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

Lignocaine is widely used as a local anaesthetic and antiarrhythmic drug. It is commonly administered to patients with acute myocardial infarction as prophylaxis for ventricular fibrillation, although its efficacy in preventing primary ventricular fibrillation is still debated. Toxicity, sometimes with serious clinical consequence, is not uncommom and is usually related to overdosage. Blood lignocaine concentrations correlate roughly with antiarrhythmic and toxic effects and might be useful as an end point for monitoring prophylactic therapy. Administration of lignocaine as a local anaesthetic may result in blood lignocaine concentration in the antiarrhythmic or even toxic ranges. Expected peak levels for various routes of local anaesthesia are tabulated so that 'safe' total doses can be calculated. Intramuscular injection of high doses results in sustained therapeutic levels but is often associated with early minor toxicity. Lignocaine is eliminated primarily by hepatic metabolism, which appears to be limited by liver perfusion. Active metabolites may contribute to therapeutic and/or toxic effects. Disease states such as cardiac failure or drugs that alter hepatic blood flow may significantly affect lignocaine clearance. Pharmacokinetic studies in man show wide variability in drug disposition between patients, even when cardiac and hepatic status is considered, making specific dosing recommendations a problem. With intravenous injection, multicompartment kinetics is observed, with an initial rapid decline phase and initial decline in antiarrhythmic activity due to redistribution. With constant infusion, steady state concentrations of lignocaine are seen after 3 to 4 hours in normal subjects and after 8 to 10 hours in patients with myocardial infarction without circulatory insufficiency. In patients with cardiac failure, blood lignocaine concentration may continue to rise for 24 to 48 hours. In the presence of cardiac failure, decreased volumes of distribution and clearance require reduction in loading and maintenance doses. Lignocaine clearance is reduced in patients with liver disease and appears to be a sensitive index of liver dysfunction. A dosing algorithm for treatment of patients with myocardial infarction is presented.
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PMID:Clinical pharmacokinetics of lignocaine. 35 Apr 70

Overt liver disease caused by left-sided heart failure is seldom recognized unless there is obvious hypotension. We now report 4 patients whose initial diagnosis was hepatitis but who were later shown to have central hepatic necrosis associated with left ventricular failure. Signs of right-sided heart failure were absent. Hepatitis was initially suspected in 3 patients because of striking transaminase elevations and in 1 patient because of jaundice and symptoms compatible with hepatitis. Liver biopsies performed on all patients revealed central hepatic necrosis without evidence of acute or chronic hepatitis. Left ventricular failure was documented in all 4 patients. One patient had coronary artery disease, and the other three patients had valvular heart disease. Liver function tests became normal or improved in all cases as the underlying heart disease was treated. We believe that liver dysfunction secondary to left ventricular failure is not uncommon and can be seen in the absence of right-sided heart failure or hypotension.
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PMID:Left-sided heart failure presenting as hepatitis. 63 89

Serum m-AST (mitochondrial isoenzyme of AST) activity in patients with acute myocardial infarction was determined quantitatively by a new immunological technique which is sensitive and easily available. All 31 patients with acute myocardial infarction showed abnormally high levels of serum m-AST (more than 5 KU/ml); the mean serum m-AST activity attained its peak (42.0 +/- 4.9 KU/ml) on the first day after the onset of infarction 5 hours later than that of serum t-AST (total AST) activity in 15 patients whose peak m- and t-AST activities were identified clearly. The individual peak m-AST activity correlated with the total CK released (r = 0.83, n = 15), indicating that the release of m-AST also reflects the infarct size. The ratio of serum m-AST/t-AST increased following myocardial infarction and showed the maximal value (average 25.7%) on the third to seventh day after onset. This ratio in the patients with acute myocardial ifarction was also greater than that in patients with liver disease or with heart failure from causes other than acute myocardial infarction. In the patients who had the additional complication of heart failure and/or cardiogenic shock the ratio was also greater than that is the patients without these hazards. These results indicate that the ratio of serum m-AST/t-AST reflects the severity of the myocardial cellular damage in acute myocardial infarction.
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PMID:Immunological determination of serum m-AST activity in patients with acute myocardial infarction. 71 64

