Surveys on the use of cardiac markers in the UK

Author(s):  
Wing Man Tsang ◽  
Avril M. Owen ◽  
Paul O. Collinson ◽  
Julian H. Barth

Background: Troponin measurements are now central to the diagnosis of acute coronary syndromes and for the stratification of the severity of cardiac disease. Some laboratories have quickly adopted the new testing strategies, which include troponin measurement for the diagnosis of acute myocardial infarction, while others are still developing appropriate protocols for cardiac testing that they can support financially. However, it is not known how widespread is the adoption of these new strategies across the UK. Methods: The National Audit Committee of the Association of Clinical Biochemists commissioned two surveys in 1999 and 2001 to assess the status of cardiac markers currently being offered by laboratories in the UK and how this service might develop in the future. Results: The results show that many laboratories are continuously adapting and improving their cardiac marker testing in line with current recommendations for acute myocardial infarction. Although most laboratories are confident in the use of troponin measurement in the diagnosis of myocardial infarction, they are less confident in the use of biochemical markers in assessing prognostic outcome in the other cardiac conditions. Conclusions: Finance, staffing and equipment constraints may offer significant impediments to troponin testing with a 1-h turnaround time.

2020 ◽  
Vol 21 (17) ◽  
pp. 6219
Author(s):  
Pei-Hsun Sung ◽  
Kun-Chen Lin ◽  
Han-Tan Chai ◽  
John Y. Chiang ◽  
Pei-Lin Shao ◽  
...  

This study tested the hypothesis that MMP-9−/−tPA−/− double knock out (i.e., MTDKO) plays a crucial role in the prognostic outcome after acute myocardial infarction (AMI by ligation of left-coronary-artery) in MTDKO mouse. Animals were categorized into sham-operated controls in MTDKO animals (group 1) and in wild type (B6: group 2), AMI-MTDKO (group 3) and AMI-B6 (group 4) animals. They were euthanized, and the ischemic myocardium was harvested, by day 60 post AMI. The mortality rate was significantly higher in group 3 than in other groups and significantly higher in group 4 than in groups 1/2, but it showed no difference in the latter two groups (all p < 0.01). By day 28, the left-ventricular (LV) ejection fraction displayed an opposite pattern, whereas by day 60, the gross anatomic infarct size displayed an identical pattern of mortality among the four groups (all p < 0.001). The ratio of heart weight to tibial length and the lung injury score exhibited an identical pattern of mortality (p < 0.01). The protein expressions of apoptosis (mitochondrial-Bax/cleaved-caspase3/cleaved-PARP), fibrosis (Smad3/T-GF-ß), oxidative stress (NOX-1/NOX-2/oxidized-protein), inflammation (MMPs2,9/TNF-α/p-NF-κB), heart failure/pressure overload (BNP/ß-MHC) and mitochondrial/DNA damage (cytosolic-cytochrome-C/γ-H2AX) biomarkers displayed identical patterns, whereas the angiogenesis markers (small vessel number/CD31+cells in LV myocardium) displayed opposite patterns of mortality among the groups (all p < 0.0001). The microscopic findings of fibrotic/collagen deposition/infarct areas and inflammatory cell infiltration of LV myocardium were similar to the mortality among the four groups (all p < 0.0001). MTDKO strongly predicted unfavorable prognostic outcome after AMI.


