Usefulness of a rapid cardiac troponin I test kit in patients with non-diagnostic chest pain or elevated CK enzyme in a Coronary Care Unit

Cardiac troponin I (cTnI) has been reported to be a highly specific marker for cardiac injury. We investigated the performance of this assay in patients admitted to a coronary care unit for suspected acute myocardial infarction (AMI), patients with extensive skeletal muscle damage, marathon runners and as a routine diagnostic test over a four week period. cTnI proved to be as sensitive a marker for AMI as creatine kinase/MB isoenzyme (CKMB) in patients admitted to the coronary care unit. In 10 patients with a proven AMI, the cTnI remained elevated from 69 to 183 h with a median time of 127 h. Cardiac troponin I had superior specificity to CKMB in patients with skeletal muscle damage. It was very useful in these patients to confirm or exclude concurrent myocardial damage. In routine diagnostic use, cTnI had greater efficiency than CKMB to classify patients as having an AMI. Consequently cTnI should replace CKMB as a marker for AMI.

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Study of Cardiac Troponin I level in Acute Coronary Syndrome and its correlation with Left Ventricular Systolic Function

Cardiovascular Journal ◽

10.3329/cardio.v12i1.43415 ◽

2019 ◽

Vol 12 (1) ◽

pp. 24-29

Author(s):

Mohammad Jakir Hossain ◽

Khondoker Asaduzzaman ◽

Solaiman Hossain ◽

Muhammad Badrul Alam ◽

Nur Hossain

Keyword(s):

Acute Coronary Syndrome ◽

Chest Pain ◽

Cardiac Troponin ◽

Troponin I ◽

Systolic Function ◽

Left Ventricular ◽

Cardiac Troponin I ◽

Left Ventricular Ejection ◽

Ventricular Ejection Fraction ◽

Coronary Syndrome

Background: In the diagnosis of acute coronary syndrome, cardiac troponin I is highly reliable and widely available biomarker. Serum level of cardiac troponin I is related to amount of myocardial damage and also closely relates to infarct size. Our aim of the study is to find out the relationship between cardiac troponin I and left ventricular systolic function after acute coronary syndrome. Methods: Total of 132 acute coronary syndrome patients were included in this study after admission in coronary care unit of Sir Salimullah Medical College, Mitford Hospital. Troponin I level was measured at admission and left ventricular ejection fraction (LVEF) was measured by echocardiography between 12-48 hours of onset of chest pain. Results: There was negative correlation between Troponin I at 12 to 48 hours of chest pain with LVEF in these study patients. With a cutoff value of troponin I e”6.8 ng/ml in STEMI patients there is a significant negative relation between 12 to 48 hrs troponin I and LVEF (p<0.001). Sensitivity of troponin I e” 6.8 ng/ml between 12 to 48 hours of chest pain in predicting LVEF <50% in STEMI was 93.75% and specificity was 77.78%. In NSTEMI sensitivity of troponin I e” 4.5 ng/ml between 12 to 48 hours of chest pain in predicting LVEF <50% was 65% and specificity was 54.05%. Conclusion: Serum troponin I level had a strong negative correlation with left ventricular ejection fraction after acute coronary syndrome and hence can be used to predict the LVEF in this setting. Cardiovasc. j. 2019; 12(1): 24-29

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Comparable detection of acute myocardial infarction by creatine kinase MB isoenzyme and cardiac troponin I

Clinical Chemistry ◽

10.1093/clinchem/40.7.1291 ◽

1994 ◽

Vol 40 (7) ◽

pp. 1291-1295 ◽

Cited By ~ 197

Author(s):

