UMLS:C0018799 - FACTA Search

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Query: UMLS:C0018799 (heart disease)
34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The fetoplacental system was studied in 80 patients with congenital heart disease by placental scintigraphy, cardiotocography, and ultrasonic examination. Disordered uteroplacental blood flow was detected in 52 of the 64 patients, small-for-date fetuses in 36 of the 80, and chronic fetal hypoxia in 48 of the 72 patients. The authors come to a conclusion that a congenital heart disease is a risk factor in respect of placental insufficiency development.
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PMID:[Diagnosis and treatment of placental insufficiency in patients with congenital heart defects]. 195 66

The feto-placental unit has been evaluated in 102 patients with acquired heart disease presenting as different circulatory states (Grade 0 insufficiency in 43, Grade I in 34 and Grade II A-B in 25 women). Placental scintigraphy was performed in 102, cardiotocography in 77, ultrasonographic fetal and placental biometry in 102 and placental pathological examination in 15 women. The neonatal study included 104 infants, with 2 twin pairs. Scintigraphy revealed utero-placental blood flow (UPBF) impairment in 72 (70.6%) pregnancies; cardiotocography showed chronic fetal hypoxia in 51 (66.1%) and ultrasonography showed intrauterine growth retardation in 44 (43.1%) pregnancies. Disorders of UPBF coexisted with chronic fetal hypoxia and intrauterine growth retardation in 33 (42.8%) pregnancies, with chronic fetal hypoxia in 18 (23.4%) pregnancies. Impairment of UPBF alone was seen in 13 (16.9%) pregnancies. The digoxin test was done concomitantly with placental scintigraphy in 28 patients; it improved diagnostic precision and provided a measure of compensation of impaired UPBF.
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PMID:[Diagnosis of placental insufficiency in patients with acquired heart defects]. 219 89

Ultrasonic diagnosis is indispensable in perinatal medicine. The applications are; 1) diagnosis of early pregnancy, 2) diagnosis of fetal life, 3) diagnosis of pregnancy weeks by fetal crown rump length, 4) evaluation of fetal growth by biparietal diameter, femur length, abdominal size, or estimated fetal weight, 5) detection of early abnormalities in blighted ovum, fetal death, hydatidiform mole, ectopic pregnancy, etc., 6) diagnosis of fetal anomalies, e.g. anencephaly, hydrocephaly, neck hygraoma, diaphragmatic hernia, congenital heart disease, intestinal obstruction, renal anomalies, obstructive uropathy, etc., 7) diagnosis of fetal diseases, e.g. hydrops fetalis, 8) diagnosis of placenta previa, hydramnios, oligohydramnios, cord coiling, excessive cord twisting, 9) detection and prediction of fetal compromise by fetal and uterine blood flow velocity wave forms, 10) further precise diagnosis by transvaginal sonography, 11) interventional ultrasound in genetic diagnosis with amniocentesis and chorionic villi sampling, fetal blood sampling with cordocentesis, 12) detection of fetal hypoxia by ultrasonic fetal monitor, fetal actocardiogram, and ultrasonic Doppler flowmetry.
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PMID:Ultrasound in fetal diagnosis and therapy. 1012 69

Cardiovascular adaptations during pregnancy are normally well tolerated in healthy women. However, 2% to 4% of women of childbearing age have some degree of concomitant heart disease, and these changes may compromise cardiac function. Of these, a few who do not respond to medical treatment may require surgical correction. In this setting, maternal mortality rate has improved to levels similar to those in non-pregnant counterparts. However, the fetal mortality rate remains high (up to 33%). Factors contributing to high fetal mortality rates include the timing of the operation, the urgency of the operation, and the fetal/fetoplacental response to cardiopulmonary bypass. Modulation of the fetoplacental response to cardiopulmonary bypass may prevent placental dysfunction and sustained uterine contractions, which underlie fetal hypoxia and acidosis.In this article, we review cardiovascular adaptations to pregnancy and the pathophysiologic effects of cardiopulmonary bypass on the mother, fetus, and fetoplacental unit, and we talk about whether manipulation of these responses can help in improving fetal outcome. Finally, approaches regarding perfusion management and off-pump cardiac surgical techniques in pregnancy are discussed.
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PMID:Cardiac surgery during pregnancy. 1894 9

Intrauterine or fetal growth restriction is best defined by using customised birth weight percentiles based upon the growth potential for an individual infant. Growth restriction in utero may be classified as asymmetric or symmetric depending upon the duration of the process. Asymmetric growth restriction is caused by placental insufficiency, maternal hypertensive conditions, long-standing maternal diabetes, smoking, living at altitude or multiple gestation. Symmetric growth restriction may be due to congenital infections, chromosomal or other abnormalities, fetal alcohol syndrome, low socioeconomic status or be constitutional. The underlying cause of growth restriction often predicts the potential adverse effects on the foetus and newborn and later effects in childhood and adulthood. With placental insufficiency, there may be chronic or acute on chronic fetal hypoxia with birth asphyxia and hypothermia, neonatal hypoglycaemia, polycythaemia and coagulopathy. Management is directed at prevention or early treatment of these conditions. In contrast, symmetrically growth-restricted infants should be examined carefully to look for congenital infections and malformations that may need specific interventions. Infants with constitutional short stature generally do not need any specific management. Feeding of growth-restricted infants is important to overcome deficiencies incurred in utero. Most infants show catch-up growth although about 10% do not. Those with excessive catch-up growth may be at greatest risk of developing insulin resistance in adulthood leading to diabetes, obesity and heart disease. The so-called fetal origins of disease may actually have a postnatal onset related more to excessive weight gain in infancy. There is still controversy over the indications for growth hormone treatment in growth-restricted infants who remain of short stature in early childhood. Intrauterine growth restriction is also associated with a five- to seven-fold increased risk of cerebral palsy probably due to chronic placental insufficiency.
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PMID:Neonatal management and long-term sequelae. 1963 99

