Serum Creatine Kinase Isoenzyme MB Research Articles

Raised CK-MB isoenzyme after exercise in a patient with alcoholic myopathy

The relation between exercise, total serum creatine kinase activity, and serum creatine kinase MB isoenzyme in a patient with alcoholic myopathy was investigated. After a short-term exercise the serum values of creatine kinase MB isoenzyme rose to high levels within hours. This finding is important for obvious differential diagnostic reasons.

Serum creatine kinase MB isoenzyme in chronic muscle disease.

Journal Article Serum creatine kinase MB isoenzyme in chronic muscle disease. Get access A A Keshgegian, A A Keshgegian Search for other works by this author on: Oxford Academic Google Scholar N V Feinberg N V Feinberg Search for other works by this author on: Oxford Academic Google Scholar Clinical Chemistry, Volume 30, Issue 4, 1 April 1984, Pages 575–578, https://doi.org/10.1093/clinchem/30.4.575 Published: 01 April 1984

Effects of coronary artery reperfusion on relation between creatine kinase-MB release and infarct size estimated by myocardial emission tomography with thallium-201 in man

The quantitative relations between serum creatine kinase-MB isoenzyme (CK-MB) release and the final infarct size estimated by myocardial emission computed tomography with thallium-201 was assessed in 37 patients with a first acute transmural myocardial infarction who underwent intracoronary thrombolysis using urokinase 4.6 +/- 1.9 hours after the onset of symptoms. Serial CK-MB determinations were used to calculate the accumulated release of CK-MB (sigma CK-MB). Myocardial emission tomography with thallium-201 was performed 4 weeks after the onset, and infarct volume was measured from reconstructed tomographic images by computerized planimetry. The results are presented for two groups of patients: 11 patients with unsuccessful thrombolysis (group A) and 26 patients with successful thrombolysis (group B). An excellent linear relation was found for group A (sigma CK-MB = 6.4 X infarct volume + 47.7, r = 0.91), whereas a different linear relation was observed for group B (sigma CK-MB = 10.5 X infarct volume + 89.1, r = 0.80). Moreover, serum CK-MB activity reached a peak at 21.1 +/- 2.2 hours after the onset in group A and reached an earlier peak at 12.5 +/- 2.9 hours in group B (p less than 0.001). These data suggest that acute coronary recanalization alters the kinetics of CK-MB release, resulting in greater CK-MB release into the serum for equivalent infarct volume estimated by myocardial emission tomography with thallium-201. Thus, serum CK-MB time-activity curves after acute myocardial infarction may be influenced considerably by acute reperfusion, which is an important factor that should be incorporated in the interpretation of enzymatic estimates of infarct size in human patients.

Elevated Skeletal Muscle Creatine Kinase MB Isoenzyme Levels in Marathon Runners

Mean serum creatine kinase MB isoenzyme (CK-MB) activity in 108 trained marathon runners after competition was 98 +/- 66 (SD) units/L measured by a quantitative electrophoretic technique (normal, less than 5 units/L), or 7.9% of total CK activity. These levels in asymptomatic runners were comparable with peak serum values reported in patients during acute myocardial infarction. Elevated serum levels of CK-MB in runners can arise from skeletal muscle through exertional rhabdomyolysis, from silent injury to myocardium, or from a combined tissue source. To investigate this directly, we analyzed skeletal muscle obtained by needle biopsy for CK isoenzymes from 25 trained male marathon runners and ten sedentary male subjects. The MB isoenzyme accounted for 8.9% +/- 1.3% (SD) of total CK activity per gram of total protein in the skeletal muscle of runners and 3.3% +/- 0.7% (SD) in control tissue, which was significant. Total CK activity was not statistically different between the two groups. Similar relative concentrations of CK-MB in skeletal muscle (8.9%) and serum after competition (7.9%) strongly suggest that elevated serum CK-MB activity in asymptomatic runners arises from a noncardiac or skeletal muscle source.

Elevated serum creatine kinase MB and creatine kinase BB-isoenzyme fractions after ultra-marathon running.

