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PubMed2003

Creatine kinase injection restores contractile function in creatine-kinase-deficient mouse skeletal muscle fibres.

Viable genetically engineered animals generally exhibit adaptations to the altered genotype, which may mask the role of the protein of interest. We now describe a novel method by which the direct effects of the altered genotype can be distinguished from secondary adaptive changes in isolated adult skeletal muscle cells. We studied contractile function and intracellular Ca2+ handling in single skeletal muscle fibres that are completely deficient of creatine kinase (CK; CK-/-) before and after microinjection of purified CK (injected together with the fluorescent Ca2+ indicator indo-1). The mean total CK activity after CK injection was estimated to be approximately 4 mM s-1, which is approximately 5 % of the activity in wild-type muscle fibres. After CK injection, CK-/- fibres approached the wild-type phenotype in several aspects: (a) the free myoplasmic [Ca2+] ([Ca2+]i) increased and force showed little change during a period of high-intensity stimulation (duty cycle, i.e. tetanic duration divided by tetanic interval = 0.67); (b) [Ca2+]i did not decline during a brief (350 ms) tetanus; (c) during low-intensity fatiguing stimulation (duty cycle = 0.14), tetanic [Ca2+]i increased over the first 10 tetani, and thereafter it decreased; (d) tetanic [Ca2+]i and force did not display a transient reduction in the second tetanus of low-intensity fatiguing stimulation. Conversely, tetanic force in the unfatigued state was lower in CK-/- than in wild-type fibres, and this difference persisted after CK injection. Injection of inactivated CK had no obvious effect on any of the measured parameters. In conclusion, microinjection of CK into CK-/- fibres markedly restores many, but not all, aspects of the wild-type phenotype.

Animals↗
PubMed2003

Creatine supplementation: a comparison of loading and maintenance protocols on creatine uptake by human skeletal muscle.

The purposes of this investigation were first to determine the impact of 3 different creatine (Cr) loading procedures on skeletal muscle total Cr (TCr) accumulation and, second, to evaluate the effectiveness of 2 maintenance regimes on retaining intramuscular TCr stores, in the 6 weeks following a 5-day Cr loading program (20 g x day(-1). Eighteen physically active male subjects were divided into 3 equal groups and administered either: (a) Cr (4 x 5 g x day(-1) x 5 days), (b) Glucose+Cr (1 g x (-1) of body mass twice per day), or (c) Cr in conjunction with 60 min of daily muscular (repeated-sprint) exercise. Following the 5-day loading period, subjects were reassigned to 3 maintenance groups and ingested either 0 g x day(-1), 2 g. day(-1) or 5 g x day(-1) of Cr for a period of 6 weeks. Muscle biopsy samples (vastus lateralis) were taken pre- and post-loading as well as post-maintenance and analyzed for skeletal muscle ATP, phosphocreatine (PCr), Cr, and TCr concentrations. Twenty-four hour urine samples were collected for each of the loading days and last 2 maintenance days, and used to determine whole body Cr retention. Post-loading TCr stores were significantly (p <.05) increased in all treatment conditions. The Glucose+Cr condition produced a greater elevation (p <.05) in TCr concentrations (25%) than the Cr Only (16%) or Exercise+Cr (18%) groups. Following the maintenance period, muscle TCr stores were still similar to post-loading values for both the 2 g x day(-1) and 5 g x day(-1) conditions. Intramuscular TCr values for the 0 g x day(-1) condition were significantly lower than the other conditions after the 6-week period. Although not significantly different from pre-loading concentrations, muscle TCr for the 0 g x day(-1) group had not fully returned to baseline levels at 6 weeks post-loading. The data suggests that Glucose+Cr (but with a much smaller glucose intake than currently accepted) is potentially the most effective means of elevating TCr accumulation in human skeletal muscle. Furthermore, after 5 days of Cr loading, elevated muscle TCr concentrations can be maintained by the ingestion of small daily Cr doses (2-5 g) for a period of 6 weeks and that TCr concentrations may take longer than currently accepted to return to baseline values after such a Cr loading regime.

