Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 43-year-old woman presented at 34 weeks' gestation with pre-eclampsia and intra-uterine growth restriction. She had a past medical history of myocardial infarction and had angina on moderate effort. She also had non-insulin dependent diabetes mellitus, chronic obstructive airways disease and hypercholesterolaemia. The onset of unstable angina, cardiac failure and a deteriorating fetal condition necessitated urgent delivery by caesarean section. General anaesthesia was chosen. High dose alfentanil was used as sole induction agent resulting in minimal haemodynamic change and a successful maternal and fetal outcome.
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PMID:High dose alfentanil as sole anaesthetic induction agent for caesarean section in a patient with severe ischaemic heart disease. 1532 Oct 90

The pathogenesis of preeclampsia stems from aberrant changes at the placental interface. The trophoblastic endovascular invasion of tonic spiral arteries that converts them to passive conduits falters. Uteroplacental insufficiency and fetoplacental hypoxemia result. Secondary maternal oxidative stress and an excessive inflammatory response to pregnancy generate the clinical syndrome of preeclampsia. Current treatment focuses on preventing seizures, controlling hypertension, preserving renal function and delivering the baby. We propose that the pathophysiological changes induced by preeclampsia in the placenta parallel those caused by persistent hypoxemia in the lungs at high altitude or with chronic obstructive pulmonary disease. Unrelenting pulmonary hypoxic vasoconstriction induces pulmonary hypertension and cor pulmonale. Inhalation of nitric oxide and phosphodiesterase-5 inhibitors opposes pulmonary hypoxic vasoconstriction, alleviates pulmonary hypertension and improves systemic oxygenation. Notably nitric oxide donor therapy also counters hypoxemic fetoplacental vasoconstriction, a biological response analogous to pulmonary hypoxic vasoconstriction. Fetal oxygenation and nutrition improve. Placental upstream resistance to umbilical arterial blood flow decreases. Fetal right ventricular impedance falls. Heart failure (cor placentale) is avoided. Emergency preterm delivery can be postponed. Other than low dose aspirin and antioxidants vitamins C and E no available therapy specifically targets the underlying disease profile. We hypothesize that, like nitric oxide donation, pharmacological inhibition of placental phosphodiesterase-5 will also protect the fetus but for a longer time. Biological availability of guanosine 3'5'-cyclic monophosphate is boosted due to slowed hydrolysis. Adenosine 3'5'-cyclic monphosphate levels increase in parallel. Cyclic nucleotide accumulation dilates intact tonic spiral arteries and counters hypoxemic fetoplacental vasoconstriction. Intervillous and intravillous perfusion pick up. Maternal to fetal placental circulatory matching improves. Enhanced placental oxygen uptake alleviates hypoxemic fetal stress. Appropriate fetal nutrition resumes. Cor placentale and severe intrauterine growth restriction are averted. Increased maternal cyclic nucleotide concentrations promote systemic vasodilatation so that blood pressures fall. Preemption of oxidative stress initiated by "consumptive" oxidation of nitric oxide stabilizes the vascular endothelium and corrects coagulopathy. Anti-inflammatory and immunosuppressant adenosine 3'5'-cyclic monphosphate offsets the extreme gestational inflammatory response. Cellular injury and multi-organ damage are prevented. One tablet a day of the new long acting phosphodiesterase-5 inhibitor, tadalafil (half life of 17.5 h) theoretically should allow a preterm pregnancy affected by preeclampsia to continue safely. Selective monitoring of vital organ functions guards against life-threatening maternal complications. Regular biophysical profiling warns the obstetrician of impending fetal compromise. Fetal growth and vital organ maturation can continue. As a result workloads imposed upon neonatal intensivists will lighten. Parental anxiety and concern will be allayed. The cost of treating preeclamptic mothers and their extremely low birth weight infants will decrease. Money saved by midwifery services in poorer states can be used to pay for better prenatal care. Severe preeclampsia/eclampsia will be less common. Maternal and perinatal morbidity and mortality will be reduced. Because the human immunodeficiency virus often infects individuals at a workforce eligible age, the global acquired immunodeficiency syndrome pandemic has already brought many nations to the brink of economic ruin. Potentially productive lives saved for the future will help restore them fiscally.
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PMID:Hypothesis: selective phosphodiesterase-5 inhibition improves outcome in preeclampsia. 1550 76

Pre-eclampsia occurs in 2-5% of pregnancies of healthy women. Here, we present a rare case of pre-eclampsia with overt acute heart failure, which was the primary manifestation of systemic lupus erythematosus with cardiac and renal involvement.
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PMID:Pre-eclampsia with acute heart failure postpartum as primary manifestation of systemic lupus erythematosus. 1622 44

