|Year : 2015 | Volume
| Issue : 4 | Page : 224-228
Maternal left ventricular systolic and diastolic function during second trimester of pregnancy with preeclampsia
Padmaja Tangeda, Neerja Shastri
Department of Physiology, Prathima Institute of Medical Sciences, Karimnagar, India
|Date of Web Publication||14-Dec-2015|
Department of Physiology, Prathima Institute of Medical Sciences, Karimnagar, Telangana
Source of Support: None, Conflict of Interest: None
Objective: This study was done to assess maternal cardiovascular function using echocardiography in normal and preeclamptic women in the second trimester of pregnancy.
Materials and Methods: This cross-sectional study was conducted at Prathima Institute of Medical Sciences (PIMS), Karimnagar, Telangana, India between February 2012 and October 2013. Doppler echocardiography was performed in 15 normotensive controls (Group I) and 15 pregnant women with hypertension (Group II) at 20-24 weeks of gestation. Baseline characteristics and maternal and fetal outcome were studied with systolic and diastolic parameters on echocardiography.
Results: The following parameters were higher in preeclamptic subjects as compared to normotensive controls: Mean cardiac output (CO) (6642 ± 1508 mL/min vs 5175 ± 1279 mL/min); mean left ventricular (LV) mass, I.E., LVM (121.15 ± 16.55 g vs 104.90 ± 23.17 g); total vascular resistance (TVR) (1286.85 ± 106.2 dyn.s/cm 5 vs 1236.5 ± 68.18 dyn.s/cm 5 ). Women with preeclampsia delivered smaller babies (2510 ± 200.16 g) as compared to normotensive controls (2895 ± 276.20 g). Student's t-test was used as a test of significance.
Conclusion: Women with preeclampsia in the second trimester have significantly high CO and systolic and diastolic dysfunction compared to normotensive controls. Blood pressure (BP) monitoring alone is insufficient to effectively identify the risk of cardiovascular complications in these subjects. Echocardiography is a noninvasive method to evaluate the maternal hemodynamic during the second trimester and can help to identify high-risk patients before development of preeclampsia, and thus it may improve the outcome of pregnancy.
Keywords: Diastolic, echocardiography, maternal, normal, preeclampsia, systolic
|How to cite this article:|
Tangeda P, Shastri N. Maternal left ventricular systolic and diastolic function during second trimester of pregnancy with preeclampsia. J NTR Univ Health Sci 2015;4:224-8
|How to cite this URL:|
Tangeda P, Shastri N. Maternal left ventricular systolic and diastolic function during second trimester of pregnancy with preeclampsia. J NTR Univ Health Sci [serial online] 2015 [cited 2020 Apr 3];4:224-8. Available from: http://www.jdrntruhs.org/text.asp?2015/4/4/224/171706
| Introduction|| |
Pregnancy causes dramatic, usually reversible changes in a woman's cardiovascular system and changes in maternal circulation, which require necessary adaptations in order to develop normally. When this adaptation fails to occur, the consequence is hypertensive disorder including preeclampsia. Normal pregnancy is accompanied by maternal cardiovascular adaptations including an increase in cardiac output (CO) with a decline in blood pressure (BP) and systemic vascular resistance.  During pregnancy the heart undergoes remodeling similar to that observed in athletes,  with increase in chamber dimensions, left ventricular (LV) wall thickness, and mass. 
Preeclampsia is a disease unique to pregnancy and is characterized by progressive hypertension, pathological edema, and proteinuria. It affects 5% of pregnancies  and preeclampsia imposes an abnormal pressure load on the heart which may result in the worsening of ventricular function.In such cases, the hemodynamic situation is different from that of the normal pregnancy and is characterized by high CO in a preeclamptic phase.  Cross-sectional studies of women with preeclampsia have revealed diverse hemodynamic findings that are different from those of normal pregnancy, such as reduced CO, reduced myocardial contractility, and in some cases elevated CO;  and high vascular resistance in the preclinical stage of pregnancy, further exaggerated during the latent phase of pregnancy. Normal, increased, and depressed functions have all been reported at various stages of gestation.  A number of studies have shown that these marked hemodynamic changes during pregnancy account for the development of several signs and symptoms of heart disease. These physiological changes in women with preeclampsia can be detected as early as possible in the first and second trimesters of pregnancy.  In orders to measure hemodynamic status in pregnancy, the noninvasive technique of echocardiography is the most useful: Simple, quick, and causing no discomfort to the patient. This study was undertaken to assess the cardiovascular hemodynamic alterations in preeclampsia on echocardiography and its impact on maternal and fetal outcome.
