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

The Pickwickian Syndrome stimulated new pathophysiological concepts in regard to control of ventilation. With the advent of sleep laboratories, the peculiar sleep apnea occurring in some of these patients has been explained on the basis of intermittent upper airway obstruction. Two patients with different manifestations of the Pickwickian Syndrome are presented. The suggestion is made that these two subsyndromes should have unique designations. The Auchincloss Syndrome is manifested by right heart failure and respiratory acidosis in obese patients who are alert and have no major abnormality of breathing pattern. The fundamental cause of this abnormality is the increased work of breathing caused by the obesity. The cost of breathing is so high that the ventilatory regulation is compromised and respiratory acidosis results. The Gastaut Syndrome is characterized principally by hypersomnia and sleep apnea. The fundamental defect is upper airway obstruction during sleep, resulting in increased work of breathing, which together with the increased work caused by obesity leads to respiratory acidosis and right ventricular failure. Hypersomnia, rather than heart failure or respiratory acidosis, is the major manifestation of this syndrome, and is the result of sleep loss.
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PMID:Pickwickian syndrome, 20 years later. 117 87

Foster child hemangioma management depends on its usual spontaneously regressive evolution as it is a transient and benign vascular tumor like lesion. Most of the time clinical follow up is the only management. Investigations are indicated if treatment is needed (for decision and follow up) concerning only hemangiomas with a bad functional or esthetic prognosis (peri-orificial lesions and large locations of the face) or complicated hemangiomas with life-risk as sub glottic hemangioma, Kasabach and Merritt Syndrome, diffuse and liver hemangiomatosis possibly associated to cardiac failure. Basic treatment remains systemic corticosteroids with indications for early surgery or intralesional corticosteroids.
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PMID:[Management of hemangioma in the infant]. 158 31

Measurement of fibronectin in ascites has been proposed for the differentiation of ascites either due to malignant growth in the peritoneal cavity or liver cirrhosis with portal hypertension. The high ascitic fibronectin concentration in patients with peritoneal carcinomatosis was thought to be due to the synthesis of this protein by neoplastic cells. Therefore in ascites of malignant origin cellular fibronectin should be present as it is synthesized by neoplastic cells. On the other side the transsudative ascites due to liver cirrhosis with portal hypertension should mainly contain plasma-fibronectin, which is secreted by hepatocytes into the bloodstream. With the aid of two different monoclonal antibodies and immunoblotting of partially digested or intact ascitic fibronectin, cellular fibronectin could be demonstrated in ascitic fluid of 10 patients with peritoneal carcinomatosis, 13 patients with liver cirrhosis, one patient with right-sided heart failure and one patient with Budd-Chiari-Syndrome. As determined by a specific ELISA 8 out of 10 samples of malignant ascites contained more than 30 mg/l of cellular fibronectin, whereas 10 out of 13 samples of ascites due to liver cirrhosis contained less than 10 mg/l. Whereas in ascites of malignant origin cellular fibronectin represented about 20% of total fibronectin, in portal ascites fibronectin represented sometimes more than 50% of total fibronectin. Cellular fibronectin of non-malignant origin is probably produced by mesothelial cells or peritoneal macrophages. Therefore, fibronectin accumulating in peritoneal carcinomatosis is only to some extent locally produced, but mainly caused by an unhindered exsudation of plasma-fibronectin.
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PMID:[Genesis of fibronectin in ascites--detection of cellular and plasma fibronectin in portal and malignant ascites]. 205 24

The report analyses clinical manifestations, preoperative preparatory procedures, variants and results of urgent and emergency surgical procedures carried out in 47 cases of advanced thyroid cancer. Syndrome of grave lung-heart failure proved a major clinical sign of the disease. It could be compensated by intensive care (in a special ward included). Cervical and cervico-transsternal access was used, and surgery was performed to an extent determined by the pattern and extension of tumor. Thirteen patients died within a few days after operation and 23 at later stages. Among immediate causes of death were lung artery embolism, obstructive tracheobronchitis and tumor progression. Development of emergencies was avoided in many cases by carrying out timely examination and treatment.
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PMID:[Emergency and urgent operations in the treatment of patients with thyroid cancer]. 246 Oct

