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clinmed/2003020003v1 (April 1, 2003)
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Maternal blood rheology and pregnancy induced hypertension

 

James Robins1, Consultant in Obstetrics & Gynaecology

Mark Woodward2, Professor of Biostatistics

Gordon Lowe3, Professor of Vascular Medicine

Pamela McCaul3, Research Technician

Helen Cheyne1, Research in Practice Development Midwife

James J. Walker1, Professor of Obstetrics & Gynaecology

 

1. Perinatal Research Unit, Glasgow Royal Maternity Hospital, Rottenrow, Glasgow, Scotland.

2. Institute for International Health, University of Sydney, Australia.

3. University Department of Medicine, Glasgow Royal Infirmary, Glasgow, Scotland.

 

 

Author for correspondence:

Dr. J. B. Robins, Inverclyde Royal Hospital, Larkfield Road, Greenock, Renfrewshire, PA16 0XN, Scotland.

Tel: 01475 633777

Fax: 01475 656188

Email: James.Robins@irh.scot.nhs.uk

 

 

 

 

Key words: antenatal care, risk assessment, rheology, viscosity, pregnancy-induced hypertension.


Abstract

 

Objective: This study evaluates the relationship between the first trimester assessment of maternal rheology and the subsequent development of pregnancy induced hypertension.

Design: Prospective observational study.

Setting: Glasgow Royal Maternity Hospital, Scotland

Population: From an original population of 744 consecutive antenatal attendees a total of 579 women were booked in at less than 14 weeks gestation. The main study group is a further subset comprising 251 primigravid women booking with a singleton pregnancy without essential hypertension. Previously published data from a group of non-pregnant women of similar age drawn from the same local community was used for external comparison.

Methods: Blood samples were collected at the booking visit, from which fibrinogen, red cell aggregation, haematocrit and plasma, whole blood, relative and corrected viscosities were recorded. Information was obtained from the case notes in retrospect starting approximately one year after the first patients had first been recruited into the trial.

Main Outcome measures: The overall outcome of the pregnancies was noted with particular reference to PIH, birth-weight, antepartum haemorrhage, pre-term labour, perinatal death, condition at delivery and neonatal complication.

Results: Pregnancy induced hypertension is associated with a significantly raised mean blood viscosity and fibrinogen at time of booking. All significance disappears after adjustment for smoking, diastolic blood pressure and age. Viscosity is, however, only marginally non-significant, (p0.07).

Conclusions: Blood rheology, in particular blood viscosity and fibrinogen, may play a predictive role in the development of pregnancy-induced hypertension. When combined with measurement of diastolic blood pressure at booking, these measurements could be used to calculate a risk score for the development of PIH, allowing targeting of antenatal care. Further data is required.

 


Introduction

There is increasing evidence to suggest that patients who develop complications of pregnancy demonstrate 'abnormal adaptation' to the pregnancy process prior to overt signs of the disorder itself. In 1986 Murphy and colleagues1 introduced the concept that the cause(s) of pregnancy-induced hypertension are operating and exerting detectable effects as early as the first trimester. It is recognized, for example, that proteinuric hypertension is associated with raised haemoglobin levels at booking.1-3 Furthermore both pregnancy induced hypertension (PIH) and intra-uterine growth retardation (IUGR) are recognised to be associated with abnormal haemostasis.4, 5 A number of researchers have shown that blood flow and blood viscosity are also abnormal in these conditions4 -12 and may in turn be related to the histological evidence of placental intravascular changes.

 

Rheology is the science of the flow and deformation of matter and describes the material properties of fluid and semi-solid materials. This study considers the parameters of maternal blood rheology in normal and abnormal pregnancies, (including blood viscosity and erythrocyte deformability), with reference to the possible use of these factors as predictors of pregnancy outcome. If certain parameters of blood rheology could be used as a predictor of pregnancy outcome then this could possibly permit selective early intervention and monitoring of at-risk patient groups.13

 


Methods

Subjects

Blood was taken from pregnant women attending for antenatal care at Glasgow Royal Maternity Hospital during a one-year period commencing in January 1989. Recruitment of patients and analysis of data was completed within 2 years. The results were recorded against the patients name, age and unit number. Data was stored and results analysed, in retrospect, following delivery. Consent was obtained from all women participating in the study. The local hospital ethics committee had granted full ethical approval.

