scholarly journals ELEVATED TROPONIN LEVEL IS NOT SYNONYMOUS WITH MYOCARDIAL INFARCTION

CHEST Journal ◽  
2005 ◽  
Vol 128 (4) ◽  
pp. 166S ◽  
Author(s):  
Nitin Mahajan ◽  
Yatin Mehta ◽  
Malcolm Rose ◽  
Jacob Shani ◽  
Edgar Lichstein
2006 ◽  
Vol 15 (3) ◽  
pp. 280-288 ◽  
Author(s):  
Wendy Lim ◽  
Deborah J. Cook ◽  
Lauren E. Griffith ◽  
Mark A. Crowther ◽  
P. J. Devereaux

• Background Levels of cardiac troponin, a sensitive and specific marker of myocardial injury, are often elevated in critically ill patients. • Objectives To document elevated levels of cardiac troponin I in patients in a medical-surgical intensive care unit and the relationship between elevated levels and electrocardiographic findings and mortality. • Methods A total of 198 patients expected to remain in the intensive care unit for at least 72 hours were classified as having myocardial infarction (cardiac troponin I level ≥1.2 μg/L and ischemic electrocardiographic changes), elevated troponin level only (≥1.2 μg/L and no ischemic electrocardiographic changes), or normal troponin levels. Events were classified as prevalent if they occurred within 48 hours after admission and as incident if they occurred 48 hours or later after admission. Factors associated with mortality were examined by using regression analysis. • Results A total of 171 patients had at least one troponin level measured in the first 48 hours. The prevalence of elevated troponin level was 42.1% (72 patients); 38 patients (22.2%) had myocardial infarction, and 34 (19.9%) had elevated troponin level only. After the first 48 hours, 136 patients had at least 1 troponin measurement. The incidence of elevated troponin level was 11.8% (16 patients); 7 patients (5.1%) met criteria for myocardial infarction, and 2 (1.5%) had elevated troponin level only. Elevated levels of troponin I at any time during admission were associated with mortality in the univariate but not the multivariate analysis. • Conclusions Elevated levels of cardiac troponin I in critically ill patients do not always indicate myocardial infarction or an adverse prognosis.


2006 ◽  
Vol 111 (3) ◽  
pp. 442-449 ◽  
Author(s):  
Nitin Mahajan ◽  
Yatin Mehta ◽  
Malcolm Rose ◽  
Jacob Shani ◽  
Edgar Lichstein

2021 ◽  
Vol 10 (Supplement_1) ◽  
Author(s):  
SR Meisel ◽  
OM Kobo ◽  
M Kleisener Shochat ◽  
M Saada ◽  
N Amsalem ◽  
...  

Abstract Funding Acknowledgements Type of funding sources: None. Background Patients frequently present to the emergency department (ED) with chest pain, dyspnea, or other symptoms with elevated troponin level. This finding prompts a provisional diagnosis of myocardial ischemia and raises the need to exclude this possibility. However, elevated blood troponin may be the result of a systemic inflammatory or infectious state merely representing cardiac injury and not myocardial ischemia. Purpose We hypothesized that the ratio of CRP/troponin could reflect the extent of the systemic inflammatory state that induces an attendant cardiac injury, which if sufficiently high could exclude myocardial ischemia. Methods Study population included 10774 patients admitted to the ED during the years 2016-2019 with cTn level higher > 14 ng/liter. CRP level was measured in all patients and CRP/troponin ratio was assessed against discharge diagnosis of myocardial ischemia, in order to evaluate its ability to exclude ischemic etiology of symptoms. The incidence of myocardial ischemia among study patients decreased with increasing CRP/troponin value. Results The prevalence of myocardial ischemia was 760/2694 patients (28.2%), 415/2694 (15.4%), 294/2695 (10.9%) and 130/2694 (4.8%) with 1st-4th CRP/troponin quartile, respectively (p < 0.0001). Logistic regression has shown that the probability of myocardial ischemia decreased by 53%, 68%, and 87% in the second to fourth CRP/troponin quartile compared with the first quartile, respectively (p < 0.0001). Conclusion The present study has shown that increased CRP level seems to modulate the specificity of simultaneous troponin as a marker of ischemia. As CRP level increases, so increases the likelihood that concomitant elevated troponin is due to myocardial injury and not due to myocardial ischemia. The clinical implication is that in the presence of a high CRP/troponin ratio, admission to the cardiology department and coronary investigation are unnecessary, whereas appropriate investigation of the actual medical problem is warranted.