To determine the incidence and range of serum creatine kinase MB (CK-MB) isoenzyme activity after ultra-marathon running, a popular test kit was used to measure total serum creatine kinase (CK) and CK MB-activity in 75 athletes immediately after they had completed an 88-km running race. Total serum CK activity was markedly elevated after the race (mean value: 637 U X 1(-1) and 45 (60%) runners showed abnormal CK-MB isoenzyme activities (greater than 4% of total CK activity - range 1-19%). Electrophoresis of 31 sera with either CK-MB to total CK activity greater than 4% or with total CK activity greater than 854 U X 1(-1) showed that 31 (100%) had visible CK-MM bands, 21 (68%) had visible CK-BB bands, but only 14 (44%) had visible CK-MB bands. We conclude that prolonged exercise increases the serum activity of all three CK-isoenzymes, and that the CK-MB test kit used in this study identified a greater number of sera with elevated post-race CK-MB isoenzyme activity than did electrophoresis. This discrepancy could result either from cross-reaction of elevated CK-BB activity with the test kit, or from relative insensitivity of the electrophoresis. The tissue source and long-term significance of the elevated serum CK-MB and CK-BB isoenzyme activity induced by ultra-marathon running are uncertain. Until these issues are resolved, these biochemical findings in ultra-marathon runners must be interpreted with the appropriate caution.

Serum creatine kinase and creatine kinase MB isoenzyme responses of post-infarction patients after a graded exercise test.

The response of total creatine kinase (CK) and the creatine kinase isoenzyme (CK MB) was studied in 22 male post-infarction patients (three to six months after myocardial infarction) after a functional graded exercise test, before entering a rehabilitation programme. Eleven subjects (group A) completed the test without developing significant electrocardiographic abnormalities. Eleven subjects (group B) showed changes that necessitated premature termination of the test. No significant differences were observed before the functional graded exercise test between the groups in serum concentration of CK, CK MB, and the percentage of CK MB to CK (MB/ CK%). The two groups were significantly different (p less than 0.01) 24 hours after the graded exercise test in CK MB and MB/CK%, but not in CK. In group B, CK and CK MB rose significantly after the graded exercise test (p less than 0.05) as did MB/CK% (p less than 0.01). In group A only CK showed a significant rise (p less than 0.05). It is probable that increases in CK MB after exercise arise from myocardial tissue efflux, reflecting reversible ischaemia. It is concluded from this study that CK MB appears to be a specific indicator of myocardial ischaemia and could, therefore, be of significant assistance in the clinical and functional assessment of the post-infarction patient.

Serum creatine kinase isoenzyme MB in acute and chronic alcoholism

Serum creatine kinase isoenzyme MB in acute and chronic alcoholism

Two‐dimensional electrophoresis of serum proteins in myocardial infarction patients and subjects at risk of developing coronary heart disease

AbstractIso‐Dalt analysis of serum from myocardial infarction patients has revealed the presence of a group of low (<23 000) molecular weight basic peptides, as yet unidentified, which were not found in the serum of healthy controls. The presence and staining intensity of these proteins correlated with the qualitatively assessed serum creatine kinase MB isoenzyme activity. The proteins were not detected in sera from patients at risk of developing coronary heart disease (smokers, hypertensive patients, subjects with a family history of developing coronary heart disease, oral contraceptive users, hyperlipidaemics, and diabetics). This excludes their possible use as a predictive test for the development of coronary heart disease. It seems probable that they originate in the cells in or near the infarct.

Sotalol and infarct size after coronary ligation in the baboon.

We investigated the hemodynamic effects and myocardial salvage actions of sotalol during experimental myocardial infarction in the baboon. Ten baboons received placebo and six were given sotalol. In anesthetized open-chest baboons base-line determinations included heart rate (HR), rate-pressure product (RPP), left ventricular dP/dt, aortic pressures, serum creatine kinase MB isoenzyme (CK-MB) activity, and a 16-point epicardial ST segment map. The left anterior descending coronary artery was then ligated and the measurements were repeated at 15-min and at 2-h intervals up to 12 h after occlusion. At 12 h, coronary blood flow and myocardial CK activity were also measured. Twenty minutes after ligation, either sotalol (3 mumol . kg-1 followed by 2 nmol . kg-1 . min-1) or placebo (saline) was administered intravenously. Sotalol reduced HR but not dP/dt or the degree of afterload. The reduction in HR resulted in a significant decrease in RPP (myocardial O2 consumption). Sotalol administration also resulted in a decrease in coronary blood flow (myocardial O2 supply). There were no significant differences between the two groups in serum CK-MB activity or in the extent of myocardial damage, as predicted by the 15-min ST-segment deviations and myocardial CK activity at 12 h. The reduction in myocardial oxygen demand caused by sotalol was accompanied by a decrease in oxygen supply. As a consequence, no significant reduction in myocardial ischemic damage was found in the group given sotalol.