| Materials and methods|| |
This study was carried out at the Department of Physiology, Cardiology, Obstetrics and Gynecology, PIMS, Karimnagar. Thirty (30) subjects were enrolled, of whom 15 were normotensive pregnant women at 19-25 weeks of gestation (Group I) and 15 were pregnant women with preeclampsia (Group II). Subjects were classified as preeclamptic if BP was ≥140/90 mmHg  with proteinuria greater than +1 on urine dipstick examination. Thirty (30) women each underwent echocardiographic and hemodynamic studies at 20 ± 5 weeks of gestation. Written informed consent was obtained from all the participants. The predetermined exclusion criteria for the study were: Diabetes, maternal cardiovascular disease, alcohol use, and tobacco use.
Gestation was confirmed by last menstrual period and ultrasound measurement in the first trimester. BP was measured using the standard auscultatory method with the help of pneumatically operated mercurial type random-zero sphygmomanometer. BP was measured in the left arm in the sitting position with the arm at the level of the heart. While recording BP, appearance of sound (Phase I Korotkoff) and disappearance of sound (Phase V) were recorded as systolic and diastolic BP respectively.
Hemodynamic measurement was carried out in the left lateral recumbent position after at least 5 min of rest, for all patients in 19-25 weeks of pregnancy. They were monitored by using Doppler echocardiography. Echocardiographic examination was performed using MEGAS CVX and MEGAS GPX equipped with Philips HD7 echocardiograph machine. Two-dimensional Doppler echocardiographic examinations were performed using 3.5 MHz. M-mode studies were performed at the level of the aorta, left atrium and LV at midposition between the tips of the mitral value and papillary muscles. Systolic parameters studied were left ventricle end systolic diameter (LV ESD), left ventricle end diastolic diameter (LV EDD), stroke volume (SV), CO, left ventricular mass (LVM), and posterior wall thickness (PWT) in long-axis parasternal view. Diastolic parameters studied were E wave, A wave, E/A ratio, isovolumetric relaxation time (IVRT), fractional shortening (FS%).
Mean arterial pressure (MAP) was calculated using the formula:
Total vascular resistance (TVR) was calculated using the formula:
TPR (dyn.s/cm 5 ) = mean BP × 80/CO
where TPR = Total peripheral resistance
Echocardiographic variables were calculated according to the American Society of Echocardiography (ASE) guidelines
LVM (ASE) = 0.8 [1.04 (IVS (intra ventricular septum) + EDD + PWT) 3 − (EDD) 3] + 0.6 g
In this study data were shown as mean ± standard deviation (SD). Analysis of variance (ANOVA) was used to compare data between normotensive pregnant and preeclamptic groups. Student's t-test was used as a test of significance. The probability value (P < 0.05) is described as significant.
[Table 1] shows the demographic characteristics of the study population. Age and body surface area (BSA) were similar in the two groups. There were no statistically significant differences between the groups. It was shown that there was statistically significant increase in systolic BP, diastolic BP, MAP, and birth weight between two groups. MAP of the subjects with preeclampsia (Group II) was 99.5 ± 7.0, higher than that of normal controls (Group I) (84.1 ± 3.89). Women with preeclampsia delivered smaller babies than did women with normotensive pregnancy.
[Table 2] shows a comparison of systolic parameters between two study groups. SV values in the preeclamptic group and in the normotensive group were 73.03 ± 19.6 and 60.49 ± 14.7 respectively, which is not statistically significant. CO in the preeclamptic group was 6642 ± 1508 mL/min as compared to 5175 ± 1279 mL/min in the normotensive group. This observation was statistically significant at P < 0.05. Thus the first null hypothesis of our study was rejected. TVR in the preeclampsia group was higher at 1.286 ± 0.47 dyn.s/cm 5 as compared to 1.236 ± 0.87 dyn.s/cm 5 in the normotensive group. This was statistically significant. Thus in this case the null hypothesis of our study was rejected. LV ESD, LV EDD, PWT, and LVM were increased but there was no statistically significant increase between the groups.
[Table 3] shows a comparison of diastolic parameters between normotensive and preeclamptic subjects. E-wave velocity, peak A-wave velocity, EF%, and FS% were higher in the preeclampsia group. But this increase was not statistically significant between the groups.
