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The Division of Cardiology, Department of Internal Medicine, Chang Gung Memorial Hospital, Lin-Kou Medical Center, Taoyuan, TaiwanInstitute of Stem Cell and Translational Cancer Research, Chang Gung Memorial Hospital, Lin-Kou Medical Center, Chang Gung University College of Medicine, Taoyuan, Taiwan
Postocclusive reactive hyperemia (PORH) is a noninvasive test for microcirculation.
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Endothelial function can be measured by PORH using laser Doppler flowmetry.
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The hormonal milieu affects microvascular function during ovarian stimulation.
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Blunting PORH indicates an early endothelial dysfunction in normoandrogenemic PCOS.
Abstract
Research question
Is there an association between post-occlusive reactive hyperaemia (PORH) and ovarian stimulation in women with normoandrogenaemic polycystic ovary syndrome (PCOS)?
Design
Women eligible for IVF at an academic fertility centre were invited to join this prospective study. Microvascular endothelial function was measured as PORH by laser Doppler flowmetry (LDF) before and after ovarian stimulation. Metabolic characteristics, hormone profiles and biochemical markers were analysed.
Results
Thirty-four normoandrogenaemic women with PCOS and 36 normoandrogenaemic women without PCOS were included. The PCOS group displayed higher C-reactive protein levels and insulin resistance (P = 0.048 and P = 0.025, respectively). No significant difference was found in microcirculatory function between the groups at baseline. After ovarian stimulation, PORH was enhanced in the control group (slope 7.1 ± 3.3 versus 9.7 ± 4.5; P = 0.007; peak flow 30.7 ± 16.3 versus 43.5 ± 17.3, P = 0.008; however, the PCOS group experienced a blunting response to supraphysiological hormone status (slope 8.2 ± 5.1 versus 7.2 ± 4.3, P = 0.212; peak flow, 38.8 ± 19.4 versus 37.0 ± 21.8, P = 0.895).
Conclusions
Impaired microcirculatory function could be found using a non-invasive LDF technique in normoandrogenaemic women with PCOS undergoing IVF, indicating early changes in vascular endothelial dysfunction. Future observational studies should clarify whether PORH measurement might help predict IVF prognosis or obstetric complications.
Polycystic ovary syndrome (PCOS) is one of the most common endocrinopathies in women of reproductive age. It is associated with metabolic disorders, including insulin resistance and dyslipidaemia, which may lead to a chronic inflammatory response, endothelial dysfunction and cardiovascular disease (
Diastolic dysfunction and increased serum homocysteine concentrations may contribute to increased cardiovascular risk in patients with polycystic ovary syndrome.
). Endothelial dysfunction, a known early sign of atherosclerosis, has been widely proposed in studies of PCOS studies, suggesting an increased risk for early onset cardiovascular events in PCOS (
Diastolic dysfunction and increased serum homocysteine concentrations may contribute to increased cardiovascular risk in patients with polycystic ovary syndrome.
). Periodic assessment of post-occlusive reactive hyperaemia (PORH) across a treatment period has been suggested as a predictive marker of microvascular function (
). Recently, PORH measurement can be conducted non-invasively by laser Doppler flowmetry (LDF), providing a real-time continuous measurement of microvascular perfusion (
). Knowledge of the relevance of PORH parameters in PCOS, however, is limited, and the number of patients studied to date is too small to enable the performance of a formal meta-analysis.
Women with PCOS have a unique hormonal milieu that is not only associated with metabolic and cardiovascular disorders but also has important implications for infertility. Reproductive potential is considered to be reduced in women with PCOS (
). Alteration in oocyte and endometrial quality influences the reproductive outcomes of infertile patients with PCOS. Regardless of ovulatory status, impaired oocyte competence among patients with PCOS ranges from altered folliculogenesis to abnormalities of oocyte morphology, which reduces the potential for oocyte maturation and fertilization (
). Furthermore, dysregulation of endometrial gene expression results in chronic inflammation, immune dysfunction and cellular abnormality, predisposing to miscarriage and pregnancy complications in women with PCOS (
). Heterogenous causes involved in PCOS lead to infertility and poor pregnancy outcomes. Although there is currently no universal recommendation to reverse endocrine disorder in PCOS, previous research has demonstrated that androgen drives endothelial dysfunction in women with PCOS (
). The aim of the present study was to investigate the association between PORH and ovarian stimulation in women with PCOS compared with women without PCOS (controls).