J E Adams ◽

K B Schechtman ◽

Y Landt ◽

J H Ladenson ◽

A S Jaffe

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Creatine Kinase ◽

Cardiac Troponin ◽

Troponin I ◽

Characteristic Curve ◽

Cardiac Injury ◽

Cardiac Troponin I ◽

Creatine Kinase Mb ◽

Coronary Care

Abstract Although measurement of cardiac troponin I (cTnI) is, in some situations, more specific for detection of cardiac injury than is measurement of the MB isoenzyme of creatine kinase (MBCK), its sensitivity and specificity relative to MBCK for detection of myocardial infarction has not been established. Accordingly, we studied prospectively 199 consecutive patients admitted to the coronary care unit. Values of MBCK and cTnI mass were determined in all samples. Of the 188 patients admitted with a suspicion of acute myocardial ischemia, 89 were diagnosed as having an acute myocardial infarction on the basis of the patterns of MBCK values. Eighty-six of these patients also had increased cTnI (concordance, 96.6%); three did not. Of the patients diagnosed as without infarction, five with unstable angina and symptoms in the day(s) prior to admission had increased cTnI, for a cTnI specificity of 94.9%. Receiver operating characteristic curve analysis indicated that cTnI and MBCK had statistically indistinguishable diagnostic accuracies for the detection of acute myocardial infarction.

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Emergency department triage of patients with acute chest pain: definition of cardiac troponin I decisional value to manage patients without electrocardiographic evidence of ischemia

Clinical Chemistry and Laboratory Medicine (CCLM) ◽

10.1515/cclm.2004.094 ◽

2004 ◽

Vol 42 (5) ◽

Cited By ~ 1

Author(s):

Pascale Beyne ◽

Erik Bouvier ◽

Patrick Werner ◽

Pierre Bourgoin ◽

Damien Logeart ◽

...

Keyword(s):

Chest Pain ◽

Cardiac Troponin ◽

Troponin I ◽

Acute Chest Pain ◽

Final Diagnosis ◽

Cardiac Troponin I ◽

Reference Limit ◽

Coronary Syndrome ◽

Definition Of ◽

Upper Reference Limit

AbstractThe aim of this study was to define the use of a new cardiac troponin I (cTnI) assay for emergency patients with chest pain and no specific electrocardiographic changes consistent with the presence of ischemia. Patients (n=106) admitted in Emergency/Cardiology Departments for chest pain and suspicion of acute coronary syndrome (ACS) were randomized into two diagnosis groups (ACS or non-ACS) by two independent cardiologists. cTnI measurements were performed at admission, and 6 hours and 12 hours later with a new generation assay (Access AccuTnI, Beckman Coulter). Using an upper reference limit of 0.04 μg/l, 27 patients had a cTnI elevation not related to the final diagnosis of ischemia; the positive predictive value (PPV) was 67% with specificity 48%. The decisional value was re-defined and set at 0.16 μg/l, a concentration corresponding to the 99th percentile of the non-ACS patient group. Precision (coefficient of variation) was 8% at this level, PPV 97% and specificity 98%. This new decisional value is now used in our institution and could be included in standard care guidelines to improve the management of patients presenting chest pain in emergency departments.

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Comparison of Myocardial Perfusion Imaging and Cardiac Troponin I in Patients Admitted to the Emergency Department With Chest Pain

Circulation ◽

10.1161/01.cir.99.16.2073 ◽

1999 ◽

Vol 99 (16) ◽

pp. 2073-2078 ◽

Cited By ~ 103

Author(s):

Michael C. Kontos ◽

Robert L. Jesse ◽

F. Philip Anderson ◽

Kristin L. Schmidt ◽

Joseph P. Ornato ◽

...

Keyword(s):

Emergency Department ◽

Chest Pain ◽

Myocardial Perfusion Imaging ◽

Myocardial Perfusion ◽

Perfusion Imaging ◽

Cardiac Troponin ◽

Troponin I ◽

Cardiac Troponin I

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Cardiac Troponin I and T Concentrations in Patients with Cocaine-Associated Chest Pain

Annals of Clinical Biochemistry International Journal of Laboratory Medicine ◽

10.1177/000456329603300301 ◽

1996 ◽

Vol 33 (3) ◽

pp. 183-186 ◽

Cited By ~ 30

Author(s):

Mary McLaurin ◽

Fred S Apple ◽

Timothy D Henry ◽

Scott W Sharkey

Keyword(s):