 

In this research we identified three study groups for analysis and comparison. Group 1 comprises of 579 consecutive women booking at less than fourteen weeks gestation. All patients routinely have an early ultrasound scan carried out to confirm menstrual dates and give an accurate assessment of gestational age. Group 2 is a subset of primigravida with a singleton pregnancy and no history of essential hypertension.

 

The third MONICA Survey in North Glasgow, which was carried out in 1992 as one of a series of cross sectional random samples of the North Glasgow community, provided a third group for external comparison. This study had been conducted within the international MONICA project14 and analyses of the complete rheological data has already been published.15 A total of 1958 men and women aged 25 - 74 years were sampled for this project. All pregnant women had been removed from this database. For Group 3 we have extracted the rheological data from 213 women aged 25 36 years for comparison with our 579 pregnant women.

 

Defined Outcomes

The pregnancy related outcomes recorded were, PIH, birth weight, ante-partum haemorrhage, pre-term labour, perinatal death, condition at delivery and neonatal complication. Information was obtained from the case notes in retrospect, starting approximately one year after the first patients had been recruited into the trial.

 

Hypertension was defined according to criteria recommended by the International Society for the Study of Hypertension in Pregnancy16 as diastolic blood pressure >110mmHg on any one occasion or diastolic blood pressure >90mmHg on two or more occasions >4hrs apart.

 

A baby is considered pre-term if delivered prior to 37 completed weeks gestation. Intrauterine growth retardation (IUGR) was defined as a birthweight of <10th centile by gestation and sex.

 

Blood viscometry

Five ml of venous blood was taken under standard conditions and anticoagulated with dry dipotassium edetate EDTA (1.5g/L). Whole-blood and plasma viscosity were measured at high shear rates (>300s-1) using a Coulter-Harkness capillary viscometer at 37C. Haematocrit was measured with a Hawksley Microcentrifuge and red cell aggregation was assessed at low shear rate by the Myrenne Photometric Aggregometer. The measured coefficient of variation for each of these variables was less than 2%. Corrected blood viscosity is a calculated variable whereby whole blood viscosity is corrected to a standard haematocrit of 45%. Relative blood viscosity (corrected blood viscosity/plasma viscosity) was calculated as a measure of red cell deformability.17

 

Identical methodologies of analysis were used for rheological variables in the MONICA 3 group with the exception of fibrinogen. No comparison is therefore made against this variable when considering the MONICA (Group 3) data.

 

Statistical Analysis

Mean values were compared using general linear models, adjusted for important confounding variables.18 Transformations were made, where necessary, to improve the approximation of a normal distribution. Fibrinogen and plasma viscosity were thus analysed on a log scale. To avoid distributional issues, rank correlations were used to describe relationships between co-variables.


Results

Of the initial study population of 744 patients, 579 women, (Group 1), were booked in at less than 14 weeks gestation of which 251, (Group 2), were in their first singleton pregnancy without essential hypertension, (Figure 1). Although not complete, reliable outcome data was available on most of these patients. The outcomes recorded were birth-weight (n=247), delivery gestation (n=251), hypertensive outcome (n=248), and severity of hypertension, (n=248).

 

Baseline rheological data

A comparison was made between the first study group and 213 non-pregnant women who had been enrolled in the MONICA (Group 3) study (Table 1). The age range of the pregnant women in our study was 15 - 36 years whereas in MONICA the women were aged 25 - 36 years. Hence, the figures quoted have been adjusted for age. Whole blood viscosity, haematocrit and red cell aggregation at time of booking were all significantly lower in the pregnant group, confirming previously published data.19-21

 

Pregnant women without essential hypertension.

Group 2 comprised of 251 primigravid women with a singleton pregnancy and no history of essential hypertension. As per the study criteria all had booked at less than 14 weeks gestation with a mean booking gestation of 10.2 weeks, (range 6 13 weeks). The mean delivery gestation was 39.1 weeks, (range 27 42 weeks) and the mean birth weight was 3257 grams, (range 860 4910 grams).

