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)

Continuous oral dimethylsulphoxide (DMSO) treatment (7-15 g/day) was given to 3 patients with amyloidosis of familial Mediterranean fever (FMF), 3 patients with idiopathic amyloidosis, and 7 patients with secondary amyloidosis. The nephrotic syndrome and various degrees of renal insufficiency were the major clinical manifestation in all case. Renal function was used as the main parameter for evaluation of therapy. DMSO treatment for 7-16 months produced no effect in the FMF patients and in the patient with idiopathic amyloidosis; they all ran the predictable clinical course of their disease and either died of cardiac failure or have been maintained on chronic haemodialysis. In the 7 patients with secondary amyloidosis an unequivocal improvement of renal function was observed following 3-6 months of DMSO treatment. It was shown by a 30-100% rise of creatinine clearance and a decline in proteinuria. This new equilibrium has been maintained as long as DMSO was administered. No serious side effects of DMSO wee encountered. Mild nausea and an unpleasant breath odour were the patients' main concern. We conclude that a therapeutic trial with oral DMSO is warranted in all patients with secondary amyloidosis. This treatment is unpleasant but bears no exceptional risks. It may significantly prolong life, though its effect on amyloid deposits themselves is doubtful.
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PMID:Prolonged dimethylsulphoxide treatment in 13 patients with systemic amyloidosis. 714 95

Rubidazone was administered to 24 children with advanced solid tumors or leukemia. The dose ranged from 80 to 150 mg/m2/IV daily to a total dose of 160 to 450 mg/m2/course. This course was repeated at intervals of approximately three weeks. Eighteen of 24 patients (75%) had received adriamycin and daunomycin as part of prior chemotherapy. The major toxic effects observed were myelosuppression, nausea, vomiting, mucositis, and skin rash. Four patients developed abnormal echocardiograms following the rubidazone therapy, 2 manifested clinical cardiac failure, of which one had anthracycline cardiomyopathic changes on autopsy. One of 7 adequately treated ALL patients achieved M2 marrow and improved peripheral counts for 3 weeks. One of the 2 neuroblastoma patients had subjective improvement of bone pain for 2 months. Rubidazone, in a previous heavily treated group of patients used in this study, had dosages of 360 and 450 mg/m2 which produced marrow hyperplasia to aplasia, with only minimal responses.
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PMID:Phase I trial of rubidazone (NSC 164011) in children with cancer. 726 27

Timolol has become so populat with ophthalmologists that it is prescribed 44% of the time when an anti-glaucoma drop is needed. This popularity is due to its newness and the publicity it has received, its effectiveness in most types of glaucoma, and the apparent scarcity of side effects. This paper looks at the first 489 patients treated with timolol at Wills Eye Hospital and the side effects encountered. These include blurring of vision, burning and pain, bradycardia and heart failure, hallucinations, dilated pupils, headaches, dizziness, hypotony, allergy, asthma, impotence, drowsiness, anxiety, emotional lability, and nausea.
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PMID:The place of timolol in the practice of ophthalmology. 740 91

We report two patients with solitary thalamic abscesses, occurring among 91 consecutive patients (2.2%) with computed tomography (CT)-diagnosed and surgically-verified brain abscess experienced in our college during 1975 to 1991. A 9-year-old girl with congenital heart disease experienced frequent vomiting followed by left hemiparesis and deterioration of consciousness. CT demonstrated a right thalamic ring-enhanced lesion. Purulent material was aspirated via a burr hole. She died of heart failure on the 5th postoperative day. Autopsy disclosed diffuse brain swelling and an encapsulated abscess in the right thalamus, which had ruptured into the third ventricle. A 30-year-old female experienced headache, nausea, and vomiting, which progressed to somnolence and right hemiparesis. CT demonstrated a left thalamic ring-enhanced lesion. Purulent material was aspirated by stereotactic procedures. All symptoms had resolved by the end of the 2nd postoperative week.
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PMID:Solitary pyogenic thalamic abscess--two case reports. 750 3

