Comparison of serum myoglobin and creatine kinase MB isoenzyme in early diagnosis of acute myocardial infarction

We compared the clinical usefulness of serum myoglobin and creatine kinase MB (CK MB) isoenzyme determinations in the early diagnosis of acute myocardial infarction in 109 consecutive patients admitted to a coronary care unit. Of these, 37 patients were diagnosed as having definite infarction, three possible infarction, and 69 no infarction, using World Heath Organisation criteria. Blood samples were taken on admission and two to four hours later, Both CK MB and myoglobin were raised in the initial serum samples in 24 of the 37 patients with definite infarction. In an additional seven patients both CK MB and myoglobin were negative in the first specimen though both were detected in the second sample. In five patients CK MB preceded the appearance of myoglobin while in the remaining patient myoglobin appeared before CK MB. We conclude that the detection of serum myoglobin does not offer any clinical advantage over CK MG as an early indicator of myocardial infarction.     

Comparison of myoglobin, creatine kinase-MB, and cardiac troponin I for diagnosis of acute myocardial infarction

Serial plasma concentrations of myoglobin, creatine kinase MB (CK-MB) isoenzyme, and cardiac troponin I (cTnI) were measured in 25 patients with a confirmed diagnosis of acute myocardial infarction (AMI), and 74 patients who were suspected of AMI but were subsequently ruled out for this diagnosis. The cutoff concentration for the cTnI assay was optimally determined to be 2.5 ng/mL. Of the three markers, myoglobin had the highest clinical sensitivity (50 percent) when blood was collected between 0 to 6 h after the onset of chest pain. Assays for all serum markers used had high clinical sensitivity (> 93 percent) 6 to 24 h after onset. The CK-MB remained highly sensitive for 48 h, while cTnI was sensitive for up to 72 h. Between 72 and 150 h, cTnI had a clinical sensitivity of 70 percent as compared to 21 percent and 18 percent for myoglobin and CK-MB, respectively. The clinical specificity of cTnI for non-AMI patients was equivalent to CK-MB and significantly higher than for myoglobin. The clinical efficiency of cTnI for all samples was better than either CK-MB or myoglobin, owing mainly to the wider diagnostic window. The specificity of cTnI for 59 patients with chronic renal failure, skeletal muscle trauma and disease was better than all of these markers including cardiac troponin T (cTnT). Results of this study show that cTnI is an effective marker for the retrospective diagnosis of AMI, and consideration should be given to its use in place of CK-MB.     

Troponin T and creatinine kinase isoenzyme MB mass in the diagnosis of myocardial infarction

The aim of this study was to compare troponin T (TnT) and creatine kinase isoenzyme MB mass (CK-MBm) with conventional enzymes, ie CK, CK-MB activity and lactate dehydrogenase isoenzyme 1, in the diagnosis of myocardial infarction (MI). 624 patients (351 men and 273 women, median age 69 years) were admitted to hospital with suspicion of an acute coronary heart disease event. TnT was elevated (> 0.10 microg/L) in 100%, CK-MBm (> 5.0 microg/L) in 99%, and both markers in 99% of the 89 patients with the diagnosis of a definite MI according to modified FINMONICA criteria. In the 60 patients with the diagnosis of a probable MI, TnT was elevated in 65%, CK-MBm in 67% and both markers in 60%. In the patients with unstable coronary artery disease (unstable angina or prolonged chest pain attack) and conventional enzymes within normal limits, TnT was elevated in 14%, CK-MBm in 17% and both markers in 9%. The use of TnT and CK-MBm did not lead to a major change in the diagnostics of definite MI. However, TnT and CK-MBm did not confirm the diagnosis of probable MI in one-third of the events. These new markers revealed a myocardial injury in about 15% of those patients who had unstable coronary artery disease and conventional enzymes within normal limits.     

Analysis of creatine kinase, CK-MB, myoglobin, and troponin T time-activity curves for early assessment of coronary artery reperfusion after intravenous thrombolysis

BACKGROUND: Thrombolysis has become the standard therapeutic approach in patients with acute myocardial infarction. To identify patients who may benefit from early invasive procedures, reliable noninvasive assessment of success or failure of thrombolytic therapy is mandatory. METHODS AND RESULTS: In a prospective study in 63 consecutive patients undergoing thrombolysis for their first myocardial infarction, serial measurements of creatine kinase (CK), its isoenzyme CK-MB, myoglobin, and troponin T were done to determine their value for noninvasive prediction of coronary artery patency. Blood samples were drawn every 15 minutes during the first 90 minutes, every 30 minutes during the first 4 hours, every 4 hours during the first 24 hours, and every 8 hours during the first 72 hours. The perfusion status of the infarct-related artery was assessed angiographically 90 minutes after initiation of thrombolysis. For each marker, time to its peak concentration and its early initial slope (start of thrombolysis to 90 minutes thereafter) were determined. Areas under receiver operator characteristic (ROC) curves were 0.83, 0.76, 0.82, and 0.80 for maxima of CK, CK-MB, myoglobin, and troponin T, respectively (p = NS by univariate Z test). The corresponding values for early slopes of CK, CK-MB, myoglobin, and troponin T were 0.79, 0.82, 0.89, and 0.80 (p = 0.23 for comparison between myoglobin and CK-MB; p = 0.07 between myoglobin and CK). Sensitivity, specificity, and positive and negative predictive values regarding noninvasive prediction of coronary artery patency after 90 minutes were 80%, 82%, 95%, and 61% for time to CK maximum; 91%, 77%, 91%, and 77% for time to myoglobin maximum; 87%, 71%, 89%, and 67% for early CK slope; and 94%, 88%, 94%, and 82% for myoglobin slope, respectively. When myoglobin slope was assessed together with other clinical reperfusion markers (resolution of chest pain or ST segment elevation, occurrence of reperfusion arrhythmias) by logistic regression analysis, only the myoglobin slope was an independent predictor of coronary artery patency (p < 0.0001). CONCLUSIONS: With regard to noninvasive prediction of coronary artery patency after thrombolytic therapy, measurement of the early initial slopes of the serum markers within only 90 minutes after the initiation of therapy is as accurate as the determination of the time to their peak concentration. Compared with the other markers examined, myoglobin appears to have advantages because of its earlier rise, yielding a better negative predictive value and a higher area under the ROC curve for determination of its early initial slopes.     

