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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 29-year-old nulliparous woman had development of hypertension, proteinuria, and congestive heart failure during the third trimester of her pregnancy. Her symptoms and cardiovascular changes were consistent with congestive heart failure and severe preeclampsia. The underlying pathophysiology was believed to be caused by the high-output state of pregnancy and by the increased peripheral vascular resistance of preeclampsia. The patient underwent an elective cesarean section, but her cardiovascular symptoms did not resolve. Soon after delivery, the patient was found to have an arteriovenous fistula of the right renal artery that caused the high-output cardiac state. Embolization and surgical removal of the arteriovenous fistula resulted in complete resolution of the patient's high-output heart failure. All previously reported cases of renal arteriovenous fistulas and malformations that have occurred during pregnancy are reviewed.
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PMID:High-output heart failure due to a renal arteriovenous fistula in a pregnant woman with suspected preeclampsia. 973 27

The endothelins are a family of endothelium-derived peptides that possess characteristically sustained vasoconstrictor properties. Endothelin-1 appears to be the predominant member of the family generated by vascular endothelial cells. In addition to its direct vascular effects, endothelin-1 has inotropic and mitogenic properties, influences homeostasis of salt and water, alters central and peripheral sympathetic activity and stimulates the renin-angiotensin-aldosterone system. Studies with endothelin receptor antagonists have indicated that endothelin-1 probably has complex opposing vascular effects mediated through vascular smooth muscle and endothelial ET(A) and ET(B)receptors. Endogenous generation of endothelin-1 appears to contribute to maintenance of basal vascular tone and blood pressure through activation of vascular smooth muscle ET(A)receptors. At the same time, endogenous endothelin-1 acts through endothelial ET(B) receptors to stimulate formation of nitric oxide tonically and to oppose vasoconstriction. In view of the multiple cardiovascular actions of endothelin-1, there has been much interest in its contribution to the pathophysiology of hypertension. Results of most studies suggest that generation of, or sensitivity to, endothelin-1 is no greater in hypertensive than it is in normotensive subjects. Nonetheless, the deleterious vascular effects of endogenous endothelin-1 may be accentuated by reduced generation of nitric oxide caused by hypertensive endothelial dysfunction. It also appears likely that endothelin participates in the adverse cardiac and vascular remodelling of hypertension, as well as in hypertensive renal damage. Irrespective of whether vascular endothelin activity is increased in hypertension, anti-endothelin agents do produce vasodilatation and lower blood pressure in hypertensive humans. There is more persuasive evidence for increased endothelin-1 activity in secondary forms of hypertension, including pre-eclampsia and renal hypertension. Endothelin-1 also appears to play an important role in pulmonary hypertension, both primary and secondary to diseases such as chronic heart failure. The hypotensive effects of endothelin converting enzyme inhibitors and endothelin receptor antagonists should be useful in the treatment of hypertension and related diseases. Development of such agents will increase knowledge of the physiological and pathological roles of the endothelins, and should generate drugs with novel benefits.
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PMID:Endothelin as a regulator of cardiovascular function in health and disease. 979 9

With recent therapeutic advances, thalassemic patients can now reach adulthood and attain reproductive capacity. Endocrine complications due to hemosiderosis and especially hypogonatotropic hypogonadism, which present either with sexual infantilism and primary amenorrhea or with secondary amenorrhea, are common in thalassemic women. The aim of this study was to estimate the frequency of fertility among our female thalassemic patients. Our population included 50 married women with thalassemia major (TM) and 12 with thalassemia intermedia (TI) who are regularly followed in our thalassemic centers. Of the 50 patients with TM, 7 had primary amenorrhea (PA), 9 had secondary amenorrhea (SA), and 34 had normal menstrual function (NM), as did all the patients with TI. Overall we had 62 women who were able to achieve 90 pregnancies and give birth to 87 healthy babies. Most of our patients became pregnant around the age of 25 years. Associated endocrine complications were rare except in the group of patients with PA, as expected. In all patients with PA and SA, the 17 pregnancies were induced (intercourse 10, insemination 3, IVF 4). In the patients with NM and TI, 66 pregnancies were achieved spontaneously and 7 following induction (insemination 3, IVF 4). There were four twin and one triple pregnancies, which all resulted in premature deliveries. Among the seven couples in which both partners had thalassemia major, sperm donation was used in 5 cases, ovum donation in one case, and one pregnancy was achieved spontaneously. These 90 pregnancies resulted in 69 full-term, 12 pre-term, 7 abortions and 2 stillbirths. No severe obstetric complication was observed except for two patients with preeclampsia. One patient with PA who carried the triple pregnancy developed severe cardiac failure, which was successfully treated. Transfusion requirements were increased during pregnancy. Discontinuation of desferrioxamine resulted in elevation of ferritin levels during the second and third trimesters of pregnancy and after delivery. Nine patients who were examined with cardiac echo had a transient increase of ESD and EDD during pregnancy, with return to normal after delivery. Labor was performed by Caesarian section in 26 births (26%) out of the 81 successful pregnancies. These collected data represent the largest number of pregnancies in thalassemic females reported so far and are clearly encouraging for the ultimate improvement of the quality of life in thalassemic patients.
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PMID:Fertility in female patients with thalassemia. 1009 Nov 68