Unexplained increase in serum creatine kinase isoenzyme MB activity in a lung cancer patient.

In this case of mixed small cell--large cell cancer of the lung in an elderly woman, creatine kinase (EC 2.7.3.2) isoenzymes were assayed serially because of chest pain. The proportions of serum CK-BB and CK-MB isoenzyme activities were persistently above normal (CK-MB 10-18%, normal less than 5%). Electrocardiograms revealed no signs of ischemia or infarction. At autopsy no gross or microscopic infarction or inflammation of the heart was seen. There was also no infarction of smooth or skeletal muscle. The tumor was the probable source of most of the circulating CK-MB isoenzyme. Future cases may pose a similar diagnostic dilemma: differentiating creatine kinase that is present as a result of myocardial infarction from tumor-related CK-MB. Whether or not CK-MB assay could be useful in detecting tumors remains to be investigated.

Elevated Creatine Kinase MB Isoenzyme Levels in Marathon Runners

Elevated serum creatine kinase MB isoenzyme (CK-MB) levels are regarded as a sensitive and specific marker for myocardial injury. Serum CK-MB was measured in male marathon runners during training and after competition. Mean serum CK-MB measured by a quantitative electrophoretic technique (normal, less than 5 IU/L) showed borderline elevation during training with peaks 24 hours after competition. Mean CK-MB in 64 serum samples from 35 runners after competition was 130 IU/L or 8.3% of total CK activity. Levels of CK-MB averaging 26 times the upper limits of normal would usually be considered indicative of massive myocardial necrosis. Myocardial scintigraphy with technetium Tc 99m pyrophosphate was performed after competition in 12 randomly selected runners with a mean postrace serum CK-MB level of 160 IU/L or 13%. Infarct-avid ("hot-spot") scintigraphy, appropriately timed to detect underlying myocardial abnormalities, was within normal limits in all subjects. Normal results of infarct-avid scintigraphy coincident with marked serum CK-MB elevations strongly suggests that CK-MB arises from a noncardiac or skeletal muscle source in these runners.

Elevated creatine kinase MB isoenzyme levels in marathon runners. Normal myocardial scintigrams suggest noncardiac source

Elevated serum creatine kinase MB isoenzyme (CK-MB) levels are regarded as a sensitive and specific marker for myocardial injury. Serum CK-MB was measured in male marathon runners during training and after competition. Mean serum CK-MB measured by a quantitative electrophoretic technique (normal, &lt;5 IU/L) showed borderline elevation during training with peaks 24 hours after competition. Mean CK-MB in 64 serum samples from 35 runners after competition was 130 IU/L or 8.3% of total CK activity. Levels of CK-MB averaging 26 times the upper limits of normal would usually be considered indicative of massive myocardial necrosis. Myocardial scintigraphy with technetium Tc 99m pyrophosphate was performed after competition in 12 randomly selected runners with a mean postrace serum CK-MB level of 160 IU/L or 13%. Infarct-avid ("hot-spot") scintigraphy, appropriately timed to detect underlying myocardial abnormalities, was within normal limits in all subjects. Normal results of infarct-avid scintigraphy coincident with marked serum CK-MB elevations strongly suggests that CK-MB arises from a noncardiac or skeletal muscle source in these runners. (<i>JAMA</i>1981;246:2049-2051)

Serum creatine kinase MB isoenzyme activity in long-term hemodialysis patients

Serum creatine kinase MB isoenzyme activity in long-term hemodialysis patients

Serum Creatine Kinase MB Isoenzyme Activity in Long-term Hemodialysis Patients

Serum creatine kinase MB isoenzyme (CK-MB) activity was determined in 46 male long-term hemodialysis patients without evidence of myocardial infarction. Thirteen (28.3%) showed mild elevations. The abnormality persisted in seven of eight patients on repeated measurement at three- to eight-month intervals. There was a significant correlation between serum CK-MB and CK-MN activity, and the activity of both enzymes rose after intramuscular injection. The reason for the abnormality is not known. It is possible that skeletal muscle is the source of elevated enzyme activity. Caution should be exercised in the interpretation of serum CK-MB activity in the diagnosis of acute myocardial infarction in this patient population.

