Elevated Cardiac Troponin in Clinical Scenarios Beyond Obstructive Coronary Artery Disease (original) (raw)
Related papers
Elevated troponin level is not synonymous with myocardial infarction
International Journal of Cardiology, 2006
Background: Elevated troponin I in the absence of angiographically visible coronary lesions is seen in up to 10 -15% of those undergoing angiography for suspected coronary artery disease. This study aims to elucidate the etiology of elevated cardiac troponin I in patients with normal coronary arteries on angiography. Methods: We identified 1551 (8.6%) patients with normal coronary arteries from our catheterization database of 17,950 patients from Jan 2000 to Jun 2004. Elevated troponin I levels were found in 217 (14%) of 1551 patients with normal coronary arteries. Of these 217 patients, 73 surgical patients were excluded, and the remaining 144 patients formed the study population. The study population was compared with age and gender matched patients with myocardial infarction and coronary artery disease (Group II). Results: The patients with elevated cardiac troponin I (cTnI) with normal coronary arteries had significantly lower prevalence of atherosclerotic risk factors and significantly higher left ventricular ejection fractions. The cTnI in patients with normal coronary arteries was elevated due to a number of causes including tachycardia, myocarditis, pericarditis, severe aortic stenosis, gastrointestinal bleeding, sepsis, left ventricular hypertrophy, severe congestive heart failure, cerebrovascular accident, electrical trauma, myocardial contusion, hypertensive emergency, myocardial bridging, pulmonary embolism, diabetic ketoacidosis, chronic obstructive pulmonary disease exacerbation and coronary spasm. Conclusions: Cardiac troponin I could be elevated in a number of conditions, apart from acute myocardial infarction, and could reflect myonecrosis. Acute myocardial infarction is a clinical diagnosis as the laboratory is an aide to, not a replacement for, informed decision making. D 2005 Published by Elsevier Ireland Ltd.
A Review of Causes and Systemic Approach to Cardiac Troponin Elevation
Clinical Cardiology, 2011
task force published recommendations for a universal definition of myocardial infarction (MI) in 2000 based on the measurement of troponin (Tn). Although this rapid and highly sensitive blood test is certainly valuable in the appropriate setting, its widespread use in variety of clinical scenarios may lead to the detection of Tn elevation in absence of thrombotic acute coronary syndrome. In 2007,
The American Journal of Emergency Medicine, 1999
This study evaluated the role of serum cardiac troponin I as a biochemical marker for the diagnosis of acute coronary syndromes in the presence of noncardiac diseases. Diagnostic characteristics were examined in 102 consecutive patients who were found to have serum cardiac troponin I levels higher than the upper reference limit of 0.6 ng/mL. Of 102 patients with cardiac troponin I levels of >0.6 ng/mL, 35 did not have the final diagnoses of acute coronary syndromes (myocardial infarction or unstable angina) but had various other final diagnoses, including nonischemic dilated cardiomyopathy, muscular disorders, central nervous systern disorders, HIV disease, chronic renal failure, sepsis, lung diseases, and endocrine disorders. The mean value of serum cardiac troponin I in the patients with diseases other than acute coronary syndromes was significantly lesser than in those with acute coronary syndromes (2.0 -+ 1.9 [SD] v 24.7 -28.2 ng/mL; P < .0001). There were significantly fewer histories of chest pain and prior myocardial infarction in patients with diseases other than acute coronary syndromes than in those with acute coronary syndromes (history of chest pain, 3 v 48 patients [P < .001]; history of prior myocardial infarction, 0 v 30 patients [P < .001]). In conclusion, elevated serum levels of cardiac troponin I, especially in the lower ranges, should be interpreted with caution, particularly in patients suffering from acute illnesses who lack other diagnostic features suggestive of acute coronary ischemic events. (Am J Emerg Med 1999;17:225-229.
Troponin elevation in coronary vs. non-coronary disease
European Heart Journal, 2010
Acute myocardial infarction is defined as myocardial cell death due to prolonged myocardial ischaemia. Cardiac troponins (cTn) are the most sensitive and specific biochemical markers of myocardial injury and with the new high-sensitivity troponin methods very minor damages on the heart muscle can be detected. However, elevated cTn levels indicate cardiac injury, but do not define the cause of the injury. Thus, cTn elevations are common in many disease states and do not necessarily indicate the presence of a thrombotic acute coronary syndrome (ACS). In the clinical work it may be difficult to interpret dynamic changes of troponin in conditions such as stroke, pulmonary embolism, sepsis, acute perimyocarditis, Tako-tsubo, acute heart failure, and tachycardia. There are no guidelines to treat patients with elevated cTn levels and no coronary disease. The current strategy of treatment of patients with elevated troponin and non-acute coronary syndrome involves treating the underlying causes. The aim of this paper is to review data from studies of non-ACS patients with acutely elevated troponin who in clinical practice may be difficult to discriminate from ACS patients.