2004 ◽  
Vol 128 (2) ◽  
pp. 158-164 ◽  
Author(s):  
David A. Novis ◽  
Bruce A. Jones ◽  
Jane C. Dale ◽  
Molly K. Walsh

Abstract Context.—Rapid diagnosis of acute myocardial infarction in patients presenting to emergency departments (EDs) with chest pain may determine the types, and predict the outcomes of, the therapy those patients receive. The amount of time consumed in establishing diagnoses of acute myocardial infarction may depend in part on that consumed in the generation of the blood test results measuring myocardial injury. Objective.—To determine the normative rates of turnaround time (TAT) for biochemical markers of myocardial injury and to examine hospital and laboratory practices associated with faster TATs. Design.—Laboratory personnel in institutions enrolled in the College of American Pathologists Q-Probes Program measured the order-to-report TATs for serum creatine kinase–MB and/or serum troponin (I or T) for patients presenting to their hospital EDs with symptoms of acute myocardial infarction. Laboratory personnel also completed detailed questionnaires characterizing their laboratories' and hospitals' practices related to testing for biochemical markers of myocardial injury. ED physicians completed questionnaires indicating their satisfaction with testing for biochemical markers of myocardial injury in their hospitals. Setting.—A total of 159 hospitals, predominantly located in the United States, participating in the College of American Pathologists Q-Probes Program. Results.—Most (82%) laboratory participants indicated that they believed a reasonable order-to-report TATs for biochemical markers of myocardial injury to be 60 minutes or less. Most (75%) of the 1352 ED physicians who completed satisfaction questionnaires believed that the results of tests measuring myocardial injury should be reported back to them in 45 minutes or less, measured from the time that they ordered those tests. Participants submitted TAT data for 7020 troponin and 4368 creatine kinase–MB determinations. On average, they reported 90% of myocardial injury marker results in slightly more than 90 minutes measured from the time that those tests were ordered. Among the fastest performing 25% of participants (75th percentile and above), median order-to-report troponin and creatine kinase–MB TATs were equal to 50 and 48.3 minutes or less, respectively. Shorter troponin TATs were associated with performing cardiac marker studies in EDs or other peripheral laboratories compared to (1) performing tests in central hospital laboratories, and (2) having cardiac marker specimens obtained by laboratory rather than by nonlaboratory personnel. Conclusion.—The TAT expectations of the ED physicians using the results of laboratory tests measuring myocardial injury exceed those of the laboratory personnel providing the results of those tests. The actual TATs of myocardial injury testing meet the expectations of neither the providers of those tests nor the users of those test results. Improving TAT performance will require that the providers and users of laboratory services work together to develop standards that meet the needs of the medical staff and that are reasonably achievable by laboratory personnel.


Author(s):  
Darshna Jain

Background: The present study was design to assess the level of altered lipid profile, lipoprotein sub fractions, oxidative stress and antioxidants in coronary artery disease with type-2 diabetes mellitus’s patients and non diabetic patients. Methods: This case–control study included 300 subjects; out of which, 100 subjects were with normal blood glucose level and with normal ECG (Normal, N), 100 subjects  were with normal blood glucose level and AMI (non-diabetic and AMI, N-AMI) and 100 subjects were with diabetes and AMI (Diabetic and AMI, D-AMI) Results: D-AMI individuals had high level of total cholesterol (TC), triglycerides (TG), low density lipoprotein (LDL), and low level of high density lipoprotein (HDL) in comparison to N-AMI individuals. The cardiac markers such as Troponin I, creatine phosphokinase (CPK), creatine kinase-MB (CK-MB), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and C-reactive protein (CRP) levels were significantly increased in patients suffering from myocardial infarction with diabetes mellitus (DM) compared to patients of myocardial infarction without DM. The antioxidant superoxide dismutase (SOD) and glutathione (GSH) were lower in D-AMI patients than in N-AMI. However, levels of malondialdehyde (MDA) and catalase (CAT) were higher in D-AMI than in N-AMI controls. Conclusion: Our study suggested that patients with D-AMI have elevated cardiac markers and reduced antioxidants levels as compared to N-AMI patient. Keywords: Diabetes Mellitus, Acute Myocardial Infarction, Creatine Phosphokinase, Glutathione


2010 ◽  
Vol 55 (4) ◽  
pp. 1088-1091 ◽  
Author(s):  
Nick I. Batalis ◽  
Bradley J. Marcus ◽  
Christine N. Papadea ◽  
Kim A. Collins

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