Evaluation of Cardiac Function of Pregnant Women with High Blood Pressure during Gestation Period and Coupling of Hearts with Peripheral Vessels by Ultrasonic Cardiogram under Artificial Intelligence Algorithm.

The research was aimed at analyzing the value of the optimized eXtreme Gradient Boosting (XGBoost) algorithm-based ultrasound cardiogram images in the diagnosis of pregnant hypertension patients. A total of 145 pregnant women (85 cases suffered from hypertension disease during pregnancy and 60 other normal women were healthy) were selected as the reference to the comparison and analysis of ultrasound cardiac function parameter, common carotid artery parameter, and the coupling relationship between hearts and cervical vessels of pregnant hypertension patients. The results demonstrated ultrasound cardiac function parameter of pregnant hypertension patients as follows. The maximum volume of the left atrium (LAVmax) was 35.65 mm, left ventricular end-systolic volume (LVESV) was 31.07 mm, and left ventricular end-diastolic volume (LVEDV) was 88.73 mm. All the above indexes were obviously higher than those of the normal control group (P < 0.05). Besides, intima-media thickness (IMT) of common carotid artery (465.84 µm), pulse wave velocity (PWV) (8.09 m/s), pressure of turning point 1 from isovolumic contraction phase to ejection phase (PT1) (126.5 mmHg), arterial enhancement pressure (AP) (6.14 mmHg), and arterial pressure enhancement index (8.58%) were all significantly higher than those of the normal control group (P < 0.05). In addition, the correlation between the coupling (E/A) of hearts and carotid artery of pregnant hypertension patients and PWV was not obvious (r = -0.08432, P > 0.05). The results of the research indicated that intima-media inside carotid artery of pregnant hypertension patients thickened obviously, and it became less elastic compared with that of normal healthy pregnant women. What is more, cardiac morphological changes were manifested mainly as the enlargement of the left atrial chamber and the thickening of the interventricular septum. Volume load and blood flow velocity both increased, and left ventricular diastolic function was damaged. XGBoost algorithm-based ultrasound cardiogram images could improve the diagnostic effects of hypertension during pregnancy effectively.

Arrhythmias in Female Patients: Incidence, Presentation and Management.

There is a growing appreciation for differences in epidemiology, treatment, and outcomes of cardiovascular conditions by sex. Historically, cardiovascular clinical trials have under-represented females, but findings have nonetheless been applied to clinical care in a sex-agnostic manner. Thus, much of the collective knowledge about sex-specific cardiovascular outcomes result from post hoc and secondary analyses. In some cases, these investigations have revealed important sex-based differences with implications for optimizing care for female patients with arrhythmias. This review explores the available evidence related to cardiac arrhythmia care among females, with emphasis on areas in which important sex differences are known or suggested. Considerations related to improving female enrollment in clinical trials as a way to establish more robust clinical evidence for the treatment of females are discussed. Areas of remaining evidence gaps are provided, and recommendations for areas of future research and specific action items are suggested. The overarching goal is to improve appreciation for sex-based differences in cardiac arrhythmia care as 1 component of a comprehensive plan to optimize arrhythmia care for all patients.

Pregnancy and Reproductive Risk Factors for Cardiovascular Disease in Women.

Beyond conventional risk factors for cardiovascular disease, women face an additional burden of sex-specific risk factors. Key stages of a woman's reproductive history may influence or reveal short- and long-term cardiometabolic and cardiovascular trajectories. Early and late menarche, polycystic ovary syndrome, infertility, adverse pregnancy outcomes (eg, hypertensive disorders of pregnancy, gestational diabetes, preterm delivery, and intrauterine growth restriction), and absence of breastfeeding are all associated with increased future cardiovascular disease risk. The menopause transition additionally represents a period of accelerated cardiovascular disease risk, with timing (eg, premature menopause), mechanism, and symptoms of menopause, as well as treatment of menopause symptoms, each contributing to this risk. Differences in conventional cardiovascular disease risk factors appear to explain some, but not all, of the observed associations between reproductive history and later-life cardiovascular disease; further research is needed to elucidate hormonal effects and unique sex-specific disease mechanisms. A history of reproductive risk factors represents an opportunity for comprehensive risk factor screening, refinement of cardiovascular disease risk assessment, and implementation of primordial and primary prevention to optimize long-term cardiometabolic health in women.

Sex Differences and Similarities in Valvular Heart Disease.

