Retinal oximetry and microvascular assessment after hypertensive pregnancy complications.

PURPOSE: Women with hypertensive disorders of pregnancy (HDP) are at increased risk of developing premature cardiovascular disease (CVD). The mechanisms behind this are not fully understood, but microvascular alterations have been documented in retinal arterioles and venules. The aim of this study was to use non-invasive retinal imaging to investigate the structural and functional properties of arterioles, venules and capillaries in this patient group. METHODS: We examined 27 women with previous HDP and 23 controls at 3 years postpartum. The retinal microvasculature was assessed by vessel calibre measurements, retinal oximetry and optical coherence tomography angiography. Differences were analysed using non-parametric tests and multiple regression analyses, adjusted for age and body mass index. RESULTS: Median arteriolar oxygen saturation (SaO2 ; 94.2% vs. 93.0%), venular oxygen saturation (SvO2 ; 60.1% vs. 62.4%) and arteriovenous saturation difference (AV-difference; 32.8% vs. 32.3%) were similar across groups. Capillary vessel density (VD; 46.2% vs. 46.3%), skeletonised VD (VSD; 21.3 vs. 21.1 mm/mm2 ) and vessel diameter index (21.65 vs. 21.86) were also comparable. In the HDP group, mean arterial pressure (MAP) was positively correlated with AV-difference (R2 = 0.209) and negatively correlated with arteriolar diameter (CRAE; r2 = 0.382). CONCLUSIONS: Structural microvascular alterations appear not to be key biomarkers for CVD risk after HDP as early as 3 years postpartum in otherwise healthy women. Further studies are needed to evaluate whether such changes occur later in life. MAP was associated with AV-difference only in the HDP group, suggesting specific mechanisms affecting functional microvascular properties in these women.

Circulating cardiovascular biomarkers during and after preeclampsia: Crosstalk with placental function?

Cardiovascular disease (CVD) is the leading cause of death in women, yet sex-specific risk factors remain understudied. Preeclampsia and other adverse pregnancy outcomes imply an increased maternal cardiovascular risk. We hypothesized that cardiac troponin T (cTnT), N-terminal pro-Brain Natriuretic Peptide (NT-proBNP) and growth differentiation factor 15 (GDF-15) are increased in such pregnancies and correlate with markers of placental dysfunction. We also investigated these cardiovascular biomarkers 1 or 3 years postpartum. Prior to delivery, we included serum from 417 pregnant women: 55 early-onset preeclampsia (EO-PE), 63 late-onset preeclampsia (LO-PE), 30 gestational hypertension (GH) and 269 healthy controls. Postpartum, we included 341 women 1 or 3 years after delivery: 26 EO-PE, 107 LO-PE, 61 GH, and 147 healthy pregnancies. Prior to delivery, median cTnT and NT-proBNP concentrations were higher in women with EO-PE, LO-PE, or GH than in controls. Median GDF-15 was higher in EO-PE and LO-PE compared to controls. Postpartum, GDF-15 was elevated in women with previous EO-PE. Markers of placental dysfunction correlated with CVD biomarkers in pregnancy, but not postpartum. Our findings underscore the cardiovascular burden of hypertensive disorders of pregnancy and the crosstalk with placental function. The upregulation of circulating GDF-15 following early-onset preeclampsia is in line with the epidemiological excessive risk of premature CVD in this group of women. GDF-15 may be explored for targeting postpartum women with most to gain from intensified preventive follow-up for CVD.

Cardiovascular biomarkers in pregnancy with diabetes and associations to glucose control.

AIM: Cardiovascular disease (CVD) is a leading cause of death in both men and women. Type 1 and 2 diabetes mellitus (DM1 and DM2) are well-known risk factors for CVD. In addition, gestational diabetes mellitus (GDM) is a female sex-specific risk factor for CVD. Here, we measure circulating concentrations of cardiac troponin T (cTNT), N-terminal pro-B-type natriuretic peptide (NT-proBNP) and growth differentiation factor 15 (GDF-15) during pregnancy-a window of time often referred to as a cardiovascular stress test for women. METHODS: This study utilized data from 384 pregnant women: 64 with DM1, 16 with DM2, 35 with GDM and 269 euglycemic controls. Blood was predominantly sampled within a week before delivery. Cardiovascular biomarker concentrations were measured in serum using electrochemiluminescence immunoassay. RESULT: Circulating cTnT levels were higher in women with DM1, DM2 and GDM as compared to controls, whereas NT-proBNP and GDF-15 levels were only increased in women with DM1. Glucose dysregulation, assessed by third trimester HbA1c levels, positively correlated with all three CVD biomarker levels, whereas pregestational body mass index correlated negatively with GDF-15. CONCLUSIONS: Our results support the presence of myocardial affection in women with diabetic disorders during pregnancy. Although pregestational DM1 in this study was associated with the most adverse CVD biomarker profile, women with GDM displayed an adverse cTnT profile similar to what we found in women with pregestational DM2. This supports that women with GDM should be offered long-term intensified cardiovascular follow-up and lifestyle advice following delivery, similarly to the well-established CV follow-up of women with pregestational DM.

