Creatine kinase-MB Mass Concentration Research Articles

SERUM cardiac-specific biomarkers and atrial fibrillation in myotonic dystrophy type I.

The aim of the present study was to evaluate the role of high-sensitivity cardiac troponin I, N terminal pro-B-type natriuretic peptide (NT-proBNP), creatine kinase-MB mass concentration (CK-MB mass) and copeptin (CP) in predicting incident atrial fibrillation (AF) in myotonic dystrophy type 1 (DM1) patients. The study enrolled 60 consecutive DM1 patients (age 50.3 ± 7.3 years, 34 male) who underwent pacemaker (PM) implantation for cardiac rhythm abnormalities and 60 PM recipients whose age and sex matched served as control group. All DM1 patients underwent a 12-lead electrocardiogram, 2D color Doppler echocardiogram, biomarkers measurements and device interrogation at implantation, 1 month after and every 6 months thereafter for a minimum of 2-year follow-up. The study population was divided into two groups according to the presence of AF (AF group vs non-AF group). The AF group was older (47.3 ± 8 vs 38.6 ± 7 years, P = .03) and showed higher serum levels of NT-proBNP (151 ± 38.4 vs 107.3 ± 24.2 pg/mL, P < .001) and CP (18.9 ± 4.5 vs 7 ± 2.3 P < .001) than non-AF Group. NT-proBNP (P < .001) and CP (P < .001) were found to be an independent predictor of AF. Based on the receiver-operating characteristics curve analysis, the cut-off value for NT-proBNP that best predicted AF event in DM1 patients was 123 pg/ml (sensitivity of 83.3% and specificity of 86.5%); the cut-off value for CP that best predicted AF event in DM1 patients was 9 pmol/L (sensitivity of 89% and specificity of 87%). NT-proBNP and CP represent two independent predictors of AF onset in DM1 population with conduction disturbances underwent PM implantation.

Effects of defibrillation shock in patients implanted with a subcutaneous defibrillator: a biomarker study.

AimsImplantable cardioverter defibrillator (ICD) shocks are associated with a subsequent increased risk of death, and an elevation of cardiac enzymes has been measured after defibrillation testing (DFT). In an experimental swine study, subcutaneous ICD (S-ICD) shocks caused less myocardial damage than traditional ICD shocks. The aim of our study was to investigate the association between S-ICD shock and acute cardiac damage in humans, as evaluated by means of sensitive and highly specific circulating biomarkers.Methods and resultsWe calculated the variation in the serum levels of high-sensitivity cardiac troponin I (hs-CTnI) and creatine kinase-MB mass concentration (CK-MB mass), measured before and after an S-ICD shock delivered during intraoperative DFT. We also measured the degree of haemodynamic stress, as the variation in the serum levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP) and copeptin (CP), after the S-ICD shock. We analysed 30 consecutive patients who received an S-ICD and who underwent DFT by means of a single 65 J shock. The levels of biomarkers did not change from baseline to 1 h post-shock, i.e. hs-CTnI (from 0.029 ± 0.005 ng/mL to 0.030 ± 0.005 ng/mL, P = 0.079) and CK-MB mass (from 1.37 ± 0.17 ng/mL to 1.41 ± 0.18, P = 0.080) and remained stable 6 and 24 h after DFT. The plasma NT-proBNP did not change, whereas CP levels were significantly higher at 1 h post-shock evaluation. However, 6 h after DFT, the levels had returned to the baseline and remained stable at 24 h.ConclusionThe S-ICD shock did not seem to cause myocardial injuries. Although CP levels temporarily rose after DFT, they returned to basal levels within 6 h, which suggests that DFT does not have long-term prognostic implications. ICD shocks are associated with a subsequent increased risk of death, and an elevation of cardiac enzymes has been measured after DFT. We showed that serum levels of biomarkers of myocardial damage did not increase after high-energy DFT in patients who had undergone S-ICD device implantation. This suggests that S-ICD shock does not have long-term prognostic implications.

