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)

The purpose of this report is to determine the role of various imaging modalities, and the outcome of early intervention in neonates with high flow pial arteriovenous malformations (AVM). This report describes 4 neonates with pial AVM associated with congestive cardiac failure, and reviews previous reports. Among the 4 infants in our series, 3 underwent early surgical resection of the AVM, complete in 2 and partial in 1. One infant suffered hemorrhagic infarction postoperatively and has a mild deficit on clinical follow-up; the other 2 patients had no worsening of mild neurologic deficits after surgery, and subsequent development has been normal. The fourth infant had absent deep venous drainage and died from intracranial hemorrhage following transvenous embolization. A single vessel arteriogram in 1 infant led to underestimation of the lesion and unexpected findings at surgery. Complete angiographic study is important in planning treatment, as the vascular anatomy of the lesions may be complex. Cranial ultrasound is useful in early diagnosis, but may miss the superficial lesions. Untreated infants with pial AVM have a poor prognosis due to cardiac failure or progressive cerebral ischemia and neurologic regression. This series illustrates the benefits of complete angiographic investigation and early treatment.
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PMID:Neonatal superficial cerebral arteriovenous malformations. 790 36

The paper describes the sequence of events typical in the pathogenesis of germinal layer hemorrhage (GLH): An initial, often prenatal, severe asphyxic event, leading to abolishment of autoregulation of cerebral perfusion, and, most likely, to hypoxic-ischemic lesions in the endothelium of the large capillaries of the germinal matrix. The hypoxia is accompanied by exhaustion of myocardial energy reserves with circulatory failure, hypotension and aggravation of cerebral ischemia. In the period immediately after birth, circulation failure proceeds with cardiac insufficiency, hypotension, cerebral ischemia, and possibly venous hypertension. Following resuscitation, arterial blood pressure gradually increases (type 3) with increased strain on the damaged germinal matrix capillary walls in the absence of autoregulation. This effect is further aggravated by arterial blood pressure increments of type 1 and 2 leading to GLH, possibly with increments of venous pressure as a contributing factor.
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PMID:On the pathogenesis of germinal layer hemorrhage in the neonate. 831 97

Topical congenital pulmonary vein stenosis is a uncommon defect, both isolated or associated to other cardiac abnormalities. Only the localization of the lesions seems to affect the survival, because 60% of survival cases has unilateral stenosis; the severity of associated cardiac lesions become the prognosis poor. We describe two cases: 1st case, a 43 days old boy presented with heart failure and convulsion and had a diagnosis of pulmonary hypertension, atrial septal defect and tricuspid regurgitation, without pulmonary abnormalities. He had recurrent pulmonary infections and a cerebral ischemia in the following months, and died at 15 months of age for sepsis. Autopsy revealed stenosis and atresia in all pulmonary veins, with venous and arterial hypertension. There was also aortic hypoplasia and aortic and tricuspid valves indifferentiation; 2nd case, a 7 days old girl had a diagnosis of aortic coarctation and atrial and ventricular septal defects. Surgical corrections, at 38 and 46 days old, firstly of the aortic coarctation and after for the septal defects, disclosed and relief a supra-valvar mitral stenosis, but she remained on heavy respiratory insufficiency. At 6 months old, she returned to the hospital with dyspnea and cianosis, heart failure and hemoptisis; a sepsis developed and she died. At autopsy, there were severe pulmonary vein stenosis on the left and in the superior right veins, with pulmonary hypertension and hemorrhage.
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PMID:[Pulmonary vein stenosis. Report of 2 cases and review of the literature]. 854 96

The objective of the investigation was an attempt to analyze some aspects of the heart-brain relationship. The group was formed by 626 patients with the diagnosis of focal cerebral ischaemia (CI) and 191 patients with the diagnosis of subarachnoidal haemorrhage (SAH). It was revealed that the CI group comprised 77.3% patients with a pathological finding on the heart. Analysis revealed moreover that in the group of patients with "congestive heart failure" there was a significantly higher percentage of patients with a severe neurological deficit as compared to the group with a "normal" ECG (p < 0.001). Atrial fibrillation causes a fivefold increase of the risk of cerebral infarction. The incidence of ECG abnormalities of various types was significantly higher in the group of patients with CI during long-term ECG monitoring, as compared to the results of conventional ECG examination (p < 0.001). The value of long-term ECG monitoring was confirmed also in an investigation of these changes in a group of patients with arterial hypertension, quari potential candidates of cerebral infarction. The relationship between cardiac and cerebral function was tested also in an investigation focused on the incidence of ectopic activity and changes of the QT interval. It was revealed that while the percentage rate of ectopic activity assessed by conventional ECG examination was in the group of "improved" patients 18.0%, long-term monitoring revealed a rate as high as 48.0%, the difference being statistically significant. Similar significant differences were observed also on analysis of the QT interval: in the group of patients with neurological "improvement" the QT interval was significantly shorter, as compared with the group with neurological "deterioration". It was assumed that the prolonged QT interval could be the cause of sudden death. A cardio-cerebral relationship was found also on analysis of changes of the cerebral circulation (CBF) in different forms of cardiac insufficiency. It was revealed that isolated ventricular extrasystoles reduced the CBF by 8.0%, isolated atrial extrasystoles by 12% and in atrio-ventricular tachyarrhythmia the CBF is reduced by as much as 25.0%. The cerebro-cardiac relationship was tested in a group of patients with SAH. ECG abnormalities of a varying type were found in 30.7% of the patients with SAH. They are described in as many as 100% of patients and were detected also other in cerebral disorders, such as contusion of the brain, intraoerebral haemorrhage and cerebral tumours.
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PMID:[The heart and the brain. Aspects of their interrelations]. 892 26

