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)

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

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