2005 ◽  
pp. 1191-1202
Author(s):  
Luciano Babuin ◽  
Allan S. Jaffe

It has been known for 50 years that transaminase activity increases in patients with acute myocardial infarction. With the development of creatine kinase (CK), biomarkers of cardiac injury began to take a major role in the diagnosis and management of patients with acute cardiovascular disease. In 2000 the European Society of Cardiology and the American College of Cardiology recognized the pivotal role of biomarkers and made elevations in their levels the “cornerstone” of diagnosis of acute myocardial infarction. At that time, they also acknowledged that cardiac troponin I and T had supplanted CK-MB as the analytes of choice for diagnosis. In this review, we discuss the science underlying the use of troponin biomarkers, how to interpret troponin values properly and how to apply these measurements to patients who present with possible cardiovascular disease. Troponin is the biomarker of choice for the detection of cardiac injury. To use it properly, one must understand how sensitive the specific assay being used is for detecting cardiac injury, the fact that elevated troponin levels are highly specific for cardiac injury and some critical issues related to the basic science of the protein and its measurement. In this article, we review the biology of troponin, characteristics of assays that measure serum troponin levels and how to apply these measurements to patients who present with possible cardiovascular disease. We also discuss other clinical situations in which troponin levels may be elevated.


2013 ◽  
Vol 2013 ◽  
pp. 1-5 ◽  
Author(s):  
O. Hammarsten

Changes in cardiac troponin (cTn) levels are often evaluated when myocardial infarction (MI) is suspected. The change in the troponin level required for diagnosis is being debated but should exceed the natural biological variation according to current guidelines. Despite this, several reports show that MI patients often present at the emergency ward with relatively stable cTn elevations. In this review we discuss the potential problem using a small cTn change as a way to exclude MI and also provide a possible solution to this diagnostic problem using long-term cTn change.


2015 ◽  
Vol 65 (10) ◽  
pp. A44
Author(s):  
Lucas Amedeo Burke ◽  
Manoj Jadhav ◽  
Carsten Schmalfuss ◽  
Carl Pepine ◽  
David Winchester

Author(s):  
Allan S Jaffe

Understanding the proper use of biomarkers requires clinicians to appreciate some critical pre-analytic and analytic issues, as well as how to use the markers properly. The bene?ts of such an approach will not only facilitate the care of patients today, but will also prepare clinicians to understand and embrace the new generation of markers that is coming and that will continue to make this area transformational for cardiology. Two fundamental concepts underlie the clinical use of biomarkers: First, biomarkers should always be used in conjunction with all other clinical information. Second, in order to maximize their diagnostic and prognostic use, biomarkers should be interpreted as quantitative variables. For example, a cardiac troponin level which is 50 times the upper limit of normal has a much higher positive predictive value for the presence of an acute myocardial infarction, compared to a level just above the upper limit of normal.


Author(s):  
Hussain Khawaja ◽  
Alexandre Makarian ◽  
Maheen Fatima ◽  
Mikhail Torosoff

Background: We have investigated clinical correlates of elevated troponin and studied contemporary management of patients with stroke and evidence suggestive for Type 2 myocardial infarction (MI). Material and Methods: Restrospective chart review was performed on 380 consecutive stroke patients referred for an echocardiographic evaluation. Of these 342 had troponin tested for chest pain and/or abnormal ECG. Patients were further divided into 3 groups according to the troponin level: Group I - 253 (74%) with normal, Group II - 72 ( 21% ) with intermediate, and Group III - 17 (5%) with level consistent with MI diagnosis. ANOVA and chi-square tests were employed. Study was approved by the institutional IRB. Results: Mortality and prolonged length of stay both strongly correlated with highest achieved troponin level (4% mortality in Gr I, 10% in Gr II, and 29% in Gr III, p<0.001). Patients with CVA and Type 2 MI (Group III) had lower hematocrit (p<0.001) and higher creatinine (p=0.009) then the rest of the cohort. However, there was no correlation between elevated troponin and patients' age, gender, history of CAD, diabetes, hypertension, dyslipidemia, peripheral vascular disease, or chronic renal failure/hemodialysis. ECG abnormalities (mostly negative T waves) were slightly, but not significantly more prevalent in Type 2 MI patients (18% vs. 9% in Gr I and 14% in Gr II, p=0.37). Prevalence of decreased ejection fraction was significantly higher in Type 2 MI, but only at initial evaluation (p=0.0001), while the follow-up echocardiograms showed no such difference (p=0.842). Abnormal, ischemic stress test result were equally common in all groups (p=0.427). Conclusion: CVA patients with abnormal troponin incur increased mortality and protracted hospital stay. Traditional CAD risk factors are poor predictors of abnormal troponin in CVA patients. Cardiac testing in this population appears to be of limited utility. Randomized studies of this important subject are needed.


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