Materials and methods
Study setting and participants
This prospective study was conducted at the reproductive centre in Chang Gung Memorial Hospital (Taoyuan, Taiwan) between June 2019 and June 2021. Patients eligible for IVF, aged between 22 and 40 years, were consecutively enrolled. All patients signed written consent forms, and the Institutional Review Board of Chang Gung Memorial Hospital approved the study protocol (Institutional Review Board number 201900400A3 on 24 April 2019).
Thirty-four women were diagnosed with PCOS based on the presence of polycystic ovaries upon transvaginal ultrasound scan and history of oligoovulatory and anovulatory menstrual cycles according to the Rotterdam consensus (
). The women were interviewed to obtain their medical history and indications of good health other than PCOS. Thirty-six healthy normoandrogenaemic women in the control group reported regular menstrual cycles with no concomitant gynaecologic pathology, such as endometriosis, uterine fibroids or ovarian cysts.
At study entry, all participants took anthropometric measurements and endothelial function evaluations. A venous blood draw was carried out for metabolic and hormonal assays initially. After ovarian stimulation, the hormonal profile and endothelial function were obtained on trigger day. A flowchart of the study is presented in Figure 1.
Weight, height, body fat and muscle mass were measured. Body mass index (BMI, kg/m2) was also calculated to assess obesity at the time of enrollment. Body fat and muscle mass percentage were obtained using a body composition monitor model: HBF-222T (OMRON Healthcare, Kyoto, Japan). The foot-to-foot bioelectrical impedance analysis was reported to be a reliable and accurate tool for body composition measurement (
). The participants were dressed in light clothing and instructed to stand upright on four electrodes with bare feet. Body fat and muscle mass percentage were automatically estimated from the manufacturer's equations.
Ovarian stimulation protocol
Protocols for ovarian stimulation were either gonadotrophin-releasing hormone (GnRH) antagonist or progestin-primed ovarian stimulation. The regimen was adjusted individually depending on the patient's age, BMI, ovarian reserve, number of antral follicles and baseline hormone levels. In general, subcutaneous gonadotrophin injections (200–250 IU per day) were started on day 2 of spontaneous or progesterone-induced menstrual cycle. Gonadotrophin doses were adjusted according to ovarian response, measured by serial transvaginal ultrasonography and serum oestradiol tests. Final oocyte maturation was carried out with either GnRH agonist (Decapeptyl® 0.2 mg) (Ferring, Kiel, Germany), recombinant HCG (Ovitrelle® 250 µg) (Merck Serono, Geneva, Switzerland), or both, when the leading follicle reached 18 mm. Transvaginal oocyte retrieval was carried out 36 h after triggering. After fresh embryo transfer or elective cryopreservation, all embryos were arranged based on clinical assessment.
Laboratory assays
Biochemistry tests were carried out in our hospital laboratory accredited by the College of American Pathologists. Venous blood samples were collected from all patients and healthy controls in the morning between 0800 and 0900 h after an overnight fast for at least 12 h. Baseline metabolic parameters were measured, including fasting glucose, fasting insulin, triglyceride, high-density lipoprotein cholesterol (HDL-C), total cholesterol and low-density lipoprotein cholesterol (LDL-C). The LDL-C/HDL-C and total cholesterol/HDL-C ratios were calculated as predictors of ischaemic heart disease risk (
Total cholesterol/HDL cholesterol ratio vs LDL cholesterol/HDL cholesterol ratio as indices of ischemic heart disease risk in men: the Quebec Cardiovascular Study.
