Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008031 (chest pain)
 17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated an immunoturbidimetric quantitation for serum myoglobin by the latex agglutination method using an automated biochemical analyzer. This method is rapid, specific, accurate, precise, and has wide dynamic range. The total assay time is 10 min and is performed at 37 degrees C with continuous monitoring at 570 nm. The assay results were compared with radioisotopic immunoassay results and showed a good correlation coefficient, r = 0.99; Y = 0.98 x + 9.3; N = 79. Sera from healthy adults has a myoglobin concentration in the range of 15-80 ng/ml(N = 362). Sex- and age-related differences were observed. The serum myoglobin levels in males and elderly people showed higher concentration than in females and younger people. The peak elevation of serum myoglobin compared with other cardiac markers was observed within 6 hours after onset of chest pain as well as the CK-isoform ratio (MM3/MM1). All of the serum from 21 patients with definite acute myocardial infarction showed increased serum myoglobin levels (100-1200 ng/ml) upon admission and within 6 hours. The results suggest that assays for serum myoglobin levels are helpful in the early diagnosis of acute myocardial necrosis.
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PMID:Measurement of serum myoglobin by a turbidimetric latex agglutination method. 154 86

The authors quantified the change of CK-MM isoforms in the first available serum sample from 16 patients each with acute myocardial infarction (AMI) and angina pectoris and 16 normal individuals as well. The average MM3/MM1 ratio in the normal group was 0.24 +/- 0.12, in angina group 0.21 +/- 0.13, and in AMI group 0.52 +/- 0.30 (P less than 0.001, as compare with the first two groups). The first blood sample of AMI was obtained in 3.0 +/- 1.9 hours after the onset of chest pain. Half of them (8/16) had a ratio of MM3/MM1 greater than 0.50 and the change occurred as early as 30 min after the attack. In contrast, the total CK and CK-MB in the three groups were within normal limits at the same time, they were 85.8 +/- 24.4 U/L for CK and 3.2 +/- 1.1% for CK-MB in patients with AMI, 66.7 +/- 18.0 U/L, 2.7 +/- 1.6% in angina pectoris and 71.4 +/- 24.5 U/L, 3.0 +/- 1.1% in normal subjects respectively. Accordingly, diagnostic change of CK-MM isoforms was the earliest among the enzymes after the onset of AMI.
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PMID:[Diagnostic changes in serum creatine kinase MM isoenzyme sub-bands after the onset of acute myocardial infarction]. 224 87

Following acute myocardial infarction, total CK and CK-MB levels begin to rise 5 to 6 hours after the onset of chest pain. The serial profile of the rise and fall of both activities is nearly always indicative of AMI. The recent increase in the use of thrombolytic agents in an attempt to attain reperfusion of occluded coronary arteries alters the enzyme profiles observed in blood after AMI. After successful reperfusion a washout phenomenon occurs in which early restoration of blood flow to damaged myocardium causes an early rise in total CK and MB levels above the normal range 2 to 4 hours after AMI, with earlier and higher peak enzyme values. Recently reports have appeared describing numerous serum and plasma CK-MM and CK-MB isoform patterns after AMI. Following release from injured myocardium CK-MM3 and CK-MB2 (designated the tissue isoforms) are converted in the circulation to post-translation products (MM2, MM1, MB1, respectively). Studies have now shown that CK-MM isoform patterns provide a unique means of assessing the time of onset of necrosis and a monitor of the duration of enzyme release from the site of injury. Following AMI, MM3, the MM3/MM1 ratio, or both rises and peaks earlier than either total CK or CK-MB levels. During successful reperfusion, the rate of rise of CK-MM3 is more rapid and the MM3/MM1 ratio peaks earlier than without reperfusion. However, any concomitant release of CK-MM3 from skeletal muscle would decrease the clinical utility of MM isoforms in detecting myocardial damage. Recent advances in technology have shown that CK-MB2 rise parallels the CK-MM increase and also rises earlier than total CK and total MB levels and provides increased specificity for the myocardium. The full potential of the diagnostic utility of MM and MB isoforms will not be realized until a reliable, sensitive, simple, and rapid quantitative assay becomes available.
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PMID:Diagnostic use of CK-MM and CK-MB isoforms for detecting myocardial infarction. 268 6

