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.

Sustaining the implementation of an evidence-based guideline for bronchiolitis.

OBJECTIVE: To describe the changes occurring over a 3-year period after implementation of an evidence-based clinical practice guideline for the care of infants with bronchiolitis. DESIGN: Before and after study. SETTING: Children's Hospital Medical Center, Cincinnati, Ohio. PATIENTS: Infants 1 year or younger admitted to the hospital with a first-time episode of typical bronchiolitis. INTERVENTION: The guideline was implemented January 15, 1997. Data on all patients discharged from the hospital with bronchiolitis, from January 15 through March 27, in 1997, 1998, and 1999, were stratified by year and compared with data on similar patients discharged from the hospital in the same periods in the years 1993 through 1996. MAIN OUTCOME MEASURES: Patient volumes, length of stay for admissions, and use of specific laboratory and therapeutic resources ancillary to bed occupancy. RESULTS: After implementation of the guideline, admissions decreased 30% and mean length of stay decreased 17% (P<.001). Nasopharyngeal washings for respiratory syncytial virus were obtained in 52% fewer patients (P<.001); 14% fewer chest x-ray films were ordered (P<.001). There were significant reductions in the use of all respiratory therapies, with a 17% decrease in the use of at least 1 beta(2)-agonist inhalation therapy (P<.001). In addition, 28% fewer repeated inhalations were administered (P<.001); mean costs for all resources ancillary to bed occupancy fell 41% (P<.001); and mean costs for respiratory care services fell 72% (P<.001). CONCLUSIONS: An evidence-based clinical practice guideline for the care of patients encountered in major pediatric care facility has been successfully sustained beyond the initial year of its introduction to practitioners in southwest Ohio.

Evaluation of a point-of-care system for quantitative determination of troponin T and myoglobin.

We present the results of a multicenter evaluation of a new point-of-care system (Cardiac Reader) for the quantitative determination of cardiac troponin T (CARDIAC T Quantitative test) and myoglobin (CARDIAC M test) in whole blood samples. The Cardiac Reader is a CCD camera that optically reads the immunochemical test strips. The measuring range is 0.1 to 3 microg/l for CARDIAC T Quantitative and 30 to 700 microg/l for CARDIAC M. Both tests are calibrated by the manufacturer. The reaction times of the tests are 12 or 8 minutes, respectively. Method comparisons were performed with 281 heparinized blood samples from patients with suspected acute coronary syndromes. The results obtained with CARDIAC T Quantitative showed a good agreement compared with cardiac troponin T ELISA (r = 0.89; y = 0.93x + 0.02). The method comparison between CARDIAC M and Tina-quant Myoglobin also showed a good agreement between both assays (r = 0.98; y = 0.92x + 1.6). Test lot-to-lot comparisons yielded differences of 2% and 6% for CARDIAC T Quantitative and of 0 to 11% for CARDIAC M. The within-run imprecision with blood samples and control materials was acceptable for CARDIAC T Quantitative (CV 10 to 15%) and good for CARDIAC M (CV 5 to 10%). The between-instrument CV was below 7% for CARDIACT Quantitative and below 5% for CARDIAC M. The cross-reactivity of CARDIAC T Quantitative with skeletal troponin T was approximately 0.003%. No significant analytical interference was detected for any of the assays in investigations with biotin (up to 100 microg/l), hemoglobin (up to 0.125 mmol/l), hematocrit (26 to 52%), bilirubin (up to 340 micromol/l), triglycerides (up to 5.0 mmol/l), and 18 standard drugs. With the Cardiac Reader reliable quantitative results can be easily obtained for both cardiac markers. The system is, therefore, particularly suitable for use in emergency rooms, coronary care units and small hospitals.

Troponin T and I assays show decreased concentrations in heparin plasma compared with serum: lower recoveries in early than in late phases of myocardial injury.

