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)

Eighteen patients with severe symptoms of the carcinoid syndrome were assessed for hepatic embolisation. Four were too ill, and one had mild symptoms; thus 13 received a periembolisation regimen of cyproheptadine, fenclonine, aprotinin, methylprednisolone, tobramycin, flucloxacillin, and metronidazole. Embolisation was not performed in one patient with an occluded portal vein and was unsatisfactory in two others, in one because she was moribund and in the other because the hepatic artery had been ligated. Dramatic improvement in symptoms occurred in the nine patients in whom embolisation was successfully carried out, with abolition of flushing, severe abdominal pain, and wheeze and reduction in diarrhoea from 10.5 (SD 7.6) to 1.6 (0.9) stools/day. Urinary excretion of 5-hydroxyindole acetic acid fell from 1048 (716) to 289 (184) mumol/24 h (200 (137) to 55 (35) mg/24 h). Complications included one death from septicaemia, a hepatic abscess requiring surgical drainage, abdominal pain in three patients, pleural effusion in two, and transient encephalopathy in one. Relief of symptoms lasted for one to 24 months, and second embolisation in two patients produced further remissions of four to six months. Five patients died, one to 40 months after embolisation, in four cases because of metastases or heart failure. Hepatic embolisation is the treatment of choice for symptoms of the carcinoid syndrome resistant to medical treatment.
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PMID:Role of hepatic arterial embolisation in the carcinoid syndrome. 641 93

Seventeen neonates received an intravenous infusion of prostaglandin E1 for an average of 39 days (range 8 to 104). Seven (group 1) had transposition of the great arteries with no ventricular septal defect or a small one; eight (group 2) had ductus-dependent pulmonary flow (pulmonary atresia or stenosis in six and tricuspid atresia in two); and two (group 3) had aortic coarctation, one with no ventricular septal defect, the other with ventricular septal defect, isthmus hypoplasia and descending aortic flow supplied mainly by the ductus. An increase in the arterial partial pressure of oxygen (PO2) was seen in groups 1 and 2. Six patients from group 1 and two from group 2 developed heart failure; cortical hyperostosis of long bones was seen in three patients from group 1 and three from group 2; one from group 1 had refractory diarrhea. Other side effects seen at the beginning improved as the rate of infusion diminished. In group 3, the patient with complex coarctation had a decrease in blood pressure in the arms, an increase in pressure in the legs and restoration of renal function; in the patient with no ventricular septal defect, heart failure worsened during therapy. Histologic changes seen in three ductus were attributed to the closing process. When delaying surgery in selected ill infants with heart defects is deemed advantageous, long-term infusions of prostaglandin E1 are feasible.
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PMID:Long-term prostaglandin E1 therapy in congenital heart defects. 653 55

Carcinoid heart disease is a rare entity and has always been hallmarked by its late appearance in the malignant carcinoid syndrome. Most cases are discovered when patients complain of typical symptoms, including flushing and diarrhea, with subsequent heart failure and valvulopathy developing years later. Only a few case reports of successful valve replacements have appeared in the literature, and the cause of the valvulopathy in those patients was known at surgery. I discuss herein a unique case of carcinoid heart disease that was diagnosed postoperatively.
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PMID:Carcinoid heart disease. A unique case of postvalvotomy diagnosis. 687 Apr 45

More than 1200 patients who received pindolol for the treatment of hypertension, angina pectoris, and various arrhythmias in studies conducted in the United States were included in the New Drug Application submitted to the FDA. Nearly 1000 of these patients received pindolol as monotherapy. The side effects reported were generally transient and of mild or moderate severity. The most frequently reported side effects seen after pindolol administration, compared to those seen after placebo, were in decreasing order of incidence: headache, dizziness, insomnia, muscle pain, fatigue, weakness, nervousness, joint pain, edema, nausea, and muscle cramps. Other side effects that occurred more frequently with pindolol than with placebo but at a rather low incidence induced weight gain, bizarre dreams, visual disturbances, lethargy, and diarrhea. Nasal congestion, throat discomfort, nocturia, impotence, pruritus, anxiety, hypotension, bradycardia, and heart failure occurred only rarely. Of the 323 patients who received pindolol alone for the treatment of mild to moderate hypertension, only 20 (6.2%) were withdrawn from the study because of side effects. Overall, 3.4% of the patients treated with pindolol were withdrawn because of side effects, most of which involved the central nervous system, that is, insomnia, anxiety, dizziness, and headache. However, a few patients manifested some edema and weight gain while receiving pindolol alone. Review of the side effects data did not reveal a tendency for the incidence of side effects to be dose related. One placebo-controlled, double-blind study designed to evaluate the fixed dosages of 15, 30, and 60 mg in the treatment of mild to moderate hypertension suggested that only the incidences of insomnia and nervousness increased with increasing doses. However, these side effects were generally transient and of mild or moderate severity. The evidence indicates that pindolol has an acceptable safety profile and that any side effects that appear are generally well tolerated and disappear with continued treatment.
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PMID:Adverse reactions to pindolol administration. 704 82