). Insulin resistance was estimated by a homeostatic model based on fasting glucose and insulin. The homeostasis model assessment-insulin resistance (HOMA-IR) index was calculated according to the formula HOMA-IR = [glucose] (mg/dl) x [insulin] (mIU/l)/405 (
Homeostasis model assessment-insulin resistance (HOMA-IR), a key role for assessing the ovulation function in polycystic ovary syndrome (PCOS) patients with insulin resistance.
). In addition, oestradiol, testosterone, free testosterone and high-sensitivity C-reactive protein (HSCRP) were measured in serial blood tests on day-2 of the menstrual cycle and the day of GnRH agonist, HCG triggering, or both.
Endothelial function evaluation
Each individual participated in two experimental sessions to assess microvascular dilation, occurring in the following order: on day-2 of the menstrual cycle and trigger day of the IVF cycle. Endothelial function was measured as PORH before and after ovarian stimulation (
). Each patient was taken into a quiet temperature-controlled room at approximately 20–25°C. After resting in the supine position for 10 min, a laser probe was applied to the left forearm skin (test site). Briefly, the reactive hyperaemic protocol consisted of a 3-min baseline recording, followed by another 3-min occlusion of brachial blood flow by upper arm pressure cuff inflation up to 200 mmHg or 60 mmHg above baseline systolic blood pressure. After releasing the pressure cuff, the PORH response was continuously recorded for the final 3 min. The procedure automatically analysed the signal through a computer algorithm using MoorSoft for Windows software package version 4.2 (Moor instruments) without interobserver variability. The following laser Doppler-derived parameters of PORH were studied (Figure. 2): PORHmax, the maximum increase in hyperaemia perfusion (peak flow above minimum rest flow), expressed as the difference between maximal perfusion flux during post-occlusive reactive hyperaemia and minimal baseline perfusion flux; time-to-peak, time after occlusion cuff decompression until the postocclusive peak perfusion flux is reached; PORHpeak, amplitude of peak perfusion flux during hyperaemia; PORHmax/time to peak, mean velocity of the post-occlusive hyperaemia increase, expressed as a ratio between PROHmax and time to peak; the PORH index, the percentage of hyperemic response, is calculated as follows: area 1 min after release/area 1 min before inflation
Figure 2Post-occlusive reactive hyperaemia (PORH) measurement. AH, area of hyperaemia; AO, area of occlusion; AU, arbitrary unit; BZ, biological zero; RL, resting level; TH, time to half decay; TP, time to peak; TR, time to recovery; T0, time to zero increase; PORHMax, maximum increase in hyperaemia perfusion flux; PORHPeak, amplitude of peak perfusion flux.
Statistical Package for Social Sciences (SPSS) version 22.0 (SPSS Inc., Chicago, IL, USA) was used for data analysis. Student's t-test was applied to continuous variables with normal distributions; the Mann–Whitney U test was used for continuous variables with non-normal distributions, and the chi-squared test was used for comparisons of qualitative data. Between-group and between-day comparisons of parameters were performed using the t-test. The results are expressed as the mean ± SD. Correlations were performed by Pearson's method. P < 0.05 were considered statistically significant.
Results
A total of 70 patients were included in this study; 34 of the patients met the Rotterdam criteria. They were classified as normoandrogenaemic PCOS (PCOS group), and the other 36 non-PCOS participants were enrolled in the control group. The mean age was 34.3 ± 3.3 years and 34.5 ± 4.5 years in the PCOS and the control groups, respectively. No significant differences were found between the two groups in age, BMI, body fat or muscle mass percentage and baseline hormone profile. The PCOS group had higher HSCRP (P = 0.048), anti-Müllerian hormone (P < 0.001), triglyceride (P = 0.014), LDL-C/HDL-C (P = 0.019), and total cholesterol/HDL-C (P = 0.011) ratios than the control group. Hyperinsulinaemia (P = 0.025) and insulin resistance (P = 0.027) were also discovered in the PCOS group. Detailed descriptions of participants are presented in Table 1.
