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

Patients with end-stage liver disease usually show a hyperdynamic circulatory state. It has previously been reported that patients who develop myocardial depression in the early post-liver transplantation period are more prone to organ failure and death. We reviewed the records of 754 adult patients undergoing liver transplantation at our institution and identified 7 patients who initially showed hyperdynamic circulation, but then developed reversible dilated cardiomyopathy in the early posttransplantation period. All identifiable causes of cardiac dysfunction, such as myocardial ischemia, thyroid dysfunction, and electrolyte imbalances, were excluded. Left ventricular ejection fraction decreased from a preoperative median baseline of 60% to 20% (P = .02), with four-chamber dilatation on echocardiogram. All these patients required supportive care, including mechanical ventilation, afterload reduction, inotropic support, and monitoring in the intensive care unit. Cardiac function subsequently improved in all patients, with ejection fraction increasing to a median of 50%. All patients were discharged from the hospital. At a median follow-up of 15 months, there was no recurrence of heart failure. The increased peripheral resistance seen after successful liver transplantation may be an important causative factor.
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PMID:Post-liver transplantation myocardial dysfunction. 972 77

Mefloquine is an effective drug for prophylaxis and treatment of malaria caused by Plasmodium falciparum. It is generally well tolerated with few side effects. Minimal elevation of liver function tests has been reported after exposure to mefloquine, especially in susceptible individuals with prior abnormal liver function tests. Our patient, who had had elevated liver function tests attributed to heart failure, experienced an acute elevation of liver transaminases 6 weeks after exposure to mefloquine 250 mg/week. Cessation of the drug caused test results to return to normal. Mefloquine should be prescribed cautiously in patients with liver disease.
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PMID:Mefloquine-induced acute hepatitis. 1113 Feb 24

Acute liver failure is a rare but potentially fatal disease. Adult definition of fulminant hepatic failure, which includes the development of hepatic necrosis and encephalopathy within 8 weeks of onset of liver disease does not apply to acute liver failure in children particularly if secondary to autoimmune or metabolic liver disease. The etiology of acute liver failure varies with the age of the child. In neonates, infection or an inborn error of metabolism are common, while viral hepatitis and drug induced liver failure are more likely in older children. The clinical presentation of acute liver failure includes jaundice, coagulopathy and encephalopathy. In neonates, encephalopathy may be subclinical. The management of acute liver failure includes assessment of prognosis for liver transplantation; prevention and treatment of complications while awaiting hepatic regeneration or a donor liver and hepatic support. The major complications of acute liver failure are sepsis, gastro-intestinal bleeding, cerebral edema, renal and cardiac failure. Selection for liver transplantation depends on the etiology of the disease, prognostic factors, the presence or absence of multisystem disease and/or reversible brain damage. Prognostic factors for survival are less well established in children than in adults but children with metabolic liver disease, prothrombin time > 50 seconds, rising bilirubin and falling transaminase, grade II or higher grade of hepatic coma indicate poor prognosis. Most children receive a reduced or split liver graft. Living related donations for acute liver failure are also carried out by some centres. Survival post liver transplantation for acute liver failure has improved and most recipients can expect a 70% five year survival.
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PMID:Acute liver failure. 1113 56

Congestive liver disease can be one of the clinical aspects of chronic heart failure. Fulminant hepatic failure can be a consequence of ischemic liver disease secondary to cardiogenic shock. We report a patient with chronic heart failure who was admitted to our hospital presenting general malaise with abnormal liver function tests, prothrombin time and renal failure. The study of viral and autoimmune liver diseases were negative. She did not consume hepatotoxic drugs. She presented encephalopathy without initial evidence of shock. On the fourth day, she presented clinical deterioration compatible with cardiogenic shock. Laboratory abnormalities were similar to those seen in congestive and ischemic liver disease. The patient died 24 hours later. The histology showed congestive and ischemic liver disease. There are several reports of chronic liver diseases without a clear etiology, caused by constrictive pericarditis or restrictive myocardiopathy. In this case, the patient presented fulminant hepatic failure without clear evidence of progressive heart failure. We emphasize the importance of cardiac diseases as possible causes of liver diseases without another clear explanation.
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PMID:[Fulminant hepatic failure. Atypical form of cardiac failure presentation]. 1118 58

Commonly prescribed antiarrhythmic agents--and several recently developed agents--are reviewed with respect to their use in patients with renal failure, hepatic failure, and congestive heart failure. Because removal of electrophysiologically active agents from the systemic circulation in most cases depends on either renal elimination, hepatic metabolism, or both, patients with preexisting kidney or liver disease may be at increased risk of treatment-related drug toxicity, including proarrhythmia. These susceptibilities should be anticipated, with drug selection and/or dosage modified accordingly. Patients with left ventricular dysfunction and heart failure also are at increased risk of treatment-related complications, including proarrhythmia and hemodynamic intolerance. In addition, the metabolism of antiarrhythmic drugs may be impaired in these patients. Preference should be given to drugs with a proven safety profile, such as amiodarone, in patients with heart failure.
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PMID:Antiarrhythmic drug therapy in patients with renal failure, liver failure, and congestive heart failure. 1172 Jun 10