Administration, Oral↗
PubMed2005

Comparison of erythrocyte and skeletal muscle creatine accumulation following creatine loading.

This study attempted to determine the relationship between creatine (Cr) accumulation in human skeletal muscle and erythrocytes following Cr supplementation. If a strong relationship exists, a blood test might provide a practical, less invasive alternative than muscle biopsy for evaluating cellular Cr accumulation. Eighteen active, but not well-trained males were supplemented with Cr (4 x 5 g/d) for 5 d. Muscle biopsies (vastus lateralis) were obtained pre- and post-loading and analyzed for Cr, phosphocreatine (PCr), and total Cr (TCr) content. Venous blood was also drawn at these times to determine erythrocyte Cr concentrations. Muscle Cr, PCr, and TCr concentrations were elevated (P < 0.05) by 39.8%, 7.5%, and 20.1% respectively following supplementation. Erythrocyte Cr concentrations were also elevated (P < 0.01) following the loading period, although to a greater relative degree than tissue concentrations (129.6%). Pre- and post-loading erythrocyte Cr concentrations were poorly and nonsignificantly correlated with that observed in skeletal muscle. Further, loading-mediated increases in erythrocyte Cr concentrations were poorly correlated with elevations in muscle Cr (r = 0.07), PCr (r = 0.06) or TCr (r = 0.04) concentrations. Erythrocyte Cr concentrations can be augmented by 5 d of Cr supplementation, however, this elevation does not reflect that observed in skeletal muscle obtained by muscle biopsy. Consequently, erythrocyte response to Cr loading is not a reliable measure of skeletal muscle Cr/TCr accumulation.

Administration, Oral↗
PubMed1994

Mouse p53 represses the rat brain creatine kinase gene but activates the rat muscle creatine kinase gene.

The creatine kinases (CK) regenerate ATP for cellular reactions with a high energy expenditure. While muscle CK (CKM) is expressed almost exclusively in adult skeletal and cardiac muscle, brain CK (CKB) expression is more widespread and is highest in brain glial cells. CKB expression is also high in human lung tumor cells, many of which contain mutations in p53 alleles. We have recently detected high levels of CKB mRNA in HeLa cells and, in this study, have tested whether this may be due to the extremely low amounts of p53 protein present in HeLa cells. Transient transfection experiments showed that wild-type mouse p53 severely repressed the rat CKB promoter in HeLa but not CV-1 monkey kidney cells, suggesting that, in HeLa but not CV-1 cells, p53 either associates with a required corepressor or undergoes a posttranslational modification necessary for CKB repression. Conversely, mouse wild-type p53 strongly activated the rat CKM promoter in CV-1 cells but not in HeLa cells, suggesting that, in CV-1 cells, p53 may associate with a required coactivator or is modified in a manner necessary for CKM activation. The DNA sequences required for p53-mediated modulations were found to be within bp -195 to +5 of the CKB promoter and within bp -168 to -97 of the CKM promoter. Moreover, a 112-bp fragment from the proximal rat CKM promoter (bp -168 to -57), which contained five degenerate p53-binding elements, was capable of conferring p53-mediated activation on a heterologous promoter in CV-1 cells. Also, this novel p53 sequence, when situated in the native 168-bp rat CKM promoter, conferred p53-mediated activation equal to or greater than that of the originally characterized far-upstream (bp -3160) mouse CKM p53 element. Therefore, CKB and CKM may be among the few cellular genes which could be targets of p53 in vivo. In addition, we analyzed a series of missense mutants with alterations in conserved region II of p53. Mutations affected p53 transrepression and transactivation activities differently, indicating that these activities in p53 are separable. The ability of p53 mutants to transactivate correlated well with their ability to inhibit transformation of rat embryonic fibroblasts by adenovirus E1a and activated Ras.

