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

Clinical, CT and EEG findings of 100 consecutive patients suffering from epileptic seizures following hemispheric cerebral infarction were evaluated retrospectively. All patients were followed up for an average of 49 months. Twelve patients suffered from cardiogenic brain embolism, 20 had an occlusive disease of the internal cerebral artery. Forty-seven patients had a single middle cerebral artery infarct, 6 each a posterior cerebral artery or watershed infarct. CT showed lacunes in only 6 cases, 8 had multiple larger infarcts and 27 were normal. Seventy-six patients suffered from generalized seizures, 54 from partial fits, predominantly focal motor seizures. Seventy-one patients had their first seizure within the 1st year after stroke, 30 within 2 weeks after the infarct. The interval between stroke and the first epileptic fit exceeded 1 year in the remaining 29 cases. If the first fit occurred in the acute phase after stroke, the risk of further ones was significantly lower than when the first fit occurred in the chronic stage. The frequency of fits mainly depended on the occurrence of epileptic potentials in the EEG and the interval between stroke and the first seizure. During follow-up 27 patients suffered a recurrent stroke, and 52 patients died. Cardiac failure was the predominant cause of death; only 4 patients died as a consequence of an epileptic fit.
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PMID:Epileptic seizures following ischaemic cerebral infarction. Clinical picture, CT findings and prognosis. 214 39

The numerous metabolic abnormalities encountered in chronic purgative abusers were investigated and the new concept of autonomous pseudo-Bartter's syndrome documented. Detailed metabolic screening tests were performed in 9 women aged 17-54 years. Two patients underwent further studies, including serum renin and aldosterone, blood volume, total body potassium, urinary chloride and prostaglandin determinations, and each underwent renal biopsy on admission and after 1 year free from laxative abuse. Clinical complications included confusion, convulsions, coma, skeletal muscle weakness with or without paralysis or rhabdomyolysis, cardiac failure, urinary tract infections and bone disease (osteomalacia, secondary hyperparathyroidism and osteoporosis). Hypokalaemia, hypomagnesaemia, hypocalcaemia and hypophosphataemia were frequent findings. Serum creatine kinase correlated inversely with the product of the potassium and serum phosphate (r = -0.86; P less than 0.03), suggesting that hypokalaemia and hypophosphataemia act synergistically to produce muscle damage. After laxative withdrawal, oedema and weight gain, followed by diuresis, ensued in 7 patients. In the other 2, ongoing chloruresis, kaliuresis, hyper-reninaemia and raised urinary prostaglandin secretion persisted. Renal biopsies in these 2 patients showed the features of juxtaglomerular apparatus hyperplasia as well as medullary interstitial cell hyperplasia. In conclusion, pseudo-Bartter's syndrome was documented in 9 chronic laxative abusers. Because patients often indulged in more than one aberrant habit, e.g. laxative and/or diuretic abuse or bulimia, the clinical syndrome produced a myriad of confounding metabolic derangements, which we termed 'metabolic madness'. Laxative withdrawal was complicated by temporary pseudo-idiopathic oedema, which persisted in 2 patients. Further studies in these 2 women strongly supported the concept of 'autonomous pseudo-Bartter's syndrome'.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic laxative abusers with pseudo-idiopathic oedema and autonomous pseudo-Bartter's syndrome. A spectrum of metabolic madness, or new lights on an old disease? 225 4

A case of familial juvenile Alzheimer's disease with apallic state at the relatively early stage and various neurological features was reported. A 33-year-old woman showed a progressive dementia followed by apallic state at the relatively early stage, and died of cardiac failure at the age of 45. Neurological examination disclosed chorea, myoclonus, rigidity, pyramidal sign, and generalized convulsion. Neuropathologically, extensive senile changes such as senile plaques, neurofibrillary tangles, and granurovascular degenerations were observed in the brain, chiefly in the cerebral cortex and limbic system. The present case was characterized by a severe neuronal loss in the subcortical gray matter such as the caudate nucleus, dentate nucleus, substantia nigra, and thalamus as well as a marked myelin loss and axonal damages in the cerebral white matter. This case suggested a combination of multisystemic degeneration and a primary degeneration of the cerebral white matter. The additional peculiar aspects in this case were the senile plaques and amyloid angiopathy in the cerebellar cortex, and the senile plaques and grumose degeneration in the cerebellar dentate nucleus. In the clinicopathological standpoint, the apallic state in this case could be attributed to a severe degeneration of the cerebral white matter in addition to the cerebral cortical deterioration. Furthermore, the occurrence of chorea and myclonus might be contributed to the severe degeneration of the caudate nucleus and to the degeneration of the dentate nucleus, particularly to the grumose degeneration, respectively.
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PMID:[A case of familial juvenile Alzheimer's disease with apallic state at the relatively early stage and various neurological features--a clinicopathological study]. 279 15

