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)

Endothelin (ET)-mediated vasoconstriction has been implicated in the pathophysiology of various disorders, e.g. hypertension, chronic heart failure, acute renal failure, pulmonary hypertension, and subarachnoid hemorrhage (SAH)-induced cerebral vasospasm. The potential involvement of ETs in cerebral vasospasm following SAH has triggered considerable interest in designing therapeutic strategies to inhibit biological effects of ET. Major approaches include: (a) reducing the levels of circulating ET- 1 by the the specific anti- ET- 1 antibodies, (b) antagonizing the ET receptors, and (c) suppressing the biosynthesis of ET-1. To date, numerous antagonists of ET(A) and/or ET(B) receptors have been discovered, and some are under clinical evaluation. Inhibitors of endothelin-converting enzymes (ECEs), which catalyze the biosynthesis of ET-1, have also been synthesized. Two types of ECE-1 inhibitors have been evaluated in various animal disease models: dual ECE-1/neutral endopeptidase 24.11 (NEP) inhibitors and selective ECE-1 inhibitors. In this article, the effects of ET receptor antagonists and ECE-1 inhibitors on the prevention and reversal of SAH-induced cerebral vasospasm in preclinical animal models are reviewed.
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PMID:Endothelin and subarachnoid hemorrhage-induced cerebral vasospasm: pathogenesis and treatment. 1527 81

The common therapeutic approach to patients, who develop vasospasm following subarachnoid hemorrhage, is usually composed of hypertension, hypervolemia, and hemodilution (HHH). This therapy often leads to cardiopulmonary complications, including significant heart failure and pulmonary edema. We describe a 40-year-old woman who developed vasospasm 8 days after surgery for clipping an aneurysm, following a large subarachnoid hemorrhage. The patient required HHH therapy with a very high blood pressure to optimize her clinical neurologic status, but she started to develop pulmonary edema resulting from this therapy. This manifested as a need for increasing oxygen to maintain a normal arterial saturation. To avoid further hemodynamic compromise, we used a new monitor of cardiac function to measure intravascular volumes and quantify pulmonary edema to help titrate the fluid management of a patient in severe vasospasm. We conclude that monitoring volumes with the PiCCO cardiac monitor can help make clinical decisions in patients requiring HHH. This enables maintaining a hypertensive and hypervolemic state while avoiding cardiopulmonary complications such as heart failure and pulmonary edema. It may also help prevent the need for mechanical ventilation in these situations.
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PMID:Monitoring intravascular volumes to direct hypertensive, hypervolemic therapy in a patient with vasospasm. 1555 35

This article describes the pharmacological properties and the overall preclinical and clinical profiling of bosentan (Ro 47-0203), a non-peptide endothelin receptor antagonist with oral activity. Bosentan is a combined and competitive antagonist of both ETA and ETB receptors that is selective for the endothelin system. In vitro and in vivo, bosentan potently antagonises the vascular response elicited by the endothelins. Preclinical efficacy is demonstrated in a variety of pathological models including pulmonary and essential hypertension, renal failure of ischaemic and nephrotic origin and cerebral vasospasm following subarachnoid haemorrhage. Effects are particularly marked in experimental models of heart failure (HF) where bosentan acts as a potent vasodilator that improves overall left ventricular performance. After chronic treatment, bosentan also improves survival in rats with HF. As a result of the first encouraging clinical results that show pulmonary and systemic vasodilation, long-term studies are ongoing in the treatment of congestive heart failure (CHF).
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PMID:The pharmacology of bosentan. 1599 23

Endothelin receptor antagonists (ERAs) have been developed to block the effects of endothelin-1 (ET-1) in a variety of cardiovascular conditions. ET-1 is a powerful vasoconstrictor with mitogenic or co-mitogenic properties, which acts through the stimulation of 2 subtypes of receptors [endothelin receptor subtype A (ETA) and endothelin receptor subtype B (ETB) receptors]. Endogenous ET-1 is involved in a variety of conditions including systemic and pulmonary hypertension (PH), congestive heart failure (CHF), vascular remodeling (restenosis, atherosclerosis), renal failure, cancer, and cerebrovascular disease. The first dual ETA/ETB receptor blocker, bosentan, has already been approved by the Food and Drug Administration for the treatment of pulmonary arterial hypertension (PAH). Trials of endothelin receptor antagonists in heart failure have been completed with mixed results so far. Studies are ongoing on the effects of selective ETA antagonists or dual ETA/ETB antagonists in lung fibrosis, cancer, and subarachnoid hemorrhage. While non-peptidic ET-1 receptor antagonists suitable for oral intake with excellent bioavailability have become available, proven efficacy is limited to pulmonary hypertension, but it is possible that these agents might find a place in the treatment of several cardiovascular and non-cardiovascular diseases in the coming future.
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PMID:Endothelin receptor antagonists. 1621 61

Aneurysms of the vein of Galen are uncommon vascular malformations. They are most frequently seen in infants and children, leading to heart failure and hydrocephalus. Exceptionally, they are detected in adults. Several theories have been proposed to explain hydrocephalus in these patients: obstruction of the cerebral aqueduct, impaired absorption of CSF after subarachnoid hemorrhage, passive ex-vacuo mechanism, or thrombosis of an aneurysm. Hydrocephalus has been treated mainly with cerebrospinal shunt procedures, but also direct surgery, radiosurgery and embolisation of the malformation have proved to be effective. We report the case of a partially thrombosed ectasia of the vein of Galen in a 44-year-old male, with huge hydrocephalus successfully treated with an endoscopic third ventriculostomy.
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PMID:Endoscopic treatment of hydrocephalus due to aneurysm of the vein of Galen: case report and literature review. 1805 45