BACKGROUND: Heparinized plasma samples allow more rapid analysis than serum samples, but preliminary studies showed lower cardiac troponin T (cTnT) results in plasma. We undertook a multicenter study to characterize this effect for cTnT and cardiac troponin I (cTnI). METHODS: Blood samples were collected with and without heparin at five hospitals. cTnT was measured by a "third generation" assay (Elecsys((R))), and cTnI was measured by a commercial immunoassay (IMMULITE((R))). RESULTS: Mean cTnT was 15% lower in heparin sampling tubes than in serum. Measured concentrations of cardiac troponins also decreased with increasing heparin concentrations added to sera. Heparin-induced losses were greater in early than in late phases after onset of chest pain. Addition of heparin ( approximately 100 IU/mL) to serial samples from nine acute myocardial infarction patients produced mean cTnT losses of 33% at 1-12 h after onset of chest pain, 17% at 13-48 h, and 7% after 48 h. The changing heparin effects were seen for both cTnT and cTnI during time courses of individual patients with myocardial infarction. CONCLUSION: We suggest that binding of heparin to troponins decreases immunoreactivity, especially in early phases of myocardial injury. The resulting losses may depend on the antibodies used in each troponin assay.

Analytical and clinical performance of an improved qualitative troponin T rapid test in laboratories and critical care units.

OBJECTIVE: To evaluate the performance of a visual troponin T rapid test in the hands of nontraditionally trained personnel of 2 critical care units in comparison to 3 laboratories. METHODS: Method comparisons of the troponin T rapid test versus cardiac troponin T enzyme-linked immunosorbent assay were performed with 804 samples from 510 patients with suspected acute coronary syndromes. Cross-reactivity with skeletal troponin T was studied up to 5000 microg/L. RESULTS: Laboratories and critical care units obtained comparable results in the analytical cutoff of the test (0.11 and 0. 10 microg/L) and in the diagnostic sensitivities in the detection of acute myocardial infarction (96% and 93% after 8 hours) and of high-risk patients with unstable angina pectoris (100% and 100%). Different percentages of false-positive results (0.2% and 3%) were found, which may reflect different objectives and strategies in these hospital units. The cross-reactivity with skeletal troponin T was less than 0.01%. CONCLUSIONS: The troponin T rapid test gives reliable results not only when used by laboratory personnel experienced in the execution of analytical methods, but also in the hands of nurses and physicians working in clinical units outside the laboratory.

Can troponin T replace CK MBmass as "gold standard" for acute myocardial infarction ("AMI")?

Diagnosis of definite "Acute Myocardial Infarction" by the old WHO criteria depends on the diagnostic sensitivity and specificity of the biochemical marker used. Troponins have higher diagnostic sensitivity and specificity than the current "gold standard" for AMI, CK MBmass. Troponin T (TnT) provides both diagnostic and prognostic information on Minor Myocardial Damage (MMD) even in patients without increases of CK MBmass. Consequently, we evaluated the possibility of replacing CK MBmass with TnT. We first re-evaluated a previous, well-documented material of 502 time series from AMI-suspected cases, 50% of which were primarily classified as AMI by CK MBmass > or = 10 micrograms/L. We found that a TnT discriminator limit of 0.40 microgram/L gave the same AMI prevalence. We then identified from our laboratory data base 1995-1998 acute patient episodes with > or = 3 pairs of CK MBmass and TnT. This resulted in 754 episodes with max CK MBmass > or = 10 micrograms/L (AMI), 93 episodes with maximal CK MBmass < 10 micrograms/L and TnT > or = 0.10 microgram/L (MMD), and 730 episodes with max concentrations below the discriminators of both markers (NOT-MMD). TnT > or = 0.40 microgram/L detected 91% of all AMI giving a posterior probability of "AMI" > 99%. The criterion: "maximal TnT within the interval 0.10-0.40 microgram/L" detected 94% of all MMD and 9% of all AMI giving posterior probabilities about half MMD and half "small AMI", the latter characterized by less than 3-fold increased maximal CK MBmass. Thus, this TnT interval confirmed the gradual transition between MMD and small AMI. We suggest gradation of myocardial damage by TnT.

[Biochemical markers enable early diagnosis of myocardial damage]. / Biokemiska markörer kan ge tidig diagnos av myokardskada.

Diagnosis of myocardial damage based on early measurement of biochemical markers is becoming an increasingly important guide in the management and treatment of suspected coronary artery disease. The new, more sensitive and/or specific markers myoglobin, CK-MB (creatine kinase and its cardiospecific isoenzyme), and the troponins T and I, are reviewed in the article, new rapid analytical tests are discussed, and modified sampling routines proposed. The combination of a marker with high early sensitivity and a marker with a broad time window and high specificity, together with modified sampling routines and analysis of whole blood can yield a reliable diagnosis within minutes or (3-6) hours of the patient's presentation. Moreover, together with other non-invasive methods, use of the markers of myocardial injury enables rapid and reliable risk analysis.