Failure of physiological transformation and spiral artery atherosis: their roles in preeclampsia.

Physiological transformation with remodeling of the uteroplacental spiral arteries is key to a successful placentation and normal placental function. It is an intricate process that involves, but is not restricted to, complex interactions between maternal decidual immune cells and invasive trophoblasts in the uterine wall. In normal pregnancy, the smooth muscle cells of the arterial tunica media of uteroplacental spiral arteries are replaced by invading trophoblasts and fibrinoid, and the arterial diameter increases 5- to 10-fold. Poor remodeling of the uteroplacental spiral arteries is linked to early-onset preeclampsia and several other major obstetrical syndromes, including fetal growth restriction, placental abruption, and spontaneous preterm premature rupture of membranes. Extravillous endoglandular and endovenous trophoblast invasions have recently been put forth as potential contributors to these syndromes as well. The well-acknowledged disturbed extravillous invasion of maternal spiral arteries in preeclampsia is summarized, as are briefly novel concepts of disturbed extravillous endoglandular and endovenous trophoblast invasions. Acute atherosis is a foam cell lesion of the uteroplacental spiral arteries associated with poor remodeling. It shares some morphologic features with early stages of atherosclerosis, but several molecular differences between these lesions have also recently been revealed. Acute atherosis is most prevalent at the maternal-fetal interface, at the tip of the spiral arteries. The localization of acute atherosis downstream of poorly remodeled arteries suggests that alterations in blood flow may trigger inflammation and foam cell development. Acute atherosis within the decidua basalis is not, however, confined to unremodeled areas of spiral arteries or to hypertensive disorders of pregnancy and may even be present in some clinically uneventful pregnancies. Given that foam cells of atherosclerotic lesions are known to arise from smooth muscle cells or macrophages activated by multiple types of inflammatory stimulation, we have proposed that multiple forms of decidual vascular inflammation may cause acute atherosis, with or without poor remodeling and/or preeclampsia. Furthermore, we propose that acute atherosis may develop at different gestational ages, depending on the type and degree of the inflammatory insult. This review summarizes the current knowledge of spiral artery remodeling defects and acute atherosis in preeclampsia. Some controversies will be presented, including endovascular and interstitial trophoblast invasion depths, the concept of 2-stage trophoblast invasion, and whether the replacement of maternal spiral artery endothelium by fetal endovascular trophoblasts is permanent. We will discuss the role of acute atherosis in the pathophysiology of preeclampsia and short- and long-term health correlates. Finally, we suggest future opportunities for research on this intriguing uteroplacental interface between the mother and fetus.

Acute Atherosis Lesions at the Fetal-Maternal Border: Current Knowledge and Implications for Maternal Cardiovascular Health.

Decidua basalis, the endometrium of pregnancy, is an important interface between maternal and fetal tissues, made up of both maternal and fetal cells. Acute atherosis is a uteroplacental spiral artery lesion. These patchy arterial wall lesions containing foam cells are predominantly found in the decidua basalis, at the tips of the maternal arteries, where they feed into the placental intervillous space. Acute atherosis is prevalent in preeclampsia and other obstetric syndromes such as fetal growth restriction. Causal factors and effects of acute atherosis remain uncertain. This is in part because decidua basalis is challenging to sample systematically and in large amounts following delivery. We summarize our decidua basalis vacuum suction method, which facilitates tissue-based studies of acute atherosis. We also describe our evidence-based research definition of acute atherosis. Here, we comprehensively review the existing literature on acute atherosis, its underlying mechanisms and possible short- and long-term effects. We propose that multiple pathways leading to decidual vascular inflammation may promote acute atherosis formation, with or without poor spiral artery remodeling and/or preeclampsia. These include maternal alloreactivity, ischemia-reperfusion injury, preexisting systemic inflammation, and microbial infection. The concept of acute atherosis as an inflammatory lesion is not novel. The lesions themselves have an inflammatory phenotype and resemble other arterial lesions of more extensively studied etiology. We discuss findings of concurrently dysregulated proteins involved in immune regulation and cardiovascular function in women with acute atherosis. We also propose a novel hypothesis linking cellular fetal microchimerism, which is prevalent in women with preeclampsia, with acute atherosis in pregnancy and future cardiovascular and neurovascular disease. Finally, women with a history of preeclampsia have an increased risk of premature cardiovascular disease. We review whether presence of acute atherosis may identify women at especially high risk for premature cardiovascular disease.