TABLE 1DEMOGRAPHIC DATA AND HORMONAL PROFILE OF WOMEN WITH POLYCYSTIC OVARY SYNDROME AND CONTROLS
Variable
PCOS (n = 34)
Control (n = 36)
P-value
Age, years
34.3 ± 3.3
34.5 ± 4.5
0.784
BMI, kg/m2
24.5 ± 4.8
23.0 ± 3.0
0.120
Body composition, %
Fat
32.5 ± 4.8
31.4 ± 3.7
0.282
Visceral fat
7.1 ± 5.8
5.3 ± 3.0
0.113
Muscle
25.9 ± 2.4
26.8 ± 2.0
0.109
AMH, ng/ml
7.0 ± 4.1
3.8 ± 1.6
<0.001
Basal LH concentration, mIU/ml
7.0 ± 6.8
5.3 ± 2.2
0.160
Basal oestradiol concentration, pg/ml
37.8 ± 22.3
38.2 ± 27.6
0.954
Basal testosterone, ng/ml
0.42 ± 0.16
0.38 ± 0.19
0.395
Basal free testosterone, pg/ml
1.10 ± 0.48
1.00 ± 0.52
0.439
Ovarian stimulation regimen, n (%)
0.241
GnRH antagonist protocol
21 (62)
27 (75)
PPOS protocol
13 (38)
9 (25)
HSCRP, mg/l
1.9 ± 2.2
1.0 ± 1.1
0.048
Lipid profile
HDL-C mg/dl
55.0 ± 12.1
60.6 ± 10.7
0.046
VLDL-C, g/dl
22.9 ± 17.2
15.2 ± 6.1
0.014
LDL-C, mg/dl
119.2 ± 31.2
107.4 ± 28.8
0.103
T-CHO, mg/dl
192.5 ± 32.0
183.7 ± 27.7
0.222
TG, mg/dl
114.4 ± 86.4
75.8 ± 30.7
0.014
Non-HDL-C, mg/dl
137.5 ± 33.6
123.2 ± 27.9
0.056
Risks of IHD, %
LDL/HDL
2.3 ± 0.9
1.9 ± 0.7
0.019
T-CHO/HDL
3.7 ± 1.1
3.1 ± 0.7
0.011
Glucose (ante cibum), mg/dl
95.4 ± 20.7
89.5 ± 20.9
0.244
Insulin, µU/ml
25.0 ± 35.5
11.0 ± 8.8
0.025
HOMA-IR index
7.2 ± 11.5
2.7 ± 3.2
0.027
HbA1c, %
5.5 ± 0.3
5.3 ± 0.4
0.166
Data are presented as mean ± SD unless otherwise indicated.
AMH, anti-Müllerian hormone; BMI, body mass index; GnRH, gonadotrophin-releasing hormone; HDL, high-density lipoprotein; HDL-C, HDL cholesterol; HOMA-IR, homeostasis model assessment-insulin resistance; HSCRP, high sensitive C-reactive protein; IHD, ischemic heart disease; LDL, low-density lipoprotein; LDL-C, LDL cholesterol; NS, not significant; PPOS, progestin-primed ovarian stimulation; T-CHO, total cholesterol; TG, triglyceride; VLDL-C, very low-density lipoprotein cholesterol.
No statistically significant differences were found in the baseline endothelial function between the two groups. The PORH index was 2.46 ± 0.74 for the PCOS group and 2.79 ± 1.02 for the controls (P = 0.119) (Table 2).
After ovarian stimulation, serum oestrogen (P = 0.018), testosterone (P = 0.007) and free testosterone (P = 0.049) were significantly higher in the PCOS group, concomitant with a lower PORH slope (7.2 ± 4.3 versus 9.7 ± 4.5, P = 0.018) compared with those in the control group (Supplementary Table 1). The changes in PORH parameters before and after ovarian stimulation demonstrated an increased slope (7.1 ± 3.3 versus 9.7 ± 4.5, P = 0.007) and a higher peak level (30.7 ± 16.3 versus 43.5 ± 17.3, P = 0.008) in the control group (Table 3). The PCOS group, however, experienced a blunting response to ovarian stimulation (change of value in slope, P for interaction = 0.003; change of value in peak, P for interaction = 0.023) (Figure 3).