When systolic and diastolic parameters were compared in subjects with preeclampsia and normal controls, TVR was significantly higher (P < 0.05) in preeclamptic subjects compared to normotensive subjects.
| Discussion|| |
The cardiovascular system undergoes significant changes in association with preeclampsia. Although most of the studies reported that high CO and low vascular resistance in early pregnancy, suggesting an increase in plasma volume, , but Duvekot et al. (1995) and Spaanderman et al. (2001) , observed that there was diminished plasma volume.
In this small and preliminary study we have assessed the role of echocardiography and found it to be a useful technique for evaluation of maternal cardiac function in preeclamptic women. Rizwana et al. (2011)  found that preeclampsia in women is characterized by high CO and a high vascular resistance state. This study confirms earlier studies that there were physiological changes in LV structure and function during normal pregnancy but that exaggerated physiological changes were seen in pregnant women with preeclampsia in second trimester. In our study CO increased significantly in preeclamptic subjects; this confirms earlier studies (Morbie et al., 1994; Vasapollo et al., 2008) , and is due to increased circulating volume and decreased TPR. Fok et al. (2006)  observed a significant change in vascular load during pregnancy.
High TPR in preeclampsia suggests elevated afterload. But elevated end systolic volume suggests that elevated end systolic pressure is generated by increased afterload.
Gilson et al. (1997)  found no change in EF% and FS%, but the current study shows nonsignificant increase in circumferential fiber shortening, which is due to increase in myocardial contractility.
In the midterm pregnancy there was increased preload as a result of increased blood volume, causing an increased E velocity and a low A velocity, but that was changed to high E-wave velocity and high A-wave velocity. The high E-wave velocity in preeclamptic subjects suggests that transmitral pressure gradient during early passive filling is greater and reflects changes in passive myocardial compliance in the hypertrophic ventricle, which confirms the reports of Mesa et al. (1999).  The higher peak A-wave velocity in preeclamptic subjects suggests the more important role of the atrial systole in filling the hypertrophied ventricle in these women. TVR of subjects with preeclampsia was significantly higher than that of normotensive pregnant women. A possible explanation for this is that the MAP of preeclamptic subjects was 99.5 ± 7.0 mmHg, while that of subjects with preeclampsia was 84.1 ± 3.89 mmHg. Zentner et al. (2009)  also observed that an increase in wall stress is accompanied by deterioration in cardiac function.
Valensise et al.  found that CO, LVM, and TVR in the preeclamptic group were higher than those of the normotensive group.
Poppas et al.  suggested that TVR should be considered as the predominant parameter to characterize the systemic arterial load, i.e., vascular afterload. Valensise et al. found that women with early gestational hypertension who have high TVR (TVR > 1286 dyn.s/cm 5 ) and concentric geometry of the LV have a higher risk of developing maternal and fetal complications. Butters et al.  reported that 67% of babies weighed less than the 10th percentile at birth after the mothers were treated for chronic hypertension. In our study we found the above changes, and also that preeclampsia in an earlier stage may lead to premature delivery and there is a higher rate of low birth weight.
One limitation of this study is that it was not possible to follow up subjects in the postpartum period to examine whether the altered cardiovascular hemodynamic state reverted to normal after pregnancy. In addition, the sample size was too small as subjects were from the rural population and were not cooperative with the echocardiography.
This study shows that there are significant structural and functional changes in the cardiovascular dynamics in subjects with preeclampsia. It appears that BP monitoring alone is insufficient to effectively identify the risk of cardiovascular complications in these subjects. Maternal echocardiography, if introduced into the routine management protocol, could help to identify women who are at high risk of developing complications.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Desai DK, Moodley J, Naidoo DP, Bhorat I. Cardiac abnormalities in pulmonary oedema associated with hypertensive crises in pregnancy. Br J Obstet Gynaecol 1996;103:523-8.
Elkayam U, Gleicher N. Haemodynamics and cardiac function during normal pregnancy and the puerperium. In: Elkayam U, Gleicher N, editors. Cardiac Problems in Pregnancy. New York: Alan R Liss; 1990. p. 5-24.
Hunter S, Robson S. Adaptation of the cardiovascular system to pregnancy. In: Oakley C, editor. Heart Disease in Pregnancy. London: BMJ Publishing; 1997. p. 5-18.
