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)

During the acute phase of myocardial infarction, the generation of thrombin is reflected in the sudden rise of fibrinopeptide A (FPA) and the thrombin-antithrombin III (TAT) complex in blood. We have systematically determined the FPA and TAT plasma concentrations over a period of 14 days after acute myocardial infarction in 100 patients. Mean levels of both thrombin markers were the highest on admission, remained elevated over the following few days, and then gradually declined after day 5. Still, by the end of the first week two thirds of the patients had distinctly elevated TAT and FPA levels, and by the end of the second week such an abnormality was present in half of them. Continuous intravenous heparin infusion at a dose of 20,000 units/day, administered for 1 week to patients who had either received (n = 21) or not received (n = 17) streptokinase, led to a significant depression (p less than 0.05) of thrombin markers over the first 48 hours, an effect that did not persist over the subsequent days of treatment. In patients not assigned to heparin treatment, those in heart failure had significantly (p less than 0.05) higher mean TAT and FPA values on days 3, 5, and 7 compared with patients in whom heart failure was absent. Infarct extension, pulmonary embolism, and death were also associated with a rise in one or both thrombin markers, often preceding the onset of clinical symptoms. Thrombinogenesis was not accompanied by changes in mean plasma concentrations of prothrombin, antithrombin III, or alpha 2-macroglobulin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Persistent generation of thrombin after acute myocardial infarction. 157 16

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

During the period 1950-1985, a total of 179 cases of clinically overt hereditary haemochromatosis (HH) were registered in Denmark, 140 males and 39 females. Median age at diagnosis was 55 years (range 29-81). Diagnostic approaches, symptoms and physical signs at discovery are described. All patients had grade 3-4 liver haemosiderin iron, and cirrhosis was present in 84%. Serum (S-) transaminase was elevated in 92%, S-alkaline phosphatase in 47% and S-bilirubin in 23%, while plasma prothrombin time was below normal in 34%. Females had higher alkaline phosphatase than males (p less than 0.05). Bone marrow haemosiderin iron (n = 81) showed no relation to iron status indicators and was unsuitable as a diagnostic tool. Skin biopsy (n = 56) was positive for haemosiderin iron in 67% and for melanin in 57%, but was of limited value in the assessment of HH. Arthropathy was registered in 44%; arthralgias and clinical joint abnormalities occurred more frequently in females than in males (p less than 0.05). Latent diabetes mellitus was found in 34% and overt diabetes in 55%, being more frequent in males than in females (p less than 0.05). Other endocrine abnormalities were seen in 66%. Cardiac failure was observed in 9% and abnormal ECG in 35%. Males had higher haemoglobin (p less than 0.0001) and S-iron (p less than 0.01) than females, while S-transferrin, transferrin saturation, S-ferritin and mobilizable iron stores showed no significant sex differences. Median transferrin saturation was 87% (range 52-100); values greater than 62% were observed in 96% of the patients. Median S-ferritin was 3,400 micrograms/l (800-12,700) and median iron stores 14.8 g (4.5-36.4).
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PMID:Hereditary haemochromatosis in Denmark 1950-1985. Clinical, biochemical and histological features in 179 patients and 13 preclinical cases. 191 39

A variant of hepatorenal syndrome occurring in patients with chronic congestive heart failure following an episode of cardiogenic pulmonary edema, and in the absence of hypotension, is described. This was observed in 13 patients during an eleven-year period. The clinical picture is characterized by hepatic injury and functional renal impairment. Increase of serum glutamic oxaloacetic transaminase levels as high as 2100 IU; prolongation of prothrombin time; elevation of serum bilirubin, creatinine, blood urea nitrogen, and potassium levels; decrease in urinary sodium excretion; and a normal urinary sediment are the salient laboratory abnormalities of this entity. Treated with conventional medication, the patients' course was fatal in 4 cases. When the splanchnic vasodilator dopamine was added to the patients' management, 5 of 9 patients recovered. Cardiogenic hepatorenal syndrome is a severe but potentially reversible complication of heart failure. The apparently beneficial effect of low-dose dopamine needs further evaluation.
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PMID:Cardiogenic hepatorenal syndrome. 224 92

The adequacy of hepatic circulation in terms of oxygen supply-demand relation was assessed by measuring hepatic venous oxygen saturation (Shvo2) in patients. Among those with congenital cardiac lesions (n = 11), Shvo2 during the early postoperative period was markedly low as less than 20% in Fontan operation group (n = 5) with subsequent clinical findings of acute hepatic dysfunction. Significant correlations were found between Shvo2 values early after surgery and subsequent peak values in serum hepatic enzymes. Serum total bilirubin and prothrombin time started to deteriorate when Shvo2 became below 30%. Cardiac index, hepatic perfusion pressure and mixed venous oxygen saturation showed positive linear correlations with Shvo2, and central venous pressure (CVP) with an inverse relation. In chronic valvular disease (n = 28), those with NYHA class IV patients showed lower Shvo2 (average; 47.4%) at cardiac catheterization than the others (class-I; 66.4%, class-II; 63.9%, p less than 0.05). These results indicate that Shvo2 monitoring appears to be useful to assess the hepatic perfusion in terms of oxygen supply-demand relation in acute and chronic heart failure, and Shvo2 of 30% seems to be a critical level.
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PMID:Analysis of acute and chronic heart failure in view of hepatic oxygen supply-demand relationship using hepatic venous oxygen saturation. 271 79

