ST elevation myocardial infarction cardiac markers: Difference between revisions
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==Clinical Application of Cardiac Markers== | ==Clinical Application of Cardiac Markers== | ||
It is important to note that it may take hours for cardiac enzymes to rise following injury to the myocardium, and that they may not be elevated on presentation. For this reason, cardiac enzymes and ECGs are checked every 6 to 8 hours over the course of the first 24 hours to "rule out" acute MI. These enzyme measures over the first 24 hours are used to gauge the size of an MI: higer peak levels and a greater area under the curve of enzyme release are associated with larger MIs and poorer prognosis. | It is important to note that it may take hours for cardiac enzymes to rise following injury to the myocardium, and that they may not be elevated on presentation. For this reason, cardiac enzymes and ECGs are checked every 6 to 8 hours over the course of the first 24 hours to "rule out" acute MI. These enzyme measures over the first 24 hours are used to gauge the size of an MI: higer peak levels and a greater area under the curve of enzyme release are associated with larger MIs and poorer prognosis. | ||
=="False Positive" Troponin Elevations That Are Not Due to Thrombotic Coronary Occlusion== | |||
It is important to note that cardiac troponins are a marker of all heart muscle damage, not just myocardial infarction. There are other "false positive" causes of troponin elevation that directly or indirectly lead to heart muscle damage can also therefore increase troponin levels:<ref name="pmid15867411">{{cite journal |author=Jeremias A, Gibson CM |title=Narrative review: alternative causes for elevated cardiac troponin levels when acute coronary syndromes are excluded |journal=Ann. Intern. Med. |volume=142 |issue=9 |pages=786–91 |year=2005 |month=May |pmid=15867411 |doi= |url=}}</ref> <ref>Ammann P, Pfisterer M, Fehr T, Rickli H. Raised cardiac troponins. ''[[British Medical Journal|BMJ]]'' 2004;328:1028-9. PMID 15117768.</ref> | |||
* Cardiac: | |||
** Cardiac [[amyloidosis]] and other cardiac infiltrative disorders | |||
** [[Cardiac contusion]] | |||
** [[Cardiothoracic surgery|Cardiac surgery]] and [[heart transplant]] | |||
** [[Defibrillation]] | |||
** Closure of [[atrial septal defect]]s | |||
** [[Coronary artery vasospasm]] | |||
** [[Dilated cardiomyopathy]] | |||
** [[Heart failure]] | |||
** [[Hypertrophic cardiomyopathy]] | |||
** [[Hypotension]] | |||
** [[Myocarditis]] | |||
** [[Angioplasty|Percutaneous coronary intervention]] | |||
** [[Pericarditis]] | |||
** [[Pulmonary hypertension]] | |||
** [[Radiofrequency ablation]] | |||
** [[Supraventricular tachycardia]] including [[atrial fibrillation]] | |||
* Non-cardiac: | |||
** Critical illness, e.g. [[sepsis]] | |||
** High-dose [[chemotherapy]] | |||
** [[Hypovolemia]] | |||
** [[Intracranial hemorrhage]] | |||
** Primary [[pulmonary hypertension]] | |||
** [[Pulmonary embolism]] | |||
** [[Renal failure]] | |||
** [[Subarachnoid hemorrhage]] | |||
** Scorpion [[venom]] | |||
** [[Stroke]] | |||
** [[Sympathomimetic]] ingestion | |||
** Very heavy [[exercise]] (e.g. marathon) | |||
==References== | ==References== | ||
Revision as of 18:23, 25 April 2009
| Myocardial infarction | |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
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For the main article on cardiac markers, please see
. For the main article on the diagnosis of STEMI, see the following chapter: Clinical classification of acute myocardial infarction
Overview
Cardiac markers or cardiac enzymes are proteins that are present in cardiac myocytes that should not be in the bloodstream. When cardiac injury occurs (such as in acute MI), these intracellular proteins are then released into the bloodstream. Along with the patient's history and the electrocardiogram, the release of these enzymes forms the basis of the diagnosis of ST elevation myocardial infarction.