Low physical activity levels 1 year after pregnancy complications.

OBJECTIVES: Women with previous preeclampsia (PE), gestational hypertension (GH), or gestational diabetes mellitus (GDM) have increased cardiovascular disease (CVD) risk. Physical activity (PA) is an important CVD risk modifier. We aimed to assess PA levels, using a validated objective method, and other modifiable CVD risk factors in women with these previous pregnancy complications. STUDY DESIGN: One year postpartum we assessed PA levels for 1 week in women with previous PE (n = 68), GH (n = 26), GDM (n = 23), and normotensive pregnancies (n = 65), using the ActiGraph-wGT3X-BT™ accelerometer. OUTCOME MEASURES: We assessed adherence to American PA guidelines (≥150 min/week of moderate or ≥75 min/week of vigorous intensity PA), and time spent in moderate and vigorous PA. We also assessed steps/day, blood pressure and anthropometric indices. RESULTS: Recommended PA levels were achieved in only 50%, 39%, and 35% following PE, GH, and GDM, respectively, not significantly different from controls (52%). Differences in moderate and vigorous PA levels and steps/day between the groups were non-significant, except from lower vigorous PA in women with previous GDM. Elevated blood pressure (systolic BP ≥ 120 mmHg and/or diastolic BP ≥ 80 mmHg) was more common after PE and GH. Overweight rates were significantly higher in PE, GH, and GDM groups compared to controls. CONCLUSIONS: Less than half of women achieved recommended PA levels 1 year postpartum. This did not differ significantly between women with previous PE, GH, or GDM compared to controls. Measures to increase PA in postpartum women are warranted, especially in women with pregnancy complications associated with high risk of premature CVD.

Circulating HLA-G and its association with cardiovascular markers in pregnancy.

Human Leukocyte Antigen-G (HLA-G) prevents the activity of immune cells and is decreased in women with preeclampsia. We aimed to investigate the associations between circulating soluble HLA-G (sHLA-G) and 92 cardiovascular disease-related biomarkers from a previously published multiplex study in women with preeclampsia and controls. We found 15 markers significantly associated with circulating sHLA-G in univariate analyses. After multivariable adjusted regression, only proto-oncogene tyrosine-protein kinase Src (SRC) and vascular endothelial growth factor D were significantly associated with sHLA-G. Low SRC, previously observed in the circulation of preeclamptic women, may be regulated by low sHLA-G, and reflect decreased trophoblast differentiation and syncytical formation.

Pregnancy and postpartum levels of circulating maternal sHLA-G in preeclampsia.

Preeclampsia is a leading cause of maternal and offspring mortality and morbidity, and predicts increased future cardiovascular disease risk. Placental dysfunction and immune system dysregulation are likely key pathophysiological factors. Soluble human leukocyte antigen G (sHLA-G) may dampen the specific immune response towards placental trophoblasts. Previous studies have shown low sHLA-G levels in preeclampsia, but postpartum, levels are unknown. Furthermore, the relationship between sHLA-G and sFlt-1 and PlGF, placental function markers, is unknown. We hypothesized that low maternal sHLA-G during pregnancy would be associated with placental dysfunction, including preeclampsia, gestational hypertension, and dysregulated sFlt-1 and PlGF, and that sHLA-G would remain decreased following preeclampsia. We included 316 pregnant women: 58 with early-onset preeclampsia (<34 weeks' gestation), 81 with late-onset preeclampsia (≥34 weeks' gestation), 25 with gestational hypertension, and 152 normotensive controls. Postpartum (1 or 3 years), we included 321 women: 29 with early-onset preeclampsia, 98 with late-onset preeclampsia, 57 with gestational hypertension, and 137 who were normotensive during their index pregnancies. In pregnancy, plasma sHLA-G was significantly lower both in the early- and late-onset preeclampsia groups compared to controls. In women with preeclampsia or gestational hypertension, sHLA-G was inversely correlated with serum sFlt-1. Postpartum, plasma sHLA-G levels were significantly higher in women who had had early-onset preeclampsia compared to controls. Our results support that sHLA-G may be important for placental function. Unexpectedly, sHLA-G was elevated up to 3 years after early-onset preeclampsia, suggesting an excessively activated immune system following this severe preeclampsia form, potentially contributing to future cardiovascular disease risk.

