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 study was designed to determine the prevalence of alcoholism/problem drinking among emergency medical admissions. Of 203 emergency admissions to two medical wards, 18% were found to be problem drinkers, using the brief Michigan alcoholic screening test (MAST) questionnaire. Problem drinking was found in 31% of males and 5% of females. Most drinking was done with friends (77%) and at the "rum shop" (62%). Fifty-one per cent of problem drinkers started between the ages of sixteen and twenty years. Seventy per cent of all problem drinkers had a first degree family relative who drank compared to 28% of non-drinkers. A high prevalence of alcoholism (48%) was found among smokers. Housestaff detected just over half of male (56%) and female (60%) alcoholics who were MAST-positive. Medical diagnoses among MAST-positive patients were gastrointestinal (cirrhosis, pancreatitis and hepatitis) in 32%, neurological (delirium tremens, seizures and subdural hematoma) in 27% and cardiovascular (cardiomyopathy, heart failure and dysrhythmias) in 16%. The detected level of problem drinking is likely to cause significant morbidity, and allows an important opportunity for intervention. The use of questionnaire methods to screen for alcoholism needs further evaluation in the region.
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PMID:Questionnaire detection of problem drinkers among acute medical admissions. 189 23

A 54 year-old man, who had a hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease; O-W-R) accompanied by pulmonary arteriovenous fistulas (PAVFs) and congestive heart failure, developed seizure, right hemiparesis and dysphasia. A brain CT scan revealed a cystic lesion with perifocal edema in left frontoparietal lobe. A contrast enhanced CT scan showed a ring-like enhancement. Dynamic CT scans disclosed that the ring in the cortical side was enhanced more thickly than that in the ventricular side. Considering the severity of the cardio-pulmonary condition, and the deep location of the abscess, we performed an echo-guided aspiration and drainage of the abscess under local anesthesia. No bacteria were demonstrated in the culture of the contents of the abscess. After the surgery, the right hemiparesis and dysphasia were much improved and a CT scan showed the marked reduction of the abscess. However, around eight days after the surgery, the patient showed severe pleural effusion due to progressive heart failure and died on the 11th postoperative day. Autopsy disclosed a shrunken brain abscess, multiple cerebral infarction, multiple PAVFs and severe constrictive pericarditis which was regarded as the cause of death in the patient. In this report, we presented the therapeutic advantage of echo-guided surgery for the treatment of brain abscess in a high-risk patient. We also discussed the mechanism of the formation of brain abscess in patients of O-W-R disease by reviewing published cases.
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PMID:[A case of Osler-Weber-Rendu disease with brain abscess; the mechanism of the formation of brain abscess and its treatment in Osler-Weber-Rendu disease]. 194 83

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 long-term clinical course of six patients with congenital central hypoventilation syndrome is described. During the neonatal period, the patients had prolonged apneas and hypoventilation, in the absence of cardiac, pulmonary, or neuromuscular disease. After an initial period of respirator dependency, they became able to sustain normal gas exchange while awake. During sleep, however, profound hypoventilation developed, and tracheostomy and mechanical ventilation were required. Ventilatory responses to hypercapnia and hypoxia were depressed or absent and did not improve with time. One patient was able, at 2 years of age, to breathe spontaneously during sleep with only moderate hypoventilation. The others, now 4 to 14 years of age, still need ventilatory support during sleep. Complications, such as cardiac failure and hypoxic seizures, mostly occurred early in the course and resolved with correction of insufficient mechanical ventilation. Speech acquisition was possible with the use of a special stoma plug. All patients were managed at home, and with appropriate support, the parents were able to provide safe ventilatory care with low morbidity and no mortality.
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PMID:Long-term follow-up of children with congenital central hypoventilation syndrome. 244 98

Since most of the toxicity associated with class 1B antiarrhythmic drugs is dose-related, this review examines adverse effects seen in both therapeutic practice and accidental or premeditated overdose. Toxicity is very common with these agents and can be life-threatening. A high percentage of patients must discontinue therapy because of adverse effects. Mexiletine and tocainide are structural analogues of lignocaine (lidocaine) and toxicity is similar with all 3 drugs. With gradual intoxication (the most common form) central nervous system effects such as lightheadedness, dizziness, drowsiness and confusion are seen first. Seizures and respiratory arrest can occur. Cardiovascular toxicity is manifested by progressive heart block, reduced cardiac contraction, hypotension and asystole. Both mexiletine and tocainide may have proarrhythmic effects. Gastrointestinal toxicity is also common. Shock, hypotension, cardiac failure and beta-blocker therapy reduce lignocaine clearance and enhance the risk of intoxication during routine therapy. Both lignocaine and mexiletine elimination is impaired in severe liver disease while tocainide clearance is reduced in renal failure. Management of toxicity is largely supportive and symptomatic. Lignocaine infusion must be discontinued and decontamination of the gut in the case of oral preparations is recommended. Serious intoxication requires intensive care unit admission. Haemodialysis or haemoperfusion may be helpful in serious lignocaine and tocainide poisoning. In institutions where extracorporeal circulatory assistance is available, massive lignocaine poisoning has been successfully treated with this intervention. In the therapeutic setting serious toxicity can be prevented by close clinical surveillance and appropriate dose reduction in patients with reduced drug clearance. Because of the large interindividual variation in lignocaine pharmacokinetic parameters, therapeutic drug monitoring is recommended if results can be reported quickly. Mexiletine and tocainide have stereoselective metabolism and assays do not distinguish the more active isomers. Therapeutic drug monitoring is less useful in this situation.
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PMID:Poisoning due to class 1B antiarrhythmic drugs. Lignocaine, mexiletine and tocainide. 251 64