As populations age worldwide, the burden of valvular heart disease has grown exponentially, and so has the proportion of affected women. Although rheumatic valve disease is declining in high-income countries, degenerative age-related causes are rising. Calcific aortic stenosis and degenerative mitral regurgitation affect a significant proportion of elderly women, particularly those with comorbidities. Women with valvular heart disease have been underrepresented in many of the landmark studies which form the basis for guideline recommendations. As a consequence, surgical referrals in women have often been delayed, with worse postoperative outcomes compared with men. As described in this review, a more recent effort to include women in research studies and clinical trials has increased our knowledge about sex-based differences in epidemiology, pathophysiology, diagnostic criteria, treatment options, outcomes, and prognosis.

Cardiovascular Disease Screening in Women: Leveraging Artificial Intelligence and Digital Tools.

Cardiovascular disease remains the leading cause of death in women. Given accumulating evidence on sex- and gender-based differences in cardiovascular disease development and outcomes, the need for more effective approaches to screening for risk factors and phenotypes in women is ever urgent. Public health surveillance and health care delivery systems now continuously generate massive amounts of data that could be leveraged to enable both screening of cardiovascular risk and implementation of tailored preventive interventions across a woman's life span. However, health care providers, clinical guidelines committees, and health policy experts are not yet sufficiently equipped to optimize the collection of data on women, use or interpret these data, or develop approaches to targeting interventions. Therefore, we provide a broad overview of the key opportunities for cardiovascular screening in women while highlighting the potential applications of artificial intelligence along with digital technologies and tools.

The Impact of Sex and Gender on Stroke.

Women face a disproportionate burden of stroke mortality and disability. Biologic sex and sociocultural gender both contribute to differences in stroke risk factors, assessment, treatment, and outcomes. There are substantial differences in the strength of association of stroke risk factors, as well as female-specific risk factors. Moreover, there are differences in presentation, response to treatment, and stroke outcomes in women. This review outlines current knowledge of impact of sex and gender on stroke, as well as delineates research gaps and areas for future inquiry.

Imaging-Based Risk Stratification for Recurrence Risk in Women with a History of Peripartum Cardiomyopathy.

OBJECTIVE: Peripartum cardiomyopathy (PPCM) affects 1:1,000 U.S. pregnancies, and while many recover from the disease, the risk of recurrence in subsequent pregnancy (SSP) is high. This study aims to evaluate the utility of left ventricular ejection fraction (LVEF) and global longitudinal strain (GLS) to predict the risk of recurrence of PPCM in SSP. STUDY DESIGN: We retrospectively evaluated outcomes in women with a history of PPCM and SSP at a large-volume cardioobstetrics program (2008-2019). RESULTS: There were 18 women who had incident PPCM and pursued SSP. Of 24 pregnancies in these women, 8 (33%) were complicated by the development of recurrent PPCM. LVEF ≥ 52% or GLS ≤ -16 was associated with a low risk of recurrent PPCM. CONCLUSION: Approximately one-third of women with PPCM developed recurrent PPCM in SSP. LVEF and GLS on prepregnancy echocardiography may predict the risk of recurrence. Additional studies evaluating risk for recurrence are required to better understand which women are the safest to consider SSP. KEY POINTS: · Peripartum cardiomyopathy affects 1:1000 US pregnancies.. · Approximately one third of women with a history of peripartum cardiomyopathy developed recurrent disease in a subsequent pregnancy.. · A left ventricular ejection fraction ≥52% or global longitudinal strain ≤-16 on echocardiogram is associated with a low risk of recurrence..

Pregnancy in Takayasu's arteritis has a high risk of hypertension-related fetomaternal complications: A retrospective study of a Turkish cohort.

