Improved detection of minor ischemic myocardial injury with measurement of serum cardiac troponin I

This study compared the diagnostic accuracy of the measurement of serum cardiac troponin I (cTnI) with creatine kinase (CK) MB mass in patients with minor myocardial injury whose measured total CK activity did not exceed twice the upper reference limit (300 U/L for men; 200 U/L for women). Forty-eight consecutive patients presenting with chest pain and with in-hospital documentation of myocardial injury were enrolled. Electrocardiogram, echocardiogram, and serial serum CK-MB mass, cTnI, and total CK were measured over 36 h after admission. Peak total CK activity was within normal limits in 28 patients (58%). The mean (+/- SD) peak CK-MB mass and cTnI concentrations were: 16.4 (11.8) micrograms/L and 132 (13.0) micrograms/L; respectively. The peak biochemical marker index (defined as CK-MB or cTnI divided by its respective upper reference limit) was significantly (P < 0.05) higher for cTnI than for CK-MB from 7 to 36 h. The clinical sensitivity for detection of myocardial injury for cTnI was 100% [95% confidence interval (CI): 87.2% to 100%], compared with 81.8% (CI: 67.3% to 91.8%) for CK-MB. Thus, cTnI was more sensitive than CK-MB mass for detection of myocardial injury in patients with small increases of total CK.     

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.     

Myoglobin in the early evaluation of acute chest pain

Two thirds of patients hospitalized to rule out acute myocardial infarction (AMI) are eventually found to have a non-AMI diagnosis, whereas 2% to 8% of patients with AMI are inappropriately discharged from the emergency department. Myoglobin has been shown to increase within 2 to 3 hours of myocardial injury. This study evaluates the usefulness of myoglobin in acute chest pain. Serial blood samples were obtained from 89 suspected AMI patients evaluated in the emergency department. Testing included creatine kinase (CK), a creatine kinase isoenzyme (CK-MB), and myoglobin. Twenty five of 89 patients (28%) had a diagnosis of AMI. The sensitivity of myoglobin for the detection of AMI was 56% at the time of admission and 100% 2 hours after admission. Thirteen of 25 AMI patients (52%) had a positive myoglobin before increases in CK or CK-MB, including one patient discharged from the emergency department. More importantly, the negative predictive value for myoglobin at the time of admission was 83% and was 100% two hours after admission. This potential for 100% predictability in excluding AMI by the use of serial myoglobin determinations will be very helpful in the correct triage of patients presenting with acute chest pain.     

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.     

Value of mass dosage of the MB isoenzyme of creatinine phosphokinase in the diagnosis of recent myocardial infarction

In 391 patients admitted 3.7 hours (h) (median) after experiencing infarct-like pain, kinetic monitoring of CK-MB "mass" (threshold: 7 micrograms/l), myoglobin (threshold: 90 micrograms/l) and total CK (threshold: 290 micrograms/l) was carried out at the time of admission and after 1.5, 3, 6, 9, 12, 24 and 48 h. When myocardial infarction (MI) was treated conventionally (102 patients). CK-MB peaked 11 h (median) after the onset of pain, later than myoglobin (9 h), but before total CK (12 h). The peak of the markers was higher in Q+ than in Q-MI (p < 0.05). When MI was treated by thrombolytic medications (44 patients), the increases in CK-MB, myoglobin and total CK were larger, and occurred sooner (peaks 9, 6 and 6 h, after the onset of pain respectively), but did not last as long. In 245 patients who had not had MI (including 123 with spontaneous angina), the levels of the three markers remained stable and well below the decision thresholds. The sensitivities of CK-MB, myoglobin and total CK were respectively 47.1, 51.8 and 34.8% at the time of admission, 67.3, 82.7 and 57.1% after 3 h and 83.1, 76.9 and 88.9% after 6 h. The combined determination of CK-MB and of myoglobin had a higher sensitivity (67.7% at the time of admission, 84.9% after 1.5% and 88.2% after 3 h: but most of this gain was due to myoglobin. The specificity of the three markers and their diagnostic accuracy are comparable. In the course of recent MI, the kinetics of CK-MB mass are thus slower than those of myoglobin, but a little faster than those of total CK. The choice of the most effective biochemical marker depends upon the interval between onset of chest pain and hospitalization of the patient. Repetition of the determinations improves the diagnostic situation.     

