troponin 高，可以 rule in ACS；低，不能exclude ACS，就醬
Troponin I 會在馬拉松後，會在腎衰竭後升高，不見得代表myocardial injury，目前認為是另一種機制讓他釋出；高，在一個病人身上，和poor prognosis相關，在正常人身上，代表的是CV risk 升高
不高，不能排除unstable angina, 這讓傳統的ECG及clinical assessment更形重要，0-4-8小時監測Tn還是重要!!!
Diagnosing Acute Coronary Syndromes: The Troponin Conundrum
As the sensitivity of Tn assays rises, electrocardiographic and clinical evidence of ACS become more — not less — important in treatment decisions.
The diagnostic criteria for myocardial infarction (MI) are obtained from the triad of clinical presentation, electrocardiogram (ECG) changes, and serial cardiac enzyme or biomarker measurements. In recent years, the emphasis on biomarkers — specifically, troponin (Tn) — has increased, while ECG findings and clinical symptoms have received relatively little attention. Nonetheless, a detectable Tn level alone does not equal a diagnosis of MI.
TROPONIN AND MYOCARDIAL DAMAGE
Acute coronary syndromes (ACS) is a general term used when clinical symptoms and signs of myocardial ischemia are caused by obstruction of flow through the coronary arteries, and it typically has included both MI and unstable angina. A European Society of Cardiology and American College of Cardiology joint consensus document (published in 2000, updated in 2007) explicitly defines MI as myocardial necrosis secondary to ischemia, which can also occur in ACS without MI. Cardiac Tn is an extremely specific marker of cardiac injury; however, myocardial damage is not specific to either MI or ACS.
Several new high-sensitivity Tn (hsTn) assays are able to detect levels of Tn that would register as zero with older, conventional assays. The advantages of the hsTn assays — greater sensitivity in identifying myocardial injury and potential for earlier detection of MI — come at the cost of a reduction in specificity for the diagnosis of ACS. Indeed, in a recent report, investigators used cardiac computed tomography to confirm a mechanistic association between elevated hsTn levels and myocardial damage, not only in patients with ACS but also in those without ACS. Even with conventional Tn assays, patients can have detectable Tn levels because of etiologies other than ACS; the use of hsTn is likely to increase such false-positive findings.
We need to reassess the currently held belief that Tn is released only from irreversibly injured myocardial cells. In a recent study, marathon runners had significant elevations in Tn levels after a race. The authors postulated two alternative mechanisms for increased Tn values after heavy exertion: true myocardial injury resulting from the breakdown of myocytes, and cytosolic release of the biomarker. In the marathon study, delayed-enhancement cardiac magnetic resonance imaging supported a cytosolic release, and the authors of a recent review concluded that increased membrane permeability is a likelier mechanism than myocardial necrosis for exercise-induced Tn release. Researchers have now determined that hsTn can be detected in healthy populations and that elevated levels are associated with increased cardiovascular risk (Am Heart J 2010; 159:972).
The goal of diagnosing any medical condition is to classify patients by prognosis, pathophysiology, and response to specific therapies. An elevated Tn level in a patient with sepsis, hypertensive emergency, pulmonary embolism, hypotension, renal failure, or any of several other conditions indicates that myocardial damage or even nonthrombotic MI (the extreme end of the spectrum of demand ischemia) has occurred, producing leakage of low levels of Tn and likely indicating a poor prognosis. However, an elevated Tn level does not mean that the patient has ACS, and therefore should not necessarily lead to ACS-directed care. To distinguish ACS from nonocclusive conditions, a compatible clinical syndrome must be accompanied by a change in Tn levels — rising, falling, or both.
CONCLUSION
High-sensitivity assays will enable physicians to both confirm and exclude MI sooner than is now possible, but serial testing at 0, 4, and 8 hours remains necessary. Moreover, the tests are useful for diagnosing ("ruling in") certain high-risk conditions (demand ischemia and MI) but not for excluding ("ruling out") the diagnosis of unstable angina — also a high-risk situation for the patient but one in which troponin leak might not occur. Overreliance on Tn and failure to consider ECG findings and clinical presentation appropriately can lead to both over- and underdiagnosis of MI, each of which carries its own set of hazards.
— J. Stephen Bohan, MD, MS, FACP, FACEP, and Joel M. Gore, MD
Published in Journal Watch Emergency Medicine August 5, 2010
Citation(s):
Thygesen K et al. Universal definition of myocardial infarction. J Am Coll Cardiol 2007 Nov 27; 50:2173.
* Original article (Subscription may be required)
* Medline abstract (Free)
Januzzi JL Jr et al. High-sensitivity troponin T concentrations in acute chest pain patients evaluated with cardiac computed tomography. Circulation 2010 Mar 16; 121:1227.
* Original article (Subscription may be required)
* Medline abstract (Free)
Mousavi N et al. Relation of biomarkers and cardiac magnetic resonance imaging after marathon running. Am J Cardiol 2009 May 15; 103:1467.
* Medline abstract (Free)
Otsuka T et al. Association between high-sensitivity cardiac troponin T levels and the predicted cardiovascular risk in middle-aged men without overt cardiovascular disease. Am Heart J 2010 Jun; 159:972.
* Medline abstract (Free)
Shave R et al. Exercise-induced cardiac troponin elevation: Evidence, mechanisms, and implications. J Am Coll Cardiol 2010 Jul 13; 56:169.