Animals↗
PubMed1985

Separation of mitochondrial creatine kinase (MiMi-CK) from cytosolic creatine kinase isoenzymes by Cibachrome-Blue affinity chromatography.

The mitochondrial isoenzyme of creatine kinase (MiMi-CK) was separated by affinity chromatography on Cibachrome-Blue-Sepharose (Sepharose-Blue, Pharmacia). While the soluble CK isoforms (BB-CK and MM-CK) were specifically eluted by raising the pH of the column buffer from pH 6.0 to pH 8.0, MiMi-CK remained bound under these conditions but was specifically eluted by subsequent addition of ADP to the pH 8.0 buffer. This one-step method allows a fast and efficient separation of MiMi-CK from MM-and BB-CK isoenzymes and at the same time an enrichment of MiMi-CK by about 50-fold. Since MiMi-CK can be assayed separately after isolation by affinity chromatography on Sepharose-Blue, this method may be of clinical importance.

Animals↗
PubMed1996

Early 'rule-in' diagnosis of acute myocardial infarction 4 h post admission for rapid risk stratification by creatine kinase increment (creatine kinase change).

The use of creatine kinase (CK) measurement on admission, CK at 4 h, percentage CK change and electrocardiography (ECG) were compared for early risk stratification in the diagnosis of acute myocardial infarction (AMI). A total of 248 patients (median age 62 years, range 26-84) were studied (187 men, 61 women) of whom 118 had a final diagnosis of AMI. Median time to presentation was 3.92 h (range 0-11.17 h). Overall, the admission ECG had a sensitivity of 72.6% [95% confidence interval (CI) 64.6-80.7] with specificity of 88.9% (CI 83.4-94.4); 4 h CK change had a sensitivity of 100% (CI 96.1-100) with a specificity of 90.4% (CI 83.5-95.1). After excluding those with contraindication to anti-thrombotic therapy there were 109 patients with an uncertain initial diagnosis. In this group, admission CK had a sensitivity of 37.5% (CI 18.8-59.4) with a specificity of 94% (CI 86.8-98.1); 4 h ECG had a sensitivity of 43.8% (CI 19.8-70.1) with specificity of 97.4% (CI 86.5-99.9%); 4 h CK had a sensitivity of 79.2% (CI 57.8-92.9) with a specificity of 96.5% (CI 90-99.3); 4 h CK increment had a sensitivity of 100% (CI 85.8-100) with a specificity of 94% (CI 86.8-98.1). The admission ECG remains the investigation of choice for early 'rule-in' diagnosis of AMI for thrombolysis. Admission measurement of CK offers a small advantage in the patient with an uncertain diagnosis but the overall benefit is low. A strategy of admission ECG plus serial testing allows diagnosis to be complete by 4 h for accurate risk stratification. Whether this can be used for selection for therapeutic options (thrombolytic, anti-coagulation, anti-platelet or anti-anginal agents) requires further clinical trials.

Adult↗
PubMed1989

Creatine kinase BB isozyme in the blood during open heart surgery--comparison with creatine kinase MB and MM isozymes.

By using a recently developed highly sensitive enzyme immunoassay method, concentrations of the 3 forms of cytoplasmic creatine kinases (CK-BB, CK-MB and CK-MM) were determined in blood samples serially taken from 18 patients who received mitral valve replacement. Blood CK-BB levels, 0.64 +/- 0.32 ng/ml at the beginning of anesthesia, rose sharply after reperfusion reaching the peak level (23.3 +/- 7.56 ng/ml) 2 hours after reperfusion, and then fell rapidly. The response of CK-BB in blood was rapider and more sensitive than that of CK-MB or CK-MM. The CK-BB concentrations were significantly higher in coronary sinus samples than in arterial samples. These results suggest that the major portion of elevated blood CK-BB level in the early phase after reperfusion are derived from the heart muscle.

Cardiopulmonary Bypass↗
PubMed1992

Determinants of elevated creatine kinase activity and creatine kinase MB-fraction following cardiopulmonary resuscitation.