Normal frontal perfusion in patients with frozen gait

With the aim to compare the diagnostic efficacy as regards acute myocardial infarction of two rapid dry-strip tests, one with both creatine kinase MB (CK-MB) and myoglobin (C + M) and the other with troponin T, and to test the reliability of bedside diagnosis by the coronary care unit (CCU) nurse, 151 patients with acute chest pain admitted to the CCU were investigated. There was no difference in diagnostic performance between rapid tests and quantitative determinations. With <6-hour duration of symptoms, the sensitivity was better for C + M than for troponin T (72% vs 33%, p < 0.05). With symptoms lasting >12 hours on arrival, troponin T performed better, with 100% sensitivity and a negative predictive value of 100% in the 6-hour retest. For exclusion of damage, the two tests have similar and reliable diagnostic capacities 12 hours after the onset of symptoms. The bedside diagnosis or exclusion of acute myocardial infarction was carried out rapidly (within 20 minutes) and reliably by the CCU nurses.     

Plasma MB creatine kinase activity and other conventional enzymes. Comparison in patients with chest pain and tachyarrhythmias

We studied 67 patients with tachycardia and chest pain admitted with suspected myocardial infarction; 29 had myocardial infarction (20 transmural, nine subendocardial) with elevated MB creatine kinase (CK) activity, as well as elevated total CK and lactate dehydrogenase (LDH) levels. However, hydroxybutyric dehydrogenase and SGOT activity remained normal in three and four patients, respectively. Despite abnormal ECGs in 84% and typical chest pain in 54%, 38 patients had normal MB CK activity. However, 15 of them had elevated MM CK levels, presumably due to release from skeletal muscle. In total, 29 patients had elevated activity of MM, CK, LDH, or SGOT, but 72% of these patients had cardiac failure, hypotension, or skeletal muscle trauma due to cardioversion. Eleven patients with normal MB CK had elevated hydroxybutyric dehydrogenase activity. Despite elevated activity of other enzymes, MB CK remained normal. Thus, elevated plasma MB CK activity appears to remain a good diagnostic marker of myocardial necrosis in patients with tachyarrhythmias.     

Myocardial infarct extension: incidence and relationship to survival

Myocardial infarct extension, defined as reelevation or reappearance of creatine phosphokinase-MB (CK-MB) 48 hours after the onset of symptoms, was evaluated prospectively in 56 consecutive patients with acute myocardial infarction. Myocardial infarct extension occurred in eight patients (14%). The sensitivity, specificity and predictive accuracy in the diagnosis of myocardial infarct extension were 63%, 85% and 42%, respectively, for recurrent chest pain requiring morphine; 50%, 65% and 19% for recurrent ST-segment elevation on routine 12-lead ECGs; and 88%, 63% and 28% for reelevation of total CK. Three of the eight episodes of extension were clinically silent. Four of eight patients (50%) with extension died, compared with one of 46 patients (2%) without extension (p = 0.0009). CK-MB persisted for 72 hours or longer in 16 patients and identified seven of eight patients who subsequently had infarct extension. We conclude that myocardial infarct extension is an infrequent complication of acute myocardial infarction and is associated with a very high mortality rate. Persistence of CK-MB for 72 hours or more identifies a subgroup of patients at high risk for subsequent infarct extension and death.     

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.     

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.     