Kawasaki disease (KD), first described in Japan in 1967 by Dr. Tomisaku Kawasaki, is an acute multi system vasculitis of infancy and early childhood characterised by high fever, rash, conjunctivitis, inflammation of the mucous membranes, erythematous induration of the hands and feet and cervical lymphadenopathy. Synonyms for Kawasaki disease include "Kawasaki syndrome" and "mucocutaneous lymph node syndrome" (MCLS, MLNS, MCLNS). Kawasaki disease was initially presumed to occur only in Japan; but now this disease is known in the whole world. The first cases in the United States were reported in Hawaii in 1976. In poland 5 cases were recognized, and first time described in 1981. The etiology of Kawasaki disease remains unknown. Toxic, allergic and immunologic causes have been suspected, but most investigators favor an infectious cause or an immune response to an infectious agent. Among classes of microorganism suspected of causing Kawasaki disease were bacteria, leptospires, fungi, rickettsiae and a number of viruses. Recently, there has been considerable interest in the possibility, that Kawasaki disease is caused by RETROVIRUSES. Although the disease is generally benign and self-limited, about 20% of children develop coronary artery aneurysms. In 5% of cases, giant aneurysm/more then 8 mm/develop, predisposing the patient to acute coronary artery thrombosis, myocardial infarction and sudden death. This is the most serious complication of KD. Other manifestations of hearth involvement, include pericarditis, myocarditis, myocardial failure and mitral regurgitation. Besides this many other clinical findings are commonly noted in KD; such as: pneumonia, diarrhea, arthritis, aseptic meningitis, otitis media, obstructive jaundice, hydrops of gallbladder and others.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Kawasaki disease]. 754 22

A crude, whole-body extract of female or male heartworms was injected IV into 28 dogs with and 22 dogs without heartworm (HW) infection. The female HW extract caused shock in 22 of 24 dogs with and 12 of 20 dogs without HW infection. The male HW extract induced shock in 4 of 4 dogs with and 1 of 2 dogs without HW infection. Prevalence of shock caused by female HW extract was significantly (P < 0.05) higher in dogs with than without HW infection; shock developed 5 to 30 minutes after HW injection. These signs were observed: marked decrease in blood pressure; collapse (initial collapse); paleness of mucous membranes; weak heart sounds; dyspnea; skin coldness; intestinal hyperperistalsis, and defecation; increases in RBC count, serum total protein concentration, serum osmolality, serum Na and blood glucose concentrations; and decreases in neutrophil, eosinophil, and platelet counts. Alanine transaminase, alkaline phosphatase, and lactate dehydrogenase activities increased substantially from the time of initial collapse to 24 hours after HW injection. Of 39 dogs with shock, 29 recovered from initial collapse, but 5 of the 29 subsequently collapsed again (secondary collapse), with bloody diarrhea followed by death. Of these 39 dogs, 6 died during initial collapse without bloody diarrhea, and 4 were euthanatized during initial collapse. It was confirmed that HW extract had, in fact, induced shock. These clinical, hematologic, and biochemical findings were fundamentally similar to those associated with shock resulting from administration of drugs, such as diethylcarbamazine and milbemycin D, in microfilaremic dogs with HW infection.
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PMID:Clinical, hematologic, and biochemical findings in dogs after induction of shock by injection of heartworm extract. 787 76

We report the case of a 28-year old asthmatic female patient, who developed an acute heart failure beginning with diarrhea, fever, and dyspnea 5 weeks after delivery. After improvement of all vital functions and dismissal from hospital care unit a marked blood hypereosinophilia, left ventricular congestive heart failure, pericardium effusion and fever up to 40 degrees C followed. Endomycardial, bone marrow and skeletal muscle biopsies and the pericardial fluid showed a marked eosinophilic infiltration or polymyositis, respectively, which could be treated successfully with steroids and azathioprin. During steroid medication cytomegalovirus-associated myocarditis developed and was diagnosed by in situ hybridization. CMV hyperimmunoglobulin treatment (Cytotect, Biotest) was started (2 ml/kg bw on day 1 and 3, and 1 ml/kg on days 5, 7 and 9), which led to the eradication of the residual infiltrate and CMV-DNA in the myocardium. After discontinuation of all medication, eosinophilia and asthma recurred so that immunosuppressive treatment was continued.
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PMID:[Eosinophilic endomyocarditis post partum or pregnancy-related cardiomyopathy]. 792 30

