Evaluation of ck-mb isoform analysis for early diagnosis of myocardial infarction

Measurement of CK-MB and its isoforms by high-voltage electrophoresis has been proposed as a sensitive test for early detection of myocardial infarction (MI). We performed a prospective study of this test in 231 patients presenting to the Emergency Department with symptoms consistent with ischemic chest pain. Blood specimens were obtained at 0, 1, and 3 h following presentation, and plasma was immediately frozen and analyzed within 1 week by high-voltage electrophoresis for total CK-MB and isoforms. The test was considered positive whenever total CK-MB was elevated (>6 U/L) or the cardiac isoform MB₂ was relatively increased (MB₂ > 2 U/L and MB₂/MB₁ > 1.7). This test had a sensitivity of 68% overall and 55% for specimens collected within 3 h of symptom onset. It was positive within 3 h of presentation in 36/39 (92%) of patients with confirmed MI. Specificity was 92% overall and did not vary with time after symptoms. The CK-MB alone, at the cutoff of 6 U/L, had lower sensitivity overall (56%; p = 0.01) and within 3 h of onset (39%; p = 0.03), and higher specificity overall (98%; p < 0.001). Lowering the cutoff for CK-MB alone to match the sensitivity of the isoform test caused a greater loss of specificity. It is concluded that analysis of CK-MB by high-voltage electrophoresis is an effective method for rapid diagnosis of MI, with the isoform analysis enhancing early sensitivity.     

Analytical and clinical evaluation of creatine kinase MB mass assay by IMx: comparison with MB isoenzyme activity and serum myoglobin for early diagnosis of myocardial infarction.

We analytically and clinically evaluated Abbott's IMx assay for creatine kinase (CK) isoenzyme MB (CK-MB) in serum. Over a 1-year period, the method was more specific but less precise than catalytic isoenzyme measurements by electrophoresis or immunoinhibition. Sera from different individuals without electrophoretic evidence of CK-MB but containing macro CK type 1 (n = 20), mitochondrial CK (n = 5), or CK-BB (n = 5) were scored as CK-MB negative by the IMx. Likewise, CK-MB-negative by the sera remained so after addition of purified human CK-MM (< or = 7600 U/L) or CK-BB (< or = 8100 U/L). For 39 patients admitted for suspicion of uncomplicated acute myocardial infarction (precordial pain for < or = 4 h), the diagnostic performance of the IMx CK-MB assay on admission and 4 h later was superior to that of total CK activity and compared well with that of CK-MB activity measured by electrophoresis or immunoinhibition. An admission, myoglobin showed a higher diagnostic sensitivity, specificity, and predictive value than did CK-MB and was the most informative test. Diagnostic performance on admission and 4 h later was further improved by considering positivity for myoglobin and for CK-MB by IMx and for the change in each over the first 4 h of hospitalization as criteria. Twelve hours after admission, diagnostic performance was further improved for all CK and CK-MB methods but began to decline for myoglobin.     

Simultaneous automated measurement of serum total CK and CK-MM lsoform ratio in serum

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?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. © 1994 Wiley-Liss, Inc.     

Monoclonal antibody inhibiting creatine kinase MM3 but not isoform MM1

Monoclonal antibody CKM-G01 inhibited greater than 99% of the activity of porcine and human creatine kinase(CK)-MM isoenzyme purified from muscle. However, it inhibited only 54% of CK-MM in human serum. Chromatofocusing of serum CK-MM showed that CKM-G01 inhibited 100% of MM3 but not isoform MM1. CKM-G01 inhibited CK-MM2 by 57%. CKM-G01 specifically inhibited only the original CK-M subunit and not the subunit modified by removal of C-terminal lysine by carboxypeptidase N. CKM-G01 can be used for assay of CK isoforms. We devised a new diagnostic reagent involving it, which requires no analytical separation of isoforms, based on the immunoinhibition method, and applied it to early diagnosis of acute myocardial infarction. The "inhibition index," (inhibited CK activity/total CK activity) x 100, increased more rapidly than did total CK and CK-MB. Evidently this diagnostic reagent can be used for easy, early diagnosis of acute myocardial infarction.     

