scholarly journals Increases of Cardiac Troponin in Conditions other than Acute Coronary Syndrome and Heart Failure

2009 ◽  
Vol 55 (12) ◽  
pp. 2098-2112 ◽  
Author(s):  
Walter E Kelley ◽  
James L Januzzi ◽  
Robert H Christenson

AbstractBackground: Although cardiac troponin (cTn) is a cornerstone marker in the assessment and management of patients with acute coronary syndrome (ACS) and heart failure (HF), cTn is not diagnostically specific for any single myocardial disease process. This narrative review discusses increases in cTn that result from acute and chronic diseases, iatrogenic causes, and myocardial injury other than ACS and HF.Content: Increased cTn concentrations have been reported in cardiac, vascular, and respiratory disease and in association with infectious processes. In cases involving acute aortic dissection, cerebrovascular accident, treatment in an intensive care unit, and upper gastrointestinal bleeding, increased cTn predicts a longer time to diagnosis and treatment, increased length of hospital stay, and increased mortality. cTn increases are diagnostically and prognostically useful in patients with cardiac inflammatory diseases and in patients with respiratory disease; in respiratory disease cTn can help identify patients who would benefit from aggressive management. In chronic renal failure patients the diagnostic sensitivity of cTn for ACS is decreased, but cTn is prognostic for the development of cardiovascular disease. cTn also provides useful information when increases are attributable to various iatrogenic causes and blunt chest trauma.Summary: Information on the diagnostic and prognostic uses of cTn in conditions other than ACS and heart failure is accumulating. Although increased cTn in settings other than ACS or heart failure is frequently considered a clinical confounder, the astute physician must be able to interpret cTn as a dynamic marker of myocardial damage, using clinical acumen to determine the source and significance of any reported cTn increase.

2009 ◽  
Vol 55 (5) ◽  
pp. 938-945 ◽  
Author(s):  
Kim Pettersson ◽  
Susann Eriksson ◽  
Saara Wittfooth ◽  
Emilia Engström ◽  
Markku Nieminen ◽  
...  

Abstract Background: Cardiac troponin (cTn) is an established marker of myocardial infarction. Pronounced heterogeneity and the minute amounts released into the circulation constitute significant challenges for cTn detection. Recently, autoantibody formation to cTn was shown to be common and to interfere with immunoassay performance. In this study, we investigated cTn autoantibodies and cardiac troponin I (cTnI) in acute coronary syndrome (ACS) patients over a 1-year period after the index event. Methods: We used a second-generation cTnI assay designed to reduce the interference of cTn autoantibodies. The assay for cTn autoantibodies used 2 anti-cTnI antibodies to capture the ternary cTnI-complex, enabling unrestricted binding of the autoantibodies, which were detected with a labeled antihuman IgG antibody. We analyzed serum samples from 81 non–ST-elevation ACS patients taken at admission and after 1 week and 3 and 12 months. Results: We found 14 cTn autoantibody–positive patients (21%) among the 67 cTnI-positive and none among the 14 cTnI-negative patients. Nine were autoantibody-positive at admission, and 5 became positive at 1 week. Autoantibody signals significantly increased in the 1-week and 3-month samples. At all time points, cTnI was significantly increased in the autoantibody-positive group relative to the negative group. Persistent cTnI elevations at 3 and 12 months were seen in the patients already autoantibody positive at admission. Conclusions: During ACS, patients with cTn autoantibodies have higher cTnI release and therefore larger myocardial damage than patients without autoantibodies. Their cTnI release also lasts longer, at least months. The possible prognostic impact of these observations must be evaluated in larger clinical cohorts.


2017 ◽  
Vol 63 (1) ◽  
pp. 223-235 ◽  
Author(s):  
Kai M Eggers ◽  
Bertil Lindahl

Abstract BACKGROUND Increased cardiac troponin concentrations in acute coronary syndrome (ACS) identify patients with ongoing cardiomyocyte necrosis who are at increased risk. However, with the use of more precise assays, cardiac troponin increases are commonly noted in other cardiovascular conditions as well. This has generated interest in the use of cardiac troponin for prognostic assessment and clinical management of these patients. In this review, we have summarized the data from studies investigating the implications of cardiac troponin concentrations in various acute and chronic conditions beyond ACS, i.e., heart failure, myocarditis, Takotsubo cardiomyopathy, aortic dissection, supraventricular arrhythmias, valve disease, pulmonary arterial hypertension, stroke, and in the perioperative setting. CONTENT Cardiac troponin concentrations are often detectable and frankly increased in non-ACS conditions, in particular when measured with high-sensitivity (hs) assays. With the exception of myocarditis and Takotsubo cardiomyopathy, cardiac troponin concentrations carry strong prognostic information, mainly with respect to mortality, or incipient and/or worsening heart failure. Studies investigating the prognostic benefit associated with cardiac troponin–guided treatments however, are almost lacking and the potential role of cardiac troponin in the management of non-ACS conditions is not defined. SUMMARY Increased cardiac troponin indicates increased risk for adverse outcome in patients with various cardiovascular conditions beyond ACS. Routine measurement of cardiac troponin concentrations can however, not be generally recommended unless there is a suspicion of ACS. Nonetheless, any finding of an increased cardiac troponin concentration in a patient without ACS should at least prompt the search for possible underlying conditions and these should be managed meticulously according to current guidelines to improve outcome.