In a 3170 g newborn with a large cavernous hemangioma at the left thigh, heart failure was evident. Echo- and angiographically a large perimembranous ventricular septal defect was found. An important a-v shunt within the hemangioma could be excluded by hemodynamic investigation and selective arteriographic examination of the vascular tumor. Thrombocytopenia present from the first day of life was only temporarily overcome by corticosteroid therapy but nevertheless consumption coagulopathy (Kasabach-Merritt-Syndrome) developed and additional therapy with heparin was necessary in order to normalize the coagulation factors. However, no regression in size of the tumor occurred over the first 8 weeks of life and a total exstirpation of the hemangioma was performed. Postoperatively no further cortison or heparin therapy was necessary. Despite vigorous medical treatment the congestive heart failure persisted. After surgical closure of the ventricular septal defect at the age of three months the infant thrived and could be discharged without pathological symptoms.
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PMID:[Cavernous hemangioma and disseminated intravascular coagulation (Kasabach-Merritt syndrome) in a newborn infant with a large ventricular septal defect]. 380 21

Over an 18 month period, 19 patients were referred for assessment of excessive daytime sleepiness and/or loud snoring. Respiratory studies during sleep were performed in 14 of these patients with additional features such as disturbed sleep, observed apnoea during sleep, morning headache, mental and personality changes, hypertension and cardiac failure. Nocturnal respiratory studies undertaken for periods of 4-8 hours confirmed a diagnosis of the Sleep Apnoea Syndrome in eight patients. In these patients apnoeas, lasting from 30-144 seconds, occurred frequently during sleep (from 35-291 episodes per patient). In one severely affected patient, tracheostomy abolished all symptoms. The use of conservative therapy such as weight loss, protriptyline or a neck collar, highlighted the inadequacies of current medical treatment. Awareness of the symptom complex and potential complications of the Sleep Apnoea Syndrome is important because the diagnosis may easily be missed if the patient presents with one or two isolated complaints.
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PMID:The importance of suspecting sleep apnoea as a common cause of excessive daytime sleepiness: further experience from the diagnosis and management of 19 patients. 693 67

Two problems in the treatment of hypertension continue to be largely unsolved. The first, and more simple, is our inability to adequately control blood pressure in the majority of hypertensive patients. This not only reflects the difficulty of retaining patients in effective treatment programs, but also of convincing physicians to strive for optimal blood pressure levels. There is a continuing need for new antihypertensive drugs and combinations to help accomplish these goals. The second major problem is that the major clinical endpoints, including coronary events and renal failure, have not been adequately reduced by traditional therapies. Standard regimens, particularly those including diuretics, have protected against strokes and heart failure. Our improved understanding of vascular biology in hypertension has directed interest to the mechanisms in hypertensive patients that might accelerate atherosclerosis and vascular events in these individuals. This involves addressing the concomitant metabolic risk factors that comprise the "Hypertension Syndrome," and, perhaps of equal importance, finding therapies that directly inhibit unwanted types of growth and proliferative activities within the walls of critical arteries. Many substances within the endothelium and the vascular wall may participate as initiators or mediators of pathology, but most information thus far has focused on the renin-angiotensin system. Angiotensin converting enzyme inhibitors (and potentially angiotensin receptor blockers) have provided coronary and renal protection in various cardiovascular conditions, though not yet in formal hypertension trials. Calcium channel blockers have also shown promise, including recent stroke and cardiovascular benefits in patients with isolated systolic hypertension, but, again, definitive coronary data in hypertension are awaited. Unless concomitant conditions mandate the selection of a particular antihypertensive drug class, physicians currently have a dilemma: should they choose drugs from older classes that have not provided full protection? Or, should they prescribe newer agents with exciting potential but with, as yet, unproved endpoint benefits in hypertension? Until currently ongoing prospective trials of antihypertensive therapy are completed, physicians must be guided by their own interpretations of the available data.
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PMID:Translating data on antihypertensive drugs into clinical practice. 965 68