Since our initial orthotopic heart transplant (OHT) in 1968, the first in Europe, 1130 patients with ages ranging from 1 month to 66 years have been referred to us. The cause of irreversible myocardial damage was idiopathic cardiomyopathy in 74%, ischemic heart disease in 19% and left ventricular failure after valvular replacement in 7%. A total of 540 transplantations, 463 orthotopic, 40 heterotopic and 37 heart-lungs were carried out. Features of the early post-operative course include temporary (first week) cardiac instability treated by isoproterenol. Later complications included rejection (95%) and side-effects of immunosuppressive therapy; infection (83%), osteoporosis, malignancy, graft atherosclerosis (2%). Cyclosporine (Cy) was responsible for diastolic hypertension, renal dysfunction, hirsutism, hyperplasia of the gingiva, hepatic dysfunction, and seizures. The survival rate of the Cy-treated patients was 68% at 7 years. All survivors have virtually normal social and professional lives, included the longest survivor 14 years after the operation. Recently in 34 patients in acute irreversible cardiac failure and who cannot have a transplant in time, we implant a total artificial heart (TAH) type JARVIK 7 during a period from 1-150 days. There has been no mechanical failure, hemolysis or thrombo-embolism and only one right ventricular device malposition; 20 patients died before transplantation, 13 were successfully transplanted, 1 is still on the artificial heart. Heart transplantation, and TAH used as a bridge to transplantation are now an accepted therapeutic means for irreversibly cardiac failure in selected patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Current problems in cardiac transplantation. 266 Sep 20

Although much has been written on the response of the heart to various intracerebral events including seizures, ischemia, intracerebral, and subarachnoid hemorrhage, less is known of the cerebral response to altered cardiac rhythm, cardiac failure, and cardiac arrest. The latter may alter central neuronal activity, cerebral blood flow, or cause ischemic damage. Such changes in cerebral function may lead to loss of consciousness, seizures, and focal neurologic deficits at the clinical level.
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PMID:Neurologic manifestations of cardiac disease. 267 32

Sudden unexpected death accounts for a substantial portion of deaths among epileptics. The incidence of this phenomenon is probably 1 in 370 to 1 in 1,110 in the general epileptic population but may be even higher in the 20- to 40-year age group, and still higher if epileptics with symptomatic epilepsy are selected. Sudden unexpected death in epileptics has been observed at least once weekly by the Office of the Medical Examiner of Cook County (Chicago), Illinois, for many years. A year-long prospective study revealed that victims of this complication of epilepsy are most commonly black males averaging 35 years of age who have infrequent generalized seizures and usually have some structural lesion in the brain responsible for their seizures. They tend to abuse alcohol and have poor compliance with anticonvulsant medication. The electroencephalograms display considerable variability from record to record. At autopsy the heart, lung, and liver weights were heavier and the brain weights were lighter than expected. The mechanisms involved in sudden unexpected death in epileptics may include autonomically mediated cardiac arrhythmia alone or in combination with sudden "neurogenic" pulmonary edema and "backward" cardiac failure.
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PMID:A prospective study on sudden unexpected death in epilepsy. 277 6

A 79-year-old white male was admitted to the hospital for treatment of a right-lower-lobe pneumonia. His past medical history included: mild congestive heart failure, asymptomatic ventricular tachycardia, and ethanol abuse. He was initially treated with furosemide for his heart failure, lidocaine for his arrhythmias, and Bactrim for his pneumonia. On day 13 of hospitalization he experienced a tonic-clonic seizure during the time he was being converted from lidocaine to tocainide. At the time of the seizure both tocainide and lidocaine were well within their respective therapeutic ranges. Since the seizure, the patient has tolerated treatment with each drug separately, and at serum concentrations similar to those preceding the seizure, without neurological complications, indicating the possibility of a tocainide-lidocaine induced seizure.
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PMID:A seizure induced by concurrent lidocaine-tocainide therapy--is it just a case of additive toxicity? 308 Feb 99

It is proposed that the vein of Galen aneurysm represents a venous ectasia secondary to an increased flow (usually caused by a deep-seated arteriovenous shunt draining either directly into the vein of Galen aneurysm or into a tributary of the vein of Galen) associated with obstruction of a dural sinus distal to the aneurysm. The closer the venous obstruction is to the vein of Galen, the better the chances are of developing obstructive (noncommunicating) hydrocephalus and the more likely it is that the venous drainage from the rest of the brain will be unaffected. The farther the venous obstruction is from the vein of Galen aneurysm, the better the chances are of developing a communicating type of hydrocephalus. The development of cardiac failure is related to the magnitude of the arteriovenous shunt. Brain damage, seizures, and hemorrhage may be related to the retrograde venous engorgement, causing impaired drainage of the healthy brain. Careful attention should be paid to the venous drainage characteristics of the lesion because the types of dural venous obstructions and anomalies vary from case to case. The term "vein of Galen aneurysm" should be abandoned in favor of the term "vein of Galen ectasia."
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PMID:The role of dural anomalies in vein of Galen aneurysms: report of six cases and review of the literature. 310 75


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