Functional and structural vascular biomarkers in women 1 year after a hypertensive disorder of pregnancy.

OBJECTIVES: Women with a previous hypertensive disorder of pregnancy (HDP: gestational hypertension and preeclampsia) have increased long-term cardiovascular disease risk. Recent meta-analyses show adverse levels of non-invasive functional and structural cardiovascular risk markers such as pulse wave velocity (PWV), heart-rate adjusted augmentation index (AIx75), carotid intima-media thickness (CIMT), and reactive hyperemia index (RHI) after HDPs, and suggest using these for cardiovascular risk stratification. However, it is not known if a previous HDP predict levels of these markers beyond classical cardiovascular risk factors. Study design and main outcome measures. We assessed PWV, AIx75, CIMT, RHI, classical cardiovascular risk factors, and pregnancy characteristics in 221 women 1 year postpartum (controls: 95, previous HDP: 126). Uni- and multi- variate regression analysis were conducted to assess associations between previous HDP and PWV, AIx75, CIMT or RHI. We adjusted for classical cardiovascular risk factors and pregnancy characteristics. A p-level < 0.05 was considered statistically significant. RESULTS: PWV was associated with previous HDP on univariate analysis. This effect was confounded by blood pressure and not significant after adjustment. We found no significant associations between AIx75, RHI, CIMT, and a previous HDP, neither before nor after adjustments. CONCLUSIONS: Associations between a previous HDP and PWV, AIx75, CIMT, or RHI 1 year postpartum can largely be explained by adverse levels of classical cardiovascular risk markers in women with a previous HDP. Women with previous HDP should receive primary prevention of cardiovascular disease, but PWV, AIx75, CIMT or RHI are unlikely to aid in cardiovascular risk stratification 1 year postpartum.

Multiplex Analysis of Circulating Maternal Cardiovascular Biomarkers Comparing Preeclampsia Subtypes.

Preeclampsia, a hypertensive pregnancy disorder, links to increased long-term maternal cardiovascular disease (CVD). The risk is further increased with early-onset preeclampsia (EPE) and delivery of a growth-restricted child. We hypothesized that circulating biomarkers associated with CVD risk differed between preeclampsia subtypes and controls. We compared EPE; n=37, delivery

Risk prediction of maternal cardiovascular disease one year after hypertensive pregnancy complications or gestational diabetes mellitus.

BACKGROUND: Previous preeclampsia, gestational hypertension and gestational diabetes mellitus show a firm epidemiological association to maternal cardiovascular disease risk. Cardiovascular disease risk assessment is recommended in women after these pregnancy complications, but not offered in most countries. We therefore wanted to evaluate the applicability of currently recommended cardiovascular disease risk scores for women one-year postpartum of such pregnancy complications. DESIGN AND METHODS: We tested applicability of three scoring systems, the Atherosclerotic Cardiovascular Disease (ASCVD) score, the Joint British Societies for the Prevention of Cardiovascular Disease (JBS3) score and Framingham 30 year Risk Score-Cardiovascular Disease (FRS-CVD) in 235 women one-year postpartum (controls: 94, gestational hypertension: 35, preeclampsia: 81, gestational diabetes mellitus: 25). Statistical analysis was performed with Mann-Whitney U test for continuous and Fisher's mid-corrected p and Pearson's r for dichotomous variables. A value of p < 0.050 was considered significant. RESULTS: Most women (87.7%) were below 40 years of age, rendering 10-year risk estimations recommended by American and European societies inapplicable. FRS-CVD could be assessed in all women. Significantly fewer could be assessed by the ASCVD (81.5%) and JBS3 (91.6%). All scoring systems showed small, but significant increases in risk scores for one or more of the pregnancy complication groups, but none at the risk magnitude for cardiovascular disease shown in epidemiological studies. CONCLUSION: We demonstrate that ASCVD, JBS3 and FRS-CVD are inadequate in assessing cardiovascular disease risk one-year postpartum. We suggest that pregnancy complications need to be considered separately when evaluating maternal cardiovascular disease risk and need for postpartum follow-up.