Skeletal Muscle ◽

Chest Pain ◽

Cardiac Troponin ◽

Muscle Injury ◽

Troponin I ◽

Troponin T ◽

Acute Chest Pain ◽

Cardiac Troponin I ◽

Skeletal Muscle Injury ◽

Rule Out

Patients with cocaine-related chest pain with electrocardiographic (ECG) abnormalities are often admitted to rule out acute myocardial infarction (AMI). Cardiac troponin I and T should be superior to measurement of creatine kinase (CK)—MB for detecting cardiac injury in patients with coexisting skeletal muscle injury. We prospectively evaluated 19 consecutive patients with acute chest pain related to cocaine use who were hospitalized to rule out AMI. The admission ECG was abnormal in 16 of 19 patients. Total CK and CK—MB were elevated during the hospital course in 14 and 3 patients, respectively. Cardiac troponin I and cardiac troponin T levels were within normal limits in all patients demonstrating that recent myocardial injury did not occur. Clinically, no patient had an AMI. Cocaine-induced thoracic skeletal muscle injury or transient cocaine-induced coronary vasospasm should be considered as alternative sources of chest pain in these patients.

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Combination of Goldman Risk and Initial Cardiac Troponin I for Emergency Department Chest Pain Patient Risk Stratification

Academic Emergency Medicine ◽

10.1111/j.1553-2712.2001.tb00187.x ◽

2001 ◽

Vol 8 (7) ◽

pp. 696-702 ◽

Cited By ~ 63

Author(s):

Alex Limkakeng ◽

W. Brian Gibler ◽

Charles Pollack ◽

James W. Hoekstra ◽

Frank Sites ◽

...

Keyword(s):

Emergency Department ◽

Chest Pain ◽

Risk Stratification ◽

Cardiac Troponin ◽

Troponin I ◽

Cardiac Troponin I ◽

Pain Patient ◽

Patient Risk ◽

Chest Pain Patient

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Autoantibody prevalence with an improved immunoassay for detecting cardiac troponin-specific autoantibodies

Clinical Chemistry and Laboratory Medicine (CCLM) ◽

10.1515/cclm-2013-0310 ◽

2014 ◽

Vol 52 (2) ◽

Cited By ~ 7

Author(s):

Tanja Savukoski ◽

Tuomo Ilva ◽

Juha Lund ◽

Pekka Porela ◽

Noora Ristiniemi ◽

...

Keyword(s):

Myocardial Infarction ◽

Emergency Department ◽

Chest Pain ◽

Cardiac Troponin ◽

Troponin I ◽

State Of The Art ◽

Cardiac Troponin I ◽

High Prevalence ◽

Sandwich Type ◽

Pain Patients

AbstractCardiac troponin-specific autoantibodies (cTnAAb) can interfere with the measurement of cardiac troponin I (cTnI) by immunoassays used for the diagnosis of myocardial infarction (MI). Here, an improved version of a previous autoantibody assay was validated and used to evaluate the cTnAAb prevalence in a cohort of consecutive chest pain patients presenting to an emergency department.Admission samples from 510 patients with suspected MI were analyzed in parallel with two sandwich-type cTnAAb assays based on different cTnI epitopes used to capture cardiac troponin-bound cTnAAbs.Sample-specific backgrounds were lower for the new assay than for the old assay (median 1225 vs. 2693 counts, p<0.001). Net signals of cTnAAb-positive samples were higher for the new assay than for the old assay (median 5076 vs. 3921 counts, p<0.001). Of all patients, 9.2% were cTnAAb-positive for the new assay and 7.3% for the old assay (p=0.013). Previous cardiac problems were not associated with cTnAAb status and cTnAAb status did not correlate with the 12-month outcome.With our new and more sensitive autoantibody assay, approximately one out of ten patients who presented to the initial cardiac triage had detectable amounts of cTnAAbs in the circulation. Because these cTnAAbs can interfere with state-of-the-art cTnI assays, their high prevalence should be acknowledged by clinical chemists, physicians, and kit manufacturers.

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