm)                  18.0 (17.0-18.0)   18.8 (17.4-18.8)   0.038
TLVPW (diastolic) (mm)    7.5 (7.2-7.5)      7.2 (7.1-7.2)     0.000
TLVPW (systolic) (mm)     9.7 (9.0-9.7)      8.4 (8.4-8.8)     0.000

Note: p is the significance level.

Table 3: The results of a comparative analysis of functional
echocardiographic parameters of the test and control groups.

Parameters                Median (25-75%)

                              Test group           Control group
                               (N = 69)              (N = 35)

LVESV ([cm.sup.3])         26.8 (26.8-28.3)      29.9 (28.0-31.9)
LVEDV ([cm.sup.3])         94.3 (85.4-100.0)     99.7 (97.3-104.9)
LVSV ([cm.sup.3])          67.6 (62.0-70.0)      70 (69.00-73.00)
LVSF (%)                   40.9 (39.0-41.0)      39.0 (38.0-39.0)
LVEF (%)                   71.5 (70.0-72.0)       70 (69.0-70.0)
Q ([cm.sup.3]/min)           5.3 (4.7-5.6)         5.6 (5.1-5.9)
SVI (l/min/[m.sup.2])        3.4 (3.1-3.4)         3.6 (3.6-3.7)
LVMM (g)                  107.1 (103.1-111.1)   104.3 (103.0-107.0)
LVEDV/LVMM                 0.89 (0.89-0.95)      0.94 (0.93-0.97)
SI ([cm.sup.3]/            43.3 (40.0-43.3)      44.0 (41.0-46.0)
  [m.sup.2])
LVDF-[V.sub.e] (m/s)       0.94 (0.90-0.94)      0.92 (0.90-0.94)
LVDF-[V.sub.a] (m/s)       0.49 (0.45-0.50)      0.51 (0.48-0.51)
[V.sub.e]/[V.sub.a]        1.97 (1.80-2.04)      1.82 (1.78-1.86)
[V.sub.max]-MV (m/s)        0.9 (0.86-0.92)      0.89 (0.87-0.89)
[V.sub.max]-AoV (m/s)      1.21 (1.12-1.21)      1.28 (1.24-1.31)
[V.sub.max]-PuV (m/s)      0.89 (0.80-0.98)      0.87 (0.87-0.88)
[V.sub.max]-TrV (m/s)      0.55 (0.52-0.56)      0.56 (0.53-0.56)
[Pg.sub.max]-MV (mmHg)     3.18 (2.90-3.30)      3.41 (3.00-3.41)
[Pg.sub.max]-AoV (mmHg)    5.72 (4.90-5.72)      6.94 (6.20-7.30)
[Pg.sub.max]-PuV (mmHg)    2.61 (2.56-2.80)      3.21 (3.10-3.21)
[Pg.sub.max]-TrV (mmHg)    1.15 (1.00-1.20)       1.2 (1.01-1.34)

Parameters                  p

LVESV ([cm.sup.3])        0.001
LVEDV ([cm.sup.3])        0.002
LVSV ([cm.sup.3])         0.005
LVSF (%)                  0.001
LVEF (%)                  0.005
Q ([cm.sup.3]/min)        0.014
SVI (l/min/[m.sup.2])     0.006
LVMM (g)                  0.006
LVEDV/LVMM                0.002
SI ([cm.sup.3]/           0.048
  [m.sup.2])
LVDF-[V.sub.e] (m/s)      0.114
LVDF-[V.sub.a] (m/s)      0.006
[V.sub.e]/[V.sub.a]       0.008
[V.sub.max]-MV (m/s)      0.044
[V.sub.max]-AoV (m/s)     0.001
[V.sub.max]-PuV (m/s)     0.297
[V.sub.max]-TrV (m/s)     0.357
[Pg.sub.max]-MV (mmHg)    0.028
[Pg.sub.max]-AoV (mmHg)   0.000
[Pg.sub.max]-PuV (mmHg)   0.000
[Pg.sub.max]-TrV (mmHg)   0.099

Note: p is the significance level.
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Title Annotation:Research Article
Author:Baev, Valery Michaylovich; Koryukina, Irina Petrovna; Kudryavtseva, Elena Nikolaevna; Gulyaeva, Inna
Publication:Biology and Medicine
Article Type:Report
Geographic Code:4EXRU
Date:Jan 1, 2014
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