Two primigravidae, 33 and 30 years of age, were admitted for pre-eclampsia after 41 and 32 weeks ofamenorrhoea, respectively. Both complained of dyspnoea that turned out to be due to heart failure. The foetuses both died before birth, but the women recovered following intensive care. Peripartum cardiomyopathy is a relatively rare but serious disease that usually develops during the last month of pregnancy or the first five months after delivery. Adequate diagnosis and treatment of pregnant women with signs of heart failure can prevent much suffering on the part of both mother and child. Because peripartum cardiomyopathy is diagnosed by exclusion, other causes of heart failure should first be ruled out. The subsequent preconceptional advice will depend on the recovery of cardiac function. Women with residual myocardial dysfunction run a severe risk of aggravated heart failure and should be strongly advised against becoming pregnant again.
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PMID:[Two pregnant women with shortness of breath due to peripartum cardiomyopathy]. 1675 32

Hyperthyroidism occurs in approximately 1 in every 1000 to 2000 pregnancies. Although the signs and symptoms of the disease are similar in the pregnant and nonpregnant patient, the complications of hyperthyroidism can have even more profound consequences for the mother and fetus during gestation. These include maternal heart failure, preeclampsia, miscarriage, and preterm labor; as well as fetal loss and low birth weight. Furthermore, thyroid function and laboratory testing for hyperthyroidism are altered in pregnancy. The gestational increase in thyroid size, increased thyroid-binding globulin levels, increased serum total T4 and total T3 levels, and decreased thyroid stimulating hormone levels often confuses the evaluation of the thyroid status in pregnancy. Worldwide, the thionamides-propylthiouracil, methimazole, and carbimazole-have been used in pregnancy for the treatment of hyperthyroidism. However, propylthiouracil has been the drug of choice in the United States because it is believed to have less potential to induce fetal/neonatal hypothyrodism, to cross the placenta and into breast milk to a lesser degree, and to be less teratogenic than methimazole or carbimazole. None of the above have been substantiated in more recent studies. The pharmacokinetics of the thionamides in the pregnant and nonpregnant states, as well as the pharmacotherapeutic recommendation for hyperthyroidism will be reviewed.
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PMID:Pharmacokinetics and pharmacotherapy of thionamides in pregnancy. 1688 14

Peripartum cardiomyopathy is a rare and under recognized form of dilated cardiomyopathy, defined as a heart failure in the last month of pregnancy or in the first five months post-partum with absence of determinable cause for cardiac failure and absence of demonstrable heart disease. The incidence of peripartum cardiomyopathy ranges from 1 in 1300 to 1 in 15,000 pregnancy. Advanced maternal age, multiparity, twin births, preeclampsia and black race are known risk factors. The etiology of peripartum cardiomyopathy remains unknown but viral, autoimmune or idiopathic myocarditis are highly suggested. The clinical presentation on patients with peripartum cardiomyopathy is similar to that of patients with systolic heart failure. The treatment is based on drugs for sympyomatic control. Studies in graeter populations are need to determine the role of immunosupressive treatment. About half patients of peripartum cardiomyopathy recover. The left ventricular ejection fraction and the left ventricular end-diastolic diameter are statistically significant prognostic factors. The risk of developing peripartum cardiomyopathy in subsequent pregnancies remains high. The place of dobutamine stress test in counseling the patients who desire pregnancy must be more studied.
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PMID:[Peripartum cardiomyopathy]. 1707 64

Nitric oxide (nitrogen monoxide) (NO) plays an important role in a wide range of physiologic processes. A major mediator of endothelial function, NO regulates vasodilatory and antithrombotic actions in the vasculature and plays a role in reproductive functions, bronchodilation, bone formation, memory, insulin sensitivity, and gastrointestinal relaxation. NO is formed from NO synthase. Impaired NO bioactivity is strongly associated with endothelial dysfunction and cardiovascular disease, but is also implicated in a broad range of other disorders, including pulmonary hypertension, insulin resistance, erectile dysfunction, and preeclampsia. Numerous therapies designed to target NO are being investigated and developed, including NO donors and stimulants. The recent African-American Heart Failure Trial (A-HeFT) showed that the NO donor isosorbide dinitrate, combined with the vasodilator hydralazine, significantly reduced morbidity and mortality in black patients with moderate-to-severe heart failure. Antihypertensive drugs, including angiotensin-converting enzyme inhibitors, calcium channel blockers, and third-generation beta-blockers, are NO stimulants that have demonstrated significant improvement of endothelial function and NO bioactivity. Other cardiovascular therapies that may improve NO bioactivity include statins, l-arginine, and nonpharmacologic approaches such as exercise and dietary changes.
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PMID:Aspects of nitric oxide in health and disease: a focus on hypertension and cardiovascular disease. 1717 Jun 2

Non-immune causes of hydrops fetalis are rare but frequently fatal. Identification of the cause for hydrops fetalis is essential to institute therapy. Chorangiomatosis and intestinal stenosis have not been previously reported as aetiological factors for the development of hydrops. We report a fetus born with hydrops associated with both of these conditions. A 1575 gms preterm neonate was born to a multigravida at 31 weeks of gestation. Emergency caesarean section was performed after detection of hydrops by prenatal ultrasonography. Baby had generalized edema at birth and died after 3 days due to progressive heart failure. At autopsy there was generalized edema and effusions. There were multiple stenotic segments in the intestine. Placenta showed numerous chorangiomas varying from 0.2 to 3 cm in diameter, hence diagnosed as diffuse multifocal chorangiomatosis. Examination of the placenta at neonatal autopsy is an essential part of assessment for hydrops fetalis. Chorangiomatosis is a rare and under reported condition which can cause prematurity, intrauterine growth retardation, pre-eclampsia and rarely hydrops fetalis.
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PMID:Diffuse multifocal chorangiomatosis of the placenta with multiple intestinal stenosis of the fetus: combination of rare causes for nonimmune hydrops fetalis. 1718 71