 

Correlations between indicies of blood rheology and other variables were made for this group, (Table 2). The observed positive correlation between body mass index and red cell aggregation, fibrinogen and the calculated variable of corrected and relative blood viscosity has been previously described.15 There is also a positive correlation between diastolic blood pressure and plasma and whole blood viscosity.

 

Seventy-three (30%), of the second study group women developed pregnancy-induced hypertension or delivered a pre-term or small for dates baby. A total of 48 (19%), developed pregnancy induced hypertension as already defined. Of this group, 13 women (5%) were considered to have gestational proteinuric hypertension (pre-eclampsia). There were no cases of eclampsia. Eighteen patients (7.2%) delivered pre-term. Twenty-four women (9.7%) delivered small for gestational age infants. Some patients had combined pathologies, for example, 4 hypertensive women delivered growth retarded infants pre-term.

 

Since PIH was by far the most common complicationthe analysis of the data was in respect of hypertensive outcome alone, (Table 3). There were too few events to analyze with respect to the other endpoints. No distinction is made between non-proteinuric and proteinuric hypertension. Diastolic blood pressure at booking was highly significantly associated with the risk of developing PIH in both raw and adjusted data. There were significant, (p<0.05) associations between CBV, PV, WBV and fibrinogen at booking and the risk of developing PIH later in pregnancy. However, significance was not maintained after adjustment.


Discussion

Rheological variables affect blood flow in both macrovessels and microvessels. These variables include whole-blood viscosity and its major determinants plasma viscosity and haematocrit. Plasma viscosity is likewise determined, at least in part, by plasma fibrinogen. Fibrinogen has both rheological and coagulation effects.

 

During pregnancy there are large-scale changes of physiological function affecting all body systems. These changes represent a positive preparation and adaptation to accommodate and support the developing fetus. They are temporary and produce no detrimental effects on the mother. The physiological changes of pregnancy confer biological advantage and if not made the pregnancy may be prejudiced.

 

Alterations in pregnancy haemodynamics start early in pregnancy and are maintained to the third trimester. Pregnancy is a hypervolaemic condition with early-expanded volume, a high cardiac output and a decrease in vascular and rheological resistance. In normal pregnancies most rheological parameters are decreased by about 10-20% due to physiological haemodilution and plasma expansion.

 

A number of studies have been performed which detail the physiological changes in blood rheology during normal pregnancy.5,7,12,19-21 It is known that fibrinogen rises, red cell aggregation increases and red cell deformability falls. These changes are balanced by haemodilution and the resultant reduction in haematocrit.

 

When normal haemodilution and fall in blood viscosity does not occur then there is evidence to suggest that this is associated with pregnancy complications. It has been demonstrated that blood viscosity, haematocrit, plasma viscosity and red cell rigidity are all increased in pregnancy-induced hypertension and fetal growth retardation.3-12 Women with diagnosed PIH show raised haematocrit, increased red cell aggregation and decreased red cell deformability.12

 

 

 

 

The majority of investigators have, however, measured rheological variables in the second and third trimester. Their studies have typically been on small numbers and have often not been prospective. Our data reveals an interesting association between early (first trimester) rheology and subsequent hypertensive outcome. Changes found in whole blood viscosity and plasma viscosity are in general agreement with the results of previous studies.5-12 However, we have now demonstrated that these changes predate the development of identifiable PIH. Differences between normal pregnancies and those that developed PIH are statistically significant. Unfortunately statistical significance is lost when the raw data is adjusted for smoking, gestation and diastolic blood pressure at booking.

 

We did, however, take particular care in this study to exclude women with essential hypertension. It is known that whole blood viscosity, plasma viscosity and erythrocyte aggregation tendency are raised in patients with untreated essential hypertension whilst erythrocyte deformability is decreased.22

 

 

 


Conclusions

One of the primary aims of antenatal care is to identify at-risk pregnancies. Any strategy that will allow increased surveillance and hence target appropriate management to the group that needs it is desirable. Our findings may shed some light on the patho-physiological processes involved in the development of PIH but do not imply a cause and effect. It is unlikely that changes in, for example, whole blood viscosity are a major determining factor in the efficacy of placental perfusion.21 Vascular changes would have a much greater role.