Sixteen cases of chronic Q fever are described. In eight there was a history of exposure to infection from farms or farm products. All had valvular heart disease, involving the mitral valve in nine and the aortic valve in seven. Infection occurred on a prosthetic valve in two patients. Arterial embolism was common. Venous thrombosis occured in three patients, and pulmonary embolism occurred in three other patients. Complement fixing antibodies to phase 1 antigen were found in a titre of 1:200 or greater in all except two patients. In one of these post-mortem examination revealed rickettsial bodies in mitral valve vegetations, and in the other Coxiella burneti was isolated from heart valve tissue. The majority presented with infective endocarditis but two presented primarily with liver disease. All patients had evidence of liver involvement and in one this led to death from cirrhosis. Abnormal tests of liver function, particularly hyperglobulinaemia, raised alkaline phsophatase and abnormal bromsulphthalein retention were found in all patients. Hepatic histology was abnormal in all eight patients in whom it was studied. The commonest features were mononuclear cell infiltration of the portal tracts and prominence of the sinusoidal Kupffer cells. Patchy focal necrosis of parenchymal cells, granulomata, fatty change, and eosinophilia of the sinusoidal walls were also noted in several patients and cirrhosis developed in one. Six patients had a purpuric rash, and in 12 there was thrombocytopenia. It is suggested that the presence of hepatomegaly and liver involvement and thrombocytopenia may help to differentiate Q fever endocarditis from bacterial endocarditis. Raised serum IgM and IgA levels occured frequently, but with only a moderate dominance of IgM. Sheep cell agglutination and latex fixation tests for rheumatoid factor were occasionally positive. Several features of the disease suggest the possibility that immune-complex mechanisms may play a role in chronic Q fever. Treatment was with prolonged courses of tetracycline usually combined with lincomycin. Seven patients underwent valve replacement surgery for haemodynamic reasons. Five patients died; two from heart failure, one from cirrhosis, one seven days after valve replacement and one from intraperitoneal haemorrhage following percutaneous liver biopsy. Three patients have survived for more than five years, and another six for more than three and a half years after diagnosis. Of these nine patients, three received medical therapy alone and six required valve replacement as well. Antibiotics have been discontinued in four patients who have had valve surgery and three others. Six patients had received antibiotics for continuous periods varying from 29-62 months. In the period after stopping therapy varying from 15-21 months, no relapse has occured. A seventh patient, who had received antibiotics for four months prior to valve replacement, has survived 43 months after the withdrawal of antibiotics...
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PMID:Chronic Q fever. 94 Sep 18

An elderly female with an acute episode of congestive heart failure, unaccompanied by any periods of hypotension, developed fulminant hepatic failure with an accompanying coagulopathy. Attempts to establish an etiology for her acute hepatic insufficiency, other than cardiac failure, proved negative. Fulminant hepatic failure as a consequence of congestive heart failure, without prolonged periods of hypotension preceding alteration in hepatic function, has not heretofore been described. Liver function is adversely effected in congestive heart failure. Hepatic ammonia clearance is impaired in cardiac failure and may be diminished to the point of resulting in hepatic encephalopathy. Coagulopathy is a frequent concomitant of fulminant hepatic failure. Establishing a clear etiology for a coagulopathy in the face of concomitant liver disease is difficult, thus making any therapeutic intervention fraught with peril.
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PMID:Fulminant hepatic failure secondary to congestive heart failure. 101 98

Despite apparently conflicting reports in the past, the bulk of evidence presently available points to a significant role for the liver in the regulation of renal function. Hepatic regulation of renal function may involve both a hepatorenal reflex and a liver-borne diuretic factor (LBDF and/or 'glomerulopressin'). The hepatorenal reflex is elicited by an increase in intrahepatic pressure, and/or certain amino acids in portal venous blood. It is transmitted by serotonin in the liver and presumably by noradrenaline in the kidney. It leads to a marked decrease in renal blood flow, glomerular filtration and urinary flow rate. The evidence for the LBDF is still circumstantial. The LBDF may be stimulated by glucagon and adenosine. It leads to a marked increase of renal blood flow, glomerular filtration rate and urinary output. Amongst the conditions presumed to be associated with altered hepatic regulation of renal function are postprandial hyperfiltration, and the deterioration of renal function which occurs in liver disease, cardiac insufficiency and cardiovascular shock.
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PMID:Hepatic regulation of renal function. 141 49

