Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.1.1.27 (lactate dehydrogenase)
 29,211 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Criteria for the retrospective diagnosis of acute myocardial infarction rely heavily on increases in lactate dehydrogenase (LD) isoenzymes. However, increases of LD isoenzyme activities are not specific for myocardial injury. Recently, increased concentrations of cardiac troponin I (cTnI) have been shown to be highly specific for myocardial damage and to have sensitivity comparable with that of creatine kinase MB isoenzyme for detecting cardiac injury. Furthermore, increases of cTnI persist in plasma for at least several days. The present study was designed to determine the relative sensitivities of cTnI and LD isoenzymes over time for the diagnosis of infarction. The results indicate that cTnI values are at least as sensitive as LD isoenzymes: 90% of patients with myocardial infarction had above-normal concentrations of cTnI on the 4th day after admission to the coronary care unit. Criteria based on cTnI should improve the accuracy of retrospective diagnoses of acute myocardial infarction.
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PMID:Comparative sensitivity of cardiac troponin I and lactate dehydrogenase isoenzymes for diagnosing acute myocardial infarction. 890 75

Cardiac troponin I (cTnI) is a highly specific marker that is elevated in the blood for several days following myocardial infarction. The lactate dehydrogenase (LD) isoenzyme 1 to isoenzyme 2 ratio (LD1/LD2) is the established marker for the late diagnosis of myocardial infarction. In this study, the sensitivity of cardiac troponin I (cTnI) and LD1/LD2 were compared as late markers of myocardial injury over a 5-day period in 36 patients admitted with a diagnosis of myocardial infarction to the coronary care unit. Over this period, the sensitivity of cTnI was significantly greater than that of LD1/LD2 (P < .05). The concurrent elevation of both cardiac markers of the five day period range from 53.1% to 79.4%. However, this low concordance was largely due to an LD1/LD2 < 1 in the presence of an increased cTnI. The average discordance over the 5-day period was 29.5%. Because cardiac troponin I (cTnI) has greater sensitivity than lactate dehydrogenase isoenzymes for delayed diagnosis of myocardial injury and is a more cost-effective test, the authors recommend it as a test of choice in this setting.
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PMID:Comparison of cardiac troponin I and lactate dehydrogenase isoenzymes for the late diagnosis of myocardial injury. 898 Mar 45

The study was designed to determine the time-course of cardiac troponin I (cTn-I) release in isolated and Langendorff-perfused rat hearts during hypoxia and reoxygenation (H/Reox), and after various durations of total ischemia and subsequent reperfusion (I/R). For this purpose, in H/Reox, cTn-I was measured with the conventional Access immunoassay (ng/ml) and a new immunoassay which operates at pg/ml, and compared with creatine kinase (CK), lactate dehydrogenase (LD) and cardiac troponin T (cTn-T). In I/R, cTn-I was compared with CK and LD. The anti-Tn-I mAbs used in cTn-I assays cross-react with cTn-I of the rat. A clear difference between time-courses and concentration levels of cTn-I in I/R and H/Reox models was found. In I/R, maximum release of cTn-I, CK and LD similarly occurred within minutes following reperfusion; however cTn-I did not return to baseline values. cTn-I levels were not linked to the duration of ischemia. In I/R, we were only able to detect small cTn-I concentrations. In H/Reox experiments, cTn-I, CK and LD increased time-dependently. We found higher cTn-I maximal peak levels detected with the Access immunoassay than with the new assay (median, 0.346 ng/ml per min/g dry wt vs 132 pg/ml per min/g dry wt). cTn-T maximal concentrations were lower than maximal cTn-I levels (median, 0.117 ng/ml per min/g dry wt). Time-courses of cTn-I release were roughly similar with both assays in the H/Reox model (r = 0.90). These data indicate that the cTn-I time-course is related to experimental model (I/R or H/Reox), but also likely depends on the sensitivity of cTn-I assays in such experimental conditions.
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PMID:Time-course of cardiac troponin I release from isolated perfused rat hearts during hypoxia/reoxygenation and ischemia/reperfusion. 1040 30

Cardiac troponins possess superior sensitivity and specificity for the detection of cardiac injury. They can be used successfully to replace measurements of MB isoenzyme of creatine kinase or lactate dehydrogenase for the retrospective diagnosis of myocardial infarction. Measurement of these proteins confers powerful prognostic information that can be used to triage patients. An increasing body of data suggests that measurement of troponin proteins can be useful to guide therapeutic decisions in patients with acute coronary artery syndromes, especially regarding treatment with low-molecular-weight heparin or IIB/IIIA inhibitors. The absence of troponins in the circulation does not necessarily indicate the absence of coronary artery disease. With current assays, a significant diagnostic difference does not appear to exist between cardiac troponin I and T in patients with acute coronary artery syndromes.
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PMID:Impact of troponins on the evaluation and treatment of patients with acute coronary syndromes. 1044 11

