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Menopause Review/Przegląd Menopauzalny
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vol. 10
Original paper

Diurnal changes of blood pressure values (24 h blood pressures) in women with polycystic ovary syndrome

Barbara Grzechocińska
Anna Cyganek
Piotr Marianowski

Przegląd Menopauzalny 2011; 3: 237–240
Online publish date: 2011/07/04
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More attention is being paid lately to polycystic ovary syndrome (PCOS) not only in the aspect of fertility but also according to long-term metabolic and cardiovascular abnormalities [1]. Although the environmental conditioning in both syndromes is similar, it is unknown whether women with PCOS are more vulnerable to blood vessel illness [2]. Ambiguous values of blood pressure in women with PCOS result from different diagnostic criteria of this syndrome. The blood hypertension, like diabetes, may be present a long time before a definite diagnosis is made [3]. During this time a lot of disorders in blood vessels may occur. Early diagnosis and implementation of proper treatment significantly decreases the risk of serious complications such as cerebral stroke or coronary heart disease.

The diurnal changes of blood pressure may be responsible for the susceptibility to blood hyper­ten­sion.


The purpose of this study was to assess the diurnal changes of blood pressure in women with PCOS.

Material and methods

A preliminary study estimating diurnal changes of blood pressure was conducted. The experimental group consisted of 26 women with PCOS diagnosed according to Rotterdam consensus criteria 2003 and Androgen Excess Society (AES) criteria: clinical and/or biochemical signs of hyperandrogenism, clinical symptoms e.g. anovulatory cycles, and typical appearance of ovaries in vaginal ultrasonography [4, 5]. They were chosen randomly from patients attending the outpatient clinic due to menstrual abnormalities. All women complained of irregular bleeding, range 35-180 days. The Ferriman Gallwey hirsutism scale score was above 7 in all patients. The control group consisted of 12 regularly menstruating women (range 26-30 days), without

hyperandrogenaemia and without ultrasound evi­dence of polycystic ovaries. The study group consisted of wo­men willing to get contraception, with no pregnancy record in the past. These women were selected according to age and body mass index (BMI). Women smoking cigarettes were excluded from the study. None of the women from either the study or control group were diagnosed with cardiac disease, primary hypertension, renal disorders or any health conditions potentially affecting the values of blood pressure. The family histories of these patients were also clean according to those conditions. The results of measurements performed in both groups are presented in Table I. The mean age in the study group was 29.5 years, and 30.8 years in the control group. The diffe­rence was not statistically significant. The mean BMI in the study group was 24.77 kg/m2, and 25.01 kg/m2 in the control group. The difference was not statistically significant. The blood samples for hormonal tests – FSH (follicle stimulating hormone), LH (luteinizing hormone), prolactin, oestradiol, testosterone, DHEAS (dehydroepiandrosterone sulfate), TSH (thyroid stimu­lating hormone), insulin, glucose, triglycerides (TG) and total cholesterol (TC) – were taken between day 3 and day 5 of the menstrual cycle from each patient.

Non-invasive blood pressure monitoring using an automatic recorder was performed in both groups, in all outpatient women every 15 min during a 24-hour study period.

The results were analysed statistically by Halberg’s cosinor method. Systolic and diastolic blood pressure were analysed separately. The mean values of systolic and diastolic blood pressure were analysed in both groups, as well as the diurnal changes of blood pressure. Calculation was performed in three stages. Data describing daily variability were presented in the form of a graph. The next stage was verification of whether deviations from the mean value were accidental or statistically significant. The third stage was statistical evaluation of diurnal values according to cosinor analysis. Halberg’s cosinor method on account of the possibility of graphic interpretation of the results clearly presents characteristics of periodic blood pressure changeability.


Clinical, endocrine and biochemical characteristics of women with PCOS and the control group are shown in Table I.

In the PCOS syndrome group in comparison with the control group there was a statistically significantly higher level of LH (9.85 ±6.00 IU/l vs. 4.03 ±1.39 IU/ml,

respectively) and testosterone (1.21 ±0.92 ng/ml vs.

0.44 ±0.22 ng/ml, respectively). A relation of fasting insulin (17.15 ±10.53 µIU/ml vs. 6.35 ±2.05 µIU/ml, respectively), level of fasting glucose (87.67 ±5.09 mg% vs. 78.0 ±9.9 mg%, respectively) and glucose/insulin ratio was not found in any of the examined women.

A chronobiological analysis of the data was per­for­med in order to test the whole-day blood pressure pattern. Halberg’s single cosinor method was used to determine the values and the confidence limits of the following parameters of 24-hour rhythmic changes: mesor (rhythm-adjusted 24-hour average), amplitude (24-hour variability estimate), and acrophase (clock hour of maximum BP level).

The variation of the above parameters during the 24-hour periods was found to be within 9 mm Hg for the systolic mesor, 9.5 mm Hg for the diastolic mesor, 6 mm Hg for the systolic amplitude and 5 mm Hg for the diastolic amplitude. Diurnal rhythm of systolic and diastolic blood pressure is shown in Figures 1 and 2 respectively.

It was confirmed that in the PCOS group of women diurnal rhythm of blood pressure is retained, with average values of systolic and diastolic blood pressure in the night time. None of the women was diagnosed with blood hypertension. Nevertheless, in 7 patients (27%) in the study group accidental measurements were above 135/85 mm Hg, and the same was found in 2 women (17%) from the control group.

Occasional increase of blood pressure occurring in some women made us analyse circadian rhythm for each woman in both groups. The detailed analysis of individual curves of blood pressure revealed single episodes of increase of systolic blood pressure in

8 (30.7%), and diastolic blood pressure in 4 (15.4%) PCOS women respectively. The curve during 24 hours is flat, indicating no physiological decrease in blood pressure in night hours.