Creatine kinase and its CK-MB isoenzyme: the conventional marker for the diagnosis of acute myocardial infarction

Biochemical markers are commonly used for detection, diagnosis, and management of various diseases. Creatine kinase (CK) is an enzyme found in most tissues, and is the best known marker for the identification of acute myocardial infarction (AMI). We review the most common techniques used to quantify creatine kinase and its cardiac specific fraction, CK-MB. Electrophoresis, immunoinhibition, monoclonal immunoassay, and CK-MB isoform assays are considered for efficacy, sensitivity and specificity, and timeliness in the setting of acute non-traumatic chest pain. Limitations of the various techniques for identifying AMI are identified. Current recommendations for CK-MB panels, including combinations with other cardiac markers, are included.     

Diagnostic use of CK-MM and CK-MB isoforms for detecting myocardial infarction

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.     

Specificity of an immunochemical reagent for quantifying the isoforms of creatine kinase-MB

Fractionation of the creatine kinase-MB isoforms is promising for use in diagnosing acute myocardial infarction and for monitoring myocardial perfusion status after thrombolytic therapy. An immunochemical reagent intended for use in fractionating the MB₁ and MB₂ isoforms of creatine kinase-MB was examined before and after immunoextraction, qualitatively by visually examining electrophoresis separation of various MB₁ and MB₂ mixtures, and quantitatively by comparing the observed and predicted enzymatic activity ofvarious MB₁ and MB₂ mixtures. Qualitatively the reagent showed greater reactivity for MB₁ than for MB₂, as demonstrated by a marked decrease in the MB₁ electrophoretic region following immunoextraction. Quantitatively, the reagent consistently eliminated about 75% of MB₁ activity; however, the assay also eliminated about 40% of MB₂ activity from isoform mixtures. Although the performance of the immunochemical reagent was not ideal, the greater reactivity for MB₁ may have clinical use. © 1993 Wiley-Liss, Inc.     

Differential diagnosis of patients with abnormal serum creatine kinase isoenzymes

For the diagnosis of myocardial injury, particularly AMI, CK-MB has become the gold standard. Changing CK-MB activities in serially collected blood from patients with suggestive signs and symptoms of AMI is almost pathognomonic for infarction. Nevertheless, an increased CK-MB cannot be equated with AMI owing to the many other types of inflammatory, traumatic, and miscellaneous forms of injury to the heart and the trace activities of CK-MB in skeletal muscle. Other enzyme tests for AMI are less efficient. In order of decreasing efficiency, the tests are CK-MB, CK, LD1 greater than LD2 or LD1/LD2 greater than 0.76, AST and LD; the latter two tests are not cost effective and add little or nothing when results for CK-MB, CK, and LD isoenzymes are available. The value of the isoforms of CK-MM and CK-MB remains to be established. Early evidence suggests that they could be helpful in the diagnosis of AMI; however, owing to the greater technical difficulties in performing these tests, their use is necessarily more restricted. Enzyme testing on admission and then every 12 hours for 2 days is sufficient and effective in making the initial diagnosis. In patients presenting early after an attack, CK and CK-MB are often normal. Decisions on AMI cannot be made on blood tests collected in the emergency department. Clot-lysing agents like streptokinase, urokinase, and tPA have changed the therapy of AMI dramatically. Enzyme tests clearly separate patients with and without successful therapeutic or spontaneous reperfusion. With successful reperfusion, the uniform finding has been a "washout" phenomenon with significantly earlier peaking times for CK and CK-MB. The isoforms of CK and myoglobin give the earliest peaks after successful reperfusion. With faster turnaround times for these tests, they may become important tools in patient management.     