Cardiac Troponin T Levels for Risk Stratification in Pediatric Open Heart Surgery

Cardiac troponin T has been found to be accurate predictor of complications and adverse clinical events after pediatric cardiac surgery. Contrary to adult cardiac surgery, the relationship of troponin T to patient survival after pediatric heart surgery has not been previously studied. The purpose of this study was to determine whether troponin T could predict death after pediatric open cardiac surgery. This was a retrospective cohort study in which data from 1001 consecutive children having cardiac surgery during a 5-year period were studied. Perioperative variables that could influence death at 30 postoperative days were evaluated. Multivariate analysis, using a forward stepwise logistic regression, showed that troponin T measured on the first postoperative day was a strong independent predictor of death at 30 days. Level of troponin T greater than 5.9 microg/L on the first postoperative day predicted death (odds ratio, 10.7; 95% confidence interval: 5.2 to 22.1) as did admission lactate level greater than 5.2 mmol/L (odds ratio, 22.2; 95% confidence interval: 9.7 to 50.8) No other variable, including postoperative creatine kinase-MB mass concentration, age, diagnosis, surgical procedure, presence of cyanosis, chromosomal anomaly or ventriculotomy, duration of cardiopulmonary bypass, or aortic cross-clamp, had any independent effect on 30-day survival. Cardiac troponin T level on the first postoperative day is a powerful independent risk marker of death in pediatric cardiac surgery.

Elevated cardiac troponin T in peritoneal dialysis patients is associated with CRP and predicts all-cause mortality and cardiac death.

Cardiac troponin T (cTnT) is a highly sensitive and specific marker of myocardial damage. In sera from patients with end-stage renal disease, cTnT may be elevated without other signs of acute myocardial injury. It has been shown that elevated cTnT in haemodialysis patients is associated with poor prognostic outcome. The aim of the present study was to test the hypothesis that elevated cTnT in a single serum sample from peritoneal dialysis (PD) patients is of prognostic importance. Blood samples were taken from 26 randomly selected PD patients without signs of acute myocardial ischaemia. Sera were analysed for: cTnT with the second generation TnT ELISA on ES 300; cardiac troponin I (cTnI) with Opus Plus; and for creatine kinase-MB (CKMB) mass and C-reactive protein (CRP). After 4 years, clinical outcomes were evaluated by chart review. The influence on survival was tested with Kaplan-Meier analysis and Cox's proportional regression analysis. Concentrations of cTnT >/=0.04 micro g/l and CRP >/=10 mg/l were strong predictors of all-cause mortality in univariate analysis. Twelve out of 14 patients with cTnT >/=0.04 micro g/l died compared with three out of 12 with cTnT <0.04 micro g/l. Other factors that influenced survival were age and the presence of ischaemic heart disease (IHD). There was a significant positive correlation between cTnT and CRP, and between cTnT and age. Cardiac troponin T was an independent predictor compared with age but not compared with CRP and IHD. Neither cTnI nor CKMB mass concentrations were related to survival. Elevated serum concentrations of cTnT significantly predicted poor outcome and there was a correlation between cTnT and CRP concentrations in samples from PD patients. Cardiac troponin I and CKMB mass had no prognostic value.

Markers of myocardial ischemia after minimally invasive and conventional coronary operation

Background. The purpose of this study was to evaluate the course of serum markers of myocardial tissue damage after two different types of minimally invasive coronary surgical procedures (MICS) as compared with conventional coronary artery bypass grafting (CABG). Methods. We enrolled 87 patients with one- or two- vessel disease scheduled for one of the three procedures: minimally invasive direct coronary artery bypass grafting (MIDCABG) by lateral thoracotomy (n = 29), the OCTOPUS method by median sternotomy (n = 27), and CABG (n = 31). Creatine kinase activity (CK), creatine kinase MB activity (CK-MB act), creatine kinase MB mass concentration (CK-MB mass), myoglobin concentration (MG), and cardiac troponin I concentration (cTnI) were measured perioperatively until the second postoperative day. Results. Creatine kinase-MB, CK-MB mass, and cTnI were significantly higher after CABG and were nearly maintained within the normal range in MICS. Creatine kinase and MG were significantly lower in the OCTOPUS group than in the MIDCABG or CABG groups. Conclusions. Minimally invasive coronary surgical procedures cause less myocardial injury than CABG as indicated by specific serum markers. However, higher CK and MG reflect more substantial skeletal muscle trauma during MIDCABG operation compared with Octopus procedures.