OBJECTIVE: We undertook this study to determine the occurrence and the determinants of elevation of serum creatine kinase (CK) levels and CK MB-fraction following cardiopulmonary resuscitation (CPR). DESIGN: Four hundred twenty consecutive adult admissions to the Long Island Jewish Medical Center from January 1989 through December 1990 with a diagnosis of cardiac arrest were reviewed. SETTING: The Long Island Jewish Medical Center, New Hyde Park, NY, the Long Island Campus for the Albert Einstein College of Medicine, Bronx, NY. PATIENTS: Sixty-three patients survived for at least 12 h following cardiac arrest for evaluation of post-CPR CK levels and were included into the study. MEASUREMENTS: Clinical features, biochemical profiles, and administered drug profiles were studied in these patients. The clinical and biochemical features of the patients with (CK greater than 224 IU/L [3.7 mu kat/L]) and without rhabdomyolysis were also compared. MAIN RESULTS: Two major determinants responsible for elevated CK levels emerged, including physical injury (number of chest compressions during CPR) and electrical injury (cumulative number of joules administered during defibrillation). Post-CPR CK levels showed positive correlations with both the number of chest compressions given (p less than 0.001) and the number of joules administered during defibrillation (p less than 0.001). Post-CPR CK-MB levels also showed a positive correlation with the number of joules administered (p less than 0.005) and the number of chest compressions (p less than 0.02). Forty-three (68.3 percent) of the 63 patients developed rhabdomyolysis. Serum CK levels were higher (p less than 0.005) in the patients who received electrical countershock therapy as well as chest compressions when compared with patients who received chest compressions alone. There were no significant differences in electrolyte levels between patients with and without rhabdomyolysis. Thirty patients had a history of coronary artery disease (CAD) and 18 (60.0 percent) of these had a positive MB-fraction post-CPR while only ten of the 33 patients without known CAD had a positive MB-fraction post-CPR (30.3 percent, p less than 0.05). Patients with no known CAD but positive CK-MB fraction had significantly higher total CK levels, physical injury, and electrical injury compared with patients with negative CK-MB fraction. Twenty patients survived CPR and were discharged from the hospital without significant neurologic sequelae. The remaining 43 either died or suffered severe neurologic injury. The patients who survived CPR had a significantly shorter duration of CPR (p less than 0.01) compared with those who did not. Patients who did not have long-term survival following CPR were more likely to have elevated serum potassium, phosphate, and creatinine values. CONCLUSIONS: CK elevation is a common finding following successful CPR after cardiac arrest and this elevation of post-CPR CK levels is related to both physical as well as electrical injury sustained during CPR. Elevation of post-CPR CK-MB fraction seems to be only a crude indicator of preexisting CAD; however, a positive CK-MB fraction in patients without CAD is related to severity of physical injury and electrical injury during CPR. Patients who survive CPR without neurologic impairment appear to be those with a shorter duration of CPR. Elevated serum potassium, phosphate, and creatinine values may be related to an adverse effect on long-term survival.

Adult↗
PubMed1992

Creatine kinase and creatine kinase-MB isoenzyme during and after exercise testing in normal and obese young people.

We report creatine kinase (CK) and CK-MB values during a cycloergometric test up to maximal work capacity in 10 normal subjects aged 20 to 39 years (mean body mass index, 22 kg/m2) and 11 obese patients aged 17 to 42 years (mean body mass index, 41 kg/m2), all without any cardiorespiratory diseases. Total CK was significantly higher in obese patients. The CK-MB was not significantly different between the two groups, except at the first recovery when it was increased in obese patients and decreased in normal subjects. These results could be due to more important total stress of the total musculature, especially cardiac, and especially cardiac musculature in obese patients during a physical effort. Considering the mean values of total CK of our obese patients, it may be possible that they have myocardial damage at percentages of CK-MB less than those of lean subjects generally accepted at more than 4 percent. Moreover, in obese heart patients myocardial distress during exercise testing may be present despite heart rate at peak exercise beneath the theoretic maximal.