Peripartum cardiomyopathy (PPCM) is a rare form of heart failure affecting women in the last month of pregnancy or the first six months post-partum. The etiology of PPCM remains poorly understood although some risk factors were described. Diagnosis is often difficult and is always necessary to exclude other prior heart disease and other cause of left ventricular dysfunction in pregnancy. Medical therapy for PPCM is similar to that for other forms of congestive heart failure; prognosis is better than in idiopathic cardiomyopathy but many authors observed that women who have had one episode of PPCM are likely to have recurrences in subsequent pregnancies. The present report describes the case of a woman presenting with severe cardiac failure immediately after cesarean section for twin pregnancy. The patient is a 35-year-old nulliparous white woman, with history of anorexia, subsequent amenorrhea, sterility and pregnancy induced with Gn-Rh. The diagnosis of PPCM was difficult for the presence of preeclampsia and acute pulmonary edema occurred four hours after delivery. The successful outcome was possible with an intensive treatment (mechanical ventilation, Swan-Ganz catheter). The whole resolution of the heart failure, six months post-partum, was demonstrated by ultrasonography.
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PMID:[Peripartum dilatative cardiomyopathy. Case report with literature review]. 1052 39

An association between moderate anemia and poor perinatal outcomes has been found through epidemiologic studies, although available evidence cannot establish this relation as causal. Anemia may not be a direct cause of poor pregnancy outcomes, except in the case of maternal mortality resulting directly from severe anemia due to hypoxia and heart failure. Preventing or treating anemia, whether moderate or severe, is desirable. Because iron deficiency is a common cause of maternal anemia, iron supplementation is a common practice to reduce the incidence of maternal anemia. Nevertheless, the effectiveness of large-scale supplementation programs needs to be improved operationally and, where multiple micronutrient deficiencies are common, supplementation beyond iron and folate can be considered. High hemoglobin concentrations are often mistaken as adequate iron status; however, high hemoglobin is independent of iron status and is often associated with poor health outcomes. Very high hemoglobin concentrations cause high blood viscosity, which results in both compromised oxygen delivery to tissues and cerebrovascular complications. Epidemiologic studies have also found an association between high maternal hemoglobin concentrations and an increased risk of poor pregnancy outcomes. Evidence does not suggest that this association is causal; it could be better attributed to hypertensive disorders of pregnancy and to preeclampsia. The pathophysiologic mechanism of these conditions during pregnancy can produce higher hemoglobin concentrations because of reduced normal plasma expansion and cause fetal stress because of reduced placental-fetal perfusion. Accordingly, higher than normal hemoglobin concentrations should be regarded as an indicator of possible pregnancy complications, not necessarily as a sign of adequate iron nutrition, because iron supplementation does not increase hemoglobin higher than the optimal concentration needed for oxygen delivery.
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PMID:Significance of an abnormally low or high hemoglobin concentration during pregnancy: special consideration of iron nutrition. 1087 93

The underlying pathophysiology in most cases of severe intrauterine growth restriction and pre-eclampsia is thought to be abnormal and inadequate conversion of the branches of the uterine arteries into low resistance uteroplacental vessels, due to poor extravillous trophoblastic invasion, leading to reduced intervillous blood flow. Since, in most vascular beds the main site of flow resistance is at the level of the small arteries/arterioles rather than the capillary bed itself it is likely that in cases of intrauterine growth restriction due to uteroplacental dysfunction with abnormal fetal umbilical artery flow velocity waveforms, the underlying pathological mechanism is primarily an initial reduction in intervillus flow leading to relative local hypoxia of some villus territories. This results initially in autocrine/paracrine mediated localized stem artery vasoconstriction to minimize intervillus/intravillus flow mismatch which, when widespread, will result in abnormal umbilical artery Doppler waveforms due to the globally increased resistance to fetoplacental flow. Since, a small reduction in vessel radius will result in an exponential increase in flow resistance and reduction in flow, the magnitude of stem vessel constriction need only be small to result in large changes in fetoplacental vascular haemodynamics. Thus, the underlying progressive pathology in this condition may be cardiac failure, secondary to chronic stem vessel vasoconstriction caused by abnormalities in oxygenation of the fetal respiratory system hence the term 'cor placentale' is proposed.
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PMID:'Cor placentale': placental intervillus/intravillus blood flow mismatch is the pathophysiological mechanism in severe intrauterine growth restriction due to uteroplacental disease. 1151 28