An autopsy case of familial juvenile Alzheimer's disease with extensive involvement of the subcortical gray and white matters is reported. A 33-year-old woman showed a progressive dementia and died of cardiac failure at the age of 45. Neurological examination disclosed choreatic movements, myoclonus, rigidity, and generalized convulsion. Gross inspection of the brain showed a diffuse cerebral atrophy and marked degenerations of both the subcortical gray and white matters. Microscopically, numerous and extensive argyrophilic changes such as senile plaques, neurofibrillary tangles, and granulovacuolar degenerations were observed in the brain. The present case was characterized by a severe neuronal loss in the basal ganglia, substantia nigra, dentate nucleus, and thalamus as well as a marked myelin loss and axonal damage in the cerebral white matter. This case suggested a combination of multisystemic degeneration and primary degeneration of the cerebral white matter. The pathological similarity of this case to Creutzfeldt-Jakob disease and Pick's disease is discussed.
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PMID:An autopsy case of familial juvenile Alzheimer's disease with extensive involvement of the subcortical gray and white matters. 292 95

Tocainide is an antiarrhythmic drug structurally related to lignocaine with similar electrophysiological, haemodynamic and antiarrhythmic effects. In contrast to lignocaine (lidocaine) it is well absorbed after oral administration and has a plasma half-life of about 15 hours. In several open and controlled therapeutic trials in patients with ventricular arrhythmias, often following a myocardial infarction, tocainide has been relatively effective and usually well tolerated. In treating ventricular ectopic beats and/or ventricular tachycardia tocainide has demonstrated effective suppression in 60 to 70% of patients in both open and controlled studies. It has an acute effect when infused in patients with ventricular arrhythmias complicating myocardial infarction, as well as a prophylactic effect when given orally. The majority of these studies have demonstrated tocainide to be more effective than placebo, but trials against other antiarrhythmic agents are few in number and vary in design. One study combining an infusion of tocainide with oral therapy compared to a bolus injection of lignocaine followed by a constant infusion in patients after myocardial infarction, found the two agents to be of similar efficacy. The most common adverse effects are neurological and gastrointestinal in nature, nausea and dizziness occurring most frequently. Adverse effects resulting in termination of therapy have been reported in about 16% of patients. Aggravation of pre-existing heart failure, increased ventricular arrhythmia, deterioration of conduction disturbances, convulsions, and cases of lupus erythematosus syndrome have occasionally been reported. Thus, tocainide appears to offer a worthwhile addition to the other antiarrhythmic agents available for ventricular arrhythmias. However, its relative place in therapy compared with other antiarrhythmic drugs is not yet clearly established.
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PMID:Tocainide. A review of its pharmacological properties and therapeutic efficacy. 641 45

Short-term (acute oral LD50 and 90-day oral subchronic) studies in mice and long-term (24 months) carcinogenesis bioassays were performed in B6C3F1 mice and Fischer 344 rats given naltrexone. The oral LD50 was approximately 1500 mg/kg; convulsions, hypopnea, and cardiac failure were dose-related. Naltrexone mixed with feed over 90 days did not evoke definitive signs of gross toxicity, and histopathology was unrelated to drug treatment. Similar drug/feed admixtures given for 24 months to mice or rats did not disturb behavior. In mice, naltrexone reduced growth rates 5-10% and food intake 9-19%, but survival rates were 70-82% for treated mice and controls. The frequency and location of predominant tumors were similar in treated and untreated mice. In the rat, the same dosages had little effect on growth or food intake. The majority of all sacrificed rats had neoplasms. Neither neoplasms nor nonneoplastic lesions in mice or rats were associated with drug treatment. It is concluded that naltrexone is not a carcinogen.
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PMID:Physiologic and morphologic changes and incidence of neoplasms in mice and rats fed naltrexone HCl for 24 months. 646 31