 

First trimester changes in the indices of blood rheology, in particular the corrected blood viscosity (CBV) and fibrinogen, antedate the development of pregnancy-induced hypertension. These simple investigations identify an evolving disease process and may provide a cheap and practical method of screening primigravidae to determine at-risk cases. When combined with measurement of diastolic blood pressure at booking these measurements could be used to calculate a risk score for the development of PIH allowing targeting of antenatal care.

 

 

 

 


References

 

1.      Murphy JF, ORiordan J, Newcombe RG, Coles EC & Pearson JF. Relation of haemoglobin levels in first and second trimester to outcome of pregnancy. Lancet 1986; i: 992-994

 

2.      Koller O, Sandvei R & Sagen N. High haemoglobin levels during pregnancy and fetal risk. Int. J. Gynaecol. Obstet. 1980; 18: 53-56

 

3.      Sagan N, Koller O & Haram K. Haemoconcentration in severe pre-ecalmpsia. Br. J. Obstet. Gynaecol. 1982; 89: 802-805

 

4.      Bonnar J, McNicol GP & Douglas AS. Coagulation and fibrinolytic systems in pre-eclampsia and eclampsia. Brit. Med. J. 1971; ii: 12-16

 

5.      Thorburn J, Drummond MM, Whigham KA, Lowe GDO, Forbes CD, Prentice CRM & Whitfield CR. Blood viscosity and haemostatic factors in late pregnancy, pre-eclampsia and foetal growth retardation. Br. J. Obstet. Gynaecol. 1982; 89: 117-122

 

6.      Mathews JD & Mason TW. Plasma viscosity and pre-eclampsia. Lancet 1974; ii: 409

 

7.      Karibara M, Marumoto Y, Taniguchi I & Kobayashi T. Blood viscosity at low shear rate in normal and abnormal pregnancies. Biorheology 1981; 18: 177.

 

8.      Buchan PC Pre-eclampsia a hyperviscosity syndrome. Am. J. Obstet, Gynaecol. 1982; 142: 111

 

9.      Hobbs JB, Oats JN, Palmer AA, Mitchell GM, Lou A & McIver MA Whole blood viscosity in pre-ecalmpsia. Am. J. Obstet. Gynaecol 1982; 142: 288-292

 

10. Lang GD, Lowe GDO, Walker JJ, Forbes CD, Prentice CRM & Calder AA Blood rheology in pre-eclampsia and intrauterine growth retardation: effects of blood pressure reduction with labetalol. Br. J. Obstet. Gynaecol. 1984; 91: 438-443

 

11. Zondervan HA, Oosting J, Smorenberg-Schoorl ME & Treffers PE. Maternal whole blood viscosity in pregnancy hypertension. Gynecol. Obstet. Invest. 1988; 25(2): 83-8

 

12. Heilmann L & Siekmann U. Haemodynamic and haemorheological profiles in women with proteinuric hypertension of pregnancy and in pregnant controls. Arch. Gynaecol. Obstet. 1989; 246(3): 159-86

 

13. Walker JJ. The case for early recognition and intervention in pregnancy induced hypertension. In Hypertension in Pregnancy. Eds. Sharp F & Symonds EM. Proc. Royal College of Obstetricians and Gynaecologists. 16th Study Group. RCOG, 1987 pp189 304.