Subcortical vascular dementia: survey of treatment patterns and research considerations

OBJECTIVE: The purpose of this study was to evaluate retrospectively the efficacy of a proposed panel of three cardiac markers (myoglobin, creatine kinase-MB mass [CK-MB], and cardiac troponin I) in the diagnosis of acute myocardial infarction (AMI) in patients with atraumatic chest pain. DESIGN: A total of 110 patients admitted for the evaluation of atraumatic chest pain were examined. Forty-one of these patients were diagnosed with AMI. RESULTS: Five of the 41 patients with AMI had abnormally elevated myoglobin levels, whereas values of CK-MB and/or cardiac troponin I remained negative. Creatine kinase-MB mass alone had a sensitivity of 92.7%, a specificity of 89.9%, a positive predictive value of 84.4%, and a negative predictive value of 95.0% for the diagnosis of AMI. Cardiac troponin I alone had a sensitivity of 90.2%, a specificity of 95.7%, a positive predictive value of 92.5%, and a negative predictive value of 94.3% for the diagnosis of AMI. Cardiac troponin I is a more specific marker for the diagnosis of AMI than CK-MB, particularly in patients with chronic renal failure who are evaluated for chest pain. The combination of CK-MB and cardiac troponin I increased the sensitivity to 100% and the negative predictive value to 100% and had a specificity of 88.4% and a positive predictive value of 83.7%. The panel was diagnostic for all patients with AMI within 12 hours after admission. CONCLUSIONS: Our preliminary results indicate that this panel is highly effective for evaluation of AMI in patients with atraumatic chest pain. Elevated myoglobin levels were useful in detecting patients at high risk for AMI who initially were not detected with other markers. The combination of CK-MB and cardiac troponin I provided much higher sensitivity and had a much higher negative predictive value for the evaluation of AMI than cardiac troponin I or CK-MB alone. The 100% negative predictive value is particularly important because it indicates that patients with negative CK-MB and cardiac troponin I values 12 hours after admission have a negligible likelihood of AMI.     

A decision tree for the early diagnosis of acute myocardial infarction in nontraumatic chest pain patients at hospital admission

STUDY OBJECTIVE: To find an accurate algorithm for the diagnosis of acute myocardial infarction in nontraumatic chest pain patients on presentation to the emergency department. DESIGN: 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. SETTING: Emergency room of a Department of Internal Medicine (University Hospital). PATIENTS: 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. MEASUREMENTS AND RESULTS: 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. CONCLUSIONS: 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 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.     

Uterine lymphoma: sonographic, Doppler, and CT findings before and after chemotherapy

We studied the performance of the CARDIAC STATus, a new rapid, easy to perform qualitative whole blood bedside test for detection of elevated CK-MB and myoglobin in the emergency room. Blood samples from 182 consecutive patients with chest pain were drawn on admission and at five and seven hours after the onset of symptoms. The CARDIAC STATus tests were performed by coronary care unit nurses and, independently, by a trained laboratory technician. The results were compared with quantitative assays for CK-MB mass and myoglobin. At the end of the study, a second test series using a new lot number of cartridges was performed on the same blood samples because of possible elution buffer contamination. Nurses produced more false negative results than the technician (CK-MB 43 vs. 27 %, p=0.01, myoglobin 31 vs. 13%, p<0.0001), but the technician produced more false positive myoglobin results (9.3 vs. 5.5%, p=0.0001). In the second test series, the nurses produced significantly fewer false negative tests both for CK-MB (19%, p<0.0001) and myoglobin (13%, p=0.0002). The false negative rate for the technician was not different between the first and the second test series. The CARDIAC STATus yields a substantial number of false negative results both for CK-MB and myoglobin when compared to a quantitative assay, and therefore at present has limited value for ruling out an acute myocardial infarction.     

Myoglobin concentration in serum as an early marker of reperfusion in patients with acute myocardial infarction after thrombolytic therapy