Immunochemical extraction and automated measurement of plasma creatine kinase MB isoenzyme and creatine kinase MB2 isoform

Measurement of creatine kinase MB (CK-MB) and its isoforms CK-MB₂ and CK-MB₁ are now applied in the diagnosis of acute myocardial infarction (AMI). The most common approach for analysis includes RIA, IRMA, and electrophoresis, all of which may be time-consuming. This study examines determination of CK-MB and CK-MB₂ by a rapid immunochemical extraction method followed by an automated measurement for both analytes. The automated method was sensitive to 2 U/L, linear to 180 U/L, and gave excellent interassay precision (<10% CV). Interference studies indicated that bilirubin, hemolysis, and lipemia caused analytical problems as did the presence of high activities of other CK isoenzymes, notably CK-MM and CK-BB, requiring dilution of samples prior to analysis. Application of immunochemical extraction gave a reference interval of CK-MB (0–2.5 U/L) and CK-MB₂ (0.1–1.4 U/L) for blood donors (20–60 years), peak levels for ruled-out AMI patients of CK-MB (0.5–7.3 U/L) and CK-MB₂ (0.3–4.9), peak levels for ruled-in AMI patients of CK-MB (80–174 U/L) and CK-MB₂ (80–155 U/L). Coronary artery bypass patients (n = 24) and all trauma patients (n = 14) also demonstrated elevations in CK-MB and CK-MB₂, whereas only five of the trauma patients demonstrated increased CK-MB by IRMA. In patients (n = 7) having increased total CK and normal CK-MB by IRMA, the extraction assay for CK-MB and CK-MB₂ yielded increased values in all patients. This new approach to CK-MB and CK-MB₂ analysis can be performed within 30 minutes of sample receipt. J. Clin. Lab. Anal. 11:163–168, 1997. © 1997 Wiley-Liss. Inc.     

Validation of NACB and IFCC guidelines for the use of cardiac markers for early diagnosis and risk assessment in patients with acute coronary syndromes

BACKGROUND: International guidelines have been established for the use of cardiac markers in the early diagnosis and risk assessment of patients with acute coronary syndromes. METHODS: A single center, prospective observational study was conducted in a tertiary care university hospital on 200 consecutive patients with suspected acute myocardial infarction (AMI). Blood was drawn on admission and after 2, 4, 8, 12 and 24 h for the measurement of CK-MB/CK activity, myoglobin, CK-MB mass and troponin I. A 6-week follow-up was undertaken for the combined end point of acute coronary syndrome and death. RESULTS: Myoglobin showed an early diagnostic sensitivity of 0.65 on admission, 0.90 after 2 h and 0.92 after 4 h compared with 0.46, 0.74 and 0.88 for CK-MB/CK activity. The combination of myoglobin and cTnI increased the diagnostic value compared with myoglobin alone on admission, 2 and 4 h later. In multivariate analysis, cTnI and CK-MB/CK mass, but not myoglobin and CK-MB/CK activity, were shown to be independent predictors on the 6-week follow-up. CONCLUSIONS: Repetitive myoglobin measurements within 4 h of admission, combined with at least one early troponin test, was shown to be the strategy of choice in early AMI diagnosis and prognosis assessment.     

Creatine kinase MB isoforms for early diagnosis and monitoring of acute myocardial infarction.

MB isoforms of creatine kinase (ATP:creatine N-phosphotransferase, EC 2.7.3.2, CK) in 848 sera obtained from 80 patients with acute myocardial infarction (AMI) were studied by agarose gel isoelectric focusing. In 173 sera (20%) from 25 patients (31%), a new isoform designated as MB3 (pI 5.4) was detected at the cathodal side of MB2 (pI 5.2) in addition to the previously known MB2 and MB1 (pI 5.1). The new isoform MB3 was found in the extract of the cardiac muscle. MB3 was dominant in the sera at an earlier stage and a shorter period of time after AMI: 1-14 h (range), 1-29.5 h and 4-154 h for MB3, MB2 and MB1 dominant, respectively. MB3 was therefore found to be an earlier and a shorter phase indicator for AMI than MB2 or MB1. However, MB2 greater than 1 was the most prevalent pattern at the time of admission to the hospital. In AMI, specificity was 96.2%, 92.4% and 90.6%, and sensitivity was 20.4%, 88.9% and 97.6%, for MB3, MB2 and MB1 isoforms, respectively. CK-MB isoform patterns were biased to MB1 dominant in the deceased group, and to MB2 dominant in the surviving group. Therefore determination of CK-MB isoforms is also useful in the course of observation of AMI. The fourth isoform, MB0 (pI 5.0), was detected at the anodal side of MB1. MB0 was a minor band of the CK-MB isoform which appeared when serum CK-MB activity increased.     