 

14. World Health Organization Principal Investigators (prepared by H Tunstall-Pedoe). The World Health Organization MONICA Project (Monitoring trends and determinants in cardiovascular disease): a major international collaboration. Journal of Clinical Epidemiology 1988; 41: 105-113

 

15. Woodward M, Rumley A, Tunstall-Pedoe H, & Lowe GDO. Associations of blood rheology and interleukin-6 with cardiovascular risk factors and prevalent cardiovascular disease. Br. J. Haematology 1999; 104: 246-257

 

16. Davey DA & MacGillivray J. The classification and definition of the hypertensive disorders of pregnancy. Am J Obstet Gynaecol 1988; 158: 892-898

 

 

17. Lowe, GDO, Smith WCS, Tunstall-Pedoe HD, Crombie IK, Lennie SE, Anderson J & Barbenel JC. Cardiovascular risk and haemorheology: results from the Scottish Heart Health Study and the MONICA project. Glasgow. Clinical Haemorheology, 1988; 8: 517-524

 

18. Woodward M. Epidemiology: Study Design & Data Analysis. Chapman & Hall/CRC Press, Boca Raton, 1999

 

19. Buchan PC. Maternal and fetal blood viscosity throughout normal pregnancy. J. Obstet. Gynaecol. 1984; 4:143-50.

 

20. Huisman A, Aarnoudse JG, Heuvelmans JHA, Goslinga H, Fidler V, Huisjes HJ & Zijlstra WG. Whole blood viscosity during normal pregnancy. Br. J. Obs. Gynae. 1987; 94: 1143-1149.

 

21. Oosterhof H, Wichers G, Fidler V & Aarnoudse JG. Blood viscosity and Uterine Artery Flow Velocity waveforms in pregnancy: A longitudinal study. Placenta 1993; 14: 555-561

 

22. Linde T, Sandhagen B, Hagg A, Morlin C, Wikstrom B & Danielson BG. Blood viscosity and peripheral vascular resistance in patients with untreated essential hypertension. Journal of Hypertension 1993; 11(7): 731-6.

 

 


Figure 1: Study Outline

 

 

 

Original Pregnant Population

744

(Total 1079 sample events)

 

 

 

 

 

 

GROUP 3

MONICA3 Group

213

Non-pregnant

Same socio-economic group

 

 

GROUP 1

Rheological Data < 14 weeks

579

(Incld. Parous, multiples and patients recruited to longitudinal study)

 

 

Table 1

 

 

 

 

 

 

GROUP 2

Primigravida with a singleton pregnancy

251

No essential hypertension

 

 

Table 2

 

 

 

 

 

 

Reliable outcome data

248

 

 

 

 

 

 

 

P.I.H

48

 

No P.I.H

200

 

Table 3

 

 

 

 

 

 


Table 1: Mean (95% confidence interval) booking values for all pregnant women with a gestation less than 14 weeks and for a random sample of non-pregnant women aged 25-34 years, (MONICA subjects).

P values compare all pregnant and non-pregnant women.

 

 

Variable

Group 3

(n=213)

Group 1

(n=579)

P value*

Age (years)

31.3

(30.7 - 31.9)

25.4

(24.9 - 25.9)

<0.0001

Systolic BP (mmHg)

111.0

(109.1 - 112.9)

114.2

(112.5 -115.8)

0.03

Diastolic BP (mmHg)

68.2

(66.8 -69.7)

70.4

(69.2 - 71.7)

0.02

Body mass index (kg/m2)

24.1

(23.5 - 24.8)

24.1

(23 - 25.1)

0.92

Whole blood viscosity

(mPas-1)

2.84

(2.78 - 2.91)

2.73

(2.69 - 2.78)

0.01

Plasma viscosity

(mPas-1)

1.28

(1.27 - 1.29)

1.27

(1.26 - 1.28)

0.45

Haematocrit (%)

41.3

(40.7 - 41.9)

38.9

(38.5 - 39.3)

<0.0001

Red cell aggregation

3.45

(3.22 -3.68)

4.84

(4.68 - 5.01)

<0.0001

Corrected blood viscosity (mPas-1)

3.05

(2.98 - 3.13)

3.08

(3.03 - 3.13)

0.54

Relative blood viscosity

2.38

(2.33 - 2.44)

2.42

(2.38 - 2.45)

0.33

* Age-adjusted (except for age itself) comparison of non-pregnant and all pregnant women. Test for plasma viscosity after a log transformation.

 

 

 


Table 2: Correlations between blood rheology and other variables for primiparous women with a singleton gestation of less than 14 weeks and recorded as not having essential hypertension (n=251).