As yet it has not been specified how often women with PCOS suffer from cardiovascular diseases. There are a few studies confirming that the influence of periodic increase of blood pressure values in young women may be the first symptom of hypertension in older age in these women [6]. Hypertension is one of the most important risk factors of cardiovascular diseases. There are also a few studies in which the results show that women of middle age with PCOS have higher risk of hypertension, cardiovascular diseases and infarcts [7, 8]. Polycystic ovary syndrome women with hypertension often have insulin resistance and hyperinsulinaemia. These disorders have a negative influence on blood vessel flow, sympathetic nerve system activation and sodium-potassium pump activation. These actions result in increased tension of vessel walls and impaired renal function, i.e. sodium excretion.

Women with PCOS and hyperinsulinaemia have higher risk of cardiovascular diseases than women with PCOS with normal levels of insulin. Accordingly, women with PCOS and normal levels of insulin have higher risk of cardiovascular diseases than women without PCOS (but with similar BMI values) [9]. In our study no significant differences in fasting glucose and insulin levels were found between the group with PCOS and controls. The glucose/insulin index was also not statistically different between those two groups (8.5 vs. 11.2, respectively). However, we found abnormal diurnal blood pressure values in 30% of women with PCOS. It has been claimed that one of the factors leading to onset of hypertension is lack of a physiological mechanism of decrease in blood pressure values during the night time [10].

Occurrence of hypertension in older age in women with PCOS may also be the result of hormonal disorders. It has been found that increased levels of testosterone, hyperinsulinaemia and insulin resistance may be risk factors of hypertension [10, 11]. Molecular and genetic studies show that enzymatic and gene disorders of steroidogenesis are the same in PCOS and hypertensive women [12-14]. The results of recent clinical studies show that early prevention of cardiovascular diseases by life style modification, and early diagnosis and treatment of hypertension as well as lipid metabolism disorders decrease the risk of coronary artery diseases and other vascular diseases, which are the most important cause of death in women [15, 16].


The results of the examination show the existence of a 24-hour rhythm of systolic blood pressure disorder in 30% and diastolic in 15% of women with PCOS in whom no physiological decrease of blood pressure in night hours was observed.


1. Legro RS, Kunselman AR, Dodson WC, Dunaif A. Prevalence and pre­dictors of risk for type 2 diabetes mellitus and impaired glucose tole­rance in polycystic ovary syndrome: a prospective, controlled study in 254 affected women. J Clin Endocrinol Metab 1999; 84: 165-9.

2. Wild RA. Long-term health consequences of PCOS. Hum Reprod Update 2002; 8: 231-41.

3. Cattrall FR, Healy DL. Long-term metabolic, cardiovascular and neo­plastic risks with polycystic ovary syndrome. Best Pract Res Clin Obstet Gynaecol 2004; 18: 803-12.

4. Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome. Fertil Steril 2004; 81: 19-25.

5. Azziz R, Carmina E, Dewailly D, et al.; Androgen Excess Society. Posi­tions statement: criteria for defining polycystic ovary syndrome as a pre­dominantly hyperandrogenic syndrome: an Androgen Excess Society guideline. J Clin Endocrinol Metab 2006; 91: 4237-45.

6. Orbetzova MM, Shigarminova RG, Genchev GG, et al. Role of 24-hour monitoring in assessing blood pressure changes in polycystic ovary syndrome. Folia Med (Plovdiv) 2003; 45: 21-5.

7. Wild S, Pierpoint T, McKeigue P, Jacobs H. Cardiovascular disease in women with polycystic ovary syndrome at long-term follow-up: a retro­spective cohort study. Clin Endocrinol (Oxf) 2000; 52: 595-600.

8. Wild S, Pierpoint T, Jacobs H, McKeigue P. Long-term consequences of polycystic ovary syndrome: results of a 31 year follow-up study. Hum Fertil (Camb) 2000; 3: 101-5.

9. Mather KJ, Kwan F, Corenblum B. Hyperinsulinemia in polycystic ovary syndrome correlates with increased cardiovascular risk independent of obesity. Fertil Steril 2000; 73: 150-6.

10. Arslainian SA, Lewy VD, Danadian K. Glucose intolerance in obese adolescents with polycystic ovary syndrome: roles of insulin resistance and beta-cell dysfunction and risk of cardiovascular disease. J Clin Endocrinol Metab 2001; 86: 66-71.

11. Godziejewska-Zawada M, Zgliczyński S, Słowińska-Srzednicka J i wsp. Zwięk­szone stężenia testosteronu i insuliny wiążą się z nadciśnieniem tętni­czym w zespole policystycznych jajników (PCO). Endokryn Polska 2003; 54: 301-7.

12. Ciechowicz A. Diagnostyka molekularna nadciśnienia tętniczego w XXI wieku. Postępy Nauk Medycznych 2003; 4: 7-16.

13. Katulski K, Warenik-Szymankiewicz A, Trzeciak WH. Ocena ekspresji genu CYP 17 na poziomie białka enzymatycznego. Gin Prakt 2001; 9: 65-7.

14. Wertheim K, Sobczyńska-Tomaszewska A, Bal J. W poszukiwaniu etiopatogenezy zespołu policystycznych jajników (PCOS). Gin Pol 2007; 78: 626-31.

15. Bittner V. Women and coronary heart disease risk factors. J Cardiovasc Risk 2002; 9: 315-22.

16. Knopp RH. Risk factors for coronary artery disease in women. Am

J Cardiol 2002; 89 (12A): 28E-34E.
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