Classical Cardiovascular Risk Markers in Pregnancy and Associations to Uteroplacental Acute Atherosis.

Uteroplacental acute atherosis (AA) is a pregnancy-specific arterial lesion resembling early stages of atherosclerosis. AA is frequent in preeclamptic pregnancies, which associate with increased long-term maternal risk of atherosclerotic cardiovascular disease. We hypothesized that AA in pregnant women associates with classical risk factors for cardiovascular disease, including hypertension, hyperlipidemia, glucose intolerance, elevated C-reactive protein, age, and body mass index. We included 237 women delivered by cesarean section (healthy pregnancies, n=94; preeclampsia, n=87; pregestational and gestational diabetes mellitus, n=39; diabetes mellitus with preeclampsia, n=17). They provided blood before delivery for biomarker analyses. AA was diagnosed by immunohistochemistry in uteroplacental (decidual) tissue collected after placental removal. Statistical analyses were performed with Mann-Whitney test. Levels of traditional cardiovascular markers were not associated with decidual AA within the groups of women with normotensive pregnancies, preeclampsia, diabetes mellitus, or diabetes mellitus superimposed with preeclampsia. However, the oldest patient age quartile (36-43 years old) with AA had significantly higher levels of LDL (low-density lipoprotein) and apolipoprotein B (both P<0.01) than women of the same age without AA. AA was associated with elevated median prepregnancy/early pregnancy systolic blood pressure ( P=0.01) in the total cohort, but as preeclampsia was strongly associated with this finding ( P<0.01), this was likely caused by a large proportion of preeclamptic pregnancies in the AA group (62.7%). Our findings demonstrate that dyslipidemia associated with cardiovascular risk is a feature of uteroplacental AA in older women, not of AA in pregnancy in general.

Dysregulation of circulating autoantibodies against VEGF-A, VEGFR-1 and PlGF in preeclampsia - A role in placental and vascular health?

OBJECTIVES: Preeclampsia is a state of antiangiogenesis, with high levels of maternal circulating sVEGFR-1 (soluble vascular endothelial growth factor receptor 1, also named sFlt1) and low levels of PlGF (placenta growth factor). Various autoantibodies have been detected in preeclamptic patients. We hypothesize that circulating autoantibodies against VEGF-A (AA-VEGF-A), VEGFR-1 (AA-VEGFR-1) and PlGF (AA-PlGF) are present in preeclamptic women, with different levels from pregnant women with normotensive pregnancies. Secondly, we wanted to analyze if autoantibody levels are associated to sFlt1 or PLGF levels. STUDY DESIGN: Retrospective cross sectional study of 88 women with singleton pregnancies who delivered at Oslo University Hospital of whom 46 had preeclampsia and 42 had uncomplicated normotensive pregnancies. Novel immunoassays for IgG-autoantibodies against VEGFA, VEGFR-1 and PlGF were developed and serum samples were assayed. MAIN OUTCOME MEASURES AND RESULTS: AA-VEGF-A, AA-VEGF-R1 and AA-PlGF were significantly lower in preeclamptic pregnancies (n=42) compared to normotensive pregnancies (n=46) (p<0.05). On unadjusted analysis, only AA-VEGFA and AA-VEGFR-1 were predictors of PE, but none were independent predictors after adjusting for BMI (body mass index) and parity. In the subgroup of normotensive and PE women with overlapping sVEGFR-1/PlGF-ratios, AA-VEGF was a significant predictor of PE with AUC: 0.735. CONCLUSION: IgG autoantibodies against VEGF-A VEGFR-1 and PlGF can be found in pregnant women. They are dysregulated in preeclampsia. The roles of these autoantibodies are unknown, but this study suggests they play a protective role in pregnancy. The levels of AA against VEGF-A, VEGFR-1 and PlGF might be important factors contributing to anti-angiogenesis regulation.

Outcome of TVT operations in women with low maximum urethral closure pressure.