Using an electrophoretic method, the changes in the catalytic activities of three CK-MM isoforms (MM1, MM2, MM3) and two CK-MB isoforms (MB1, MB2) in the serum of 13 patients with acute myocardial infarction (AMI) have been monitored for 3 days after the onset of chest pain. In post-AMI period, MM3 reaches a peak first, 17 h after infarction (394 U/l), followed by MB2 (17.3 h, 190 U/l), MB1 (20.6 h, 82 U/l), MM2 (28.7 h, 637 U/l), and MM1 (32 h, 780 U/l). According to their faster decay from circulation, MB2 and MM3 have higher fractional disappearance rates (-0.035 and -0.026 per hour, respectively). The MM3/MM1 activity ratio rises beyond the upper limit found in healthy subjects within about 3 h after onset of symptoms and peaks 9.3 h after AMI, even earlier than peaks of isoforms. These characteristics make the ratio an earlier and more sensitive indicator of acute enzyme release from necrotic myocardium.
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PMID:Serum isoforms of creatine kinase MM and MB in myocardial infarction. An appraisal of quantitative, clinical and pathophysiological information. 360 11

Serum creatine kinase (CK, EC 2.7.3.2) isoenzymes MM and MB were resolved, respectively, into three (MM1, MM2, MM3) and two (MB1, MB2) isoforms (subforms derived from the same isoenzyme) by electrophoresis and the isoform patterns were determined in multiple sequential serum samples, timed from the onset of chest pain, from 58 patients with acute myocardial infarction (AMI). During the first 3 h after the onset of chest pain, the serum isoform activity resembled the pattern seen in normal volunteers. Specimens obtained 6 h after AMI showed predominantly MM3 and MB2 (45% and 11% of the total CK activity, respectively). Between 10 and 72 h, there was a gradual shift in which MM3, MM2 and MB2 decreased, while MM1 and MB1 increased. MB2 and MB1 disappeared from the pattern for samples collected after 24-48 h, while MM1 was always the most prominent band at the end of the observation period (66%, range 41-77%, at 48 h). These data suggest that a single determination of CK isoform pattern, drawn between 6 and 48 h after AMI, may provide an effective means of predicting the time of onset of necrosis. There were no significant differences in the CK isoform patterns according to infarct location and functional status of patients.
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PMID:Isoforms of creatine kinase MM and MB in acute myocardial infarction: a clinical evaluation. 369 4

Using an isoelectric-focusing (IEF) method developed to quantitate MM isoenzyme-creatine kinase (CK) sub-band activity, we identified a reproducible time-varying pattern of these sub-bands in the serum of eight patients with acute myocardial infarction (MI). Our observations are consistent with the view that MM3-CK (the M2-CK dimer, the pure gene product) is converted intravascularly to MM2-CK, and then to MM1-CK (the M1-CK dimer, the pure postsynthetic sub-band). The MM3-CK reaches a peak first, 16 hours after infarction, followed by MM2-CK, and then by MM1-CK. The MM3-CK is the dominant sub-band in normal myocardium; there is much less MM2-CK and virtually no MM1-CK. The MM3-CK sub-band peak may indicate the time at which enzyme ceases to be released from the injured myocardium. The ratio MM3-CK:MM1-CK rises within 6 hours after onset of chest pain from a baseline of 0.38 and peaks 10 hours after MI. The peak ratio was between 1.1 and 4.2, and the value correlated with the time when total CK activity peaked after MI. The 10-fold change in the MM3:MM1 ratio after MI, as well as the early period at which this ratio peaks (10 hours), makes this an earlier and more sensitive indicator of enzyme release.
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PMID:Serum creatine kinase MM isoenzyme sub-bands after acute myocardial infarction in man. 685 Oct 22

We automated a two-step kinetic procedure for determining serum CK-MM isoform ratio using an immunoinhibition method. By measuring the total CK activity and the residual CK activity (serum CK-MM isoform) remaining after the inhibition by tissue CK-MM isoform specific monoclonal antibody reagent (CK-M01) the CKMM isoform ratio is calculated using the difference between total CK and residual CK activities divided by the residual CK activity. Linearities of total CK and residual CK assays were < or = 7750 U/L and 2,500 U/L, respectively; within-run CVs of isoform ratio (N = 10) were 2.8 and 7.0% (mean 0.14 and 0.60), respectively. The MM3/MM1 isoform ratio obtained with the proposed method (X) correlated well with the results of electrophoretic method (Y) according to the equation: Y = 0.98X-0.3, r = 0.988. The normal reference range of isoform ratios obtained by assaying 1,222 serum samples from healthy subjects was 0.09-0.75. The isoform ratio increased after onset of chest pain, peaking at 2-6 hr thereafter. A mean isoform ratio of 1.86 was obtained with serum sample from 86 patients diagnosed as having an acute myocardial infarction (AMI). This method is accurate and highly sensitive, as the detection and early diagnosis of AMI can be completed in 10 min.
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PMID:Simultaneous automated measurement of serum total CK and CK-MM isoform ratio in serum. 780 81