Adolescent↗
PubMed2004

Mg2+-creatine chelate and a low-dose creatine supplementation regimen improve exercise performance.

We tested the hypotheses that, compared with a placebo group or creatine (Cr) group, a Mg(2+)-Cr chelate group would demonstrate improvements in the 1 repetition maximum (1RM) on the bench press and be able to perform more work at 70% of the 1RM for the bench press. Thirty-one weight-trained men were randomly assigned in a double-blind manner to a placebo group (multidextran), a Cr group (2.5 g of Cr daily), or a Mg(2+)-Cr group (2.5 g of Cr daily). Baseline data were collected for the bench press 1RM and maximal work completed during a fatigue set at 70% of the 1RM. Following 10 days of Cr supplementation, follow-up tests were completed for the dependent variables. Groups were similar when the change in 1RM was evaluated either absolutely or relatively. Both the Cr and the Mg(2+)-Cr groups had significantly larger increases in work, both absolutely and relatively, when compared with the placebo group. Partial support for the hypothesis suggests that low doses of Cr are effective at increasing fiber Cr content, and consequently, performance. Further, the Cr and Mg(2+)-Cr groups were similar in both performance tests, suggesting that the proposed mechanism of entry is no better than the conventional method when 2.5 g of Cr is administered and performance is measured as work. This study raises the possibility that a low dose of Cr may be an effective means of enhancing performance after short-term ingestion.

Adolescent↗
PubMed1993

Creatine kinase-MB protein mass is a better indicator for the assessment of acute myocardial infarction in the lower range of creatine kinase level.

The theoretical and clinical validity of immunochemiluminometric assay of creatine kinase (CK)-MB protein mass was assessed in patients with acute myocardial infarction and the results were compared with those of immunoinhibition assay of CK activity. Serial changes of both CK-MB protein mass and CK-MB activity were analyzed in 20 consecutive patients. In all 312 samples from 20 patients, protein mass and activity of CK-MB showed good correlation. The exponential fitting of the time-value curve of CK-MB protein mass showed a better correlation coefficient than that of CK-MB activity (0.97 +/- 0.02 vs 0.93 +/- 0.07, p < 0.05), indicating that the CK-MB level measured by the immunochemiluminometric assay was less scattered than that measured by the immunoinhibition method. This finding was most evident at lower CK-MB values (< 500 IU/l). The rate of disappearance from serum of CK-MB protein mass was faster than that of CK-MB activity (0.54 +/- 0.23 hr-1 vs 0.28 +/- 0.13 hr-1, p < 0.001). This may indicate that some amount of the CK-MB activity may be inactivated in the early phase of the release into the serum from the necrotic myocardium. Thus, the immunochemiluminometric assay of CK-MB protein mass has superiority in the diagnosis of acute myocardial infarction compared with the immunoinhibition method, especially when the measured CK-MB level is low. This feature may be useful to distinguish a small myocardial infarction from severe ischemia without myocardial necrosis.

Aged↗
PubMed1999

[Effect of macro-creatine kinase in serum on dry chemistry methods results for total creatine kinase activity].

Most enzymes in serum that are measured in clinical laboratories can occur in macro-molecular forms in a significantly number of patients. Within dry chemistry (DC) multilayer film, physical barriers may prevent contact macro-molecular enzyme forms with the active reagent ingredients. Here, serum samples with macro-creatine kinase (macro-CK) type 1: CK-immunoglobulin complex or type 2: oligomer mitochondrial CK (CKm) were analyzed for total CK activity on three different DC analyzers: VITROS 700XR, FUJIDRYCHEM 5000, SPOTCHEM SP4410 and a classic wet chemistry (WC) analyzer: HITACHI 7350. Macro-CKs were detected and identified by electrophoresis on cellulose acetate. Serum with high amounts of oligomer CKm gave CK values by all of DC methods significantly lower than that by the WC method (p < 0.05). Oligomer CKm gradually converts into monomer forms in serum after storage. With increase in day after storage at 4 degrees C, there was a gradual shift in which percent of total CK activity for oligomer CKm decreased while the ratio of total CK activity, DC method/WC method increased. The principle of analytical method for CK activity determination is commonly to all of the DC methods, the WC method and the electrophoretic analysis. These suggest that oligomer CKm is sieved by DC multilayer film elements. In contrast, each of DC method produced highly corrected CK activities for sample containing CK-immunoglobulin complex. This difference in the effects of macro-CKs may depend upon physicochemical characteristics of analytical DC elements.