Serum creatine kinase isoenzyme MB activity: Evaluation of a kit employing agarose-gel electrophoresis with overlay paper fluorescence scanning

A commercial kit for determining serum creatine kinase isoenzyme MB activity was evaluated. The kit employed agarose-gel electrophoresis followed by incubation of overlay paper on the agarose and then fluorescence scanning of the paper. Within-day coefficients of variation ranged from 24.9% for a specimen with no elevation of MB activity to 6.6% for a specimen with moderately elevated MB activity. The kit appeared to demonstrate MB in all sera and showed higher than expected values in recovery studies. The kit performed in a relatively linear fashion from 50 to 500 I.U./1 total creatine kinase activity. Hemolysis appeared to lower measured MB. For comparison with another method, specimens were also analyzed by microcolumn chromatography, which was found to incompletely separate isoenzymes. The kit produced lower values than microchromatography for specimens with low MB activities and higher values for specimens with elevated MB activities. Patients without corroborative evidence of myocardial injury showed a somewhat hyperbolic relationship between per cent MB and total creatine kinase activity, but MB activity was generally 4 I.U./1 or less. Although the kit had serious laboratory shortcomings, it may be as clinically useful as other methodologies.

Serum CK-KB Kinetics in Acute Myocardial Infarction and After Coronary Bypass Operations

Serum creatine kinase (CK) isoenzyme MB and total CK activity concentrations in 11 patients with acute myocardial infarction (AMI) were compared with the corresponding enzyme activities in 25 patients after coronary bypass surgery, not complicated clinically by AMI. Peak CK-MB occurred 2 +/- 0 (mean +/- SEM) hours after the end of surgery (mean duration of operation 6 hours), but 17 +/- 1 hours from the onset of symptoms in AMI. The plasma half"life for CK-MB was 11 +/- 1 hours under both conditions. Peak total CK was found after about 20 hours in both series of patients. Total CK half-life was 17 +/- 2 hours in AMI, but 30 +/- 3 hours following surgery. CK kinetics were thus different in these two situations, indicating different mechanisms for the elevations of serum CK-MB activity. In conclusion, the time course for the transient CK-MB elevation following bypass surgery should be considered in the diagnosis of peri operative infarction.

Relative merits of two electrophoretic and two column-chromatographic kets for determining serum creatine kinase isoenzyme MB activity.

Prospective analysis (by use of commercially available kits) of 339 validated admission specimens from patients consecutively admitted to a cardiac monitoring unit revealed sensitivities of 68 and 63% for two electrophoretic assays (Bioware and Helena) and up to 73 and 77% for two chromatographic assays (Roche and Worthington). Specificities were 94.8, 96,6, 90.2, and 89.7% and efficiencies were 90.2, 90.7, 87.0, and 87.0, respectively. Although these results differ from early reports, they agree well with several recent studies. However, 86 (25%) of the specimens gave at least one discrepant result based on clinical evaluation of the patients, and 68 (20%) gave at least one discrepant result between methods.

Determination of creatine kinase isoenzyme MB (CK-MB): Comparison of methods and clinical evaluation

An ion-exchange chromatography method based on the method of Mercer is advocated for the routine determination of serum CK-MB. This method has some prominent advantages over other methods with which it is compared, and which include electrophoresis and an immunological technique. This method proves to be reliable and highly reproducible, while it allows a rather large number of samples to be analyzed within a relatively short period of time. Some parameters of the release pattern of CK-MB after acute myocardial infarction are characterized: normal values, time of first rise, time of peak value and rate-constant of inactivation. The clinical significance of serum CK-MB determination is evaluated.