The most important strategies in pharmacogenomics are gene expression profiling and the network analysis of human disease models. We have previously discovered novel drug target candidates in cardiovascular diseases through investigations of these pharmacogenomics. The significant induction of S100C mRNA and protein expression was detected in the rat pulmonary hypertension and myocardial infarction model. We also found increased taurine in hypoxia, a calcium-associated cytoprotective compound, to suppress the hypoxia-induced S100C gene expression and vascular remodeling. These results suggest that S100C may be one of the potential novel drug targets in hypoxic or ischemic diseases. Delayed cerebral vasospasm after aneurysmal subarachnoid hemorrhage causes cerebral ischemia and infarction. Using a DNA microarray, a prominant upregulation of heme oxygenase-1 (HO-1) and heat shock protein (HSP) 72 mRNAs were observed in the basilar artery of a murine vasospasm model. Antisense HO-1 and HSP 72 oligodeoxynucleotide inhibited HO-1 and HSP 72 induction, respectively, and significantly aggravated cerebral vasospasm. Moreover, we have also developed a unique heart failure model in zebrafish and identified several candidate genes as novel drug targets. These results suggest that pharmacogenomic network analysis has the potential to bridge the gap between in vitro and in vivo studies and could define strategies for identifying novel drug targets in various cardiovascular diseases.
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PMID:Pharmacogenomics of cardiovascular pharmacology: pharmacogenomic network of cardiovascular disease models. 1849 Aug 53

Treating patients with aneurysmal subarachnoid haemorrhage is taking care of acutely ill patients, and should be performed in centres where a multidisciplinary team is available 24 hours a day 7 days a week, and where enough patients are managed to maintain and improve standards of care. There is no medical management that improves outcome by reducing the risk of rebleeding, therefore occlusion of the aneurysm, nowadays preferably by means of coiling, remains an important goal in treating patients with aneurysms. Because the poor outcome after subarachnoid haemorrhage is caused to a large extent by complications other than rebleeding, proper medical management to prevent and treat these complications is therefore essential. On basis of the available evidence, oral (not intravenous) nimodipine should be standard care in patients with subarachnoid haemorrhage. It is rational to refrain from treating hypertension unless cardiac failure develops and to aim for normovolaemia, even in case of hyponatraemia. There is no evidence for prophylactic hypervolaemia, and the strategy of hypervolaemia and hypertension in patients with secondary cerebral ischaemia is based on case reports and uncontrolled observational series of patients. Magnesium sulphate and statins are promising therapies, and large trials on effectiveness in improving clinical outcome are underway. There is no evidence for prophylactic use of anti epileptic drugs, and routine use of corticosteroids should be avoided.
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PMID:Medical management of patients with aneurysmal subarachnoid haemorrhage. 1870 99

Cerebral arteriovenous fistula (AVF) is a vascular malformation that is rare in the pediatric population. Older children with cerebral AVF tend to present with neurologic problems related to intracranial venous hypertension or intracranial hemorrhage. Cardiac and pulmonary complications following acute neurologic injury such as subarachnoid hemorrhage are common in adults, but are rarely reported in children. However, complications have been reported in cases of enterovirus 71 rhombencephalitis in infants and children and can cause high morbidity and mortality. Here, we report a 14-year-old boy who presented with cardiac failure associated with pulmonary edema following cerebral hemorrhagic stroke due to AVF. After aggressive investigation and management, we intervened before significant hypoxia and hypotension developed, potentially reducing the risk of long-term adverse neurologic consequences in this patient.
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PMID:Hemorrhagic stroke associated with pulmonary edema and catastrophic cardiac failure. 1894 7

We present the case of a 13-year-old boy with a ruptured cerebral arteriovenous malformation who had rapidly progressive cardiac failure leading to death. Serial electrocardiograms, cardiac enzymes, echocardiograms, and pulmonary artery catheter data confirmed severe ventricular dysfunction related to myocardial ischemia and infarction. Cardiac dysfunction after cerebral insult is commonly described in adults with aneurysmal subarachnoid hemorrhage and has been termed "neurogenic stunned myocardium" because of its transient nature in most of patients. In children, cardiovascular dysfunction has been described in a few reports and only after traumatic brain injury. No deaths have been reported. This case report illustrates the potentially lethal consequences of cardiovascular dysfunction in children after ruptured cerebral arteriovenous malformation with subarachnoid hemorrhage. Compromised cardiac function should be considered during the early evaluation and management of these patients and supportive care instituted to limit secondary brain injury from poor perfusion.
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PMID:Death from cardiac failure in a child with ruptured cerebral arteriovenous malformation. 1944 33

The field of Emergency Care Medicine is a very dynamic part of the Medical Science. That is why there is a huge amount of publications on this topic every year. This article is my personal selection of recently published scientific work on pulmonary embolism, classification of circulatory shock, betablockers in acute decompensated heart failure, advanced cardiac life support, subarachnoid hemorrhage, inhalation therapy with ipratropium-bromide, community acquired pneumonia, diverticulosis, gout and pancreatitis. Last but not least there is a choice of prophylactic interventions, you might not yet be aware of. Some of the discussed publications may help you manage the next patient you'll encounter, when you're on call next time.
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PMID:[News in emergency medicine 2009]. 1984 80


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