2020 ◽  
Vol 24 (6) ◽  
pp. 28-39
Author(s):  
E. A. Vorobyev ◽  
O. V. Galkina ◽  
I. M. Zubina ◽  
E. O. Bogdanova ◽  
E. N. Levy`kina ◽  
...  

2017 ◽  
pp. 101-106
Author(s):  
Thi Thanh Hien Bui ◽  
Hieu Nhan Dinh ◽  
Anh Tien Hoang

Background: Despite of considerable advances in its diagnosis and management, heart failure remains an unsettled problem and life threatening. Heart failure with a growing prevalence represents a burden to healthcare system, responsible for deterioration of patient’s daily activities. Galectin-3 is a new cardiac biomarker in prognosis for heart failure. Serum galectin-3 has some relation to heart failure NYHA classification, acute coronary syndrome and clinical outcome. Level of serum galectin-3 give information for prognosis and help risk stratifications in patient with heart failure, so intensive therapeutics can be approached to patients with high risk. Objective: To examine plasma galectin-3 level in hospitalized heart failure patients, investigate the relationship between galectin-3 level with associated diseases, clinical conditions and disease progression in hospital. Methodology: Cross sectional study. Result: 20 patients with severe heart failure as NYHA classification were diagnosed by The ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure (2012) and performed blood test for serum galectin-3 level. Increasing of serum galectin-3 level have seen in all patients, mean value is 36.5 (13.7 – 74.0), especially high level in patient with acute coronary syndrome and patients with severe chronic kidney disease. There are five patients dead. Conclusion: Serum galectin-3 level increase in patients with heart failure and has some relation to NYHA classification, acute coronary syndrome. However, level of serum galectin-3 can be affected by severe chronic kidney disease, more research is needed on this aspect Key words: Serum galectin-3, heart failure, ESC Guidelines, NYHA


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
S El-Deek ◽  
A.R Meki ◽  
A Hassan ◽  
M Gaber ◽  
O Mohamed

Abstract Introduction Acute coronary syndrome (ACS) is a leading cause of mortality and morbidity worldwide. Despite being the gold standard biomarkers, cTn and CK-MB have a major drawback as they are less sensitive in the first 3 hours of the onset of symptom. So, there is still a need for novel biomarkers, which can reliably rule in or rule out this disease immediately on admission. Aim of the work To evaluate the role of copeptin, miRNA-499 and miRNA-208 as novel biomarkers for early detection of unstable angina (UA) and non-ST-segment elevation myocardial infarction (NSTEMI) Patients and Methods: A total of 65 patients presenting within 4 h of onset of chest pain suggestive of ACS were enrolled in the study. They included 23 UA, 42 NSTEMI. Also 25 apparently healthy controls were included. Blood samples (first set within the first 3 hours and second set at 6 hours) were taken for estimation of copeptin by ELISA and miRNA-499 and miRNA-208 expression levels by real time PCR. Results Copeptin, miRNA-499 and miRNA-208 expression levels were significantly increased in UA and NSTEMI patients compared to controls (P<0.001 each). Also these biomarkers were significantly increased in NSTEMT compared to UA (P<0.001 each). They also significantly elevated in UA and NSTEMI patient in the first 3 hours who had negative cardiac troponin (p<0.001 each). ROC curve analysis revealed that the area under curve (AUC) for prediction of ACS was 0.96 for copeptin, 0.97 for miRNA-499 and 0.0.97 for miRNA-208. Interestingly, combining copeptin with miRNA-499 and miRNA-210 significantly improved the diagnostic value by increasing the AUC to 0.98, P<0.001. The sensitivity and specificity within the first 3 hours were 90%, 86% for copeptin, 95%, 94% for miRNA-499 and 93%, 98% for miRNA-208. The sensitivity and specificity were 81% and 86% for cardiac troponin within 6 hours. There was a positive correlation between copeptin and miRNA-499 and miRNA-208 (r=0.75, P<0.001 and r=0.76, P<0.001 respectively) Also, there was a positive correlation between these biomarkers and cTn (r=0.7. P<0.001, r=0.64, P<0.001 and r=0.68, P<0.001 respectively). Conclusions Copeptin, miRNA-499 and miRNA-208 expression might be novel biomarkers as they are associated with UA and NSTEMI presented in the first 3 hours of onset of pain. The combination of copeptin and miRNA with cTn accelerate the diagnosis of ACS and avoiding the gray zone of cTn. Copeptin and miRNAs representing a potential aid in early diagnosis as they have different pathogenesis and site of liberation. Funding Acknowledgement Type of funding source: None


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