Troponin T: a sensitive and specific diagnostic and prognostic marker of myocardial damage.

Cardiac troponin T (cTnT) in serum is a highly sensitive and specific marker for myocardial damage. Quantitative immunoassays take 9 min. A rapid test (TropT, CardiacT) using plasma detects cTnT concentrations above 0.10 microg/l within 15 min. Both assays are specific for the cardiac isoform. In a study using the maximal values from serial sampling in 502 infarction-suspected patients, we found a diagnostic sensitivity for non-Q- and Q-wave infarctions of 100%, with a specificity of 99%. cTnT has been shown to be a powerful prognostic marker for risk stratification in acute coronary syndromes. In 30-40% of patients with unstable angina, cTnT > or = 0.10 microg/l detects minor myocardial damage (MMD) with poor prognosis. False positives may be found in certain skeletal muscle diseases, such as polymyositis and Duchenne's muscular dystrophy. Constantly increased values in renal failure may be due to uremic cardiomyositis. Even in uremia, a rapid increase of cTnT will indicate acute myocardial damage. We propose a diagnostic strategy based on timed, parallel determinations of myoglobin + cTnT.

The use of biochemical markers in ischaemic heart disease: summary of the roundtable and extrapolations.

Acceptable biochemical markers of ischaemic heart disease are now considered to include myoglobin, CK-MB isoforms, CK-MB, and cardiac troponins T and I. AST (SGOT), total LD and LD isoenzymes, and total CK activity measurements are regarded as obsolete for this purpose. All acceptable biochemical markers must be available, if required, with a turnaround time of < 20 min. Such a service can either be provided by quantitative assays in a well-equipped laboratory or by qualitative point-of-care (bedside) devices (except for the CK-MB isoform assay) which can also be used in patients' homes and ambulances. There is, however, a pressing need for the careful side-by-side assessment of the relative merits of each of these biochemical markers to permit definitive conclusions about their future usage. A particular problem is the lack of primary standards for CK-MB and troponin I assays. The sensitivity of the initial ECG is about 50% for detecting myocardial damage; thus the use of biochemical markers may contribute to the early diagnosis and monitoring of thrombolytic therapy and these possible applications are examined. In addition, biochemical markers are presently the gold standard for the diagnosis of minor myocardial damage. There is now good evidence that biochemical markers, particularly the cardiac troponins, have a prognostic function in ischaemic heart disease although such findings pose unanswered clinical management questions. At the same time, it is recognized that there is often no need at all for the use of any biochemical marker when the clinical diagnosis is unequivocal, other than for prognosis, monitoring thrombolytic therapy, or diagnosing reinfarction.

An improved rapid troponin T test with a decreased detection limit: a multicentre study of the analytical and clinical performance in suspected myocardial damage.

In a multicentre study, we evaluated the analytical and diagnostic performance of the second version of the TROPT rapid test (TROPT 2, CARDIACT in the US). We tested TROPT 2 on 796 blood samples from 487 patients admitted on suspicion of myocardial infarction between 1 and 72 h after onset of symptoms and determined cTnT ELISA and CK MB mass in the corresponding serum samples. Frequency distributions of the results with TROPT 2 showed a detection limit of 0.18 microgram/l (for 50% positive results) as determined by the quantitative cTnT ELISA method. In a total of 796 samples the sensitivities in the detection of myocardial infarction (WHO criteria) 8-12 h after onset of symptoms were highest for cTnT ELISA (98%), followed by the rapid assay and CK MB mass (92%). A subgroup of 87 patients was primarily classified by the WHO criteria for definite infarction. Based on the maximum values within each patient time-series, diagnostic sensitivities for infarction were 100% for TROPT2, cTnT ELISA and CK MB mass. The corresponding specificities were 90%, 82% and 100%, respectively. After reclassification summarizing all cases of myocardial damage (acute and subacute myocardial infarctions and minor myocardial damage) the sensitivities were 87% (TROPT2), 100% (cTnT ELISA) and 71% (CK MB mass). The specificities of all three markers were 100%. Over 50% of all cases of minor myocardial damage were detected by TROPT 2. The clinical evaluation showed that the diagnostic performance of TROPT 2 is only slightly lower than that of cTnT ELISA.