BACKGROUND: This study aimed to examine fetomaternal outcomes in pregnant women in a large Turkish Takayasu arteritis (TAK) cohort and to evaluate the effects of pregnancy on the disease in those patients. METHODS: This is a cohort study involving 296 pregnancies of 112 TAK patients from 8 tertiary rheumatology centers in Turkey. Pregnancies were divided into 2 groups as pre-d (before disease onset) and post-d (after disease onset). In addition, post-d pregnancies were further divided into 2 subgroups according to fetomaternal complications (FMC) development status. Finally, patients were grouped into those with and without a history of pregnancy after disease onset. RESULTS: In post-d pregnancies, rates of worsening hypertension, new-onset hypertension, and preeclampsia were higher than in pre-d pregnancies (0.9% vs 16%, P < .001, 0.5% vs 5.3%, P = .012, and 0% vs 4%, P = .013, respectively). Patients with FMC were more likely to have renal artery involvement (65% vs 21%, P = .003). The patients who had post-d were younger, had longer disease duration, and had more relapses number than other patients (P < .001, P = .028, P = .016, respectively). Vasculitis Damage Index (VDI) results were similar in patients with or without post-d pregnancies. CONCLUSION: Pregnancies after disease onset were found to be associated with HT and preeclampsia/eclampsia. HT-related FMCs are increased in TAK, and patients with renal artery involvement are at higher risk. The number of relapses increases in patients who become pregnant after disease onset, but pregnancy was not an independent risk factor for relapse. Pregnancy after the onset of disease had no negative effect on VDI.

An integrated model of preeclampsia: a multifaceted syndrome of the maternal cardiovascular-placental-fetal array.

Maternal tolerance of the semiallogenic fetus necessitates conciliation of competing interests. Viviparity evolved with a placenta to mediate the needs of the fetus and maternal adaptation to the demands of pregnancy and to ensure optimal survival for both entities. The maternal-fetal interface is imagined as a 2-dimensional porous barrier between the mother and fetus, when in fact it is an intricate multidimensional array of tissues and resident and circulating factors at play, encompassing the developing fetus, the growing placenta, the changing decidua, and the dynamic maternal cardiovascular system. Pregnancy triggers dramatic changes to maternal hemodynamics to meet the growing demands of the developing fetus. Nearly a century of extensive research into the development and function of the placenta has revealed the role of placental dysfunction in the great obstetrical syndromes, among them preeclampsia. Recently, a debate has arisen questioning the primacy of the placenta in the etiology of preeclampsia, asserting that the maternal cardiovascular system is the instigator of the disorder. It was the clinical observation of the high rate of preeclampsia in hydatidiform mole that initiated the focus on the placenta in the etiology of the disease. Over many years of research, shallow trophoblast invasion with deficient remodeling of the maternal spiral arteries into vessels of higher capacitance and lower resistance has been recognized as hallmarks of the preeclamptic milieu. The lack of the normal decrease in uterine artery resistance is likewise predictive of preeclampsia. In abdominal pregnancies, however, an extrauterine pregnancy develops without remodeling of the spiral arteries, yet there is reduced resistance in the uterine arteries and distant vessels, such as the maternal ophthalmic arteries. Proponents of the maternal cardiovascular model of preeclampsia point to the observed maternal hemodynamic adaptations to pregnancy and maladaptation in gestational hypertension and preeclampsia and how the latter resembles the changes associated with cardiac disease states. Recognition of the importance of the angiogenic-antiangiogenic balance between placental-derived growth factor and its receptor soluble fms-like tyrosine kinase-1 and disturbance in this balance by an excess of a circulating isoform, soluble fms-like tyrosine kinase-1, which competes for and disrupts the proangiogenic receptor binding of the vascular endothelial growth factor and placental-derived growth factor, opened new avenues of research into the pathways to normal adaptation of the maternal cardiovascular and other systems to pregnancy and maladaptation in preeclampsia. The significance of the "placenta vs heart" debate goes beyond the academic: understanding the mutuality of placental and maternal cardiac etiologies of preeclampsia has far-reaching clinical implications for designing prevention strategies, such as aspirin therapy, prediction and surveillance through maternal hemodynamic studies or serum placental-derived growth factor and soluble fms-like tyrosine kinase-1 testing, and possible treatments to attenuate the effects of insipient preeclampsia on women and their fetuses, such as RNAi therapy to counteract excess soluble fms-like tyrosine kinase-1 produced by the placenta. In this review, we will present an integrated model of the maternal-placental-fetal array that delineates the commensality among the constituent parts, showing how a disruption in any component or nexus may lead to the multifaceted syndrome of preeclampsia.

The placenta and preeclampsia: villain or victim?