It is well known in patients with aortitis syndrome that the clinical features and prognosis vary with location, spread, and degree of the lesion in the affected artery. Therefore, both an indication for surgery and suitable surgical procedures are very manifold in each case. The indication of surgical management for aortitis syndrome is mainly to prevent the cerebral ischemia, cardiac failure and for aneurysm. We reviewed the current status of surgical treatment for aortitis syndrome on the cases reported in Japan and some cases surgically treated in our institute.
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PMID:[Present status of aortitis syndrome surgery in Japan]. 930 92

Endothelial-derived nitric oxide (NO) is an important mediator of vascular function. Clinical studies indicate that HMG-CoA reductase inhibitors (statins) improve endothelial function and reduce the incidence of stroke and myocardial infarction. Treatment of human endothelial cells with statins increased the expression of endothelial NO synthase (eNOS) protein and mRNA expression. Statins increased eNOS mRNA half-life but did not change eNOS gene transcription. Inhibition of mevalonate synthesis by statins not only blocks the formation of cholesterol but also of isoprenoids. The upregulation of eNOS expression by statins was independent of cholesterol but mediated via the inhibition of the isoprenoid geranylgeraniol, whereas farnesiol had no effect on eNOS. Immunoblot analyses, (35S)-GTP gamma S-binding assays and transfection studies revealed that statins upregulate eNOS expression by blocking the geranylgeranylation of the GTPase Rho which is necessary for its membrane-associated activity. Studies with mice showed, that statin treatment upregulates eNOS expression and function independent of serum cholesterol levels. Prophylactic treatment with statins augmented cerebral blood flow and reduced cerebral infarcts in normocholesterolemic mice. These effects of statins were completely absent in eNOS-deficient mice indicating that enhanced eNOS activity by statins is the predominant mechanism by which these agents protect against cerebral injury. Our results suggest that statins provide a novel prophylactic treatment strategy for increasing blood flow and reducing brain injury during cerebral ischemia. Upregulation of eNOS by inhibiting Rho may provide a new pharmacologic target for the treatment of arteriosclerosis, pulmonary hypertension, and heart failure.
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PMID:[Regulation of endothelial NO production by Rho GTPase]. 1037 57

BACKGROUND: We investigated the association of cigarette smoking with high-grade carotid artery stenosis in patients with ischemic stroke and transient ischemic attacks. METHODS: Prospectively collected data from 404 patients with focal brain ischemia were used for a cross-sectional study estimating the association between cigarette smoking and high-grade carotid artery stenosis (diagnosed by Doppler-ultrasound and defined as a luminal narrowing of > or = 70%). Cerebral ischemia patients with normal sonographic findings served as a comparison group. Multivariate logistic regression models were used for statistical tests to determine the association between smoking and high-grade carotid stenosis. Age, gender, hypertension, diabetes mellitus, hypercholesterolemia and co-existing heart disease (myocardial infarction, angina, heart failure) were considered potential confounders. RESULTS: High-grade carotid stenoses were found in 25% (n = 101) of the patients; 39% (n = 156) were classified as smokers. Smoking (odds ratio 3.6, 95% confidence interval [CI] 2.2 to 5.8), hypercholesterolemia (odds ratio 1.8; CI 1.1 to 2.8) and preexisting heart disease (odds ratio 1.7; CI 1.1 to 2.7) were significantly associated with carotid stenosis > or = 70%. The impact of smoking augmented with increasing degree of stenosis (odds ratio for stenoses > or = 80%: 4.3, CI 2.3 to 7.7), whereas the association with hypercholesterolemia, and co-existing heart disease decreased in strength for stenoses greater than 80%. Hypertension and diabetes mellitus were not found to be significantly with high-grade carotid artery stenoses. CONCLUSION: Smoking is an independent determinant of severe carotid artery stenosis in patients with focal cerebral ischemia.
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PMID:[In Process Citation] 1059 30