Detection of coronary artery reperfusion in patients after thrombolytic therapy because of acute myocardial infarction includes, except angiography, disappearance of anginal pain, regression of electrocardiographic and echocardiographic myocardial ischaemia symptoms, increased activity of creatine kinase (CPK) and its isoenzyme CK-MB. The aim of the study was to check whether changes in myoglobin serum concentration could be an early marker of coronary artery reperfusion after thrombolysis in patients with acute myocardial infarction. The studies comprised 50 patients treated by thrombolysis due to threatening myocardial infarction, including 29 men and 21 women aged 43-84 years. The patients were divided into 2 groups: the first (i)-patients without symptoms of coronary artery reperfusion and the second (ii)-those with symptoms of coronary artery reperfusion. It was assumed that the basis for successful reperfusion would be the reduction of total elevations of the ST segment 70% or more in electrocardiographic recording performed 3 hours after the start of thrombolytic treatment. Reperfusion was considered completely unsuccessful when reduction of total elevations was less than 30%. In patients with reperfusion after thrombolysis the concentrations of myoglobin were much higher and the activity of CPK and CK-MB significantly more intensive in comparison with patients without reperfusion symptoms in electrocardiographic assay. The evaluation of myoglobin concentration, CPK and CK-MB activity in the 3rd hour after the start of thrombolytic treatment in relation to maximum values is characterised by high sensitivity and specificity in the prediction of reperfusion onset Maximum myoglobin concentration in serum appears significantly earlier than maximum CPK and CK-MB activity and this marker is characterised by higher sensitivity and specificity in the evaluation of coronary artery reperfusion than the activity of CPK and CK-MB.     

Gallbladder volume and contractility in term and preterm neonates: normal values and clinical applications in ultrasonography

BACKGROUND: Normovolemic hemodilution is a well-accepted method for intraoperative blood salvage. However, some controversy exists concerning the possible risk of myocardial fiber injury as consequence of the reduced oxygen content. Laboratory diagnosis of perioperative myocardial fiber injury is difficult, since biochemical markers are elevated postoperatively due to the surgical trauma. Cardiac troponin I (cTnI) is a new, highly sensitive and specific marker for the detection of myocardial injury. The aim of our study was to investigate whether normovolemic hemodilution in patients with major orthopedic surgery (13 hemodiluted patients, 15 control) induces a release of cTnI. METHODS: cTnI as a highly specific and sensitive cardiac parameter, as well as total creatine kinase (CK), creatine kinase isoenzyme MB mass (CKMB mass) and myoglobin were measured after induction of anesthesia, after normovolemic hemodilution, prior to retransfusion of blood components, 3 h after surgery, and on the first and third postoperative days. RESULTS: Prior to retransfusion of blood components the hematocrit was decreased to 25.4 +/- 1.2% (mean +/- SEM; range: 18%-34%) in the control group and to 20.2 +/- 0.8% (mean +/- SEM; range: 17%-24%) in the hemodilution group. Total CK, CKMB mass as well as myoglobin concentration increased significantly in both groups, reaching their maxima within the first day of surgery. In contrast, cTnI was below the detection limit of assay (< 0.5 micrograms/L) at any time. CONCLUSIONS: We suggest that pre- and intraoperative hemodilution to a hematocrit of approximately 20% by maintaining normovolemia does not induce myocardial fiber injury in patients without preexisting cardiac diseases.     

Troponin T as a marker for myocardial ischemia in patients undergoing major noncardiac surgery

To assess the diagnostic performance of cardiac troponin T as a marker for myocardial injury in patients undergoing major noncardiac surgery, we prospectively collected preoperative and postoperative clinical data, including measurements for creatine kinase (CK), CK-MB, and troponin T for 1,175 patients undergoing major noncardiac surgery. Acute myocardial infarction was diagnosed in 17 patients (1.4%) by a reviewer who was blinded to troponin T data and who used CK-MB and electrocardiographic criteria to define acute myocardial infarction. Other predischarge major cardiac complications were detected for another 17 patients. Troponin T elevations (>0.1 ng/ml) occurred in 87% of patients with and in 16% of patients without myocardial infarction. Among patients without myocardial infarction, troponin T was elevated in 62% of patients with and in 15% of patients without major cardiac complications. Receiver-operating characteristic analysis indicated that troponin T had a performance for the diagnosis of acute myocardial infarction similar to CK-MB, and a significantly better correlation with other major cardiac complications in patients without definitive infarction. Future research should seek to determine the significance of troponin T elevations in patients without complications.     

