Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

I describe a simple, single-tube batch fractionation procedure for separating MM and MB isoenzymes of creatine kinase on a macroporous strong anion exchanger (AG MP-1, Bio-Rad Laboratories). The isoenzymes can be separated in less than 3 min, with a resulting dilution of the serum with no more than an equal volume of buffer. Without sample concentration or spectrofluorometric measurement, the procedure detects 4 U of MB isoenzyme per liter. Sensitivity is limited by the sensitivity and precision of the method of measurement. The CV for the fractionation can be held to less than 4.0% at 65 U of MB per liter. Current fractionation methods are compared to the proposed procedure. With use of a discrete analyzer (Du Pont aca) the mean MB activity in a population free of heart disease was 3.2 +/- 3.0 U/liter (range, 0 to 8 U/liter). The kinetics and stability of isolated isoenzymes are reported, indicating that advisability of storing or pre-incubating samples with mercaptoethanol.
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PMID:Improved separation of creatine kinase cardiac isoenzyme in serum by batch fractionation. 0 Nov 60

Lactate dehydrogenase (LD) isoenzymes 1 and 2 in human serum were separated on a column of diethylaminoethyl-Sephadex. Samples layered on mini-columns were eluted with buffered sodium chloride (100, 150, and 200 mmol/liter). Lactate dehydrogenase activity in column effluents was measured by the Wacker method, and their isoenzyme content was evaluated by electrophoresis on polyacrylamide gel. Results for column-fractionated LD-1 and LD-2 were expressed in two ways: LD-1/LD-2 ratios and total LD-1 + LD-2 activities. The former is a more specific indicator of myocardial infarction than the latter. Sera from 10 patients with acute myocardial infarction (increased creatine kinease isoenzyme MB activity) exhibited ratios in the range of 0.92 to 1.56, ratios for 10 patients without heart disease (normal creatine kinase MB) ranged from 0.33 to 0.69.
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PMID:Improved column method for separating lactate dehydrogenase isoenzymes 1 and 2. 63 Jul 10

The diagnostic value of creatine kinase (CK) and lactate dehydrogenase isoenzymes was investigated in a prospective study of 201 patients with suspected acute myocardial infarction (AMI). The isoenzymes were analyzed with a column chromatographic method. The patients' final diagnoses were made according to the WHO criteria without knowledge of the isoenzyme results. The prevalence of AMI was 50%. The diagnoses were predicted with significantly greater reliability with the isoenzyme than with the total enzyme determinations in most of the patients. However, the greater diagnostic reliability had sufficient therapeutic consequence to justify the extra analytical cost only in patients for whom the diagnosis must be based mainly on the enzyme results. The CK isoenzyme specificity for myocardial damage was studied in populations with low prevalence of heart disease. In a group of 39 patients who had elevated total CK due to noncardiac disease there were five with elevated isoenzyme values, but since among 69 young healthy persons none had elevated isoenzymes, this was taken to indicate that the isoenzymes may be leaked into the blood from other organs than the heart.
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PMID:Diagnostic value for acute myocardial infarction of creatine kinase and lactate dehydrogenase isoenzymes compared with total enzymes. Creatine kinase isoenzyme specificity for myocardial damage. 63 12

Serum activity of creatine kinase and creatine kinase-MB have been investigated in 129 patients of various etiology in overt heart failure. Elevations in CK-MB were found in 19 patients, most frequently in patients with inflammatory heart disease. We found no correlation between CK-MB activity in serum and the severity of heart failure. CK-MB elevation in patients with chronic heart failure may be interpreted as a sign of progressive as well as regressive processes in the myocardium.
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PMID:[Determination of creatine kinase and CK-MB in heart failure (author's transl)]. 72 68

A young man without heart disease with a metastatic carcinoma of the pancreas received a 5-Fluorouracil therapy (25 mg per kilogram body weight/24 h by continuous infusion over a period of 5 days). Approximately 56 h after beginning of the first cycle of therapy (after 36 h of the second cycle) he complained of severe chest pain, which did not respond to nitrates, improved after application of opioids, and subsided definitely after termination of the 5-FU infusion. During the periods of pain, the ECG and the creatine kinase were normal. At a later time, finally, a scar in the posterior wall of the myocardium was detectable in the ECG. When repeating the 5-FU infusion, similar problems arose with less intensity. The patient died as a consequence of the progress of the tumor disease. At autopsy, two myocardial infarctions were detectable. There was no demonstrable stenosis of the coronary arteries. Spasms of the coronary arteries are discussed as a cause of this side effect of 5-FU-therapy.
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PMID:[Myocardial infarcts within the scope of 5-fluorouracil therapy]. 209 85