Early Diagnostic Efficiency of Cardiac Troponin I and Troponin T for Acute Myocardial Infarction

Objective : To compare the early diagnostic efficiency of the cardiac troponin I (cTn-I) level with that of the cardiac troponin T (cTn-T) level, as well as the creatine kinase (CK), CK-MB, and myoglobin levels, for acute myocardial infarction (AMI) in patients without an initially diagnostic ECG presenting to the ED within 24 hours of the onset of their symptoms. Methods : A prospective, observational, cohort study was performed involving chest pain patients admitted to a large urban community hospital. Participants were consecutive consenting ED chest pain patients ≥30 years of age. Exclusions included duration of symptoms >24 hours, inability to complete data collection, receipt of CPR, and ST-segment elevation on the initial ECG. Measurements included levels of cTn-I, cTn-T, CK, CK-MB, and myoglobin at the time of presentation and 1, 2, 6, and 12–24 hours after presentation as well as presenting ECG and clinical follow-up. Confirmation of the diagnosis of AMI was based on World Health Organization criteria. Results : Of the 177 patients included in the study, 27 (15%) were diagnosed as having AMIs. The sensitivities of all 5 biochemical markers for AMI were poor at the time of ED presentation (3.7–33.3%) but rose significantly over the study period. The sensitivity of cTn-T was significantly better than that of cTn-I over the initial 2 hours, but both markers' sensitivities were low (<60%) during this time frame. The cTn-I was significantly more specific for AMI than was the cTn-T, but not significantly better than CK-MB or myoglobin. Likelihood ratio analysis showed that the biochemical markers with the highest positive likelihood ratios for AMI during the first 2 hours following ED presentation were myoglobin and CK-MB. From 6 through 24 hours, the positive likelihood ratios for cTn-I, CK-MB, and myoglobin were superior to those of CK and cTn-T. Conclusions : cTn-I, CK-MB, and myoglobin are significantly more specific for AMI than are CK and cTn-T. Myoglobin is the biochemical marker having the highest combination of sensitivity, specificity, and negative predictive value for AMI within 2 hours of ED presentation. Neither cTn-I nor cTn-T offers significant advantages over myoglobin and CK-MB in the early (≤2 hours) initial screening for AMI. The cardiac troponins are of benefit in identifying AMI ≤6 hours after presentation.     

影响肌酸激酶同工酶活性检测结果的因素探讨

目的探讨应用酶免疫抑制法检测血清肌酸激酶（CK）同工酶——CK—MB酶活力单位时,引起临床假阳性的因素,以科学合理地解释每一检测结果及解决方法。方法采用回顾性研究,分析125例非心肌梗死患者,应用酶免疫抑制法检测血清标本中CK、CK—MB酶活力单位,分析可能引起检测值CK—MB酶活力单位假性升高的影响因素。结果86例成人非心肌梗死患者中,总CK活力相对较低,癌症患者、脑梗死患者、变态反应疾病患者CK—MB假阳性比例较大,其中CK—MB占CK总活力大于5％有59例,其中53例在6％～21％,6例大于38％;38例新生儿中CK活性范围为145～1974U／L,其中1例新生儿呼吸窘迫综合征患儿CKMB占CK总活力达90％;另1例溶血标本也引起假阳性。结论应用酶免疫抑制法检测非心肌梗死患者CK—MB酶活力单位假性升高的影响因素,可能是血清中存在巨CK、CK—BB、AK等,影响试剂单克隆抗体与肌酸激酶中的M亚基结合,存在未被抑制的CK—M、M亚基同时与B亚基参加酶促反应,而且因计算时结果乘以2,更加扩大误差,是该方法学缺点造成的错误结果,不能作为诊断依据。     

Serum free L-carnitine in association with myoglobin as a diagnostic marker of acute myocardial infarction