Multicenter evaluation of a second-generation assay for cardiac troponin T.

We report on the evaluation of the second-generation assay for cardiac troponin T (cTnT) on the Enzymun system. This new assay is completely specific for the cardiac isoform of TnT, utilizing two cardiospecific monoclonal antibodies. The assay time is reduced to 45 min. The interassay precision shows a median CV of 5.5%; 20% interassay CV was found between 0.05 and 0.1 microg/L. The cardiosensitivity of the second-generation cTnT assay in patients with ischemic myocardial injury appears equivalent when compared with the first-generation assay. We found no falsely positive results in patients with skeletal muscle damage including multitraumas, surgery patients, and marathon runners who showed highly increased values with the unspecific first-generation assay. In Duchenne disease cTnT was still increased, but to a much lower extent. cTnT remains increased in renal failure, but to a lesser degree than with the first-generation assay. The cause of this increase remains unclear. Although a cross-reactivity of skeletal muscle TnT in the second-generation assay could be excluded by our findings, minor myocardial damage or expression of the cardiac isoform of TnT in regenerating muscles cannot be ruled out in those cases with apparently falsely increased cTnT values. The second-generation cTnT assay is a step forward in the combination of cardiosensitivity and cardiospecificity in biochemical markers for diagnosis of heart disease.

Detection of myocardial damage by serial measurements of cardiac troponin T, CK MBmass, and TROPT rapid test.

Detection of cardiac damage is greatly facilitated by serial blood measurements of myocardial cell markers. In many hospitals creatine kinase MBmass concentration (CK MBmass) constitutes the biochemical criterion (WHO) for acute myocardial infarction (AMI). Cardiac troponin T (TnT) is an even more sensitive and specific marker for myocardial damage. With discriminator levels of 10.0 and 0.10 micrograms/l, respectively, serial measurements of both markers provide a useful diagnostic strategy for ischemic heart disease. This survey reviews representative cumulated time curves in individual patients covering the spectrum of myocardial damage, including unstable angina pectoris (UAP), non-Q-wave and Q-wave infarctions with and without early reperfusion, re-infarction, and subacute infarction. Increased TnT detects minor myocardial damage (MMD) in over 30% of patients with UAP, although CK MBmass remains below its discriminator. Subacute infarction is detected by the wide diagnostic time window of the serum TnT at a time when CK MBmass has already returned to normal. In a substudy of 502 suspected cases of AMI, the distributions of maximum serum TnT concentrations within each patient series demonstrated that TnT had a diagnostic sensitivity of 100% and a specificity of 99%. Median, 5th and 95th percentiles of maximum TnT values within the diagnostic subgroups showed that serum TnT was increased five-fold more than CK MBmass. Median values of Q-wave AMI were higher than in non-Q-wave AMI. A diagnostic strategy using TROPT, a rapid test specific for the cardiac isoform of TnT with a detection limit 0.10 microgram/l, is presented.

Improved troponin T ELISA specific for cardiac troponin T isoform: assay development and analytical and clinical validation.

The first generation of troponin T ELISA (TnT 1) can yield false-positive results in patients with severe skeletal muscle injury. Therefore, a cardiac-specific second-generation troponin T ELISA (TnT 2) was developed, in which the cross-reactive antibody 1B10 has been replaced by a high-affinity cardiac-specific antibody M11.7. No cross-reactivity of TnT 2 was observed with purified skeletal muscle troponin T (1000 micrograms/L) or in test samples from 43 marathon runners and 24 patients with rhabdomyolysis and highly increased creatine kinase. TnT 2 was increased > 0.2 microgram/L in 5 of 40 patients with renal failure and in 4 of 20 muscular dystrophy patients. The detection limit is 0.012 microgram/L. Day-to-day imprecision (CV) within the range 0.19-14.89 micrograms/L was < 5.8%. In 4955 patients without myocardial damage, 99.6% had TnT < 0.10 microgram/L. Assay comparison (TnT 1 vs TnT 2) over the whole concentration range (i.e., in 323 samples from AMI-suspected patients) showed a slope, intercept, and standard error of estimate (Sey) of 1.18, 0.01 micrograms/L, and 0.81 microgram/L, respectively.