AIMS: (i) To establish whether low maximal urethral closure pressure (MUCP) is associated with a poorer prognosis after TVT-surgery, and if so to establish an MUCP cut-off value for poor outcome. (ii) To characterize the population with a low MUCP. METHODS: Retrospective analysis of data from 6,646 women with stress/mixed urinary incontinence included in the Norwegian Female Incontinence Registry. Postoperative subjective (degree of satisfaction), objective (leakage on stress test) and composite cure according to preoperative MUCP were analyzed in unadjusted and adjusted analysis. Preoperative variables were compared between women having a low or normal MUCP. Non-parametric tests were used on continuous variables and χ2 tests on categorical variables. Logistic regression was used for the adjusted analysis. Level of significance: P < 0.05. RESULTS: An analysis of centiles of preoperative MUCP showed that a cut-off at 20 cm H2 O did best identify women at risk of not being cured. In unadjusted analysis MUCP ≤20 cm H2 O (n = 422) was associated with objective (OR: 2.48), subjective (OR: 1.60), and composite failure (OR: 1.95) compared to MUCP >20 cm H2 O. In adjusted analysis MUCP ≤20 cm H2 O was associated with neither objective, subjective, nor composite failure. Women with MUCP <20 cm H2 O were preoperatively significantly older, had larger leakage on stress and 24 h pad test, lower mean voided volume and maximum flow rate and higher stress and urge indices. CONCLUSIONS: Women with MUCP ≤20 cm H2 O have similar objective, subjective, and composite outcomes after TVT-surgery compared to women with MUCP >20 cm H2 O after adjusting for preoperative variables. Neurourol. Urodynam. 36:1320-1324, 2017. © 2016 Wiley Periodicals, Inc.

Sling mobilization in the management of urinary retention after mid-urethral sling surgery.

OBJECTIVE: To compare intermittent catheterization, sling mobilization, and sling transection for treatment of urinary retention after mid-urethral sling surgery. METHODS: Data registered in the Norwegian Female Incontinence Registry from 1998 to 2013 were analyzed in this cohort study to compare subjective and objective outcomes after intermittent catheterization, sling mobilization, and sling transection as management of postoperative urinary retention after mid urethral sling surgery. Subjective outcomes were degree of symptom bother and the percentage of women stating "very satisfied" at the postoperative follow-up. The objective outcome was leakage at a cough-jump pad stress test. RESULTS: Intervention due to urinary retention was performed in 585 of 18,772 women (3.1%). Women who had their sling mobilized or had intermittent catheterization, scored better on all postoperative outcomes than those who had their sling transected (P < 0.001). Sling transection was more often needed after intermittent catheterization than after mobilization (P = 0.023). No outcome differences were found between intermittent catheterization only and sling mobilization only. Intention to treat analysis showed that women who underwent sling mobilization as the primary procedure significantly more often had a negative stress test (P = 0.033) and were more often "very satisfied" with the treatment (P = 0.006) than those who were primarily catheterized. CONCLUSIONS: Sling mobilization is a more successful treatment than intermittent catheterization or transection for urinary retention after mid-urethral sling surgery. CLINICAL TRIAL REGISTRATION: Clinical trial registration was not applicable because this study is based on an analysis of anonymous data from The Norwegian Female Incontinence Registry. Neurourol. Urodynam. 36:1091-1096, 2017. © 2016 Wiley Periodicals, Inc.

How often does detrusor overactivity cause urinary leakage during a stress test in women with mixed urinary incontinence?

INTRODUCTION AND HYPOTHESIS: The study examined how often detrusor overactivity (DO) causes leakage during a stress test in women with mixed urinary incontinence (MUI) and whether there are differences between those who do and those who do not have DO during the stress test. METHODS: A retrospective study was performed in 100 women who had an ambulatory urodynamic recording done where bladder, urethral, and vaginal pressures, and leakage were recorded. The stress test consisted of 20 jumping jacks and three forceful coughs. RESULTS: All the women leaked during the stress test: five due to simultaneous stress test and DO, 87 due to the stress test only, and eight during the stress test as well as due to DO before or after the stress test. CONCLUSIONS: During the stress test, 5 % of women with MUI leaked due to the coughs and jumps and simultaneous DO. Women in whom DO was detected had significantly higher Urgency Incontinence Index and leakage during the 24-h pad test.