BackgroundEarly diagnosis of acute myocardial infarction (AMI) in patients with chest pain is necessary to initiate appropriate treatment. Elevation of ST-segment in ECG is the only marker that cardiologists depend on in diagnosis. The aim of this study was to monitor the level of serum free L-carnitine in combination with myoglobin (Myo) and creatine kinase (total activity and CK-MB level) for usefulness as a predictor of AMI in ICU patients.Design and methodsIn the present study serum total CK activity and CK-MB, Myo, and free L-carnitine levels were determined in 90 patients admitted to the ICU at Ain Shams University Hospital and correlated the sensitivity and specificity of each parameter.ResultsObtained data revealed that, 47/90 who were diagnosed as AMI showed a highly significant reduction in serum free L-carnitine level in all cases as compared to normal control (P < 0.001), 24/90 diagnosed as unstable angina showed a non significant reduction of serum carnitine and 19/90 who were diagnosed as noncardiac showed non significant changes in the level of serum free carnitine as compared to normal control. In addition, serum free L-carnitine level was negatively correlated to CK-MB and Myo (r = ? 0.61 and ? 0.52) respectively. The sensitivity of carnitine assay was considerably higher (95.5%) compared to CK-MB (87%) and Myo (89.5%) even considering patients with a short delay until admission.ConclusionComparing the changes in serum total CK, levels of CK-MB, Myo and carnitine, the sensitivity and specificity were significantly higher for serum free L-carnitine. For this reason, serum free L-carnitine can be used as a good predictor for AMI diagnosis from other diseases.     

Myoglobin,creatine kinase MB isoforms and creatine kinase MB mass in early diagnosis of myocardial infarction in patients with acute chest pain

OBJECTIVES: Measurements of myoglobin and creatine kinase (CK)-MB isoforms have been suggested to be sensitive tests for the early diagnosis of myocardial infarction (MI). We have investigated the utility of myoglobin, creatine kinase (CK)-MB isoforms and creatine kinase MB mass (CK-MBm) in early diagnosis of MI using cardiac troponin T (cTnT) positivity as a reference. DESIGN AND METHODS: The study population comprised 440 patients who had had chest pain for less than 12 h. Patients were divided into cTnT negative (cTnT-) or cTnT positive (cTnT+) patients (concentration of cTnT >0.1 microg/L at two different time points during 72 h). RESULTS: At the time of admission to the emergency department receiver operating characteristics (ROC) curves of CK-MB isoforms and CK-MBm were not better than that of myoglobin. Six hours after admission CK-MB isoforms and CK-MBm provided statistically significantly larger areas under the curve (AUC) than myoglobin (p < 0.01). When ROC curves were related to the onset of chest pain (< 3 h, 3-6 h, and > 6 h) there were no significant differences between the cardiac markers studied. CONCLUSIONS: According to the present findings, CK-MB isoforms or myoglobin offer no advantage over CK-MBm as early markers of myocardial infarction.     

肌酸激酶同工酶检测在急性心肌梗死中的临床价值

目的 探讨肌酸激酶（CK）MB和MM同工酶（CK-MB和CK-MM）亚型在急性心肌梗死（AMI）患者中的变化规律与其预后的关系,评价CK同工酶的亚型检测在AMI心肌早期再灌注、梗死延迟或再梗死诊断中的临床价值。方法 采用琼脂糖凝胶电泳系统将血清CK同工酶亚型分离为CK-MM3、CK-MM2、CK-MM1、CK-MB2和CK-MB1,并分析比较21例AMI患者血清CK同工酶亚型在发病后0～6小时、24小时和72小时的动态变化。结果 AMI患者血清CK-MB和CK-MM在发病后6h开始升高,其中以CK-MB2和CK-MM3升高为主,MB2／MB1〉1．36,MM3／MM1〉0．7;12-24小时达峰值,CK-MB／CK〉30％。15例早期再灌注的AMI患者血清CK、CK-MB和CK-MM在72小时下降至正常,但6例无早期再灌注患者仍处于较高水平,其中MB2／MB1〉1．29,MM3／MM1〉0．65。结论 CK同工酶的亚型检测能反映AMI患者心肌组织损伤的动态过程,可作为一项较灵敏的生化指标,有助于诊断AMI心肌早期再灌注、梗死延迟或再梗死。     