This study tested the hypothesis that membrane transport is the major biochemical system of the myocardium altered in furazolidone-induced cardiomyopathy (round heart disease), before the development of myocardial failure, and that metabolic enzymes and contractile proteins are less affected. Compared with controls, maximal percentage depression of activities of myocardium from furazolidone-treated birds were 40 for creatine kinase, 30 for glycolysis, 30 for glycogen, 20 for myofibrils, 20 for Krebs's cycle enzymes, 15 for fatty acid oxidation and 10 for total soluble protein. Sodium and potassium transport, antioxidant system activity, myosin, myosin isoenzyme patterns and amino acid aminotransferases were unaffected. In marked contrast, the calcium-transport ATPase activity of the sarcoplasmic reticulum had undergone a 60 per cent compensatory increase in activity. The pattern of biochemical changes observed is consistent with a role of ischaemia in the pathogenesis of round heart disease and indicates that calcium transport by the sarcoplasmic reticulum is the major biochemical system affected.
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PMID:Myocardial biochemical changes in furazolidone-induced cardiomyopathy of turkeys. 232 37

The concentration of brain type creatine kinase (CK-BB) was measured in blood from the internal jugular vein in 32 children (less than 1 year old) with congenital heart disease. In transposition of the great arteries the CK-BB levels were significantly higher than in children without cyanosis (10.1 +/- 4.1 vs. 3.0 +/- 0.5 ng/ml). A negative correlation was found for CK-BB concentration and arterial oxygen saturation (r = -0.41, p less than 0.02 for all children and r = -0.62, p less than 0.05 for those with tetralogy of Fallot). It is suggested that the increased CK-BB levels in the blood of cyanotic children reflect chronic cerebral hypoxia, which may explain other reports of reduced psycho-intellectual function in patients with cyanotic heart disease.
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PMID:Brain type creatine kinase in relation to oxygen desaturation in the blood of children with congenital heart disease. 235 87

To investigate biochemical characteristics of hypertrophic myocardium of young and adult humans, we analysed myocardial biopsies obtained from 28 mainly young patients undergoing cardiac surgery for congenital heart disease and 41 autopsied hearts from 18 adult normal and 23 hypertrophic human subjects. Myocardial activities of the enzymes creatine kinase and lactate dehydrogenase were independent of age during childhood, but decreased significantly with hypertrophy at adult age. Myocyte nuclei showed increased polyploidization during childhood which was progressive with age, and in the adult stage polyploidization was correlated with heart weight. Nevertheless myocardial DNA concentration fell under both conditions, which is to be ascribed to the 'diluting' effect of myocyte hypertrophy. Before an age of 8 years DNA concentration in the child heart material studied has reached the value found in adult nonhypertrophic hearts, although at that time polyploidization of myocyte nuclei in child hearts was only half the value found in adult non-hypertrophic hearts. Biochemical measurement of DNA concentration in peroperatively taken myocardial biopsies may contribute to the in vivo diagnosis of ventricular hypertrophy in quantitative terms, in combination with radiology, echocardiography and histology.
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PMID:Myocardial (iso)enzyme activities, DNA concentration and nuclear polyploidy in hearts of patients operated upon for congenital heart disease, and in normal and hypertrophic adult human hearts at autopsy. 252 96

The biochemical diagnosis of myocardial infarction is mainly based on assays of serum enzymes. The most commonly used markers are creatine kinase, lactic dehydrogenase and aspartate amino-transferase. They are useful to diagnose the infarction, determine its time of onset and evaluate its importance. Changes in concentration of these enzymes are measured during their release from cells, their diffusion and their elimination in order to establish their characteristic profile in the acute phase of the disease. The diagnostic value and contribution to the prognosis of these tests are detailed. Heart diseases other than myocardial infarction, and other diseases in which serum levels are raised are described. The other laboratory abnormalities associated with myocardial infarction are listed.
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PMID:[Biological diagnosis of myocardial infarction]. 296 89

We compare a "second-generation" immunoenzymometric assay (Tandem-E CKMB II) for creatine kinase (EC 2.7.3.2) MB with its electrophoretic (Beckman Paragon system) determination. In the former, two monoclonal antibodies are directed against the B and M subunits. We evaluated 502 samples from 253 patients. Precision, linearity, and analytical recovery for both assays were excellent. The two methods correlated well (r = 0.936). The reference interval for individuals with no suspected cardiac disorder was 0-6.0 micrograms/L; that for non-infarct patients was 0-18.0 micrograms/L. Peak CK-MB values determined by the two assays agreed for 95% of the patients, in terms of exceeding the normal reference interval or not. Diagnostic efficiencies were 86% (Tandem) and 88% (electrophoresis). The immunoenzymometric assay showed no cross reaction with other CK isoenzymes. Both assay methods performed well in detecting CK-MB, although there were some false positives by both methods, as judged from electrocardiographic results. When total CK for the Tandem assay exceeds 2000 U/L, we recommend calculation of a ratio (CK-MB, micrograms/L:total CK, U/L).
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PMID:Immunoenzymometric assay of creatine kinase with monoclonal antibodies to the MB isoenzyme compared with electrophoresis. 265 4


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