Blood Chemical Analysis↗
PubMed2000

Correlation of antemortem serum creatine kinase, creatine kinase-MB, troponin I, and troponin T with cardiac pathology.

BACKGROUND: Spurious increases in serum troponins, especially troponin T, have been reported in patients with and without acute myocardial syndromes. METHODS: We studied 78 autopsied patients without clinical myocardial infarction (MI) and correlated histologic cardiac findings with antemortem serum creatine kinase (CK), its MB isoenzyme (CK-MB), cardiac troponin I (cTnI), and cardiac troponin T (cTnT). RESULTS: There was no significant myocardial pathology in 15 patients. Cardiac pathologies were in five groups: scarring from previous MI or patchy ventricular fibrosis (n = 9), recent MI (n = 27), healing MI (n = 7), degenerative myocyte changes consistent with congestive heart failure (CHF; n = 12), and other cardiac pathologies (n = 8). The median concentrations in the five groups were not significantly different for either CK or CK-MB. Compared with the no-pathology group, only the MI group was significantly different for cTnI, and the MI and other pathology groups were significantly different for cTnT. For patients with MI, 22%, 19%, 48%, and 65% had increased CK, CK-MB, cTnI, and cTnT, respectively; for CHF and other cardiac pathologies combined, the percentages were 28%, 17%, 22%, and 50%. For patients with increased cTnI, 72% and 28% had MI and other myocardial pathologies, respectively; patients with increased cTnT had 64% and 36%, respectively. Patients without myocardial pathology had no increases in CK-MB, cTnI, or cTnT. CONCLUSIONS: All patients with increased serum CK-MB, cTnI, and cTnT had significant cardiac histologic changes. The second-generation cTnT assay appears to be a more sensitive indicator of MI and other myocardial pathologies than the cTnI assay used in this study.

Autopsy↗
PubMed1992

Ratio of creatine kinase 2 mass concentration to total creatine kinase activity not altered by heavy physical exercise.

Serum creatine kinase isoenzyme 2 concentrations (CK 2 mass) were measured in marathon runners during training and 1 and 2 days after a race and compared with values from 36 acute myocardial infarction (AMI) patients whose total CK and (or) CK 2 activities were similar to those of runners in the basal state. During training, runners had CK and CK 2 activities 53% and 43% above reference values, respectively, and 36% had CK 2 activity > 5% of total CK. Nine runners (26%) showed CK 2 mass values > 6 micrograms/L but < or = 10 micrograms/L; 35 of the AMI subjects, despite having CK activities similar to those of runners, had values > 10 micrograms/L. The ratio of CK 2 mass to total CK activity was significantly (P < 0.0002) different between sexes for runners. At 1 and 2 days after racing, 100% of CK and CK 2 activities and 71% and 57% of the percentages of CK 2 activity, respectively, were abnormally high; 57% and 43% of CK 2 mass values were > 10 micrograms/L, being comparable with those observed for the AMI group. Basal CK 2 mass values of the runners appeared only slightly higher than that for sedentary subjects, but after exercise half the subjects presented increased values similar to those observed for AMI subjects. The ratio of CK 2 mass to total CK activity appeared unaltered by exercise in all but one of the samples assayed, indicating its utility in evaluating CK 2 mass increases originating in skeletal muscle.

Adult↗
PubMed1985

Appearance of M-band attached MM-creatine kinase in differentiating chicken heart cells after injection of M-type isoprotein or poly (A+)-RNA enriched for M-type creatine kinase message.