Creatine kinase isoenzymes in human cerebrospinal fluid and brain

Extracts of normal brains obtained at autopsy and cerebrospinal fluid (CSF) from patients with global brain ischemia were analyzed for creatine kinase (CK; EC 2.7.3.2) isoenzymes. We used both qualitative and quantitative assays (electrophoresis and immunoinhibition). Brain extracts contained CK-BB isoenzyme and mitochondrial CK. In 54 CSF samples free of blood contamination and with total activities ranging from 7 to 2010 U/L (mean 202 U/L), virtually all of the CK activity was due to CK-BB, and none to CK-MM or CK-MB. We conclude that brain contains CK-BB and mitochondrial CK, but lacks CK-MM and CK-MB. After cardiac arrest, CK-BB is released into the CSF. Any CK-MM in the CSF is probably from blood contamination, in which case immunoinhibition with anti-CK-M antibodies accurately quantifies CK-BB.     

At what level of serum total creatine kinase activity can measurement of serum creatine kinase MB isoenzyme activity be omitted in suspected myocardial infarction?

The purpose of this study was to establish a discriminatory limit for serum total creatine kinase activity (CK activity) below which CK isoenzyme fractionation is unnecessary. We looked at 2610 serum samples from 1077 consecutive patients with suspected acute myocardial infraction (AMI). The CK activity was determined according to the Scandinavian recommended method. Isoenzymes of CK were separated by agarose gel electrophoresis, followed by fluorometric scanning. When the threshold for CK activity was 150 U/l, none of the samples had a creatine kinase MB isoenzyme activity (CK-MB activity) equal to or higher than 30 U/l (the diagnostic level), which has been found to differentiate between patients with AMI and those without AMI. Only 14 patients (1.3% of all patients investigated) had CK-MB activity peaks between 10 U/l (detection limit) and 30 U/l. Of these, AMI was only diagnosed in one. We recommend that CK-MB activity should be measured only when CK activity is higher than 150 U/l. This would make about 50% of all CK-MB measurements unnecessary.     

The levels of serum myoglobin in cardiac patients with elevated creatine kinase-MB and suspected acute myocardial infarction

A monoclonal antibody enzyme immunoinhibition assay was used to quantitate serial serum myoglobin (Mb) levels in 121 patients who had ?5% creatine kinase-MB (CK-MB) and suspected acute myocardial infarction (AMI). Serum Mb levels higher than 0.16 μg/ml were considered abnormal. In 94% of these patients who were finally diagnosed with AMI, Mb levels were higher than 0.16 μg/ml, whereas all 30 normal control blood donors had lower Mb levels. Patients with anterior or inferior wall infarcts had higher Mb levels (?0.64 μg/ml) than patients with lateral or subendocardial infarction. Only 68% (82/ 121) of patients evaluated by elevated CK-MB alone had a final diagnosis of AMI. In contrast, 94% (77/83) of patients who in addition showed elevated Mb had AMI. It is suggested that analysis of Mb levels allows a more accurate diagnosis of AMI in patients with elevated CK-MB than does reliance on CK-MB values alone. © 1993 Wiley-Liss, Inc.     

Mass concentration and activity concentration of creatine kinase isoenzyme MB compared in serum after acute myocardial infarction

We compared three current methods (immunoinhibition, "Isomune-CK" immunoprecipitation, and the Tandem-E CKMB II immunoenzymometric assay) for determination of creatine kinase (CK; EC 2.7.3.2) isoenzyme MB in serum. Although results inter-correlated well, the immunoinhibition assay gave higher activity values. Atypical CK forms did not interfere with the immunoprecipitation and immunoenzymometric methods. In acute myocardial infarction the catalytic properties of CK decreased with the enzyme's age, as reflected by a steady increase in activation energy of the catalyzed reaction. In septicemia patients with very low CK and CK-MB catalytic activity, mean CK-MB mass concentration exceeded the upper reference limit, suggesting an increased rate of loss of activity concentration in these patients' sera. Because of the assay's lesser susceptibility to conformational changes at the active site of the enzyme, we suggest that measurement of CK-MB mass concentration is better suited for infarct sizing than measurement of catalytic activity.