The detection of cardiac troponin I(cTnI), including serum or plasma, was evaluated in 114 patients with ischemic heart diseases or other heart diseases. The results were that the sensitivity of cTnI detection(qualitative analysis, cutoff is 0.2 ng.ml-1) was higher than that of creatine kinase(CK), creatine kinase-MB(CK-MB), alpha-hydroxybutyrate dehydrogenase(alpha-HBD), lactic dehydrogenase(LDH), and aspartic transaminase(AST) for diagnosing acute myocardial infarction (AMI) (93.2% vs 68.2%, 68.2%, 65.9%, 65.9%, and 75.0%; P < 0.05; respectively). The specificity of cTnI detection was higher than that of alpha-HBD, LDH, and AST(95.2% vs 81.0%, 73.8%, and 54.0%; P < 0.05; respectively) and similar to CK and CK-MB(95.2% vs 83.3% and 83.3%; P > 0.05; respectively). On the other hand, the sensitivity of cTnI in patients with unstable angina pectoris was 45.5%. It was higher than stable angina pectoris and lower than AMI. The results suggest that the cardiac troponin I is a better cardiac injury marker than other cardiac markers for diagnosing AMI.
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PMID:[Clinical evaluation of cardiac troponin I in ischemic heart diseases]. 1080 70

In the present study, 41 children in Upper Egypt were admitted to Pediatric Intensive Care Unit, Assiut University Hospital, for scorpion envenomation. They were compared with 15 apparently healthy children of matching age as controls. The victims and controls were subjected to complete clinical examination, full blood count and arterial blood gases analysis. According to severity of scorpion envenomation, 17 children had manifestations of severe envenomation and clinical signs of toxic myocarditis (severe cases), 14 children had moderate manifestations of envenomation without clinical evidence of carditis (moderate cases) and 10 cases showing only mild symptoms of envenomation (mild cases). The serum levels of cardiac troponin I (cTnI) and interleukin-8 (IL-8) beside the enzymatic activities of creatine phosphokinase (CPK), CPK-isoenzyme-MB (CPK-MB) and lactate dehydrogenase (LDH) were determined once for mild cases and controls on admission and twice for severe and moderate cases on admission and after 24. Electrocardiography and measurements of echocardiographic (Echo) of % fractional shortening of left ventricule (% SF), left ventricular ejection fraction (LVEF) and cardiac chambers dilatation were done for severe and moderate cases. All the envenomed victims showed significantly higher mean values of CPK, CPK-MB, LDH, and IL-8 on admission in comparison to control group. cTnI was not detectable in the sera of control group as well as patients of mild envenomation. The mean values of CPK, CPK-MB, LDH, and IL-8 were significantly higher in severe cases while only IL-8 and CPK-MB were significantly higher in moderate cases in comparison with mild cases. The mean values of IL-8, cTnI, CPK, CPK-MB and LDH were significantly higher in severe cases both on admission and on follow-up comparing with moderate cases. The case fatality rate was 12.5% and all were from severe cases with toxic myocarditis. The non-survivors victims showed significant higher mean values of only cTnI on admission and both cTnI and IL-8 on follow up in comparison to the survivors. Significant reduction of % SF and LVEF were noticed among the non-survivors in comparison to survivors. The cTnI showed 100% specificity and sensitivity for diagnosis of myocardial injury in relation to Echo finding in the envenomed victims. In severe cases, cTnI was positively correlated with IL-8 while negatively correlated with %SF and LVEF. In conclusion, cTnI is a specific marker for diagnosis of myocardial injury in scorpion envenomation while other biochemical markers did not show such specificity. Also, IL-8 may be involved in the pathogenesis of myocardial injury of scorpion envenomation. Both cTnI and IL-8 may be useful to forecast the fatal outcome in scorpion envenomation.
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PMID:Significance of assessment of serum cardiac troponin I and interleukin-8 in scorpion envenomed children. 1256 31