The 4q-Syndrome: Here we report four cases of interstitial and terminal deletions of the long arm of chromosome 4. Case 1 is a 16 month old boy with del(4)(q12q21) who has soft dysmorphic features, tetralogy of Fallot, and severe developmental delay. Case 2 is a male infant with the same deletion and congenital cardiomyopathy. He suffered severe birth asphyxia and died at the age of 6 months. His father was found to have a complex chromosome 4 rearrangement. Case 3 is a female infant with del(4)(q33) who died of aspiration pneumonia. She was mildly dysmorphic and presented with heart failure and hypercalcaemia. Case 4 is a 8 month old girl who has del(4)(q33) and Pierre-Robin sequence. So far about 70 patients with microscopically visible deletions of chromosome 4q have been described. Although they vary in their phenotypes, they have several features in common. We suggest to use the term 4q-syndrome for all macrodeletions of the long arm of chromosome 4.
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PMID:The 4q-Syndrome. 1183 1

The role of glycoprotein IIb/IIIa platelet receptor antagonist therapy for patients with an acute coronary syndrome (ACS) and a history of coronary artery bypass grafting (CABG) remains incompletely defined. We examined the outcomes of patients with an ACS and prior CABG who were treated with tirofiban versus placebo among subjects with prior CABG in the Platelet Receptor Inhibition in Ischemic Syndrome Management in Patients Limited by Unstable Signs and Symptoms (PRISM-PLUS) trial. Of 1,570 patients treated with tirofiban plus heparin (n = 773) or heparin alone (n = 797), 231 had prior CABG. Compared with patients without prior CABG, those with prior CABG were more likely to have risk factors for a complicated ACS course, including severe coronary artery disease and heart failure (all p <0.0001), typically had clinical predictors of benefit from tirofiban, such as ST-segment depression (p = 0.01) or a TIMI risk score >or=4 (p <0.001), and were more likely to die or have a myocardial infarction or refractory ischemia at all time points examined (p <0.0001). Among patients with prior CABG, decreases in the incidence of death, myocardial infarction, or refractory ischemia with tirofiban and heparin versus heparin alone were noted at 7 and 30 days (7 days: 16.9% vs 29.0%, p = 0.035; 30 days: 25.0% vs 40.2%, p = 0.015). Trends toward a decrease in death, myocardial infarction, and refractory ischemia with tirofiban and heparin versus heparin alone in the prior CABG subgroup were noted at 48 hours and 180 days (48 hours: 6.5% vs 14.0%, p = 0.09; 180 days: 37.1% vs 48.6%, p = 0.057). Bleeding rates were similar in patients with and without prior CABG. Tirofiban was well tolerated and tended to decrease the considerable risk for ischemic ACS complications in patients with prior CABG.
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PMID:Tirofiban therapy for patients with acute coronary syndromes and prior coronary artery bypass grafting in the PRISM-PLUS trial. 1505 Apr 86

The differentiation of haemangiomas and vascular malformations is histological, clinical and prognostic. Although the majority of haemangiomas evolve towards spontaneous resolution, as many as 10% of cases can develop complications with ulceration, pain and haemorrhaging. Besides, the localisation of haemangiomas in the head and neck, next to vital structures, can compromise their functions. Hence, compression of the airway might be a vital emergency. Periorbital haemangiomas can give rise to amblyopia due to sensory deprivation or due to a restrictive strabismus. Lumbosacral haemangiomas must be studied with Nuclear Magnetic Resonance because of their frequent association with alterations in the midline at the level of the spine, anus, genitals or kidneys. Amongst visceral haemangiomas, hepatic haemangiomas are the most serious due to their association with congestive cardiac insufficiency. The association of extensive facial haemangiomas with anomalies of the central nervous system, vascular, cardiac, ocular and sternal anomalies, is denominated PHACE syndrome and is frequently complicated by mental deficiency, convulsions or ictus. Vascular malformations of trigeminal localisation are associated in up to 15% of cases with glaucoma or choroidal or leptomeningeal haemangiomas (Sturge-Weber syndrome). Combined vascular malformations localised in the extremities can become complicated with thrombophlebitis, regional osteolysis and even distant thromboembolisms (Klippel-Treneaunay Syndrome). On the other hand, there is a coagulopathy due to consumption (Kassabach-Merrit Syndrome) that can complicate some vascular tumours such as the Kaposiform haemangioendothelioma and the tufted angioma. Finally, the complications of the treatments employed are reviewed.
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PMID:[Complications in the evolution of haemangiomas and vascular malformations]. 1514 12


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