Myocardial damage after minimally invasive coronary artery bypass grafting on the beating heart

Background. In conventional coronary artery bypass grafting, the rate of perioperative myocardial infarction is reported in the 2% to 6% range; however, significantly higher rates are observed if sensitive myocardial marker proteins are used to detect perioperative myocardial damage. For minimally invasive direct coronary artery bypass grafting, few data are available concerning myocardial marker protein release. Methods. Fifteen consecutive patients (11 male, 4 female; mean age, 59.6 ± 8.5 years) received minimally invasive direct coronary artery bypass grafting procedures via minithoracotomy on the beating heart. Electrocardiography and transesophageal and transthoracic echocardiography as well as determination of creatine kinase-MB mass concentration and cardiac troponin I level were used for ischemic monitoring. Results. One patient had a perioperative myocardial infarction according to standard criteria and died despite mechanical circulatory support. Determination of cardiac troponin I level showed small but definitive ischemic damage in 4 of 9 patients (44%) who presented transient ischemic signs intraoperatively or postoperatively. In 2 of these 4 patients pathologic findings could be detected on angiographic restudies. Conclusions. Subclinical myocardial injury is a common event in minimally invasive coronary artery bypass grafting on the beating heart. Cardiac troponin I could serve as an adequate diagnostic tool for diagnosis of perioperative myocardial infarction in minimally invasive direct coronary artery bypass grafting.

Cardiac markers in the early hours of acute myocardial infarction: clinical performance of creatine kinase, creatine kinase MB isoenzyme (activity and mass concentration), creatine kinase MM and MB subform ratios, myoglobin and cardiac troponin T.

We compared early markers of acute myocardial infarction (AMI) in the first 6 h from the onset of symptoms in 133 non-traumatized patients arriving at the emergency department with chest pain suggestive of AMI. Clinical performance parameters were calculated on the basis of 45 patients with AMI and 88 patients with a non-AMI diagnosis. At admission and in the first 0-3 h after the onset of chest pain the creatine kinase-MB (CK-MB) subform ratio was the most sensitive test at a comparable specificity level of 0.95. In the time interval of 3-5 h, myoglobin, the CK-MB mass concentration and the CK-MB subform ratio were associated with the greatest areas under receiver operating characteristic (ROC) curves, but differences between these tests were small and non-significant. At 6 h from the onset of pain, differences in clinical performance between the same three tests were even smaller whether or not samples drawn after the start of thrombolytic treatment were included in the test comparison. For confirmation of AMI at 6 h after onset of pain, CK-MB (activity and mass concentration) demonstrated the highest positive likelihood ratio, and for exclusion of AMI at 6 h the CK-MB subform ratio was associated with the highest negative likelihood ratio. However, differences between the CK-MB subform ratio, CK-MB mass concentration and myoglobin were not significant as estimated by the substantial overlap between the confidence intervals of the likelihood ratios and the ROC areas at 6 h. Cardiac troponin T (cTnT) demonstrated an ROC area equal to the CK-MB isoform ratio and myoglobin at 6 h. However, the likelihood ratio for ruling out AMI was lower, mostly due to the elevated cTnT in unstable coronary disease not defined as AMI. We conclude that the CK-MB subform ratio, CK-MB mass concentration and myoglobin do not demonstrate any significant differences in clinical performance for ruling in or ruling out acute myocardial infarction at 6 h after the onset of chest pain.

A Decision Tree for the Early Diagnosis of Acute Myocardial Infarction in Nontraumatic Chest Pain Patients at Hospital Admission