The pericardial fluid was examined in 26 patients without morphological signs of severe damage to cardiac histiocytes, who died unexpectedly from ischemic heart disease (IHD)--main group. The control group comprised 26 persons, who died from other (not heart diseases-asphyxia, acute blood loss, crania-cerebral trauma). The mean age of the died was 57.4 +/- 1.5 years in the main group and 51.8 +/- 2.7 years in the control group. Cardiac markers were examined in the pericardial fluid of the died in both groups, i.e. the activity of aspartate aminotransferase (AsAT), of creatine kinase (CK), of isoenzyme KK-MB, of lactate dehydrogenase (LDG), and its isoenzyme spectrum, and, finally, the content of the cardiac troponin I (cTnI). The statistically reliable differences were found between the two groups according to the activity of AsAT, LDG, its isoenzyme spectrum and the cTnI content. Isoenzymes LDG1 and LDG2 constituted up to 60% of the LDG activity in the pericardial fluid of those who unexpectedly died from IHD. As for the control group, the LDG activity was virtually evenly distributed between all isoenzymes. No differences were found in the activity of CK and isoenzyme KK-MB between the main and control groups. Thus, the obtained data are indicative of the "cardiac" origin of enzymes in the pericardial fluid. Finally, a number of assumptions were put forward on mechanisms of hyper-fermentation in the ischemic damage of the cardiac muscle.
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PMID:[Cardiac markers in the pericardial fluid in sudden coronary death]. 1282 98

The postmortem diagnostics of acute forms of coronary heart disease showed that third-degree cardiomyocytic damages, primary lumpish destruction, and intracellular myocytolysis are attended by elevated cardiac troponin I levels in pericardial fluid and by enhanced activity aspartate aminotransferase and lactate dehydrogenase.
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PMID:[Relationship of microscopic myocardial changes to the biochemical parameters of pericardial fluid in acute forms of coronary heart disease]. 1683 Jun 18

Different molecules have been studied as biochemical markers in heart transplantation. However, their utility is under discussion as results in human and animal models are controversial. In this work, lactate dehydrogenase (LDH), creatine kinase (CK) and cardiac troponin I (TnI) were studied as serologic markers of acute rejection after heterotopical heart transplantation in rats. In predictable rejection experiments, animals were divided into three groups: nonoperated (Lewis rats), control group (Lewis-Lewis isografts) and rejection group (Brown Norway-Lewis allografts). Nonpredictable rejection experiments were performed using nonconsanguineous Sprague-Dawley allografts. In predictable rejection experiments, LDH activity was similar between control and rejection groups. TnI values were heterogeneous in control and rejection groups. In contrast, the rejection group showed CK activity increased 4.5-fold compared with the control group. In addition to these predictable studies, we also presented novel nonpredictable experiments in which rats were divided into groups based on low and high CK activity. Histologic studies in these rats showed that none of those with low CK activity presented rejection signs, while all animals with high CK levels showed grade 2R rejection. These results suggest that CK might be an excellent marker for prediction of rejection in heart transplantation.
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PMID:Increased serum creatine kinase is a reliable marker for acute transplanted heart rejection diagnosis in rats. 1723 27

The aim of the present study was to investigate the protective effect of total flavones of rhododendra (TFR) pharmacological preconditioning against myocardial ischemia-reperfusion (I/R) injury and its probable mechanisms in rats. Rat myocardial I/R injury was induced by ligating and untying the left anterior descending coronary artery. Male Sprague-Dawley rats were anesthetized and the chests were opened. All animals were subjected to 30 min of occlusion and 1 h of reperfusion. Twenty-four hours before the 30-minute occlusion, rats received 3 cycles of 5 min intravenous perfusion of TFR (10, 20, 40 mg/kg) or morphine hydrochloride (0.3 mg/kg) or normal saline interspersed with drug-free periods. Changes in the ST segment of ECG, the content of cardiac troponin I (cTnI), malondialdehyde (MDA), and nitric oxide (NO), and the activity of superoxide dismutase (SOD), lactate dehydrogenase (LDH), creatine phosphokinase (CK), and nitric oxide synthase (NOS) in serum were measured. Infarct size (IS), as a percentage of the area at risk (AAR), was determined by TTC staining. The expression of inducible nitric oxide synthase (iNOS) mRNA in rat myocardium was detected by RT-PCR and the expression of iNOS protein was detected by Western blot. Pretreatment with TFR (10, 20, 40 mg/kg) markedly inhibited I/R-induced ST segment elevation of ECG. TFR (20, 40 mg/kg) pretreatment decreased I/R-induced IS/AAR, markedly inhibited the increase of MDA content and the activity of CK and LDH, and also significantly inhibited the decline of NO content and the activity of NOS and SOD in serum. TFR (40 mg/kg) preconditioning significantly inhibited the increase of serum cTnI induced by I/R injury and increased the expression of iNOS both at mRNA and protein levels in rat myocardium. Our findings indicate that TFR preconditioning has a protective effect against myocardial I/R injury in rats. The cardioprotection involves the stimulation of NO release and the inhibition of lipid peroxidation.
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PMID:Late protective effect of pharmacological preconditioning with total flavones of rhododendra against myocardial ischemia-reperfusion injury. 1841 40


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