Multicentre evaluation of an immunological rapid test for the detection of troponin T in whole blood samples.

In a multicentre study we assessed the analytical and diagnostic performance of a rapid test (TROPT rapid test, Boehringer Mannheim; in the USA: CARDIACT) for cardiac troponin T compared to quantitative troponin T ELISA and creatine kinase-MB mass determinations. The rapid test requires 150 microliters of heparinized or EDTA whole blood; serum is not suitable. Interference testing with biotin, haemoglobin and 27 standard drugs yielded no significant influence in the physiological range. Skeletal muscle troponin T concentrations > or = 40 micrograms/l gave positive results with the rapid test. We used the rapid test for 369 samples from 203 patients with suspected acute coronary syndromes and compared the results to troponin T ELISA and creatine kinase-MB mass. 90 patients (44%) were primarily classified as having myocardial infarction by the WHO criteria. Twenty-two (20%) of the 113 non-myocardial infarction patients were unstable angina pectoris cases showing increased troponin T ELISA but not increased creatine kinase-MB mass values. Consequently, these were classified as minor myocardial damage cases. The rapid test was positive in 99% of all samples with a troponin T ELISA value > or = 0.30 micrograms/l and negative in 95 to 96% of all samples below this value. Diagnostic sensitivities for the detection of acute myocardial infarction within the first 12 hours after onset of pain were the same, 90%, for the rapid test, troponin T ELISA and creatine kinase-MB mass. After 48 hours, diagnostic sensitivity of creatine kinase-MB mass sharply decreased whereas that of the troponin T assays remained close to 100% beyond 72 hours after onset of symptoms. Diagnostic specificities for acute myocardial infarction (WHO) of all markers remained between 80 and 100% over this time. The diagnostic sensitivity of the rapid test for the detection of high risk unstable angina pectoris patients with minor myocardial damage was nearly the same as for troponin T ELISA. A major advantage of the rapid test is the ease of use and 20 minute turn around time. This facilitates the detection of increased troponin T at alternate sites.

[Troponin T in acute myocardial infarction. Diagnosis and prognosis in patients admitted for suspected acute myocardial infarction]. / Troponin T ved akut myokardieinfarkt. Diagnostik og prognostik hos patienter indlagt til observation for akut myokardieinfarkt.

Cardiac troponin T (TnT) is a new serological marker for use as a diagnostic tool for myocardial damage. A blinded prospective multicentre study representing 298 patients who on admission were suspected of acute myocardial infarction (AMI) to the coronary care units of six Scandinavian hospitals was undertaken to assess the diagnostic performance and prognostic efficacy of a new cardiospecific TnT immunoassay. We used a discriminator value of TnT of 0.20 micrograms/l. One hundred and fifty-five patients (52%) had definite AMI, based on WHO criteria (all had peak S-TnT values > or = 0.20 micrograms/l); 127 patients (43%) had ischaemic heart disease (IHD) without AMI; and 16 patients (5%) had non-IHD (all had peak S-TnT values < 0.20 micrograms/l). The 127 IHD-patients without definite AMI could be subdivided into a group of 44 patients with S-TnT peak values > or = 0.20 micrograms/l, and a group of 83 patients with TnT below this level. A follow-up study was able to define the clinical significance of these findings. The cumulative six months probability of suffering cardiac death or AMI was significantly higher in the subgroup with increased TnT values (14% (6/44)) as compared to the other subgroup (4% (3/83)) (Log-rank test, p = 0.025). The probability of cardiac events was 15% for the patients with definite AMI. We conclude that increased troponin T in serum can detect a subgroup of IHD-patients in whom AMI has been ruled out, but who still have a prognosis as serious as that of patients with definite AMI.

Diagnostic performance and prognostic value of serum troponin T in suspected acute myocardial infarction.