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

A 77 year-old male mistakenly ingested an estimated 30 g of boric acid as a single oral dose to stop hiccups. On admission, he had vomiting, diarrhea, and hiccups. Laboratory data was diagnostic of acute renal failure. Hemodialysis and charcoal hemoperfusion were performed in series. The serum concentration of boric acid was reduced by the therapy, but the patient died due to cardiac insufficiency. Acute boric acid poisoning resulting from a single oral dose in adults has rarely been reported. Our case is the fourth fatal case in adults since the 1920s following a single, acute ingestion of boric acid.
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PMID:A fatal case of acute boric acid poisoning. 849 48

We report a rare case of non-menstrual toxic shock syndrome (TSS) in the course of Staphylococcus aureus sepsis in a 31-year-old primigravida who developed high fever and severe pulmonary and cardiovascular failure within a few hours at the end of the 29th week of a twin pregnancy. Mechanical ventilation was necessary due to signs of adult respiratory distress syndrome (ARDS) and catecholamines were needed to maintain a somewhat adequate blood pressure. A forceps delivery was performed immediately. Postoperatively, the patient was brought to the intensive care unit (ICU) due to the suspicion of severe septic shock. In addition to the extreme cardiovascular instability and massive disturbance of pulmonary gas exchange, the clinical picture was characterised by a disseminated intravascular coagulopathy (DIC) with marked petechial bleeding and ecchymoses on all extremities. Moreover, a confluent, spotty exanthem of the trunk and extremities could be seen. Despite all therapeutic efforts, the patient died within a few hours after admission to the ICU with signs of multiorgan failure. Post-mortem, multiple staphylococcal abscesses were found in the kidneys, liver, and uterus. Moreover, acute ulcerous endocarditis of the mitral valve and septic myocardial foci with myocarditis were seen. The Staph. aureus strain isolated from the blood cultures was shown to produce TSS toxin 1 (TSST-1) and enterotoxin B. In summary, the clinical picture can be interpreted as severe staphylococcal sepsis complicated by TSS. TSS is a specific type of infectious disease, occurring mainly in young women during the menstrual period (80%-90%), but it has also been reported in non-menstrual cases (10%-20%). It is characterised by sudden-onset high fever, hypotension, rash, mucosal hyperaemia, and various additional symptoms such as myalgia, vomiting, and diarrhoea. The clinical course depends on the extent of the organ failure due to decreased tissue perfusion during hypotension. Severe cases are accompanied by multiple organ-system failure including impaired renal function, which is reversible in nearly all cases. Respiratory failure ranges from interstitial and alveolar aedema to ARDS in 10% of cases; severe DIC is seen in 10%-15%. Another severe clinical complication is cardiac insufficiency. The etiology of TSS is based on a localized or, rarely, systemic infection with certain Staph. aureus strains that are capable of producing toxins, the most important one being TSST-1. Staph. aureus strains can also produce various other enterotoxins that may be involved in the pathogenesis of TSS. The pathogenetic importance of the toxins is supported by the antibody titers in TSS patients: more than 80% of healthy adults show high levels of antibody titers, whereas 90% of TSS patients exhibit low levels in the acute phase followed by a significant increase during convalescence. It is not clear whether the toxins cause TSS by a direct effect or by release of mediators due to their function as superantigens. The clinical characteristics of non-menstrual TSS are identical to those of menstrual TSS, but it can occur in many clinical settings in both sexes at any age. Severe clinical courses are more frequent in non-menstrual TSS: the mortality is about 8%-11% in non-menstrual TSS compared to 2%-5% in menstrual TSS. The diagnosis is based mainly on clinical signs and the isolation of toxin-producing Staph. aureus strains. Besides antibiotic therapy, treatment is primarily directed to the correction of hypotension and additional organ-system failure. Other therapeutic measures such as the elimination of toxins by plasma separation or the administration of antibodies or gamma-globulins are subjects of investigation with no general recommendations at this time.
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PMID:[Lethal, non-menstrual toxic shock syndrome associated with Staphylococcus aureus sepsis]. 859 62


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