Preeclampsia is a disease whose characterization has not changed in the 150 years since the cluster of signs associated with the disorder were first described. Although our understanding of the pathophysiology of preeclampsia has advanced considerably since then, there is still little consensus regarding the true etiology of preeclampsia. As a consequence, preeclampsia has earned the moniker "disease of theories," predominantly because the underlying biological mechanisms linking clinical epidemiologic findings to observed organ dysfunction in preeclampsia are far from clear. Despite the lack of cohesive evidence, expert consensus favors the hypothesis that preeclampsia is a primary placental disorder. However, there is now emerging evidence that suboptimal maternal cardiovascular performance resulting in uteroplacental hypoperfusion is more likely to be the cause of secondary placental dysfunction in preeclampsia. Preeclampsia and cardiovascular disease share the same risk factors, preexisting cardiovascular disease is the strongest risk factor (chronic hypertension, congenital heart disease) for developing preeclampsia, and there are now abundant data from maternal echocardiography and angiogenic marker studies that cardiovascular dysfunction precedes the development of preeclampsia by several weeks or months. Importantly, cardiovascular signs and symptoms (hypertension, cerebral edema, cardiac dysfunction) predominate in preeclampsia at clinical presentation and persist into the postnatal period with a 30% risk of chronic hypertension in the decade after birth. Placental malperfusion caused by suboptimal maternal cardiovascular performance may lead to preeclampsia, thereby explaining the preponderance of cardiovascular drugs (aspirin, calcium, statins, metformin, and antihypertensives) in preeclampsia prevention strategies. Despite the seriousness of the maternal and fetal consequences, we are still developing sensitive screening, reliable diagnostic, effective therapeutic, or improvement strategies for postpartum maternal cardiovascular legacy in preeclampsia. The latter will only become clear with an acceptance and understanding of the cardiovascular etiology of preeclampsia.

Impact of autoantibodies against the M2-muscarinic acetylcholine receptor on clinical outcomes in peripartum cardiomyopathy patients with standard treatment.

OBJECTIVES: To evaluate the impact of autoantibodies against the M2-muscarinic receptor (anti-M2-R) on the clinical outcomes of patients receiving the standard treatment for peripartum cardiomyopathy (PPCM). METHODS: A total of 107 PPCM patients who received standard heart failure (HF) treatment between January 1998 and June 2020 were enrolled in this study. According to anti-M2-R reactivity, they were classified into negative (n = 59) and positive (n = 48) groups, denoted as the anti-M2-R (-) and anti-M2-R (+) groups. Echocardiography, 6-min walk distance, serum digoxin concentration (SDC), and routine laboratory tests were performed regularly for 2 years. The all-cause mortality, cardiovascular mortality, and rehospitalisation rate for HF were compared between the two groups. RESULTS: A total of 103 patients were included in the final data analysis, with 46 in the anti-M2-R (+) group and 57 in the anti-M2-R (-) group. Heart rate was lower in the anti-M2-R (+) group than in the anti-M2-R (-) group at the baseline (102.7 ± 6.1 bpm vs. 96.0 ± 6.4 bpm, p < 0.001). The initial SDC was higher in the anti-M2-R (+) group than in the anti-M2-R (-) group with the same dosage of digoxin (1.25 ± 0.45 vs. 0.78 ± 0.24 ng/mL, p < 0.001). The dosages of metoprolol and digoxin were higher in the anti-M2-R (-) patients than in the anti-M2-R (+) patients (38.8 ± 4.6 mg b.i.d. vs. 27.8 ± 5.3 mg b.i.d., p < 0.0001, respectively, for metoprolol; 0.12 ± 0.02 mg/day vs. 0.08 ± 0.04 mg/day, p < 0.0001, respectively, for digoxin). Furthermore, there was a greater improvement in cardiac function in the anti-M2-R (-) patients than in the anti-M2-R (+) patients. Multivariate analysis identified negativity for anti-M2-R as the independent predictor for the improvement of cardiac function. Rehospitalisation for HF was lower in the anti-M2-R (-) group, but all-cause mortality and cardiovascular mortality were the same. CONCLUSIONS: There were no differences in all-cause mortality or cardiovascular mortality between the two groups. Rehospitalisation rate for HF decreased in the anti-M2-R (-) group. This difference may be related to the regulation of the autonomic nervous system by anti-M2-R.

Cardiac Complications in Pregnant Women With Isolated Mitral Stenosis and Their Association With Echocardiographic Changes During Pregnancy.