We describe a successful episode of anesthesia management in a parturient affected with Takayasu's disease who underwent elective cesarean section under combined spinal-epidural anesthesia. Takayasu's disease is characterized by chronic occlusive inflammation of the arteries (panarteritis) of unknown origin that usually involves the aorta and its main branches. Progression of the disease may be marked by aneurysmal dilation of the affected arteries and may lead to a fatal outcome, usually from cerebral ischemia or heart failure. The impact of pregnancy on Takayasu's disease is unclear, but worsening of ischemic symptoms, cardiac failure, aggravation of hypertension and cerebral hemorrhage have been reported in sufferers who are in the later stages of pregnancy. Nonetheless, anesthesia management of a parturient with advanced Takayasu's disease presents a challenge to anesthetists.
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PMID:Combined spinal-epidural anesthesia for cesarean section in a patient with Takayasu's disease. 1064 54

During the past 20 years, several bioactive peptides have been identified in teleost fishes that subsequently have been shown to play important regulatory roles in mammalian physiology. The urophysis, corpuscles of Stannius and Brockmann body are anatomical structures particular to fish that have no obvious counterpart in mammals. Extracts and/or cDNA libraries prepared from these tissues have been used to identify for the first time urotensin II (U-II), urotensin-I (U-I), stanniocalcin and glucagon-like peptide-1 (GLP-1). Although U-II and U-I were originally regarded as exclusively the products of the teleost urophysis, the peptides have a wide phylogenetic distribution across the vertebrate lineage, including mammals. U-II is localized to motor neurones in the human spinal cord and is a potent vasoconstrictor that may be implicated in the pathogenesis of heart failure. The human ortholog of urotensin-I is urocortin which is synthesized in selected regions of the brain and is the endogenous ligand for the CRF type 2 receptor. Urocortin is believed to important in mediating the effects of stress on appetite. Stanniocalcin is involved in maintaining calcium and phosphate homeostasis in teleost fish. An ortholog of stanniocalcin has a widespread distribution in mammalian tissues and is postulated to regulate renal phosphate excretion and to protect neurons against damage during cerebral ischemia. The biological actions and therapeutic potential of GLP-1 in humans are now fully appreciated but the peptide was first identified as a domain in a preproglucagon cDNA prepared from anglerfish Brockmann bodies. In contrast to mammalian preproglucagons, GLP-1 is present in anglerfish preproglucagon as the bioactive, truncated sequence [corresponding to human GLP-1(7-37)] rather than the inactive, N-terminally extended form [corresponding to GLP-1(1-37)]. Failure to appreciate the significance of this fact retarded progress in the field for several years.
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PMID:Singular contributions of fish neuroendocrinology to mammalian regulatory peptide research. 1103 47

Dexanabinol is a non-psychotropic cannabinoid NMDA receptor antagonist under development by Pharmos Corp for the potential treatment of cerebral ischemia, glaucoma, Alzheimer's disease, cardiac failure, head injury and multiple sclerosis (MS) [311522]; it is in phase III trials for traumatic brain injury (TBI) [388709]. Dexanabinol was licensed to Pharmos for development from its originator, the Hebrew University of Jerusalem [180441]. Pharmos is seeking to enter into a strategic agreement with another company to develop and commercialize dexanabinol [317369]. Unlike its enantiomer, HU-210 (Yissum Research Development Co), dexanabinol does not interact with cannabinoid receptors [223330]. It has also exhibited more effective antioxidant and anti-inflammatory properties than MK-801 (dizocilpine; Merck & Co Inc) [167980], [168212]. In addition, dexanabinol is generally well tolerated and appears toxicologically safe [170116]. Pharmos has been awarded a Small Business Innovation Research grant from the National Institutes of Health (NIH) National Institute of Neurological Disorders and Stroke, Division of Stroke and Trauma. The grant covers the development of new prodrugs and novel formulations of dexanabinol and will support additional study of dexanabinol compounds for various indications. The prodrugs being studied are part of the group of compounds that include dexanabinol [247958]. A Notice of Allowance was received in March 1999 on a patent covering the use of the drug in the treatment of MS [324163]. The use of dexanabinol and its derivatives to treat MS is described in US-05932610 [358503]. An oral formulation of dexanabinol is claimed in US-05891468. Dexanabinol analogs with special utility in acute and chronic pain are claimed in US-04876276, while dexanabinol analogs for neuroprotection are claimed in US-06096740. Pharmos estimates that the worldwide market for dexanabinol in the treatment of severe head trauma may reach $1 billion per year [319244].
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PMID:Dexanabinol Pharmos. 1124 4


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