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Sensitivity and specificity of troponin T and creatine kinase as non-invasive markers of infarct artery patency. Values are per cent (lower 95% confidence limit)
Source publication
To confirm the validity of a previously described method for assessment of infarct artery patency involving serial measurements of creatine kinase activity by use of troponin T concentration as an independent plasma marker.
Streptokinase (1.5 x 10(6) units) was given intravenously to 60 patients within 6 h of onset of prolonged chest pain and ST se...
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A consecutive series of 56 patients with chest pain but no evidence of previous myocardial infarction was prospectively studied by radionuclide ventriculography to determine the value of global and regional radionuclide indices in detecting coronary artery disease. The results were correlated with the clinical judgment of chest pain, the results of...
Citations
... The rapid peaking of myoglobin seems to be the earliest marker of a successful recanalization, whilst the rate of troponin T rise over 3 h post-thrombolysis has revealed very high (94%) sensitivity as well as specificity (100%) in this situation [22] . There is only limited evidence that any of these markers can predict failure to achieve TIMI 3 flow at 60–90 min with any degree of similar accuracy [23,24] . Even though rapid assessment of myoglobin and kits for troponin for bedside diagnosis have recently become available, creatine kinase-MB assessment is still the marker most frequently used in community hospitals. ...
There remain some questions concerning the specifity of the troponins, especially cardiac troponin T. Nonetheless, they represent a substantial advance in both specificity for cardiac injury and improved sensitivity. Thus, it is likely that these markers will lead to the definition of new clinical syndromes by unmasking false positive elevations in MBCK and by identifying elevations indicitave of cardiac abnormalities that could not be detected by any other means. The development of new more sensitive assays should further improve our understanding of disease processes that involve the heart by allowing for more subtle abnormalities to be detected.
Comparing the performance of one biochemical marker of myocardial damage with another is bedeviled with many problems, including a lack of uniform calibration between instruments providing measurements of the same analyte and differing reference ranges and decision thresholds. Diagnostic groupings and various gold standards create difficulties in comparing analytic results. There is a lack of uniformity in test assessments and their use for diagnostic and prognostic purposes. Finally, there is an almost complete absence of data from economic and decision analyses of test usage. It is argued that a much more stringent and rigorous approach to these aspects is essential. The use of biochemical markers of cardiac damage is in a dynamic state, with new applications continually appearing and new markers being developed. It is therefore essential that a uniform and rigorous outlook be maintained to ensure both optimal and economic test utilization based on the previously outlined principles.
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.
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 cardiac troponins (cTns), cTnT and cTnI, are currently regarded as being the most useful diagnostic and prognostic biochemical markers of myocardial damage in patients with suspected acute coronary syndromes (ACSs). In spite of the evidence-based nature of this observation, the uptake of serum cTn measurement in routine clinical practice--in both the UK and elsewhere, is patchy, indeed, there still exists wide variability in the range of testing and sampling strategies involving usage of the many existing cardiac markers. For evaluating suspected acute myocardial infarction (AMI) and other ACSs, international opinion favours either serum cTnT or cTnI (measured 12-24 h after admission to the emergency room)--together with a short-time window marker such as serum creatine kinase (CK) (measured on admission and perhaps again within the 12-24 h window). Translation of this strategy into universal clinical practice would require not only formulation of, but also strict adherence to, agreed clinical decision-making protocols which, in turn, would need to be backed by adequate funding.
The relationship between the admission troponin T (TnT) level and the response to streptokinase (SK) was examined in 76 patients with acute myocardial infarction (AMI). Of 27 TnT positive patients, 10 (37%) showed a response to SK as suggested by a non-invasive criterion for reperfusion, while 24 (49%) were ‘responders’ among 49 TnT negative patients. There appeared to be a trend towards a better response to SK in the TnT negative group but the difference lacked statistical power due to the small sample size.
The mean time-interval between the onset of symptoms and thrombolytic treatment among TnT positive ‘non-responders’ was significantly ( P <0.005) higher than the TnT negative ‘non-responders’ (5.23 ±3.42 h versus 2.38 ± 1.37 h). An 18 month follow up on 61 patients revealed a higher mortality (33%) among TnT positive patients than TnT negative patients (10%). Mortality among TnT positive ‘non-responders’ was significantly higher ( P=0.0494) than mortality among TnT-negative ‘non-responders’ (43% versus 9%), indicating that TnT positive patients, non-responsive to SK were at a greater risk of cardiac death. The data suggest that the admission TnT level can be of value in risk stratification of patients with AMI.
The presence of plasminogen activator inhibitor-1, angiotensin-converting enzyme and others may play a role in unsuccessful recanalization after thrombolytic therapy.
To find out the clinical and biochemical predictors that may affect the choice and short-term outcomes following different thrombolytic agents in acute myocardial infarction.
Angiotensin-converting enzyme and plasminogen activator inhibitor-1 plasma levels of 184 patients with acute myocardial infarction, treated with streptokinase, metalyze or reteplase, were determined. Failure of thrombolysis was assessed by noninvasive reperfusion criteria. Prolonged hospitalization, impaired left ventricular ejection fraction and reinfarction were considered as short-term outcomes.
Patients who received streptokinase developed higher incidence of >50% resolution of ST-segment elevation (82.5 vs. 64.7%, P-value<0.05, in comparison with metalyze and 82.5 vs. 55.7%, P-value 0.001, in comparison with reteplase) than those who received other thrombolytic agents. High plasma angiotensin-converting enzyme was associated with prolonged hospitalization (55, 63 and 94%, P<0.02) following streptokinase, metalyze and reteplase, respectively. High plasma plasminogen activator inhibitor-1 is associated with impaired left ventricular ejection fraction (55.3, 76.7 and 68.5%, P<0.09), ST resolution<50% (13.2, 36.7 and 37.5%, P=0.03), ST resolution>50% (86.8, 63.3 and 62.5%, P=0.03) following streptokinase, metalyze and reteplase, respectively.
Rapid determination of pretreatment angiotensin-converting enzyme and plasminogen activator inhibitor-1 plasma levels in patients with acute myocardial infarction may influence the choice and outcomes of the thrombolytic agents. The presence of a high plasma level of either angiotensin-converting enzyme or plasminogen activator inhibitor-1 is significantly associated with adverse short-term outcomes after treatment with reteplase or metalyze.