The calcium ion plays a decisive role in the effect and regulation of several cellular processes. The heart muscle cells, pacemaker and channel systems and vascular smooth muscle are functionally dependent on Ca2+ influx mainly via potential sensitive L (long lasting)-Ca(2+)-channels, which are blocked by Ca(2+)-channel blockers, a group of organic substances binding to specific sites at the Ca2+ channels. The Ca2+ channel blockers are now well established in the treatment of angina pectoris, arterial hypertension, supraventricular arrhythmia and subarachnoidal haemorrhage. On the basis of chemistry and pharmacodynamics the Ca2+ channel blockers are divided into three groups, with verapamil, nifedipine and diltiazem representing 1. generation derivatives and prototypes for groups I, II and III, respectively. All Ca2+ channel blockers act as vasodilators, while group I (verapamil) and to a lesser degree group III (diltiazem) also have antiarrhythmic effects. All Ca(2+)-channel blockers are contraindicated in hypotension. In cases of pronounced bradycardia, sinoatrial and atriventricular block Ca2+ channel blockers with antiarrhythmic effects are contraindicated and must be used with care in combination with beta-blocker treatment and in heart failure. Headache, flushing, reflex tachycardia, nausea, obstipation and ankle oedema are the most important secondary effects. With respect to pharmacodynamics the newly marketed 2. generation derivatives do not differ essentially from the 1. generation derivatives. The clinical potential of the Ca2+ channel blockers is not fully explored and the possibilities for extending their indications are still to be elucidated.
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PMID:[Calcium channel blockers (calcium antagonists). Background, effects and use]. 764 18

A 65-year-old woman, known to have peptic ulcers, developed nausea and retching. Clinical examination demonstrated pain on pressure in the epigastrium with otherwise normative findings for age. Two gastric ulcers and gastritis with erosions were seen at endoscopy. The patient, who was being treated with digitoxin for heart failure, reported having taken up to four digitoxin tablets (0.07 mg each) daily because she had insomnia. The plasma digitoxin level was between 150 and 160 nmol/l (therapeutic range 17-33 nmol/l), while the ECG showed no signs of digitalis intoxication. Initially the platelet count was 40,000/microliter: there had been no history of thrombocytopenia or symptoms of abnormal haemostasis. Other laboratory tests were within normal limits. After digitoxin had been discontinued, the platelet count rose without further treatment to 373,000/microliter 3 weeks after hospital admission by which time the digitoxin level had fallen to 48.9 nmol/l. The gastrointestinal symptoms regressed completely on treatment with omeprazole (40 mg three times daily for 8 days) and ranitidine (150 mg twice daily).
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PMID:[Reversible thrombocytopenia due to digitoxin overdose]. 800 65

The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage of sotalol hydrochloride are reviewed. The chemical name of sotalol hydrochloride is 4'-[1-hydroxy-2-(isopropylamino)ethyl]methanesulfonanilide monohydrochloride. Sotalol is a class III antiarrhythmic that prolongs the action potential and refractoriness of cardiac tissue and has potent nonselective beta-blocking activity. Sotalol is well absorbed after oral administration. The pharmacokinetics of sotalol can be described by an open, linear, two-compartment model. The drug is eliminated primarily by the kidneys; mean elimination half-life is 12 hours. Sotalol has been found to be effective in controlling life-threatening ventricular arrhythmias, including sustained ventricular tachycardia, ventricular fibrillation, and premature ventricular complexes. Although sotalol has FDA-approved labeling for use in the treatment of ventricular arrhythmias only, it is also effective against a variety of supraventricular arrhythmias. Noncardiac adverse effects include fatigue, impotence, depression, headache, nausea, diarrhea, and increased triglyceride levels. Cardiovascular adverse effects include atrioventricular block, bradycardia, hypotension, exacerbation of heart failure, and polymorphic ventricular tachycardia. Overall, 11-21% of patients experience adverse effects; 6-18% of these patients have reactions serious enough to warrant the discontinuation of sotalol therapy. The initial dosage of oral sotalol hydrochloride in adults is 80 mg twice daily or 160 mg once daily; the dosage can be increased every three to four days in increments of 40-160 mg/day to a maximum of 480 mg/day. Sotalol is useful in the control of intractable, life-threatening ventricular arrhythmias, as well as a variety of supraventricular arrhythmias, in patients who do not respond to or are intolerant of more conventional antiarrhythmics.
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PMID:Sotalol: a new class III antiarrhythmic agent. 813 5