In women with mitral stenosis (MS), mitral valve gradients and right ventricular systolic pressure (RVSP) can increase in response to the physiologic stress of pregnancy. The prognostic significance of these echocardiographic changes has not been well studied. Pregnancy outcomes and serial echocardiograms were collected in women with MS prospectively recruited as part of a larger study on pregnancy outcomes. Third trimester echocardiograms were compared with baseline echocardiograms. Changes in mitral valve area (MVA), transmitral mean gradient (MG), and RVSP during pregnancy and their relationship to adverse cardiac events (CE) were examined. Fifty-six pregnancies in 47 women with MS were included. The MVA did not change during pregnancy (1.6 ± 0.6 cm2 at baseline vs 1.7 ± 0.6 cm2 in the third trimester, p = 0.46). There was an increase in the MG (8 ± 3 vs 11 ± 6 mm Hg, p <0.001) and the RVSP (39 ± 14 vs 47 ± 20 mm Hg, p <0.001) during the third trimester. Adverse CE occurred in 45% (25/56) of pregnancies. CE were associated with baseline MG>10 mm Hg, baseline RVSP >40 mm Hg, third-trimester MG>10 mm Hg, and RVSP >40 mm Hg. Women with mitral valve MG ≤10 mm Hg who had a normal RVSP at baseline and in the third trimester were at lowest risk for CE (11%) with a negative predictive value of 89%. In conclusion, baseline echocardiographic assessment of MS severity as well as changing echocardiographic parameters during pregnancy can help identify women at risk for cardiac complications during pregnancy.

Obesity, not a high fat, high sucrose diet alone, induced glucose intolerance and cardiac dysfunction during pregnancy and postpartum.

Cardiovascular disease is the leading cause of death in women during pregnancy and the postpartum period. Obesity is an independent risk factor for cardiovascular diseases. Nearly 60% of women of reproductive age are considered overweight or obese, cardiovascular disease morbidity and mortality continue to be pervasive. The objective of this study was to determine the effects of an obesogenic diet on the cardiometabolic health of dams during pregnancy and postpartum. Female mice were fed either a high-fat, high-sucrose diet (HFHS) or a refined control diet (CON) for 8 weeks before initiation of pregnancy and throughout the study period. Mice in the HFHS showed two distinct phenotypes, obesity-prone (HFHS/OP) and obesity resistance (HFHS/OR). Pre-pregnancy obesity (HFHS/OP) induced glucose intolerance before pregnancy and during postpartum. Systolic function indicated by the percent fractional shortening (%FS) was significantly decreased in the HFHS/OP at late pregnancy (vs. HFHS/OR) and weaning (vs. CON), but no differences were found at 6 weeks of postpartum among groups. No induction of pathological cardiac hypertrophy markers was found during postpartum. Plasma adiponectin was decreased while total cholesterol was increased in the HFHS/OP. Our results suggested that obesity, not the diet alone, negatively affected cardiac adaptation during pregnancy and postpartum.

Echocardiographic Assessments for Peripartum Cardiac Events in Pregnant Women with Low-Risk Congenital Heart Disease.

This retrospective cohort study aimed to explore the relationship between temporal changes in the cardiac function and peripartum cardiac events in pregnant women with low-risk congenital heart disease.We performed echocardiography at early and late pregnancy and postpartum in 76 pregnant women with low-risk congenital heart disease, and compared echocardiographic parameters between subjects with and without peripartum cardiac events. Median age at delivery was 27 (range, 24-31) years. The ZAHARA and CARPREG II scores suggested that most women were found to be at low-risk for pregnancy. Fifteen subjects had cardiac events that included heart failure in 10, arrhythmia in 4, and pulmonary hypertension in one subject. The left ventricular and atrial volumes significantly increased from early pregnancy toward late pregnancy, and the E/A ratio and global longitudinal strain significantly decreased from early pregnancy toward late pregnancy. The left atrial volume (67 [53-79] versus 45 [35-55] mL, P = 0.002) and plasma brain natriuretic peptide level (58 [36-123] versus 34 [18-48] pg/mL, P = 0.026) at late pregnancy were significantly higher in subjects with cardiac events than in those without cardiac events.An increase in the left atrial volume followed by mild left ventricular diastolic dysfunction is related to peripartum cardiac events in women with congenital heart disease who are at low risk for cardiac events during pregnancy.

The 9-Month Stress Test: Pregnancy and Exercise-Similarities and Interactions.