The molecular mechanism of antenatal hypoxia impacting on fetal heart development and elevated risk of heart disease of adult offspring is poorly understood. We present a dataset integrating DNA methylome and transcriptome analyses of antenatal hypoxia affecting rat fetal and adult offspring hearts to understand hypoxia-mediated epigenomic reprogramming of the heart development. We showed that antenatal hypoxia not only induced DNA methylomic and transcriptomic changes in the fetal hearts, but also had a delayed and lasting effect on the adult offspring hearts. Of interest, antenatal hypoxia induced opposite changes in DNA methylation patterns in fetal and adult hearts, with a hypermethylation in the fetus and a hypomethylation in the adult. An extensive preprocessing, quality assessment, and downstream data analyses were performed on the genomic dataset so that the research community may take advantage of the public resource. These dataset could be exploited as a comprehensive resource for understanding fetal hypoxia-mediated epigenetic reprogramming in the heart development and further developmental programming of heart vulnerability to disease later in life.Figshare doi: https://doi.org/10.6084/m9.figshare.9948572.
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PMID:Prenatal hypoxia-induced epigenomic and transcriptomic reprogramming in rat fetal and adult offspring hearts. 3166 36

Antenatal hypoxia caused epigenetic reprogramming of methylome and transcriptome in the developing heart and increased the risk of heart disease later in life. Herein, we investigated the impact of gestational hypoxia in proteome and metabolome in the hearts of fetus and adult offspring. Pregnant rats were treated with normoxia or hypoxia (10.5% O₂) from day 15 to 21 of gestation. Hearts were isolated from near-term fetuses and 5 month-old offspring, and proteomics and metabolomics profiling was determined. The data demonstrated that antenatal hypoxia altered proteomics and metabolomics profiling in the heart, impacting energy metabolism, lipid metabolism, oxidative stress, and inflammation-related pathways in a developmental and sex dependent manner. Of importance, integrating multi-omics data of transcriptomics, proteomics, and metabolomics profiling revealed reprogramming of the mitochondrion, especially in two clusters: (a) the cluster associated with "mitochondrial translation"/"aminoacyl t-RNA biosynthesis"/"one-carbon pool of folate"/"DNA methylation"; and (b) the cluster with "mitochondrion"/"TCA cycle and respiratory electron transfer"/"acyl-CoA dehydrogenase"/"oxidative phosphorylation"/"complex I"/"troponin myosin cardiac complex". Our study provides a powerful means of multi-omics data integration and reveals new insights into phenotypic reprogramming of the mitochondrion in the developing heart by fetal hypoxia, contributing to an increase in the heart vulnerability to disease later in life.
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PMID:Multi-Omics Integration Reveals Short and Long-Term Effects of Gestational Hypoxia on the Heart Development. 3183 78

Chronic fetal hypoxia and infection are examples of adverse conditions during complicated pregnancy, which impact cardiac myogenesis and increase the lifetime risk of heart disease. However, the effects that chronic hypoxic or inflammatory environments exert on cardiac pacemaker cells are poorly understood. Here, we review the current evidence and novel avenues of bench-to-bed research in this field of perinatal cardiogenesis as well as its translational significance for early detection of future risk for cardiovascular disease.
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PMID:Impact of Chronic Fetal Hypoxia and Inflammation on Cardiac Pacemaker Cell Development. 3219 15

Hypoxia is one of the most frequent and severe stresses to an organism's homeostatic mechanisms, and hypoxia during gestation has profound adverse effects on the heart development increasing the occurrence of congenital heart defects (CHDs). Cardiac progenitor cells (CPCs) are responsible for early heart development and the later occurrence of heart disease. However, the mechanism of how hypoxic stress affects CPC fate decisions and contributes to CHDs remains a topic of debate. Here we examined the effect of hypoxic stress on the regulations of CPC fate decisions and the potential mechanism. We found that experimental induction of hypoxic responses compromised CPC function by regulating CPC proliferation and differentiation and restraining cardiomyocyte maturation. In addition, echocardiography indicated that fetal hypoxia reduced interventricular septum thickness at diastole and the ejection time, but increased the heart rate, in mouse young adult offspring with a gender-related difference. Further study revealed that hypoxia upregulated microRNA-210 expression in Sca-1⁺ CPCs and impeded the cell differentiation. Blockage of microRNA-210 with LNA-anti-microRNA-210 significantly promoted differentiation of Sca-1⁺ CPCs into cardiomyocytes. Thus, the present findings provide clear evidence that hypoxia alters CPC fate decisions and reveal a novel mechanism of microRNA-210 in the hypoxic effect, raising the possibility of microRNA-210 as a potential therapeutic target for heart disease.
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PMID:Fetal Hypoxia Impacts on Proliferation and Differentiation of Sca-1⁺ Cardiac Progenitor Cells and Maturation of Cardiomyocytes: A Role of MicroRNA-210. 3224 1