To find an accurate algorithm for the diagnosis of acute myocardial infarction in nontraumatic chest pain patients on presentation to the emergency department. In a prospective clinical study, we compared the diagnostic performances of clinical symptoms, presenting ECG, creatinine kinase, creatine kinase MB activity and mass concentration, myoglobin, and cardiac troponin T test results of hospital admission blood samples. By classification and regression trees, a decision tree for the diagnosis of acute myocardial infarction was developed. Emergency room of a Department of Internal Medicine (University Hospital). One hundred fourteen nontraumatic chest pain patients (median delay from onset of chest pain to hospital admission, 3 h; range, 0.33 to 22): 26 Q-wave and 19 non-Q-wave myocardial infarctions, 49 patients with unstable angina pectoris, and 20 patients with chest pain caused by other diseases. Of each parameter taken by itself, the ECG was tendentiously most informative (areas under receiver operating characteristic plots: 0.87 +/- 0.04 [ECG], 0.80 +/- 0.08 [myoglobin], 0.80 +/- 0.04 [creatine kinase MB mass], 0.77 +/- 0.04 [creatine kinase activity], 0.69 +/- 0.06 [clinical symptoms] 0.67 +/- 0.06 [creatine kinase MB activity], 0.67 +/- 0.05 [troponin T]). In patients presenting 3 h or less after the onset of chest pain, ECG signs of acute transmural myocardial ischemia were the best discriminator between patients with and without myocardial infarction. In patients presenting more than 3 h, however, creatine kinase MB mass concentrations (discriminator value, 6.7 micrograms/L) were superior to the ECG, clinical symptoms, and all other biochemical markers tested. This algorithm for diagnosing acute myocardial infarction was superior to each parameter by itself and was characterized by 0.91 sensitivity, a 0.90 specificity, a 0.90 positive and negative predictive value, and a 0.90 efficiency. We found an algorithm that could accurately separate the myocardial infarction patients from the others on admission to the emergency department. Therefore, this classifier could be a valuable diagnostic aid for rapid confirmation of a suspected myocardial infarction.

Cardiac troponin T and creatine kinase MB mass concentrations in children receiving anthracycline chemotherapy

Anthracyclines (doxorubicin, daunorubicin, and derivatives) are among the most effective antineoplastic drugs for pediatric cancer with dose-limiting acute and long-term cardiotoxicity. The exact mechanism of the development of cardiomyopathy is still not clear. Anthracyclines may induce subclinical acute myocardial injury leading to lysis of a limited number of myocytes. Alternatively, myocytes may experience a transient loss of cytoplasmic membrane integrity. Both conditions may lead to a transient efflux of small amounts of cytoplasmic enzymes and other proteins specific to the heart muscle fibers. To test these hypotheses we assayed plasma creatine kinase (CK) MB mass and cardiac specific troponin T (TnT). CKMB may be released even in case of reversible cell membrane injury, while prolonged elevation of TnT is the most sensitive and specific marker of limited myocardial necrosis. Thirty-five anthracycline-containing chemotherapy courses in 22 children with cancer were analyzed. CKMB mass and TnT concentrations were within the normal range in all children before anthracycline therapy. Within 72 hours from anthracycline therapy no increment of one of these two marker proteins was detected (ANOVA for repeated measures, P = 0.94 [TnT] and 0.25 [CKMB]). We conclude that only minimal if any acute necroses of cardiac myocytes occur after anthracycline therapy. Even membrane integrity appears to be maintained within the first 3 days after anthracycline therapy, in the absence of electrocardiographic or echocardiographic signs of acute cardiotoxicity.

Exclusion of acute myocardial infarction. The value of measuring creatine kinase slope.

For the exclusion (and diagnosis) of acute myocardial infarction, we studied timed sequential (slope) measurements of creatine kinase and creatine kinase-MB catalytic activity concentration, creatine kinase-MB mass concentration, troponin T and myoglobin, using data from 242 patients consecutively admitted for evaluation of suspected acute myocardial infarction in the 12 hours before admission. Three biochemical strategies based on measurements in two consecutive samples obtained within 12 hours after admission were evaluated. The highest sensitivities were encountered for a biochemical strategy based on the sole measurement of creatine kinase mass concentration (98%) or troponin T (96%) and a strategy based on measurements of creatine kinase activity concentrations, which includes creatine kinase slope calculation and measurement of creatine kinase mass concentration (95%). Both strategies were applied in subgroups of patients based on the electrocardiographic findings. In patients with a normal electrocardiogram, the sensitivity of the strategy using sole measurements of creatine kinase mass concentration was 100%, but this was true for the strategy based on creatine kinase slope measurements, which is the cheaper and therefore preferred procedure for excluding myocardial infarction. This approach, however, does not account for detecting minor myocardial cell damage in patients not yet fulfilling the criteria of the World Health Organization for diagnosing acute myocardial infarction.