International Journal of Cardiology, 2005
Objectives: Cardiac troponins are highly sensitive and specific markers of myocardial cell injury. We wished to determine the clinical relevance of raised troponins in the absence of significant angiographic coronary artery disease. Design and methods: We assessed patients admitted to our hospital over the past 3 years with troponin-positive chest pain and no angiographically significant coronary disease. Results: The study included 67 patients, all of whom had symptoms of bchest painQ and elevated (N0.2 Ag/L) troponin I on admission. Thirtyfour (51%) patients had alternative causes for myocyte injury other than coronary ischaemia. In the remaining 33 (49%) patients we could find no other associated features or diagnoses. Follow up was obtained in 29 (88%) of these 33 patients (mean follow up 58F13 weeks, range 17-156 weeks). During the follow up period, three (4.5%) patients were readmitted with further ischaemic events. Conclusions: Myocardial damage can occur in the absence of significant angiographic coronary disease and other causes of raised troponins should be considered according to the clinical presentation. Troponin-positive cases with angiographically bnormalQ coronary arteries can represent with future cardiac events and should still be considered for aggressive risk management. D
The clinical significance of cardiac troponins in medical practice
Journal of the Saudi Heart Association, 2011
Troponins are regulatory proteins that form the cornerstone of muscle contraction. The amino acid sequences of cardiac troponins differentiate them from that of skeletal muscles, allowing for the development of monoclonal antibody-based assay of troponin I (TnI) and troponin T (TnT). Along with the patient history, physical examination and electrocardiography, the measurement of highly sensitive and specific cardiac troponin has supplanted the former gold standard biomarker (creatine kinase-MB) to detect myocardial damage and estimate the prognosis of patients with ischemic heart disease. The current guidelines for the diagnosis of non-ST segment elevation myocardial infarction are largely based on an elevated troponin level. The implementation of these new guidelines in clinical practice has led to a substantial increase in the frequency of myocardial infarction diagnosis.
Increased Troponin Levels in Nonischemic Cardiac Conditions and Noncardiac Diseases
Journal of Interventional Cardiology, 2008
Elevated cardiac troponin levels often lead to a diagnosis of acute coronary syndrome (ACS). However, this finding may occur also in other conditions, both nonischemic and noncardiovascular, leading to an incorrect diagnosis of ACS and, sometimes, invasive tests. We describe various cardiovascular diseases other than ACS (heart failure, pulmonary embolism, etc.) and noncardiovascular diseases (renal failure, etc.) that may cause elevated troponin levels and give possible explanations and prognostic relevance for this rise.
High-sensitive cardiac troponin: friend or foe?
Swiss Medical Weekly, 2011
Cardiac troponin I and T (cTn) are structural proteins unique to the heart. Detection of cTn in peripheral blood indicates cardiomyocyte necrosis. As acute myocardial infarction (AMI) is the most important cause of cardiomyocyte necrosis, cTns have become an integral part in the diagnosis of AMI. In this indication, cTns are superior to all other biomarkers indicating cardiomyocyte necrosis such as CK-MB and myoglobin, and are therefore considered the preferred marker in the diagnosis of AMI. It is important to highlight that cTn indicates and quantifies cardiomyocyte necrosis irrespective of its cause? The major limitation of contemporary cTn assays is a sensitivity deficit in the first few hours of AMI due to a delayed increase of circulating levels. Recent advances in assay technology have lead to a refinement in cardiac troponin (cTn) assays that have had a profound impact on clinical practice. High-sensitive cTn assays have two differentiating features from contemporary cTn assays: 1) detection of cTn in healthy persons and 2) a precise definition of what is "normal" (= the 99th percentile). Recent multicentre studies have shown that high-sensitive cTn assays improve the early diagnosis of AMI. To achieve the best clinical use, cTn has to be interpreted as a quantitative variable. Rising and/or falling levels differentiate acute from chronic cardiomyocyte necrosis. The term "troponin-positive" should Figure 1
International Journal of Clinical Cardiology, 2019
Background: Several studies have linked elevated cardiac troponin to increased overall risk in patients with acute coronary syndrome but the prognostic significance of elevated troponin in non-cardiac conditions remains scanty. Objectives: The primary aim of this study was to investigate the prognostic significance of elevated high sensitivity troponin T (TnT-HS) in non-cardiac disorders outside the remit of an acute coronary syndrome (ACS). Secondarily we aimed to investigate the impact of cardiovascular comorbidities and other clinical presentations in the release of cardiac biomarkers in non-cardiac disorders. Methodology: This was a retrospective electronic patient record pilot review where all patients with elevated TnT-HS without acute coronary syndrome, recent angioplasty or heart failure within a three month period were enrolled into the study and subsequently followed prospectively for a six month period. From January 1, 2016 to June 30, 2016, a total of 2535 patients were screened of which 306 patients had elevated TnT-HS and 162 patients met the study inclusion criteria. Data were encrypted and collected in Google database format, exported into excel spreadsheet, analyzed and computed using SPSS (version 24) to identify clinical associations with increased values of TnT-HS. Results: Most troponin TnT-HS samples (77.1%) were obtained from emergency room (ER) attendance and 63.4% of patients were male. The mean age was 72 years and no Conclusions: TnT-HS positivity should be cautiously interpreted in patients exhibiting non acute cardiac conditions associated CKD, infections, and CVAs. This troponin elevation in non-cardiac conditions still carries a significant adverse prognosis. After adjusting for age and renal insufficiency, we can suggest a new cut off level of TnT-HS > 30 ng/l to have increased risk of MACCE within 180 days in non-cardiac conditions.