Thirty-four cases of SLE treated during the past seven years (1974-1981) in Taipei Municipal Jen-Ai Hospital are reported and analyzed. Diagnosis of SLE was based on ARA preliminary criteria and Hahn's preliminary criteria. There were 32 females (94.2%) and 2 males (5.8%). The mean age at diagnosis was 28.5 years (range 14-51). Clinical manifestations were as follows: facial erythema 24 cases (70.6%), Raynaud's phenomenon 4 cases (11.4%), oral or nasopharyngeal ulceration 7 cases (20.6%), arthritis without deformity 22 cases (64.7%), proteinuria 21 cases (61.8%), pleural or pericardial effusions 13 cases (38.2%), psychosis or convulsions 9 cases (26.5%), hematological abnormalities 25 cases (73.5%). Laboratory findings were as follows: positive ANA test 33/34 (97.0%), hypocomplementemia 10/13 (76.9%), direct Coombs' test 4/18 (22.2%), indirect Coombs' test 1/13 (7.6%), LE cell 19/34 (55.9%), RA Latex 7/17 (41.7%), polyclonal gammopathy 15/17 (88.2%), anemia 25/34 (73.5%), leukopenia 12/34 (35.3%), thrombocytopenia 10/34 (29.4%). Three cases were complicated by herpes zoster, one by hyperthyroidism, and one by autoimmune thyroiditis. Ten cases died, including 4 renal failure, 2 heart failure, 2 cases of committed suicide and 1 case of CNS involvement.
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PMID:[Clinical experience in systemic lupus erythematosus (author's transl)]. 709 84

Among the 94 tricyclic antidepressant intoxications received in 3 years in the intensive care unit of Edouard Herriot Hospital, 16 with cardio-vascular manifestations are studied. The criteria of selection is the presence on the electrocardiogram (ECG) of a ventricular trouble in conduction excitability or automaticity. Eight times, the ingested dose exceeds 20 mg/kg. 10 times several toxics are taken explaining the severity of coma and the rarity of convulsions. 2 collapses, 1 shock, 1 cardiac arrest occur. The most frequent ECG abnormalities are: T modifications, (90 p. 100), prolongation of QT interval (60 p. 100), right bundle branch block (50 p. 100) or left one (25 p. 100). Only one death occurs; (1 p. 100 of this series). Ventricular dysrythmia or myocardial failure represent the main criteria in the evaluation of severity of the tricyclic antidepressant intoxication. For the treatment, a complete digestive evacuation is needed, Hemodialysis, plasmapheresis, or hemoperfusion cannot be actually recommended. The treatment of cardiac troubles involves essentially sodium. and eventually intra-cardiac pace maker.
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PMID:[Acute tricyclic antidepressant intoxication. Evaluation of severity and treatment. A study of 16 patients with cardiovascular manifestations (author's transl)]. 711 55

Fluoroacetate was dosed per stomach tube to 17 Merino sheep at the rate of 0,05-1,0 mg/kg/day. The clinical signs, haemodynamic changes, chemical pathology and pathology of acute, subacute and chronically intoxicated cases are described. Tetanic convulsions were seen in acutely intoxicated animals and in them respiratory failure, occurring concomitantly with cardiac failure, may have been the cause of death. Subacute intoxication resulted in less conspicuous clinical signs when the sheep were at rest, but they developed apparent nervous signs on being handled, and later tended to lie down. Chronically intoxicated animals were only mildly affected. At all levels of intoxication changes in the chemical pathological parameters were either absent or were mild and transient. The microscopic lesions in the hearts of acutely intoxicated sheep included degeneration as well as necrosis of individual or small groups of myocardial fibres. In the subacutely and chronically intoxicated animals the multifocal myocardial lesions were more widespread and in various stages of development or resolution.
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PMID:Observations on the clinical, cardiac and histopathological effects of fluoroacetate in sheep. 718 40

Forty patients with idiopathic hypertrophic subaortic stenosis have been studied. It was established that these patients had early signs of cardiac insufficiency (cardiac palpitations, fainting fits, dyspnoea) as a result of morphological changes in the myocardium (micro- and macrofocal cardiosclerosis). With the aid of contrast methods of investigation and phonography it was shown that in microfocal cardiosclerosis the index of the systolic murmur varies from 0.5 to 3, the planimetric index from 0.8 to 1.0. In macrofocal cardiosclerosis from 1.5 to 0 and less than 0.8, respectively.
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PMID:[Clinicodiagnostic aspects of idiopathic hypertrophic subaortic stenosis]. 719 66


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