TABLE 3CHANGES IN POST-OCCLUSIVE REACTIVE HYPERAEMIA PARAMETERS DURING OVARIAN STIMULATION
Ovarian stimulation
PCOS (n = 34)
Control (n = 36)
P for interaction
Before
After
P-value
Before
After
P-value
Clinical parameters
LH, mIU/ml
7.0 ± 6.8
3.6 ± 3.4
<0.001
5.3 ± 2.2
3.5 ± 3.5
0.005
0.100
Oestradiol, pg/ml
37.8 ± 22.3
4436.9 ± 3603.3
<0.001
38.2 ± 27.6
2769.9 ± 1908.6
<0.001
0.016
Testosterone, ng/ml
0.42 ± 0.16
0.74 ± 0.38
<0.001
0.38 ± 0.19
0.52 ± 0.25
<0.001
0.004
Free testosterone, pg/ml
1.10 ± 0.48
1.51 ± 0.66
<0.001
1.00 ± 0.52
1.20 ± 0.58
0.019
0.038
HSCRP, mg/l
1.9 ± 2.2
2.0 ± 2.2
0.465
1.0 ± 1.1
1.4 ± 1.6
0.068
0.266
PORH parameters
Time to peak, s
27.4 ± 44.2
24.1 ± 37.0
0.668
16.9 ± 28.3
12.8 ± 14.5
0.461
0.938
Slope
8.2 ± 5.1
7.2 ± 4.3
0.212
7.1 ± 3.3
9.7 ± 4.5
0.007
0.003
PORHIndex
2.46 ± 0.74
2.5 ± 0.9
0.649
2.79 ± 1.02
2.7 ± 0.9
0.675
0.543
PORHMax, AU
38.8 ± 19.4
37.0 ± 21.8
0.895
30.7 ± 16.3
43.5 ± 17.3
0.008
0.023
Data are reported as mean ± SD.
AU, arbitrary unit; HSCRP, high sensitive C-reactive protein; NS, not significant; PORH, post-occlusive reactive hyperaemia.
Figure 3Changes in post-occlusive reactive hyperaemia (PORH) parameters during ovarian stimulation. ap for interaction; AU, arbitrary unit; PCOS, polycystic ovarian syndrome; PORHMax, maximum increase in hyperaemia perfusion flux.
In the present study, the PCOS group had significantly higher inflammatory factors, such as HSCRP, ischaemic heart risk predictors, hyperinsulinaemia and insulin resistance than the control group.
The diagnosis of PCOS has changed over the years. Using the Rotterdam criteria (
), PCOS can be characterized into three different phenotypes: hyperandrogenism and chronic anovulation; hyperandrogenism and polycystic ovaries but with ovulatory cycles; chronic anovulation and polycystic ovaries, without requiring clinical hyperandrogenism. The clinical presentation of chronic anovulation and hyperandrogenism, however, has been stressed as the major diagnostic criteria (
), and the occurrence of normoandrogenaemic PCOS has been acknowledged in recent years. For Taiwanese patients, polycystic ovary morphology is the most common PCOS component (
). In addition, normoandrogenaemic PCOS, a typical phenotype in Korean women, was reported to be less likely to have metabolic dysfunction, insulin resistance or elevated blood pressure (
). The present study was not initially designed to assess different phenotypes of PCOS; however, the enrolled patients presenting to our fertility centre primarily had normoandrogenaemia with PCOM and irregular menstrual cycles.