Easterling TR, Benedetti TJ, Schmucker BC, Millard SP. Maternal hemodynamic in normal and preeclamptic pregnancies: A longitudinal study. Obstet Gynecol 1990;76:1061-9.
Carr DB, McDonald GB, Brateng D, Desai M, Thach CT, Easterling TR. The relationship between hemodynamics and inflammatory activation in women at risk for preeclampsia. Obstet Gynecol 2001;98:1109-16.
Escudero EM, Favaloro LE, Moreira C, Plastino JA, Pisano O. Study of the left ventricular function in pregnancy-induced hypertension. Clin Cardiol 1988;11:329-33.
Simmons LA, Gillin AG, Jeremy RW. Structural and functional changes in left ventricle during normotensive and preeclamptic pregnancy. Am J Physiol Heart Circ Physiol 2001;283:H1627-33.
Look Wood C, Peter J. Increase plasma level of EDT cellular fibrinogen precede the clinical sign of preeclampsia. Am J Obstet Gynecol 1990;162:357-62.
Easterling TR, Watis DH, Schmucker BC, Benedetti TJ. Measurement of cardiac output during pregnancy: Validation of Doppler technique and clinical observations in preeclampsia. Obstet Gynecol 1987;69:845-50.
Brown MA, Zammit VC, Mitar DM. Extracellular fluid volume in pregnancy-induced hypertension. J Hypertens 1992;10:61-8.
Duvekot JJ, Cherix EC, Pieters FA, Peeters LL. Severely impaired fetal growth is preceded by maternal hemodynamic maladaptation in very early pregnancy. Acta Obstet Gynecol Scand 1995;74:693-7.
Spaanderman ME, Aardnburg R, Ekhart TH, van Eyndhoven HW, van der Heijden OW, van Eyck J, et al
. Non-pregnant circulatory volume status predicts subsequent pregnancy outcome in normotensive thrombophilic formerly preeclamptic women. Eur J Obstet Gynecol Reprod Biol 2001;95:218-21.
Solanki R, Maitra N. Echocardiographic assessment of cardiovascular hemodynamics in preeclampsia. J Obstet Gynaecol India 2011;61:519-22.
Morbie WC, DiSessa TG, Crocker LG, Sibai BM, Arheart KL. A longitudinal study of cardiac output in normal human pregnancy. Am J Obstet Gynecol 1994;170:849-56.
Vasapollo B, Novelli GP, Valensise H. Total vascular resistance and left ventricular morphology as screening tools for complications in pregnancy. Hypertension 2008;51:1020-6.
Fok WY, Chan LY, Wong JT, Yu CM, Lau TK. Left ventricular diastolic function during normal pregnancy: Assessment by spectral tissue Doppler imaging. Ultrasound Obstet Gynecol 2006;28:789-93.
Geva T, Mauer MB, Striker L, Kirshon B, Pivarnik JM. Effects of physiologic load of pregnancy on left ventricular contractility and remodelling. Am Heart J 1997;133:53-9.
Mesa A, Jessurun C, Hernandez A, Adam K, Brown D, Vaughn WK, et al
. Left ventricular diastolic function in normal human pregnancy. Circulation 1999;99:511-7.
Zentner D, du Plessis M, Brennecke S, Wong J, Grigg L, Harrap SB. Deterioration in cardiac systolic and diastolic function late in normal human pregnancy. Clin Sci (Lond) 2009;116:599-606.
Valensise H, Novelli GP, Vasapollo B, Di Ruzza G, Romanini ME, Marchei M, et al
. Maternal diastolic dysfunction and left ventricular geometry in gestational hypertension. Hypertension 2001;37:1209-15.
Poppas A, Shroff SG, Korcarz CE, Hibbard JU, Berger DS, Lindheimer MD, et al
. Serial assessment of the cardiovascular system in normal pregnancy. Role of arterial compliance and pulsatile arterial load. Circulation 1997;95:2407-15.
Valensise H, Vasapollo B, Novelli GP, Pasqualetti P, Galante A, Arduini D. Maternal total vascular resistance and concentric geometry: A key to identify uncomplicated gestational hypertension. BJOG 2006;113:1044-52.
Butters L, Kennedy S, Rubin PC. Atenolol in essential hypertension during pregnancy. BMJ 1990;301:587-9.
[Table 1], [Table 2], [Table 3]