Cardiac troponin T (TnT) is a new serological marker for use as a diagnostic tool for myocardial damage. A blinded prospective multicentre study representing 298 patients suspected of having acute myocardial infarction (AMI), and admitted to the coronary care units of six Scandinavian Hospitals was undertaken to assess the diagnostic performance and prognostic efficacy of a new cardiospecific TnT immunoassay. We used a discriminator TnT value of 0.20 microgram l-1. One hundred and fifty five patients (52%) had definite AMI, based on WHO criteria (all had peak S-TnT values of > or = 0.20 micrograms l-1); 127 patients (43%) had ischaemic heart disease (IHD) without AMI; and 16 patients (5%) had non-IHD (all had peak S-TnT values of < 0.20 microgram l-1). The 127 IHD-patients without definite AMI could be subdivided into a group of 44 patients with S-TnT peak values of > or = 0.20 microgram l-1, and a group of 83 patients with TnT below this level. An equal identification of these patients among the centres was seen (mean +/- SD 35 +/- 13%; range 20-55%). A follow-up study was able to define the clinical significance of these findings. The cumulative 6 months probability of suffering cardiac death or AMI was significantly higher in the subgroup with increased TnT values (14% (6/44)) as compared to the other subgroup (4% (3/83)) (Log-rank test, p = 0.025). The probability of cardiac events was 15% for the patients with definite AMI.(ABSTRACT TRUNCATED AT 250 WORDS)

Troponin-T and CK MB (mass) in early diagnosis of ischemic myocardial injury. The Helsingborg Study, 1992.

We evaluated cardiac troponin T (S-troponin T) versus CK MB in serum (S-CK MB) sampled 4, 10, 16, and 22 h after onset of acute symptoms in 207 consecutive cases admitted to our coronary care unit in Helsingborg, Sweden, May-October 1992. These were primarily classified into 106 acute myocardial infarctions (AMI) and 101 NOT-AMI cases by conventional cardiological criteria plus S-CK MB (mass). Time curves of S-troponin T and S-CK MB data were plotted for each individual case. Twelve of the 101 cases in the NOT-AMI group showed increased S-troponin T indicating ischemic myocardial injuries. The same cases also showed changes of S-CK MB (mass), though below its discriminator. Seven of these cases were reclassified as minor myocardial damage, constituting 25% of our 28 cases of unstable angina. The remaining five cases showed a combination of constantly increased S-troponin T and decreasing or low S-CK MB mass values as seen after a recent infarction. Consequently, the patient material was reclassified into 118 cases of ischemic myocardial injury (106 conventional AMI + 7 minor myocardial damage + 5 postinfarctions) and 89 cases of NOT-ischemic myocardial injury. The frequency distributions of the maximal S-troponin T and S-CK MB (mass) values of each case were plotted in double test evaluation histograms. For troponin T, discriminator 0.20 micrograms/L, clinical sensitivity for ischemic myocardial injury was 97% and specificity 99%. With a lower discriminator of 0.10 micrograms/L, sensitivity increased to 99% and specificity decreased to 89%. For S-CK MB (mass), discriminator 10 micrograms/L, sensitivity was 91%, specificity 98%. With a lower discriminator of 5 micrograms/L sensitivity increased to 96% and specificity decreased to 78%. We conclude that as a single routine test, S-troponin T is the marker of choice for early diagnosis of ischemic myocardial damage. The combination S-troponin T and S-CK MB (mass) provides additional, detailed information in reinfarction and postinfarction unstable angina pectoris.

A programme for assigning target values for external quality assessment schemes in countries with no authorized reference laboratories. Annex. Experiences with deviating results on Ektachem 700 XR.

The use of consensus values in external quality assessment schemes (EQAS) involves several problems and should preferably be replaced with target values obtained by methods of high metrological level. However, such values are difficult to obtain. In the present study we transferred values from the NIST (former NBS) certified reference serum SRM 909 to lyophilized and frozen test sera for various inorganic components using flame absorption or flame emission spectrometry. Enzyme values were assigned by laboratories of members of the former Scandinavian Enzyme Committee. The assignment was based on 2-4 determinations each day through 3 days of experiment. A total of 10 laboratories participated in the work. The results were utilized in a Danish EQAS. One practical concern is the fairly long time (9 months) which was needed for production, collection and compiling all data. To get an impression of how much dry chemistry analysers, e.g, could influence consensus values a Kodak Ektachem 700 XR was studied using lyophilized and frozen sera. The results are reported in the annex. On NIST SRM 909 the values found for sodium(I) were 6% too high even though the findings on frozen human sera were accurate. For aspartate aminotransferase a result three times the target values was found on a human lyophilized serum, while the values on the frozen sera only were slightly too high.