Twenty-seven patients underwent reoperation because of thrombotic obstruction of a disc-type cardiac valve prosthesis. Preoperative clinical features included effort dyspnea in 81%, new-onset angina in 44%, a new murmur in 89%, and an abnormal opening or closing sound associated with the prosthetic valve in 56%. Symptoms were present for 1 week or more before reoperation in 86%, although many patients were referred only after acute exacerbation of heart failure and development of pulmonary edema. Noninvasive studies confirmed prosthetic valve malfunction in only 33%, but cardiac catheterization documented thrombotic obstruction in all 15 patients in whom it was performed. In 14 of the 27 patients, prothrombin time was in the therapeutic range at the time of admission. Prompt reoperation for valve replacement or thrombectomy was performed with an operative mortality of 11%, and long-term outcome was satisfactory in all but 1 hospital survivor. These findings emphasize the importance of considering the diagnosis of thrombosed heart valves in patients with mechanical heart valves who are seen with nonspecific symptoms.
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PMID:Thrombotic obstruction of disc valves: clinical recognition and surgical management. 276 2

A flexible loading dose schedule for inducing anticoagulation with warfarin was assessed in 31 consecutive patients. 55% reached the therapeutic range (prothrombin ratio between 2 and 4:1) by Day 2 (40 hours after the first dose) and this figure rose to 77% on Day 3 and to 87% on Day 4. All patients had a PTR between 1.7 and 4.2 on Day 5. Patients with evidence of cardiac failure and abnormal liver function, and those taking medications known to interact with warfarin required lower doses and ran a higher PTR when compared with the total group of patients. This schedule offers a useful means of safely and rapidly inducing warfarin therapy in all patients.
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PMID:A flexible loading dose schedule for warfarin therapy. 332 67

Indications and the type of antithrombotic therapy for the prevention of thromboembolism in patients with valvular heart disease, mechanical prosthetic heart valves and bioprosthetic heart valves are discussed. The evidence for these clinical recommendations is described and graded into five levels. The indications for anticoagulation in patients with valvular heart disease are chronic or paroxysmal atrial fibrillation, sinus rhythm with a very large left atrium, severe left ventricular dysfunction or presence of heart failure or a history of previous thromboembolism. Anticoagulant therapy is administered to prolong the prothrombin time to 1.5 to 2.0 times control, using rabbit brain thromboplastin (standardized international normalized ratio = 3.0 to 4.5). Risk factors for thromboembolism in patients with prosthetic heart valves are discussed. Because intracardiac thrombus formation may start during and continues early after operation, restarting heparin therapy 6 hours after operation and continuing it for the duration of the hospitalization is advised. For mechanical prosthetic heart valves, oral anticoagulation as outlined plus dipyridamole is advised indefinitely. Platelet inhibitor therapy alone is insufficient. For bioprosthetic heart valves, heparin is followed by oral anticoagulation as outlined for 3 months after mitral or aortic valve replacement and indefinitely after mitral valve replacement if there is atrial fibrillation or a very large left atrium; aspirin may be recommended indefinitely after aortic valve replacement. Antithrombotic therapy is also considered for four special situations: noncardiac surgery, prosthetic valve endocarditis, anticoagulation after a thromboembolic event, and antithrombotic therapy during pregnancy.
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PMID:Antithrombotic therapy in patients with valvular heart disease and prosthetic heart valves. 353 70

Two adolescent patients referred for evaluation of severe "hepatitis" were found to have clinically unsuspected cardiac failure. Clinical profiles were characterized by anorexia, malaise, right upper quadrant pain, mild jaundice, initially predominantly indirect hyperbilirubinemia, profound elevations of transaminases, and prolonged prothrombin time. Left ventricular failure and low cardiac output were documented by clinical examination, echocardiography, and measurements of pulmonary capillary wedge pressure and cardiac index. Acute and chronic intrinsic liver disease was ruled out by appropriate tests. At autopsy, pathologic lesions of centrilobular necrosis characteristic of hepatic hypoxia were noted, and there was evidence of marked myocardial degeneration. These two cases emphasize the need for careful cardiac examination when evaluating acute hepatitis.
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PMID:Severe cardiomyopathy simulating hepatitis in adolescence. 369 46

The influence of oral amiodarone on the anticoagulant effect of the coumarin derivative acenocoumarol has been investigated prospectively in 10 patients with normal renal, hepatic and haematological function and who were not in cardiac failure. The daily dose of acenocoumarol was sufficient to produce a prothrombin activity of 25 to 35%. When the prothrombin time had become stable amiodarone 600 mg/d was administered for 1 week followed by 400 mg/d for the next 3 weeks. A decrease in prothrombin activity from 30.5 to 20.2% was observed, associated with a decrease in vitamin K coagulation factors, after a mean of 4 days following commencement of amiodarone. In 6 patients a prothrombin activity less than 20% required a 60% reduction in the dose of acenocoumarol after 1 week of amiodarone 600 mg, and a 33% reduction after 3 weeks of amiodarone 400 mg. There was no correlation between the plasma amiodarone and the decrease in prothrombin activity. Inhibition of acenocoumarol metabolism by amiodarone is the most likely explanation of these findings.
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PMID:Prospective study of the potentiation of acenocoumarol by amiodarone. 406 85


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