* Original article (Subscription may be required)
* Medline abstract (Free)
https://docs.google.com/fileview?id=0B278nGJMQBk7NDdiMTgwZjQtYzIzMi00YzVlLTgzYzYtMWY4MzNhMGUxOGZm&hl=zh_TW
不高，不能排除unstable angina, 這讓傳統的ECG及clinical assessment更形重要，0-4-8小時監測Tn還是重要!!!
Diagnosing Acute Coronary Syndromes: The Troponin Conundrum
As the sensitivity of Tn assays rises, electrocardiographic and clinical evidence of ACS become more — not less — important in treatment decisions.
The diagnostic criteria for myocardial infarction (MI) are obtained from the triad of clinical presentation, electrocardiogram (ECG) changes, and serial cardiac enzyme or biomarker measurements. In recent years, the emphasis on biomarkers — specifically, troponin (Tn) — has increased, while ECG findings and clinical symptoms have received relatively little attention. Nonetheless, a detectable Tn level alone does not equal a diagnosis of MI.
TROPONIN AND MYOCARDIAL DAMAGE
Acute coronary syndromes (ACS) is a general term used when clinical symptoms and signs of myocardial ischemia are caused by obstruction of flow through the coronary arteries, and it typically has included both MI and unstable angina. A European Society of Cardiology and American College of Cardiology joint consensus document (published in 2000, updated in 2007) explicitly defines MI as myocardial necrosis secondary to ischemia, which can also occur in ACS without MI. Cardiac Tn is an extremely specific marker of cardiac injury; however, myocardial damage is not specific to either MI or ACS.
Several new high-sensitivity Tn (hsTn) assays are able to detect levels of Tn that would register as zero with older, conventional assays. The advantages of the hsTn assays — greater sensitivity in identifying myocardial injury and potential for earlier detection of MI — come at the cost of a reduction in specificity for the diagnosis of ACS. Indeed, in a recent report, investigators used cardiac computed tomography to confirm a mechanistic association between elevated hsTn levels and myocardial damage, not only in patients with ACS but also in those without ACS. Even with conventional Tn assays, patients can have detectable Tn levels because of etiologies other than ACS; the use of hsTn is likely to increase such false-positive findings.
We need to reassess the currently held belief that Tn is released only from irreversibly injured myocardial cells. In a recent study, marathon runners had significant elevations in Tn levels after a race. The authors postulated two alternative mechanisms for increased Tn values after heavy exertion: true myocardial injury resulting from the breakdown of myocytes, and cytosolic release of the biomarker. In the marathon study, delayed-enhancement cardiac magnetic resonance imaging supported a cytosolic release, and the authors of a recent review concluded that increased membrane permeability is a likelier mechanism than myocardial necrosis for exercise-induced Tn release. Researchers have now determined that hsTn can be detected in healthy populations and that elevated levels are associated with increased cardiovascular risk (Am Heart J 2010; 159:972).
The goal of diagnosing any medical condition is to classify patients by prognosis, pathophysiology, and response to specific therapies. An elevated Tn level in a patient with sepsis, hypertensive emergency, pulmonary embolism, hypotension, renal failure, or any of several other conditions indicates that myocardial damage or even nonthrombotic MI (the extreme end of the spectrum of demand ischemia) has occurred, producing leakage of low levels of Tn and likely indicating a poor prognosis. However, an elevated Tn level does not mean that the patient has ACS, and therefore should not necessarily lead to ACS-directed care. To distinguish ACS from nonocclusive conditions, a compatible clinical syndrome must be accompanied by a change in Tn levels — rising, falling, or both.
CONCLUSION
High-sensitivity assays will enable physicians to both confirm and exclude MI sooner than is now possible, but serial testing at 0, 4, and 8 hours remains necessary. Moreover, the tests are useful for diagnosing ("ruling in") certain high-risk conditions (demand ischemia and MI) but not for excluding ("ruling out") the diagnosis of unstable angina — also a high-risk situation for the patient but one in which troponin leak might not occur. Overreliance on Tn and failure to consider ECG findings and clinical presentation appropriately can lead to both over- and underdiagnosis of MI, each of which carries its own set of hazards.
— J. Stephen Bohan, MD, MS, FACP, FACEP, and Joel M. Gore, MD
Published in Journal Watch Emergency Medicine August 5, 2010
Citation(s):
Thygesen K et al. Universal definition of myocardial infarction. J Am Coll Cardiol 2007 Nov 27; 50:2173.
* Original article (Subscription may be required)
* Medline abstract (Free)
Januzzi JL Jr et al. High-sensitivity troponin T concentrations in acute chest pain patients evaluated with cardiac computed tomography. Circulation 2010 Mar 16; 121:1227.
* Original article (Subscription may be required)
* Medline abstract (Free)
Mousavi N et al. Relation of biomarkers and cardiac magnetic resonance imaging after marathon running. Am J Cardiol 2009 May 15; 103:1467.
* Medline abstract (Free)
Otsuka T et al. Association between high-sensitivity cardiac troponin T levels and the predicted cardiovascular risk in middle-aged men without overt cardiovascular disease. Am Heart J 2010 Jun; 159:972.
* Medline abstract (Free)
Shave R et al. Exercise-induced cardiac troponin elevation: Evidence, mechanisms, and implications. J Am Coll Cardiol 2010 Jul 13; 56:169.
* Original article (Subscription may be required)
* Medline abstract (Free)
https://docs.google.com/fileview?id=0B278nGJMQBk7NDdiMTgwZjQtYzIzMi00YzVlLTgzYzYtMWY4MzNhMGUxOGZm&hl=zh_TW
留言
張貼留言