Hyperandrogenism is a primary driver of endothelial dysfunction in women with androgen-excess PCOS. Compromised endothelial-mediated vasodilatation was found in young women with androgen-excess PCOS (
). The study demonstrated that suppressing androgens in women with PCOS improved endothelial-mediated microvascular response and enhanced vasodilator tone through increasing endothelin-1 (ET-1) mediated endothelin-B receptor mechanism. It was considered a prominent endothelial function abnormality in obese and non-obese patients with hyperandrogenic PCOS (
Metabolic characteristics of women with polycystic ovaries and oligo-amenorrhoea but normal androgen levels: implications for the management of polycystic ovary syndrome.
) showed that normoandrogenaemic women with PCOS were metabolically similar to controls, with significantly fewer metabolic features than women with PCOS who were also hyperandrogenaemic. In the present study, baseline endothelial function was identical between normoandrogenaemic PCOS and controls.
Insulin resistance and resultant hyperinsulinaemia are cardinal features of PCOS. Specifically, insulin-stimulated secretion of ET-1, independent of obesity, is a predictor of coronary artery disease in PCOS (
). In the present study, hyperinsulinaemia was found in the PCOS group, implicating insulin resistance and glucose intolerance. Besides, subclinical dyslipidaemia with increased ischaemic heart risk and elevated HSCRP were also observed in the PCOS group, which were reported as circulating biomarkers of cardiovascular risk (
Changes in the skin microvasculature have been found to occur many years before the appearance of symptoms of the microvascular disease of other organs in young patients with type 1 diabetes (
). Despite epidemiological evidence suggesting increased cardiovascular morbidity and coronary artery mortality in women with PCOS, data on endothelial dysfunction in patients with PCOS were poor and conflicting (
). In-vivo studies of endothelial function are fraught with difficulties, and no gold standard currently exists. Measuring endothelial dysfunction in peripheral arteries has the advantage over direct evaluation in the coronary arteries of being less invasive and more amenable to complex study protocols, yielding more detailed mechanistic data (
). Forearm ischaemia is induced by a tourniquet, the release of which results in hyperaemia of the distal vascular bed. The magnitude of flow-mediated diameter is thought to be proportional to endothelial function in the coronary arteries (
). In FMD of the brachial artery, dilatation is measured by ultrasonography after inducing brachial artery ischaemia, which leads to the release of endothelial nitric oxide and relaxation of vascular smooth muscle.
showed no difference in FMD between patients with PCOS and controls, despite the hyperandrogenism and insulin resistance in patients with PCOS. Conversely,
found markedly diminished endothelium-dependent and insulin-mediated flow responses in the femoral artery of women with PCOS. A meta-analysis encompassing 21 studies with 908 women with PCOS and 281 control women suggested that endothelial dysfunction is inherent in women with PCOS, even if they are young and non-obese (
The evaluation of endothelial function with flow-mediated dilatation and carotid intima media thickness in young nonobese polycystic ovary syndrome patients; existence of insulin resistance alone may not represent an adequate condition for deterioration of endothelial function.
Increased arterial stiffness in nonobese women with polycystic ovary syndrome (PCOS) without comorbidities: one more characteristic inherent to the syndrome?.
) previously published studies. The disparity in the extant literature might be related to the different methods used to assess FMD, the considerable variability between participants, with varying definitions of diagnosis, disease duration, severity and comorbidities, or the poorly matched control groups.
Although FMD is one of the most common tests in vascular research, high technique-demanding and inter-observer variation should be overcome. Recently, LDF has become a promising model for studying microvascular reactivity. It uses the Doppler shift of laser light as the information carrier. A previous study (
) showed that PORHmax, time to peak, PORHpeak, and PORHmax/time to peak are highly reproducible laser Doppler-derived parameters and reliable non-invasive clinical application indices of microvascular function. Indeed, vascular research related to numerous diseases and conditions was successfully conducted through LDF studies of the forearm-based reactive hyperaemia response (
Statins enhance postischemic hyperaemia in the skin circulation of hypercholesterolemic patients: a monitoring test of endothelial dysfunction for clinical practice?.
). The laser Doppler PORH method, however, has not been optimized and standardized. In the present study, we proposed several parameters to characterize better the microvascular response to PORH assessed with LDF in participants with PCOS.