History
Until the 1980s, the enzymes SGOT and LDH were used to assess cardiac injury. In the early 1980s it was found that disproportional elevation of the MB subtype of the enzyme creatine kinase (CK) was very specific for myocardial injury. More recently, troponin has been used as an even more specific marker of myonecrosis. Current guidelines are generally in favor of troponin sub-units I or T, which are very specific for damage to myocytes.[1] [2][3]
Clinical Application of Cardiac Markers
It is important to note that it may take hours for cardiac enzymes to rise following injury to the myocardium, and that they may not be elevated on presentation. For this reason, cardiac enzymes and ECGs are checked every 6 to 8 hours over the course of the first 24 hours to "rule out" acute MI. These enzyme measures over the first 24 hours are used to gauge the size of an MI: higer peak levels and a greater area under the curve of enzyme release are associated with larger MIs and poorer prognosis.
"False Positive" Troponin Elevations That Are Not Due to Thrombotic Coronary Occlusion
It is important to note that cardiac troponins are a marker of all heart muscle damage, not just myocardial infarction. There are other "false positive" causes of troponin elevation that directly or indirectly lead to heart muscle damage can also therefore increase troponin levels:[4] [5]
- Cardiac:
- Cardiac amyloidosis and other cardiac infiltrative disorders
- Cardiac contusion
- Cardiac surgery and heart transplant
- Defibrillation
- Closure of atrial septal defects
- Coronary artery vasospasm
- Dilated cardiomyopathy
- Heart failure
- Hypertrophic cardiomyopathy
- Hypotension
- Myocarditis
- Percutaneous coronary intervention
- Pericarditis
- Pulmonary hypertension
- Radiofrequency ablation
- Supraventricular tachycardia including atrial fibrillation
- Non-cardiac:
- Critical illness, e.g. sepsis
- High-dose chemotherapy
- Hypovolemia
- Intracranial hemorrhage
- Primary pulmonary hypertension
- Pulmonary embolism
- Renal failure
- Subarachnoid hemorrhage
- Scorpion venom
- Stroke
- Sympathomimetic ingestion
- Very heavy exercise (e.g. marathon)
References
- ↑ Eisenman A (2006). "Troponin assays for the diagnosis of myocardial infarction and acute coronary syndrome: where do we stand?". Expert Rev Cardiovasc Ther. 4 (4): 509–14. doi:10.1586/14779072.4.4.509. PMID 16918269. Unknown parameter
|month=ignored (help) - ↑ Aviles RJ, Askari AT, Lindahl B; et al. (2002). "Troponin T levels in patients with acute coronary syndromes, with or without renal dysfunction". N. Engl. J. Med. 346 (26): 2047–52. doi:10.1056/NEJMoa013456. PMID 12087140. Unknown parameter
|month=ignored (help) - ↑ Summary of "Troponin T levels in patients..." for laymen
- ↑ Jeremias A, Gibson CM (2005). "Narrative review: alternative causes for elevated cardiac troponin levels when acute coronary syndromes are excluded". Ann. Intern. Med. 142 (9): 786–91. PMID 15867411. Unknown parameter
|month=ignored (help) - ↑ Ammann P, Pfisterer M, Fehr T, Rickli H. Raised cardiac troponins. BMJ 2004;328:1028-9. PMID 15117768.
External links
- The MD TV: Comments on Hot Topics, State of the Art Presentations in Cardiovascular Medicine, Expert Reviews on Cardiovascular Research
- Clinical Trial Results: An up to date resource of Cardiovascular Research
- Risk Assessment Tool for Estimating Your 10-year Risk of Having a Heart Attack - based on information of the Framingham Heart Study, from the United States National Heart, Lung and Blood Institute
- Heart Attack - overview of resources from MedlinePlus.
- Heart Attack Warning Signals from the Heart and Stroke Foundation of Canada
- Regional PCI for STEMI Resource Center - Evidence based online resource center for the development of regional PCI networks for acute STEMI
- STEMI Systems - Articles, profiles, and reviews of the latest publications involved in STEMI care. Quarterly newsletter.
- American College of Cardiology (ACC) Door to Balloon (D2B) Initiative.
- American Heart Association's Heart Attack web site - Information and resources for preventing, recognizing and treating heart attack.