Using the electrophoretic method, the changes in the catalytic activities of three CK-MM isoforms in multiple sequential serum samples of 12 patients with acute myocardial infarction (AMI) were monitored for 3 days after the onset of chest pain. In post-AMI period, MM3 reached a peak (518.6 U/L) first, on the average 14.0 hours after AMI, followed by MM2 (19.8 h, 640.5 U/L) and MM1 (28.7 h, 641.3 U/L). According to their faster decay from circulation, MM3 had higher fractional disappearance and appearance rates, followed by MM2 and MM1. The MM3/MM1 activity ratio rose beyond the upper limit, found in health subjects, about 3.5 hours after onset of symptom and peaked on an average 10.6 hours after AMI, even earlier than the peaks of all isoforms, CK and CK-MB. On the other hand, our findings indicated these changes in isoform composition can be of value in estimating the time elapsed since the onset of tissue damage; MM3 is the predominant isoform when the tissue necrosis is of relatively recent origin (5-15 h); MM2 is the dominant subband between 15 and 24 hours after AMI, whereas a predominant MM1 band would indicate a significantly longer time period since the injury occurred (24 hours or more). Thus, these characteristics make CK-MM isoforms an earlier and more sensitive indicator of acute release from necrotic myocardium and an effective mean of predicting the time of the onset of AMI.
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PMID:Serum isoforms of creatine kinase MM isoenzyme in acute myocardial infarction. 822 90

The diagnostic efficacy of creatine kinase (CK) isoforms (CK-3 and CK-2) was compared with measurement of CK-2 mass concentrations for the early diagnosis of myocardial infarction (MI). Serial serum samples drawn from 76 patients with confirmed MI and 55 non-MI patients were used for determining CK-2 mass concentrations and the MM3/MM1 (CK-3 isoforms) and MB2/MB1 (CK-2 isoforms) ratios. We compared the diagnostic utility of each by receiver-operating-characteristic (ROC) curve and likelihood ratio analyses. Our results indicate that all three tests were ineffective within the first 4 h after the onset of chest pain. All three were most effective at 4-18 h after onset, but both CK-3 and CK-2 isoform ratios were less effective than CK-2 mass concentrations in the next 6-h period (18-24 h). In the critical time between 3 and 6 h, the diagnostic performance of all three was comparable.
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PMID:Diagnostic evaluation of creatine kinase-2 mass and creatine kinase-3 and -2 isoform ratios in early diagnosis of acute myocardial infarction. 844 62

Measurement of creatine kinase (CK) isoforms enables the clinician to detect myocardial tissue damage at an early stage after myocardial infarction. According to the manufacturer's specifications, it should be possible to perform CK isoform analysis automatically using the new Cardio Rep analyser. In order to investigate the suitability of this new analyser we measured the CK MM1-3, and CK MB1 and 2 isoform patterns, firstly in 30 patients with acute myocardial infarction (AMI), for whom total CK and CK-MB levels were ordered, and secondly in 23 patients with chest pain suspected as having AMI (n = 11) or with unstable angina pectoris (UAP) (n = 12). The total time for analysis, including 5 min pre- and 10 min post-analyser run time, was found to be 40 min. For elevated MB2/MB1 ratios there is a discrepancy between the MB2/MB1 ratios determined from the densitometric scans concerning the surface and the peak height ratios. The MB2/MB1 ratios of the studied AMI patients exceeded the upper reference limits approximately 2 h after the onset of symptoms, whereas the CK-MB and total CK levels increased after about 6 h. The MB2/MB1 ratios from the patients with UAP were either below the detection limit or these patients could be discriminated from patients with AMI when low CK-MB and total CK levels were considered in conjunction. From our results we conclude that assessment of CK isoforms can be performed relatively simply with the new analyser within 40 min. However, for reliable calculation of the MB2/MB1 ratios, the curve monitoring of the MB2-MB1 densitometric scans should be improved. The CK isoforms are useful as an early marker for AMI as their reference interval is already exceeded approximately 2 h after an AMI. Moreover, CK isoform analysis might prove to be useful in discriminating at an early stage between AMI and other causes of chest pain. This could decrease the number of patients with a false-positive diagnosis admitted to coronary care units, resulting in a reduction of costs.
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PMID:Implications of automated creatine kinase (CK)-MM1,2,3/CK-MB1,2 isoform analysis as an early marker for the detection of myocardial tissue damage. 898 58


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