Levosimendan belongs to a new group of heart failure drugs, the calcium sensitizers. Because these compounds are not yet available for clinical use, the adverse drug events (ADEs) during levosimendan treatment cannot be predicted in detail. To evaluate the tolerability of levosimendan in human subjects, ADEs, safety laboratory values before and after treatment, and ambulatory ECG findings have been collected from several phase I and phase II clinical studies. By June 1994, approximately 200 subjects had received levosimendan. The most common ADE seen in healthy volunteers is headache, reported by some 40% of subjects in oral dosing but only 10% in i.v. dosing. The incidence of headache does not correlate well with the total daily dose of the drug. However, the controlled release formulations tested appear to cause vasodilatory symptoms more frequently than i.v. or rapid release oral formulations. The other typical vasodilatory ADEs seen in healthy volunteers are nausea, palpitation, and dizziness. Symptomatic hypotension is rarely encountered. It appears that heart failure patients tolerate the vasodilatory actions of the drug better than healthy volunteers. Only individual cases of headache, vertigo, and flushing have been reported, and injection site irritation has been the most commonly reported ADE (with an incidence <5%). However, because the longest administration of the i.v. infusion has been only 24 h, the duration of exposure to the drug is too short to allow any definitive conclusions to be drawn. All patients who have received levosimendan have been monitored with an ambulatory ECG. Even though some increase in heart rate is seen with high doses of the drug, there are thus far no signs of an increased incidence of ventricular tachyarrhythmias, nor have there been any noteworthy changes in the clinical laboratory safety tests. The experience with levosimendan is limited thus far and long-term data are lacking. It can be concluded, however, that at least in i.v. dosing the drug is devoid of ADEs with significant medical seriousness.
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PMID:Safety of levosimendan and other calcium sensitizers. 890 34

Sudden cardiac death is a common cause of mortality in patients with congestive heart failure. Asymptomatic ventricular arrhythmia has been attributed as the cause for increased overall mortality in such patients. We conducted a prospective randomised single-blind placebo-controlled trial with low-dose amiodarone to assess its efficacy in reducing mortality in severe congestive heart failure and its effect on exercise tolerance, left ventricular systolic function and ventricular ectopic activity. Patients were randomised to receive amiodarone (n = 36) 400 mg/day orally for one month followed by a maintenance dose of 200 mg/day, or to a standard treatment (n = 40) according to intention-to-treat principle. There were 10 cardiac deaths in the amiodarone-treated group and 16 in the control group. Significant improvement was noted in exercise time in the treadmill test (modified Bruce Protocol) among patients in the amiodarone-treated group while no such statistical difference was detectable in the placebo group. Side-effects in the amiodarone group included asymptomatic rise in hepatic enzymes (three-fold) in 6 percent and proarrhythmia in 3 percent of patients. Nausea was reported in one patient and rash in one. Though low-dose amiodarone proved to be an effective antiarrhythmic agent, it failed to live up to the expectation of improving sudden cardiac death in patients with severe chronic heart failure and asymptomatic ventricular ectopy.
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PMID:Low-dose amiodarone in severe chronic heart failure. 890 21

Forty chemotherapy naive patients with metastatic or locally advanced breast cancer were treated in a randomized trial comparing mitozantrone 14 mg/m2 with epirubicin 75 mg/m2 given intravenously at 3-weekly intervals. There was a 40% (95% confidence interval (CI) 8-72; P = 0.013) higher partial response rate with epirubicin (11/18) than with mitozantrone (4/19). Epirubicin caused significantly more alopecia (difference 76%; 95% CI 57-96; P < 0.0001) and nausea/vomiting (difference = 38%; 95% CI 10-67; P = 0.01). Three patients who received long courses of epirubicin experienced cardiac failure; two were proved to have cardiomyopathy. The median survival for the epirubicin and mitozantrone groups were 9.5 and 8 months respectively. Thus, although epirubicin gave a higher response rate it also caused more toxicity.
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PMID:Comparison of mitozantrone and epirubicin in advanced breast cancer. 897 51


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