Contribution of creatine kinase MB mass concentration at admission to early diagnosis of acute myocardial infarction.

To assess the diagnostic value at admission of creatine kinase MB mass concentration, alone or in combination with electrocardiographic changes, in suspected myocardial infarction. Prospective study of all consecutive patients admitted within 12 hours after onset of chest pain to a coronary care unit for evaluation of suspected myocardial infarction. Large regional hospital. In 297 patients creatine kinase and creatine kinase MB activities and creatine kinase MB mass concentration were determined. Myocardial infarction according to the criteria of the World Health Organisation was diagnosed in 154 patients and excluded in 143 patients (including 70 with unstable angina pectoris). Sensitivity/specificity for creatine kinase MB mass concentration in patients admitted within 4 hours and 4-12 hours after onset of chest pain were 45%/94% and 76%/79% respectively. Corresponding values for creatine kinase activity were 20%/89% and 59%/83%, and for creatine kinase MB activity 16%/87% and 53%/87%. Raised creatine kinase MB mass concentration was seen in 17% of patients with unstable angina pectoris. Stepwise logistic regression analysis showed that independent predictors of acute myocardial infarction in patients admitted within 4 hours after onset of chest pain were electrocardiographic changes and creatine kinase MB mass concentration on admission; in patients admitted 4-12 hours after the onset of pain independent predictors were electrocardiographic changes and creatine kinase MB mass concentration and activity. Creatine kinase MB mass concentration is a more sensitive marker for myocardial infarction than the activity of creatine kinase and its MB isoenzyme. Electrocardiographic changes on admission in combination with creatine kinase MB mass concentration (instead of creatine kinase and creatine kinase MB activities) are best in diagnosing myocardial infarction.

Early release of glycogen phosphorylase in patients with unstable angina and transient ST-T alterations.

To determine whether transient ST-T alterations in patients with unstable angina are associated with an increase in plasma glycogen phosphorylase BB concentrations on admission to hospital. Prospective screening of patients with unstable angina for markers of myocardial cell damage. Accident and emergency department of university hospital. 48 consecutive patients admitted for angina pectoris (18 with transient ST-T alterations). None of the patients had acute myocardial infarction according to standard criteria. Creatine kinase and creatine kinase MB activities, creatine kinase MB mass concentration, and myoglobin, cardiac troponin T, and glycogen phosphorylase BB concentrations on admission. All variables except for creatine kinase and creatine kinase MB activities were significantly higher on admission in patients with unstable angina and transient ST-T alterations than in patients without. However, glycogen phosphorylase BB concentration was the only marker that was significantly (p = 0.0001) increased above its discriminator value in most patients (16). In the 18 patients with transient ST-T alterations creatine kinase MB mass concentration and troponin T and myoglobin concentrations were significantly (p = 0.0001) less commonly increased on admission (in five, three, and two patients, respectively). The early release of glycogen phosphorylase BB may help to identify high risk patients with unstable angina even on admission to an emergency department. Glycogen phosphorylase BB concentrations could help to guide decisions about patient management.

Immunoreactive creatine kinase-MB and creatine kinase isozyme concentrations during treatment of hypothyroid patients.

Using a highly sensitive enzyme immunoassay (EIA) system, we determined creatine kinase isozymes, namely creatine kinase-MB and creatine kinase-MM, in sera of patients suffering from primary hypothyroidism with concomitant signs of myocardial affections before and during treatment. After oral administration of L-thyroxine, the augmented mass concentrations of serum creatine kinase-MB and creatine kinase-MM, and the increased catalytic activity concentrations of serum total creatine kinase and creatine kinase-MB gradually decreased in inverse proportion to the increased concentrations of serum triiodothyronine (T3) and thyroxine (T4). By the 6th to 8th week after treatment, the elevated levels of serum total creatine kinase and creatine kinase-MB catalytic activity concentrations (assayed by a routine method) and serum creatine kinase-MM mass concentrations (assayed by EIA) declined to normal values, while serum T3, T4, and thyroid stimulating hormone attained normal values. Serum creatine kinase-MB mass concentrations (assayed by EIA), however, still remained at the higher level, without complete recovery from myocardial damage, as shown by electrocardiogram (ECG). These data indicate that metabolic distortion still exists in the myocardium, as revealed by the high creatine kinase-MB mass concentration, especially as assayed by EIA, even though the plasma levels of thyroid hormones had returned to normal.