In each cell of the table, the first line shows the Spearman correlation coefficient, the second (in italics) gives the p value for the test of this correlation being zero and the third gives the number of subjects from which the correlation has been computed. The exception is for smoking status, where the first line shows the difference between mean values, smokers minus non-smokers; the other two lines are as elsewhere.

 

Whole blood viscosity

Plasma viscosity

Haematocrit

Red cell aggregation

Corrected blood viscosity

Relative blood viscosity

Fibrinogen

Age

0.006

0.05

-0.002

0.16

0.01

-0.04

-0.01

 

0.93

0.43

0.97

0.03

0.87

0.58

0.86

 

221

216

226

188

212

212

213

 

 

 

 

 

 

 

 

Booking

-0.09

0.02

-0.23

0.04

0.0009

-0.03

0.09

Gestation

0.17

0.74

<0.001

0.55

0.99

0.71

0.18

 

228

222

233

194

218

218

219

 

 

 

 

 

 

 

 

Systolic BP

0.13

0.13

0.03

-0.02

0.14

0.05

0.11

 

0.06

0.08

0.65

0.76

0.06

0.46

0.12

 

203

196

206

172

194

194

191

 

 

 

 

 

 

 

 

Diastolic BP

0.19

0.19

0.13

0.04

0.15

0.04

0.07

 

0.008

0.009

0.06

0.60

0.04

0.54

0.33

 

203

196

206

172

194

194

191

 

 

 

 

 

 

 

 

Body mass

0.08

-0.05

-0.09

0.30

0.22

0.26

0.30

index

0.53

0.70

0.44

0.01

0.08

0.04

0.02

 

68

65

69

65

64

64

63

 

 

 

 

 

 

 

 

Smoking

0.159

0.007

1.26

-0.294

0.187

0.175

0.233

status

0.59

0.17

0.85

0.001

0.52

0.19

0.98

 

169

164

173

139

161

161

162


Table 3: Mean (95% confidence interval) booking values for pregnant women with gestation less than 14 weeks recorded as not having essential hypertension, by hypertensive outcome.

P values compare those with and without pregnancy-induced hypertension.

 

Pregnancy induced hypertension?

P value

Variable

No (n=200)

 

Yes (n=48)

 

Raw

Adjusted*

Age (years)

25.1

(24.5 - 25.7)

26.7

(25.4 - 27.9)

0.03

0.47

Systolic BP (mmHg)

112.0

(110.2 - 113.8)

117.4

(113.3 - 121.5)

0.01

0.14

Diastolic BP (mmHg)

68.3

(67.0 - 69.6)

74.2

(71.6 - 76.8)

<0.0001

0.01

Body mass index

(kg/m2)

22.7

(21.9 - 23.4)

24.1

(22.2 - 26.0)

0.11

0.24

Whole blood viscosity (mPas-1)

2.70

(2.65 - 2.75)

2.83

(2.72 - 2.94)

0.03

0.18

Plasma viscosity

(mPas-1)

1.27

(1.26 - 1.28)

1.29

(1.27 - 1.32)

0.04

0.55

Haematocrit (%)

38.8

(38.3 - 39.2)

38.9

(37.8 - 40.0)

0.80

0.82

Red cell aggregation

4.71

(4.52 - 4.89)

5.04

(4.60 - 5.48)

0.15

0.83

Corrected blood viscosity (mPas-1)

3.04

(2.99 - 3.10)

3.22

(3.10 - 3.34)

0.007

0.07

Relative blood viscosity

2.40

(2.36 - 2.44)

2.49

(2.40 - 2.57)

0.08

0.12

Fibrinogen (g/l)

3.04

(2.94 - 3.14)

3.33

(3.14 - 3.53)

0.02

0.20

* adjusted for smoking, age (except for age) and (except for BP) diastolic blood pressure at booking

 

 

 





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Related Collections
Right arrow Cardiovascular Medicine:
Hypertension

Right arrow Pathology:
Haematology Incl Blood Transfusion

Right arrow Obstetrics and Gynaecology:
Pregnancy


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