Cardiac troponin I and minor cardiac damage: biochemical markers in a clinical model of myocardial lesions

Radiofrequency (RF) catheter ablation is the curative treatment of choice for many cardiac arrhythmias. After RF ablation there is always a small localized endomyocardial necrosis, necessary to abolish the arrhythmia. We designed this study to determine the serum concentrations of several cardiac markers in patients who underwent RF catheter ablation. The study shows a higher frequency of increase of serum cardiac troponin I (cTnI) than of creatine kinase (CK), the CK MB isoenzyme (CK-MB), or myoglobin. A pathological value of cTnI was found in 47 of 51 patients (92%) in the ablation group. The area under the ROC curve for cTnI was 0.9375, significantly higher than for the other biochemical markers (0.86, 0.76, and 0.75 for CK-MB, myoglobin, and CK, respectively), with P <0.05. We conclude that the serum concentration of cTnI is the best biochemical marker for detecting the minor myocardial damage produced by RF ablation.     

Comparative sensitivities and specificities of the mass measurements of CK-MB2, CK-MB, and myoglobin for diagnosing acute myocardial infarction

We evaluated the clinical utility of the mass measurement of the tissue isoform of creatine kinase MB isoenzyme (CK-MB2) in the diagnosis of an acute myocardial infarction (AMI) by determining its sensitivity, specificity, and predictive value relative to those of CK-MB mass and myoglobin. Samples were obtained at 0, 4, 8, and 16 h postpresentation from 100 patients (41% with AMI). The order of sensitivity for the sample proportions taken at 0-2 h from the onset of symptoms was myoglobin > CK-MB2 > CK-MB. At all other time points, the sensitivity of CK-MB2 either equaled or surpassed that of both CK-MB and myoglobin, although the 95% confidence intervals for the population proportions each of these markers overlapped. Of the 41 AMI patients, 31 (76%) exhibited concurrent abnormal increases of CK-MB and %CK-MB2; the other 10 (24%; 8 non-Q wave, 2 Q wave) exhibited abnormal values for %CK-MB2 before their CK-MB exceeded the upper limit of normal. The specificity of myoglobin was statistically lower than that for either CK-MB2 or CK-MB at all time points.     

Levels of CK MB mass in patients with acute myocardial infarct treatedwith fibrinolysis. Comparison with levels of CK, CKMB, CKMB mass and troponin T in the diagnosis of coronary ischemia]

In a group of 26 patients with AIM the CKMB value was raised above the discrimination level already on admission--on average 2.7 +/- 1.4 hours after development of ischaemic pain--in 46% patients. The maximal value of CKMB mass was achieved in the group with probable reperfusion 12.1 +/- 3.8 hours after the development of ischaemic pain and this value was elevated in relation to the discrimination value 41.5 +/- 17x and in relation to the so-called basal value 145 +/- 117x. In the group without probable reperfusion the maximal value was achieved significantly later, after 19.8 +/- hours and was elevated in relation to the discrimination value 31 +/- 17x and in relation to the final value 84 +/- 42 times. The value of CKMB mass increased above the discrimination limit from the onset of ischaemic pain after 4.0 +/- 1.5 and after 5.7 +/- 3 hours in the group with probable and without probable reperfusion and declined below the discrimination limit after 00 +/- 60 and 119 +/- 98.0 hours in the same groups. On comparison of CK, CKBM, CKBM mass and troponin T on admission the CKMB mass value was elevated in 46% patients, the value of CK in 23%, of CKMB in 27% and the troponin T value in 96% patients. With regard to the assembled experience that haemolytic serum raises false troponin T values, the percentage of elevated troponin T values on admission declines from the original 96% to 81% when all haemolytic samples are eliminated. The time of reaching maximal values of CKMB mass in patients with AIM and probable reperfusion was significantly shorter than in CK values and is similar as in CKMB values. The time taken to raise the CKBMB mass value above the discrimination value is significantly shorter than the time taken by CK levels, but significantly longer than the time before troponin T levels are raised. The time of total elevation of CKMB mass levels above the discrimination limit does not differ from the time taken to raise CK values, it is however shorter than the increase of troponin T values, although the exact time of persistence of raised levels of troponin T was not assessed in our work. The time of increase above and decrease below the discrimination limit was not assessed in CKMB values. Based on mutual comparison of the impact of indicators for assessment of the diagnosis of ischaemic heart attacks the authors consider it best regardless of financial costs--to assess troponin T, possibly along with levels of CKMB mass.