Failure of new biochemical markers to exclude acute myocardial infarction at admission

Summary In a substantial proportion of patients with suspected myocardial infarction, biochemical markers are needed for clinical decision-making at the time of admission, because electrocardiographic (ECG) recordings are inconclusive. We have assessed the usefulness for exclusion of myocardial infarction at admission of the newer markers creatine kinase MB (CK-MB) mass concentration, troponin T, and myoglobin in comparison with the routinely used markers creatine kinase (CK) and CK-MB activity. 290 consecutive patients were enrolled. Acute myocardial infarction was diagnosed on the basis of clinical history, ECG criteria, and time-dependent changes in CK and CK-MB activity. 153 patients had definite acute myocardial infarction. Troponin T had the highest sensitivity for prediction of acute myocardial infarction; high concentrations (above the upper reference limits) were found in 98 (64%) of the patients with infarctions compared with 92 (60%) for CK-MB mass concentration, 76 (50%) for myoglobin, 61 (40%) for CK activity, and 53 (35%) for CK-MB activity. However, troponin T also had the highest "false-positive" rate; of 137 patients without myocardial infarction, 36 (26%) had high troponin T concentrations. Sensitivity, specificity, and positive and negative predictive values were calculated in relation to time between onset of chest pain and hospital admission. Although CK-MB mass concentration was, by a small margin, the best marker in patients admitted within 8-10 h of onset of chest pain, all the markers had negative predictive values too low to allow exclusion of acute myocardial infarction at admission in patients with symptoms suggestive of myocardial infarction of less than 10 h duration.

Plasma immunoreactive endothelin in the acute and subacute phases of myocardial infarction in patients undergoing fibrinolysis

Endothelin is a potent vasoconstrictor of coronary arteries. We measured plasma concentrations of immunoreactive endothelin (irET) in 46 patients with confirmed acute myocardial infarction (AMI). When compared with irET concentrations in healthy individuals who served as controls, irET concentrations in patients were already significantly elevated at the time of admission (P = 0.002) and remained significantly elevated for at least 2 days after AMI (P < 0.01). IrET concentrations peaked 1 h (mean) after admission (8.5 +/- 3.9 ng/L, P = 0.02 compared with values at time of admission). Reperfusion of the infarct-related artery markedly influenced irET release. Before the start of thrombolytic therapy, irET concentration in patients with early reperfusion did not differ significantly from that of those without early reperfusion. However, irET time courses were significantly (P = 0.03 by analysis of variance) different in patients who did and did not have early reperfusion. In the latter, peak irET concentrations correlated closely with the angiographic left ventricular ejection fraction (r = -0.71, P = 0.03), maximum creatine kinase MB mass concentrations (r = 0.69, P = 0.01), and creatine kinase activities (r = 0.59, P = 0.03). Reflow and reversion of myocardial ischemia are associated with a reduced irET release in patients with AMI.

Does Low Total Creatine Kinase Rule Out Myocardial Infarction?

Letters15 March 1992Does Low Total Creatine Kinase Rule Out Myocardial Infarction?Laura Bilodeau, MD, Lynne M. Preese, MBA, Fred S. Apple, PhDLaura Bilodeau, MDSearch for more papers by this author, Lynne M. Preese, MBASearch for more papers by this author, Fred S. Apple, PhDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-116-6-523_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editors: Serial creatine kinase and creatine kinase-MB measurements with clinical history findings, physical examination findings, and electrocardiographic (ECG) changes are the standards for diagnosing acute myocardial infarction (1, 2). Whether creatine kinase-MB measurements should be quantified when total creatine kinase activity never rises above the upper limit of the normal range is unclear (3, 4). We wondered whether there truly was an upper limit of the normal range for creatine kinase-MB measurements and whether percent relative index (creatine kinase-MB mass concentration/ total creatine kinase activity) might misdiagnose acute myocardial infarction when the total creatine kinase activity is normal....