The SHHF/Mcc-fa(cp) (spontaneous hypertension and heart failure) rat is advanced as a novel and suitable non-primate model of pregnancy-associated hypertension and fetal growth restriction because it simultaneously has spontaneous pregnancy-associated hypertension, small for gestational age (SGA) offsprings, and altered placental gene expression. Pregnancy-associated hypertension is a major contributor to maternal and fetal morbidity and mortality with the potential to result in maternal death and the need for iatrogenic preterm delivery. It has been reported to develop spontaneously in humans, but not in animals; consequently, progress in identifying the cause and pathogenesis of this disorder has been hampered. Spontaneous hypertension and heart failure rats develop hypertension spontaneously as they age, therefore we sought to determine whether these rats developed hypertension and SGA offsprings during pregnancy. Our results show that systolic blood pressure (BP) increased >40 mm Hg by the end of the first trimester and remained at this elevated level for the remainder of pregnancy, but decreased after parturition. Placenta weights of SHHF rats (0.60 +/- 0.02 g, n = 36) were significantly higher than Wistar-Kyoto (WKY) rats (0.42 +/- 0.01 g, n = 22, P < .05), but pup weights were significantly lower (2.68 +/- 0.06 g for SHHF rats compared to 3.24 +/- 0.06 g for WKY controls, P < .05). Histologic examination revealed pathologic lesions in neither heart, liver, placenta, nor kidney. L-Arginine administered in drinking water prevented the elevation of BP, particularly during the third trimester. Placentas from SHHF rats displayed altered expression of several genes whose protein products have been implicated in preeclampsia, including serotonin receptor, sodium channel, carbonic anhydrase, estrogen receptor regulator, major histocompatibility complex proteins, superoxide dismutase, and angiotensiogen. In addition, gene expression profiling showed alteration of a number of subcellular putative myristoylproteins not previously associated with preeclampsia, particularly those engaged in post-translational modifications in the placenta. Thus, SHHF rats may be a valuable tool, because it simultaneously has spontaneous pregnancy-associated hypertension, SGA offsprings, and altered placental gene expression.
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PMID:Spontaneous pregnancy-induced hypertension and intrauterine growth restriction in rats. 1171 Jul 86

Peripartum cardiomyopathy is an under-recognized form of dilated cardiomyopathy of unknown cause and is associated with excess morbidity and mortality in women of childbearing age. Incidence of peripartum cardiomyopathy ranges from 1 in 1,300 to 1 in 15,000 pregnancies. The diagnostic criteria are onset of heart failure in the last month of pregnancy or in first 5 months postpartum, absence of determinable cause for cardiac failure, and absence of a demonstrable heart disease before the last month of pregnancy. Multiparity, twin births, advanced maternal age, preeclampsia, gestational hypertension, and black race are known risk factors. The exact cause of peripartum cardiomyopathy is unclear. The clinical presentation of patients with peripartum cardiomyopathy is similar to that of patients with systolic congestive heart failure. Little is known about the therapy of this disease, and the medical treatment is limited to the use of drugs for symptomatic control. Prospective, randomized, double-blind studies are needed to define the role of immunosuppressive treatment and to evaluate the role of conventional treatment of dilated cardiomyopathy in reducing the mortality rate of peripartum cardiomyopathy. About half the patients of peripartum cardiomyopathy recover without any complications. The prognosis is poor in patients with persistent cardiomyopathy. Persistence of disease after 6 months indicates irreversible cardiomyopathy and portends worse survival. The risk of developing peripartum cardiomyopathy in subsequent pregnancies remains high. The clinical and therapeutic aspects of the peripartum cardiomyopathy are discussed.
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PMID:Peripartum cardiomyopathy: clinical and therapeutic aspects. 1171 28

Hyperuricemia (HU) is present in 5-30% of the general population, although the prevalence is higher among some ethnic groups and seems to be increasing worldwide. Classically, chronic HU has been considered a risk factor for gout or lithiasis and is associated with alcoholism, obesity, hypertension, dyslipidemia, hyperglycemia/diabetes mellitus, renal failure and intake of certain drugs. HU is also associated with cardiovascular diseases such as hypertension, vascular disease, pre-eclampsia, pulmonary arterial hypertension, stroke, heart failure, ischemic heart disease and also metabolic syndrome, renal disease and increased mortality. It is uncertain if these associations are dependent or not, especially cardiovascular and renal diseases. Patients with chronic HU and also those with gout require both medical investigation for associated diseases or drugs as well as nutritional counseling and life-style changes. HU should alert physicians to possible complications.
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PMID:Primary prevention in rheumatology: the importance of hyperuricemia. 1512 Oct 34

The majority of sacrococcygeal teratomas diagnosed before birth can be managed by planned delivery and postnatal surgery. However, large tumors early in gestation may result in placentomegaly, hydrops and fetal death and a preeclampsia-like syndrome in the mother. This is due to high output cardiac failure in the fetus caused by arteriovenous shunting through the tumor. In these cases, in utero treatment may offer improved chances of survival, and emerging technologies should lower fetal and maternal morbidity. Nevertheless, these therapeutics need to be correctly evaluated.
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PMID:[Sacrococcygeal teratomas: is there a place for in utero treatment of complicated forms? About three cases]. 1521 67


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