Volume 6, Number 55;  December 4, 2006 - Troponin - Normal Arteries

 

Clinical Question: 

1) What are the possible causes of elevated troponin in persons with angiographically normal coronary artieries?

 

Recommended reading:

Patient:

Session Handout:

 

Readings:

 

 

 

Link Directly to Fulltext Article at Publisher

 

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Unique Identifier [PMID]: 15867411

Authors: Jeremias A. Gibson CM.

Institution: Division of Cardiology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA. ajeremia@bidmc.harvard.edu

Title: Narrative review: alternative causes for elevated cardiac troponin levels when acute coronary syndromes are excluded. [Review] [48 refs]

 

Source: Annals of Internal Medicine. 142(9):786-91, 2005 May 3.

Abstract: Current guidelines for the diagnosis of non-ST-segment elevation myocardial infarction are largely based on an elevated troponin level. While this rapid and sensitive blood test is certainly valuable in the appropriate setting, its widespread use in a variety of clinical scenarios may lead to the detection of troponin elevation in the absence of thrombotic acute coronary syndromes. Many diseases, such as sepsis, hypovolemia, atrial fibrillation, congestive heart failure, pulmonary embolism, myocarditis, myocardial contusion, and renal failure, can be associated with an increase in troponin level. These elevations may arise from various causes other than thrombotic coronary artery occlusion. Given the lack of any supportive data at present, patients with nonthrombotic troponin elevation should not be treated with antithrombotic and antiplatelet agents. Rather, the underlying cause of the troponin elevation should be targeted. However, troponin elevation in the absence of thrombotic acute coronary syndromes still retains prognostic value. Thus, cardiac troponin elevations are common in numerous disease states and do not necessarily indicate the presence of a thrombotic acute coronary syndrome. While troponin is a sensitive biomarker to "rule out" non-ST-segment elevation myocardial infarction, it is less useful to "rule in" this event because it may lack specificity for acute coronary syndromes. [References: 48]

Publication Type: Journal Article. Review.

 

 

Link Directly to Fulltext Article at Science Direct

 

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Unique Identifier [PMID]: 15823642

Authors: Nageh T. Sherwood RA. Wainwright RJ. Shah AM. Thomas MR.

Institution: Department of Cardiology, King's College Hospital, Denmark Hill, London, UK. tmageh@hotmail.com

Title: The clinical relevance of raised cardiac troponin I in the absence of significant angiographic coronary artery disease.

 

Source: International Journal of Cardiology. 100(2):325-30, 2005 Apr 20.

Abstract: 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 "chest pain" and elevated (>0.2 microg/L) troponin I on admission. Thirty-four (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 58+/-13 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 "normal" coronary arteries can re-present with future cardiac events and should still be considered for aggressive risk management.

Publication Type: Journal Article.

 

 

Link Directly to Fulltext Article at Publisher

 

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Unique Identifier [PMID]: 12412934

Authors: Bakshi TK. Choo MK. Edwards CC. Scott AG. Hart HH. Armstrong GP.

Institution: North Shore Hospital, Auckland, New Zealand.

Title: Causes of elevated troponin I with a normal coronary angiogram.

 

Source: Internal Medicine Journal. 32(11):520-5, 2002 Nov.

Abstract: BACKGROUND: The new definition of myocardial infarction (MI) emphasizes the pre-eminent role of troponin for diagnosis. Troponin rise indicates myocardial injury, but is not synonymous with infarction or ischaemia. AIMS: To review the precipitating event for troponin elevation in patients with angiographically normal coronary arteries, in a district general hospital. METHODS: Consecutive patients with elevated troponin I (TnI) who underwent angiography for suspected coronary disease were included in the present study if they had normal or mild disease (<50% diameter loss without complex features or thrombus). Precipitating event for TnI elevation was assigned on the totality of clinical evidence. RESULTS: Twenty-one patients qualified, with an average age of 50 years (range 33-73). Sixty-two per cent of participants were female. Troponin release was attributed to tachycardia in six patients, only two of whom had haemodynamic compromise. Physical exertion was the precipitating factor in two patients; pericarditis in two patients; and severe congestive heart failure in one patient. Ten of 21 patients had no identifiable cause for a rise in TnI concentration. Five of 21 patients had left-ventricular wall motion abnormalities. There were no deaths or MI at 41 +/- 24 weeks follow up. CONCLUSION: Troponin is a sensitive marker of myocardial injury and may rise following apparently minor insults. A rise in TnI concentration may have a cause other than acute coronary syndrome and may occur without significant angiographic coronary artery disease.

Publication Type: Journal Article.

 

 

 

Resident Report / Department of Medicine & Grady Branch Library

Emory University School of Medicine

2006 Edition

Participating Faculty:  Carlos Del Rio MD  / Joyce Doyle MD / Lorenzo Difrancesco MD / Joel Mermis MD / Maunank Shah MD

Contact: Karl Woodworth 

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