Thirteen out of 268 children (less than 18 years old) underwent hepatic transplantation (OLT) for end-stage liver disease (ESLD) associated with arteriohepatic dysplasia (AHD). Seven children are alive and well with normal liver function. Six children died, four within 11 days of the operation and the other two at 4 and 10 months after the OLT. Vascular complications with associated septicemia were responsible for the deaths of three children. Two died of heart failure and circulatory collapse, secondary to pulmonary hypertension and congenital heart disease. The remaining patient died of overwhelming sepsis not associated with technical complications. Seven patients had a portoenterostomy or portocholecystostomy early in life; five of these died after the OLT. Severe cardiovascular abnormalities in some of our patients suggest that complete hemodynamic monitoring with invasive studies should be performed in all patients with AHD, especially in cases of documented hypertrophy of the right ventricle. The improved quality of life in our surviving patients confirms the validity of OLT as a treatment of choice in cases of ESLD due to AHD.
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PMID:Liver transplantation for arteriohepatic dysplasia (Alagille's syndrome). 162 41

It is common for general practitioners (GPs) to refer patients suspected of impaired liver function for laboratory tests (alkaline phosphatase, lactate dehydrogenase, bilirubin, prothrombin, aspartate aminotransferase). In a prospective multipractice study over a six-month period, including 30 GPs, 55 patients were recorded as having, for the first time, a high level of alkaline phosphatase (AP) as an isolated finding, 14 with an increase of aspartate aminotransferase (ASAT), eight with an increase of both AP and ASAT, three with an increase of ASAT, AP, and bilirubin, two with an isolated increase of lactate dehydrogenase (LDH), one with an increase of ASAT, AP, and bilirubin, combined with a low prothrombin (PP), and, finally, one patient with a low prothrombin in isolation. In most cases the tests were requested because of unspecific symptoms. The most common causes of abnormal test results were neoplasms, alcoholic liver disease, and heart failure. Thirty patients were referred to hospital for further investigations. During the same study period, 50 patients with known abnormal liver function tests were recorded, and the most common causes of these abnormalities were neoplasms, rheumatoid arthritis, and alcoholic liver disease.
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PMID:Epidemiology of abnormal liver function tests in general practice in a defined population in Denmark. 180 31

Multiple linear regression techniques were utilized to determine models for the renal clearance and urinary excretion rate of furosemide. Models for the renal clearance were formulated based on data collected from the literature. The best model predicted that the weight-normalized renal clearance was a function of the weight-normalized creatinine clearance, with coefficient values dependent on the presence or absence of heart, liver, and/or kidney failure. The predictive performance of this model was evaluated using a separate verification data set, and, prospectively, for a group of cardiac patients. The urinary excretion rate of furosemide is the primary determinate of response. Models for the furosemide excretion rate were formulated from data collected prospectively from a group of patients with cardiac disease. The best model predicted that the dose-normalized morning urinary excretion rate was a function of the blood urea nitrogen concentration (BUN), with modifications for the presence of liver failure and/or decompensated heart failure. The oral dosage required to produce a clinically optimal furosemide excretion rate in cardiac patients without liver disease was dose (mg) = 42.1/(0.925-0.0151 BUN).
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PMID:Multiple linear regression modeling of furosemide renal clearance and urinary excretion rate. 181 62

Enoximone, a new phosphodiesterase-inhibitor with positive inotropic and vasodilating activities is available for intravenous use in patients with severe heart failure. A review of the current knowledge regarding the adverse effects of this substance reveals that they are characterized by cardiovascular, central nervous, and gastrointestinal side effects. Adverse effects occurred in 20% of patients and were mostly due to the pharmacological properties of enoximone. Cardiovascular side effects (10%) were the most frequent; ventricular and supraventricular arrhythmias were most common. Two to three percent of the patients experienced hypotension due to the vasodilator activity of enoximone. Headache, insomnia, and anxiety were the most frequent adverse effects on the central nervous system. Three percent of the patients treated experienced vomiting, nausea, abdominal pain, and diarrhea. An increase of liver enzymes and serum glucose could be observed, mostly in patients with previous liver disease or diabetes. Pharmacokinetic drug interactions are not known; possible pharmacodynamic interactions result from the pharmacological properties of the drugs. Intravenous therapy with enoximone causes a few serious side effects that can only be controlled by careful observation of the patients treated.
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PMID:[Tolerance of enoximone in patients with heart failure]. 183 4


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