Pregnancy is contraindicated in cases of maternal pulmonary hypertension, a highly morbid disease affecting young women of childbearing age. The rate of heart failure increases gradually with the severity of pulmonary hypertension. In certain instances, the severity of maternal pulmonary hypertension in rheumatic heart diseases can be higher than in congenital heart diseases. Placenta accreta is an important cause of bleeding in the second half of pregnancy and in labor. In severe cases, hysterectomy is the only way to manage the bleeding during cesarean section. A 33-year-old gravida, G2P0AA1, suffering from rheumatic heart disease with mitral valve stenosis and pulmonary hypertension, was referred to our high-risk pregnancy center at 10(+3) weeks of gestation due to lower abdominal pain and brownish vaginal bleeding. She had received 2 mitral valve replacements in Shenzhen, China, at the ages of 22 and 26, respectively. Ultrasound scan of the abdomen at 12(+2) gestational weeks showed that the internal cervix was completely covered with the placenta, and a retroplacental hypoechoic space measuring 35 x 13 mm was observed at the upper posterior margin of the placenta. On color Doppler scan, an area of lacunar lake flow was observed in the hypoechoic space of the placenta and a spiral artery with low blood flow resistance was detected. The pulsation of the placental flow was synchronized with the maternal pulse rate. Team specialists, including neonatologists, pulmonary physicians, pediatric cardiologists, hematologists, anesthesiologists, psychiatrists and social workers, as well as high-risk obstetricians were consulted in an effort to minimize fetal and maternal morbidity and mortality. At 29(+2) weeks, the patient developed preeclampsia and delivered a healthy newborn by cesarean section, the uterus being preserved by square compression sutures. The gravida tolerated the procedures and was discharged in stable condition.
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PMID:Pregnancy complicated with maternal pulmonary hypertension and placenta accreta. 1759 87

Cardiac glycosides have been used for decades to treat congestive heart failure. The recent identification of cardiotonic steroids such as ouabain, digoxin, marinobufagenin, and telocinobufagin in blood plasma, adrenal glands, and hypothalamus of mammals led to exciting new perspectives in the pathology of heart failure and arterial hypertension. Biosynthesis of ouabain and digoxin occurs in adrenal glands and is under the control of angiotensin II, endothelin, and epinephrine released from cells of the midbrain upon stimulation of brain areas sensing cerebrospinal Na(+) concentration and, apparently, the body's K(+) content. Rapid changes of endogenous ouabain upon physical exercise may favor the economy of the heart by a rise of intracellular Ca(2)(+) levels in cardiac and atrial muscle cells. According to the sodium pump lag hypothesis, this may be accomplished by partial inhibition of the sodium pump and Ca(2+) influx via the Na(+)/Ca(2+) exchanger working in reverse mode or via activation of the Na(+)/K(+)-ATPase signalosome complex, generating intracellular calcium oscillations, reactive oxygen species, and gene activation via nuclear factor-kappaB or extracellular signal-regulated kinases 1 and 2. Elevated concentrations of endogenous ouabain and marinobufagenin in the subnanomolar concentration range were found to stimulate proliferation and differentiation of cardiac and smooth muscle cells. They may have a primary role in the development of cardiac dysfunction and failure because (i) offspring of hypertensive patients evidently inherit elevated plasma concentrations of endogenous ouabain; (ii) such elevated concentrations correlate positively with cardiac dysfunction, hypertrophy, and arterial hypertension; (iii) about 40% of Europeans with uncomplicated essential hypertension show increased concentrations of endogenous ouabain associated with reduced heart rate and cardiac hypertrophy; (iv) in patients with advanced arterial hypertension, circulating levels of endogenous ouabain correlate with BP and total peripheral resistance; (v) among patients with idiopathic dilated cardiomyopathy, high circulating levels of endogenous ouabain and marinobufagenin identify those individuals who are predisposed to progressing more rapidly to heart failure, suggesting that endogenous ouabain (and marinobufagenin) may contribute to toxicity upon digoxin therapy. In contrast to endogenous ouabain, endogenous marinobufagenin may act as a natriuretic substance as well. It shows a higher affinity for the ouabain-insensitive alpha(1) isoform of Na(+)/K(+)-ATPase of rat kidney tubular cells and its levels are increased in volume expansion and pre-eclampsia. Digoxin, which is synthesized in adrenal glands, seems to counteract the hypertensinogenic action of ouabain in rats, as do antibodies against ouabain, for example, (Digibind) and rostafuroxin (PST 2238), a selective ouabain antagonist. It lowers BP in ouabain- and adducin-dependent hypertension in rats and is a promising new class of antihypertensive medication in humans.
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PMID:Endogenous and exogenous cardiac glycosides and their mechanisms of action. 1761 Mar 45


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