Effects of benzodiazepine agonists on punished responding in pigeons and their relationship with clinical doses in humans

We evaluated the AxSYM troponin I (cTnI) immunoassay for assisting in the detection of acute myocardial infarction (AMI). At four sites, the total imprecision (CV) over 20 days was 6.3-10.2%. The minimum detectable concentration was 0.14 +/- 0.05 microgram/L. Comparison of cTnI measurements between the AxSYM and Stratus (n = 406) over the dynamic range of the AxSYM assay demonstrated good correlation, r = 0.881, with a proportional bias: AxSYM cTnI = 3.50(Stratus cTnI) - 1. 10. The confidence intervals (95%) for the slope and intercept were 3.39-3.64 and -1.32 to -0.95, respectively. The expected cTnI concentration in healthy individuals was /=96%, in skeletal muscle injury, chronic renal disease, and same-day noncardiac surgery patients.     

Interference of CK-BB isoenzyme in the determination of CK-MB using the immunoinhibition method in patients with pulmonary diseases

An increase in serum creatine kinase-MB (CK-MB) isoenzyme is regarded as a specific indicator of acute myocardial infarction. We analyzed retrospectively the clinical data of 94 patients whose serum creatine kinase MB (CK-MB) was measured with immunoinhibition kit which measures all residual CK activity following inactivation of M-subunit. There were 21 patients with chronic obstructive lung disease (COLD), 17 patients with pneumonia, 17 patients with pulmonary tuberculosis (TBC), 16 patients with non-small cell lung cancer (NSCLC), 10 patients with small cell lung cancer (SCLC), 8 patients with malignancies of other origin (NPL), and 5 patients with chronic heart diseases. The results revealed that serum concentrations of CK-MB in SCLC, NSCLC and TBC were significantly greater than those in other groups (P < 0.1). Clinical examination showed no evidence of myocardial infarction, injury, or tumor involvement of the heart. We assumed that those results are due to interference of the CK-BB isoenzyme in the immunoinhibition method. So we suggest that in clinical practice, markedly elevated levels of CK-MB measured with immunoinhibition kit, after the exclusion of the myocardial injury, may point toward the existence of a malignancy or TBC of the lungs.     

QT dispersion may be a useful adjunct for detection of myocardial infarction in the chest pain center

BACKGROUND: QT dispersion has been proposed as a noninvasive measurement of the degree of inhomogeneity in myocardial repolarization. Increased QT dispersion has been reported after myocardial infarction. We hypothesized that increased QT dispersion may be a useful adjunct for risk stratification in patients being evaluated in a chest pain center. METHODS AND RESULTS: Patients were admitted to the chest pain center for evaluation of chest pain. Exclusion criteria included (1) systolic blood pressure <90 mm Hg, (2) ischemia or infarction on the initial electrocardiograph (ECG), (3) elevated creatine kinase or MB fraction, and (4) chest pain associated with cocaine use. Serial creatine kinase and MB levels and ECGs were obtained at 0, 6, and 9 hours. Patients were monitored for (1) creatine kinase and MB rise, (2) ECG changes for infarction, (3) ST-segment changes, and (4) rest angina. A negative evaluation at the chest pain center led to an exercise stress test. Patients with a positive exercise stress test were admitted for further evaluation and patients with a negative exercise stress test result were discharged home. Patients were divided into 3 groups. Group 1 consisted of patients who were found to have an acute myocardial infarction (AMI), group 2 consisted of patients with prior history of coronary artery disease but no evidence of AMI, and group 3 consisted of patients without prior coronary artery disease or AMI. QT dispersion was measured on the initial ECG in all patients. A total of 586 patients were evaluated. Group 1 consisted of 13 patients with mean QT dispersion of 44.6+/-18.5 ms, group 2 consisted of 267 patients with a mean QT dispersion of 10.0+/-13.8 ms, and group 3 consisted of 303 patients with a mean QT dispersion of 10.5+/-10.0 ms. Analysis of variance showed a significantly higher QT dispersion in patients who had AMI compared with other patients with chest pain (P< .001). CONCLUSIONS: QT dispersion can be a useful diagnostic adjunct for detection of AMI in patients with chest pain with a normal ECG and normal cardiac enzymes.