Myofibrils of chicken heart cells do not contain the electron-dense material of the so-called m-bridges which transverse the sarcomere in the M-region. It has been shown that the M-isoform of creatine kinase (MM-CK) which is mainly responsible for the m-bridge material is not expressed during differentiation of chicken heart cells. No transition from the embryonic BB-CK to the muscle-specific MM-CK takes place in chicken heart, thus no MM-CK is available for m-bridge formation. Here we report on chicken heart cells microinjected with either MM-CK protein or with poly(A+)RNA enriched for M-CK message. In both cases appearance of MM-CK within the M-band of heart myofibrils could be observed by immunofluorescence, indicating translation of the injected message as well as specific binding of the translation product to the M-band of myofibrils. The M-band protein myomesin which is regularly found in heart myofibrils served as specific marker for assembled myofibrils in double immunofluorescence experiments.

Animals↗
PubMed1989

Study on heart mitochondrial creatine kinase using a cross-linking bifunctional reagent. II. The binding sites for the creatine kinase octamer on mitochondrial membranes have different properties.

Beef heart mitochondria suspended in 0.25 M sucrose were treated with 0.3% glutaraldehyde (GA). The membranes were disintegrated by ultrasonication in 0.25 M KCl and precipitated by centrifugation. The relative amount of the membrane-bound mitochondrial creatine kinase (CKm) does not depend on the time course of membrane disruption. The enzyme is not removed by repeated washing of the pellet. It is concluded that this part of CKm is cross-linked to mitochondrial membranes. The maximum amount of the enzyme capable of cross-linking to the membrane with an increase in GA concentration or incubation time makes up to about 50% of the total CKm activity present in the mitochondria. It is concluded also that the CKm binding sites differ with respect to their environment.

Adenylate Kinase↗
PubMed1989

[The change of creatine kinase bb isozyme in patients undergoing mitral value replacement--comparison with creatine kinase MB and MM isozymes].

By using highly sensitive enzyme immunoassay method recently developed, concentrations of the three forms of cytoplasmic creatine kinases (CK-BB, CK-MB and CK-MM) were determined in blood plasma samples serially taken from 18 patients, who received mitral valve replacement. Plasma CK-BB levels, that were 0.64 +/- 0.32 ng/ml at the beginning of anesthesia, increased sharply after reperfusion reaching peak levels (23.3 +/- 7.56 ng/ml) at 2 hours after reperfusion, and then decreased rapidly. The response of CK-BB in plasma was more rapid and sensitive than that of CK-BB or CK-MM. The CK-BB concentrations were significantly higher in coronary sinus samples than in arterial samples. These results suggest that the major portion of elevated plasma CK-BB levels at early phase after reperfusion were considered to be derived from the heart muscle.

Creatine Kinase↗
PubMed1988

Creatine kinase:aspartate aminotransferase activity ratio as an indicator of the source of an increased creatine kinase activity.

Although measurements of creatine kinase isoenzyme 2 (CK-MB) are often used to diagnose acute myocardial infarction, their sensitivity and specificity are less than 100%. Because skeletal muscle contains more CK and less aspartate aminotransferase (AST) than cardiac muscle, the CK/AST ratio might provide a useful adjunct in evaluating the source of a supranormal value for CK. I established the following decision levels in a retrospective study of 342 patients: ratios less than 14 (if total CK was 300-1200 U/L), less than 20 (CK 1201-2000 U/L), or less than 25 (CK greater than 2000 U/L) suggested myocardial infarction, with a sensitivity of 95% and a specificity of 65%. In a validation study with 277 additional patients, liver disease and alcohol abuse caused erroneous results, leading to exclusion of 22% of these patients. In the remaining cases, sensitivity was 94%, specificity 90%. The CK/AST ratios changed little with time, suggesting that a single value would be adequate for evaluating patients with increased CK.

Aspartate Aminotransferases↗