Of all physiological systems, the cardiovascular system takes on the most profound adaptation in pregnancy to support fetal growth and development. The adaptations that arise are systemic and involve structural and functional changes that can be observed at the cerebral, central, peripheral, and microvascular beds. This includes, although is not limited to, increased heart rate, stroke volume, and cardiac output with negligible change to blood pressure, reductions in vascular resistance, and cerebral blood flow velocity, systemic artery enlargement, and enhanced endothelial function. All of this takes place to accommodate blood volume expansion and ensure adequate fetal and maternal oxygen delivery. In some instances, the demand placed on the vasculature can manifest as cardiovascular maladaptation and thus, cardiovascular complications can arise. Exercise is recommended in pregnancy because of its powerful ability to reduce the incidence and severity of cardiovascular complications in pregnancy. However, the mechanism by which it acts is poorly understood. The first of our aims in this review was to describe the systemic adaptations that take place in pregnancy. Our second aim was to describe the influence of exercise on these systemic adaptations. It is anticipated that this review can comprehensively capture the extent of knowledge in this area while identifying areas that warrant further investigation.

Links Between Maternal Cardiovascular Disease and the Health of Offspring.

Maternal cardiovascular disease (CVD) during pregnancy is on the rise worldwide, as both more women with congenital heart disease are reaching childbearing age, and conditions such as diabetes, hypertension, and obesity are becoming more prevalent. However, the extent to which maternal CVD influences offspring health, as a neonate and later in childhood and adolescence, remains to be fully understood. The thrifty phenotype hypothesis, by which a fetus adapts to maternal and placental changes to survive a nutrient-starved environment, may provide an answer to the mechanism of maternal CVD and its impact on the offspring. In this narrative review, we aim to provide a review of the literature pertaining to the impact of maternal cardiovascular and hypertensive disease on the health of neonates, children, and adolescents. This review demonstrates that maternal CVD leads to higher rates of complications among neonates. Ultimately, our review supports the hypothesis that maternal CVD leads to intrauterine growth restriction (IUGR), which, through the thrifty phenotype hypothesis and vascular remodelling, can have health repercussions, including an impact on CVD risk, both in the immediate newborn period as well as later throughout the life of the offspring. Further research remains crucial in elucidating the mechanism of maternal CVD long-term effects on offspring, as further understanding could lead to preventive measures to optimise offspring health, including modifiable lifestyle changes. Potential treatments for this at-risk offspring group could mitigate risk, but further studies to provide evidence are needed.

Outcomes of women with congenital heart disease admitted to acute-care hospitals for delivery in Japan: a retrospective cohort study using nationwide Japanese diagnosis procedure combination database.

BACKGROUND: The number of women with congenital heart disease (CHD) who are of childbearing age is increasing due to advancements in medical management. Nonetheless, data on the outcomes of delivery in women with CHD remain limited. Therefore, we conducted a retrospective cohort study using a nationwide database of deliveries by women with CHD. METHODS: Deliveries by women with CHD discharged from acute-care hospitals between April 2017 and March 2018 were identified based on the Diagnosis Procedure Combination database which covers almost all acute-care hospitals in Japan. By using this database, we tried to include relatively high-risk deliveries by women with CHD. Subjects were divided into three groups according to the underlying disease complexity: simple, moderate, and great complexity. The clinical characteristics and incidence of peripartum cardiovascular events were compared among the three groups. RESULTS: A total of 249 deliveries from 107 hospitals were included. The largest facility had 29 deliveries per year. Given the uncertainty of underlying cardiac anomalies, 48 women were excluded, and the remaining 201 women (median age, 32 years) were analyzed. In-hospital maternal death, use of extracorporeal membrane oxygenation, intra-aortic balloon pump, pacemaker, and direct current cardioversion were not observed. Nine patients (4.5%) required intravenous diuretic administration. However, the difference in the frequency of diuretic use was not significant among the three groups (simple, 1.9%; moderate, 7.2%; great, 6.9%; P = 0.204). One participant required valve replacement surgery at 22 days after a successful cesarean section. As the disease complexity increased, deliveries occurred more frequently at university hospitals (simple, 41.7%; moderate, 52.2%; great, 72.4%; P = 0.013) and the length of hospitalization was significantly longer, with median durations of 9.0 (interquartile range [IQR] 7.0-11.0) days, 10.0 (IQR 8.0-24.0) days, and 11.0 (IQR 8.0-36.0) days in the simple, moderate, and great complexity groups, respectively (P = 0.002). CONCLUSIONS: Appropriate patient selection and management by specialized tertiary institutions may contribute to positive outcomes in pregnancies in women with CHD.