Beriplex, a prothrombin complex concentrate (PCC), was administered to 42 patients requiring immediate reversal of their oral anticoagulant therapy. The dose administered was determined using the pretreatment International Normalized Ratio (INR). Blood samples were obtained before treatment and at 20, 60 and 120 min after treatment. The following investigations were performed on all samples - INR, clotting factors II, VII, IX and X, coagulation inhibitors protein C (PC) and antithrombin (AT), and other markers of disseminated intravascular coagulation, plasma fibrinogen, D-dimer and platelet count. Immediate reversal of the INR, the vitamin K-dependent clotting factors and PC was achieved in virtually all patients. Reduced AT levels were present in 18 patients before treatment. Further slight AT reductions occurred in four patients, but other associated abnormalities of haemostasis were observed in only one of the four patients. One patient with severe peripheral vascular disease, sepsis and renal and cardiac failure died of a thrombotic stroke following leg amputation, 48 h after receiving Beriplex. No other arterial and no venous thromboembolic events occurred within 7 d of treatment. Beriplex is effective in rapidly reversing the anticoagulant effects of warfarin, including PC deficiency, without inducing coagulation activation. Caution should continue to be exercised in the use of these products in patients with disseminated intravascular coagulation, sepsis or liver disease.
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PMID:Rapid reversal of oral anticoagulation with warfarin by a prothrombin complex concentrate (Beriplex): efficacy and safety in 42 patients. 1184 21

An increased concentration of fibrin(ogen) degradation products (FDPs) commonly is used in conjunction with other hemostatic test abnormalities to identify patients with disseminated intravascular coagulation (DIC). Positive FDP results, however, have been observed in dogs without clinical evidence of DIC. The purpose of this study was to evaluate FDP concentrations in a group of clinically ill dogs with a variety of disorders. Dogs included in the study had the following hemostatic parameters evaluated: prothrombin time, activated partial thromboplastin time, fibrinogen concentration, platelet count, and FDP concentration. Two rapid latex agglutination methods were compared for detecting FDP in serum samples (Thrombo-Wellcotest, International Murex Technologies Corp) and plasma samples (FDP Plasma, American Bioproducts Inc). Results of the serum FDP method were positive in 8% (4/50) of the dogs tested: 3 with DIC and 1 with immune-mediated hemolytic anemia and liver disease. Results of the plasma FDP test were positive in 60% (30/50) of the animals tested: 6 with DIC, 3 with confirmed thrombosis, and 21 with a variety of conditions, including neoplasia, immune-mediated hemolytic anemia, pancreatitis, gastric dilatation-volvulus, heat stroke, severe trauma, sepsis, protein-losing nephropathy, liver disease, hyperadrenocorticism, and chronic heart failure. Because the plasma FDP test was positive more frequently than the serum FDP test in ill dogs, it may be more sensitive for the detection of canine FDP.
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PMID:Serum and plasma latex agglutination tests for detection of fibrin(ogen) degradation products in clinically ill dogs. 1202 12

The cachexia syndrome is characterised by progressive weight loss and depletion of lean body mass and has long been recognised as a poor prognostic sign. Whilst the clinical features of the wasting process are readily apparent, its pathogenesis is complex and poorly understood. There is increasing evidence that the immune system, in particular inflammatory cytokines, may play an important role in the development of cachexia. The cytokine considered to be the most relevant to this process is tumor necrosis factor alpha (TNF), although other mediators such as interleukin (IL) 1, IL-6 and interferon gamma have also been implicated. Apoptosis represents a potential pathway by which wasting can occur in chronic diseases. Cytokines and their corresponding receptors are known to be important regulators of cell death. Apoptosis has been demonstrated in the skeletal muscle of patients with chronic heart failure (CHF) and is thought to be partly responsible for the significant impairment of functional work capacity associated with this condition. An understanding of the mechanisms that regulate muscle protein breakdown is essential for the development of strategies for treating or even preventing muscle cachexia in patients. It is the aim of this article to review the role of inflammatory cytokines, particularly TNF, in the pathogenesis of wasting and also the potential for anti-cytokine therapy. Although this review will concentrate predominantly on the syndrome of CHF, other chronic illnesses such as liver disease, cancer, and sepsis will also be discussed.
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PMID:Cytokines, apoptosis and cachexia: the potential for TNF antagonism. 1216 21

We performed liver resection for focal liver disease in 266 patients between January 1, 1992 and December 31, 2001 at the University of Debrecen Medical and Health Science Center, Medical School of Medicine, 2nd Department of Surgery in Debrecen, Hungary. The indication was primary liver cancer in 35 cases, liver metastasis in 97 cases. The primary tumour and its liver metastases were removed synchronously in 28 patients (29.9%). Comparing the results of different operating methods we found the need of transfusion significantly less in "anterior" liver resections. Regarding operating time, complications and survival time there were no significant differences between the different operations. One patient died in the perioperative period because of cardiac failure and one because of DIC (1.5%). There were 4 complications which needed reoperation in the early postoperative period. Eighty of the patients were treated with systemic adjuvant chemotherapy (Mayo protocol), with added chemoembolisation in another 26 patients. This has not increased life expectancy significantly. Thirty-two patients are still alive, their average survival time is 21.2 (5 to 59) months. The average survival time of the 78 patients' who died is 16.5 (3 to 58) months. Twenty-two patients were lost out of our follow-up.
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PMID:[Surgical treatment for primary and secondary tumors of the liver]. 1223 80

Taurine is not only present in foods, tonics and nutrient drinks but is also used as a medicinal agent mainly for treatment of chronic heart failure and liver disease. However, little is known about its influence on drug-metabolizing enzymes, especially cytochrome P450 (CYP), in human. We examined whether taurine could affect the expression of CYP3A4 mRNA in the presence or absence of rifampicin (RFP), which is a potent inducer of CYPs, with HepG2 cells. Taurine enhanced twice the induction of CYP3A4 mRNA by RFP, but did not affect the expression by itself. This effect was both concentration- and time-dependent. On the other hand, taurine did not affect the induction by phenobarbital. Taurine did not increase intracellular uptake of RFP. Therefore, we conclude that taurine is an enhancer for the induction of CYP3A4 by RFP.
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PMID:Taurine modulates induction of cytochrome P450 3A4 mRNA by rifampicin in the HepG2 cell line. 1243 88


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