Ovarian stimulation
Women undergoing ovarian stimulation may represent a model for studying the complex interaction between the hormonal milieu and microvascular function. Changes in PORH during an IVF cycle in PCOS were described for the first time in this study. Before ovarian stimulation, resting cutaneous vascular conductance was similar between the groups, suggesting normal baseline endothelial function despite insulin resistance in normoandrogenaemic PCOS. Endogenous oestrogen in IVF (approximately 10-fold increase in oestradiol levels at the time of ovulation) enhanced post-ischaemic skin blood flow in healthy women relative to resting PORH parameters (
). In the present study, ovarian stimulation increased microvascular responses to temporary ischaemia in the control group. Serum oestradiol rose during ovarian stimulation and was significantly higher on trigger day in the PCOS group than in the control group. The increase in post-ischaemic blood flow was blunted in the PCOS groups. We demonstrated the obscure endothelial dysfunction in normoandrogenaemic PCOS compared with healthy controls induced by ovarian stimulation during artificial reproductive therapy.
The limitations of our study included the relatively small number of participants. Nevertheless, our data demonstrated changes in sex hormone concentrations and cutaneous microcirculatory function related to ovarian stimulation. This study strengthened the possibility that early endothelial dysfunction in PCOS could be measured by LDF, a simple, non-invasive method for PORH.
In conclusion, to the best of our knowledge, this was the first study to assess endothelial function from an ovarian stimulation cycle in normoandrogenaemic patients with PCOS. Non-invasive LDF investigated functional vascular damage in PCOS as an early cardiovascular risk marker. The results demonstrated that normoandrogenaemic women with PCOS and a blunted PORH response after pronounced oestrogen stimulation compared with healthy controls.
Funding
This research was funded by Chang Gung Foundation (Research Grant number CMRPG3J0451).
The evaluation of endothelial function with flow-mediated dilatation and carotid intima media thickness in young nonobese polycystic ovary syndrome patients; existence of insulin resistance alone may not represent an adequate condition for deterioration of endothelial function.
Metabolic characteristics of women with polycystic ovaries and oligo-amenorrhoea but normal androgen levels: implications for the management of polycystic ovary syndrome.
Statins enhance postischemic hyperaemia in the skin circulation of hypercholesterolemic patients: a monitoring test of endothelial dysfunction for clinical practice?.
Total cholesterol/HDL cholesterol ratio vs LDL cholesterol/HDL cholesterol ratio as indices of ischemic heart disease risk in men: the Quebec Cardiovascular Study.
Homeostasis model assessment-insulin resistance (HOMA-IR), a key role for assessing the ovulation function in polycystic ovary syndrome (PCOS) patients with insulin resistance.
Increased arterial stiffness in nonobese women with polycystic ovary syndrome (PCOS) without comorbidities: one more characteristic inherent to the syndrome?.
Diastolic dysfunction and increased serum homocysteine concentrations may contribute to increased cardiovascular risk in patients with polycystic ovary syndrome.
Liang-Hsuan Chen graduated in medicine and completed her residency in obestetrics and gynaeology in 2013 and 2018, respectively. She works as a clinical researcher in reproductive endocrinology and infertility at Linkou Chang Gung Memorial Hospital, Taiwan. Her main areas of interest are reproductive medicine, gynaecological disease and infertility treatment.
Key message
Impaired microcirculatory function could be found using non-invasive laser Doppler flowmetry. Normoandrogenaemic women with polycystic ovary syndrome (PCOS) had a blunted post-occlusive reactive hyperaemia (PORH) response after pronounced oestrogen stimulation, indicating early changes in vascular endothelial dysfunction. The study supports PORH as an early marker for impaired microcirculation in PCOS.
Article info
Publication history
Published online: November 25, 2022
Accepted:
November 21,
2022
Received in revised form:
November 5,
2022
Received:
September 6,
2022
Declaration: The authors report no financial or commercial conflicts of interest.
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