Clinical classification of acute myocardial infarction
| Myocardial infarction | |
 | |
|---|---|
| Acute Myocardial infarction; Posterior wall. Image courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology | |
| ICD-10 | I21-I22 |
| ICD-9 | 410 |
| DiseasesDB | 8664 |
| MedlinePlus | 000195 |
| eMedicine | med/1567 emerg/327 ped/2520 |
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 Discuss Clinical classification of acute myocardial infarction further in the WikiDoc Cardiology Network |
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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]
Prior MI Classification Schemes
There have been several prior classification schemes for characterizing MI:
1. Transmural (necrosis of full thickness of ventricle) vs. non transmural (necrosis of partial thickness of ventricle)
2. Q wave vs. non Q wave: Based upon the development of electrocardiographic Q waves representing electrically inert tissue.
3. ST elevation MI (STEMI) and Non ST elevation myocardial infarction (NSTEMI)
At one time it was thought that Transmural MI and Q wave MI were synonymous. However, not all Q wave MIs are transmural, and not all transmural MIs are associated with Q waves.
Likewise, not all ST elevation MIs go on to cause q waves. Non ST elevation MIs can result in q waves.
Thus, ST elevation MI should not be equated with transmural MI or q wave MI. Likewise, Non ST elevation MI should not be equated with non transmural MI or non q wave MI. These 3 designations reflect three separate but overlapping characterization schemes.
New MI Clinical Classification System
A new clinical evidence based classification system has been introduced by Thygesen K, Alpert JS, White HD, et al. and jointly sponsored by the American College of Cardiology (ACC), American Heart Association (AHA), European Society of Cardiology (ESC), and the World Heart Federation (WHF).[1]
Criteria for Diagnosis of Acute Myocardial Infarction
The term myocardial infarction should be used when there is evidence of myocardial necrosis in a clinical setting consistent with myocardial ischemia. Under these conditions any one of the following criteria meets the diagnosis for acute myocardial infarction. [1]
- Detection of rise and/or fall of cardiac biomarkers (preferably Troponin) with at least one of the following
- Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischemia, accompanied by presumably new ST segment elevation, or new LBBB, and/or evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy, if death has occurred before blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the blood
- In patients with normal baseline troponin values, a greater than 3 times increase above the 99th percentile of the upper limit of normal of cardiac biomarkers has been designated as the definition of PCI related myocardial infarction. A subtype related to documented stent thrombosis is recognized.
- For patients with CABG surgery; (In patients with normal baseline troponin values) increases of cardiac biomarkers greater than 5 times, (> 5 times the 99th percentile upper limit of normal) and either new pathological Q waves or new LBBB or angiographically evidence of new graft or native vessel occlusion have been designated as defining CABG surgery related myocardial infarction.
- Pathological findings of acute myocardial infarction.
Criteria for Prior Myocardial Infarction
Any of the following criteria meets the diagnosis for prior myocardial infarction:[1]
- Development of new pathological Q waves with or without symptoms
- Imaging evidence of a region of loss of viable myocardium that is thinned and fails to contract in the absence of a non ischemic cause.
- Pathological findings of healed or healing myocardial infarction.
Classification
Clinically the various types of myocardial infarction can be classified as follow: [1]
- Spontaneous myocardial infarction related to ischemia due to a primary coronary event, such as plaque erosion and/or rupture, fissuring, or dissection.
- Myocardial infarction secondary to ischemia due to an imbalance of O2 supply and demand, as from coronary spasm or embolism, anemia, arrhythmias, hypertension, or hypotension
- Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggesting ischemia with new ST segment elevation; new left bundle branch block; or pathologic or angiographic evidence of fresh coronary thrombus (in the absence of reliable biomarker findings)
-
- a. Myocardial infarction associated with Percutaneous Coronary Interventions (PCI)
- b. Myocardial infarction associated with documented in stent thrombosis.
- Myocardial infarction associated with Coronary Artery Bypass Graft surgery
Diagnostic Applications for Acute Myocardial Infarction
Differential Diagnosis for EKG in Acute Myocardial Infarction
Conditions that confound the EKG diagnosis of myocardial infarction are the following: [1];
- A QS complex in lead V1 is normal.
- A Q wave <0.03 s and <1/4 of the R wave amplitude in lead III is normal if the frontal QRS axis is between 30 and 0°.
- The Q wave may be normal in aVL if the frontal QRS axis is between 60 and 90°. Small septal Q waves are non pathological Q waves if <0.03 s and <1/4 of the R wave amplitude in leads I, aVL, aVF, and V4-V5-V6
- The following may be associated with Q/QS complexes in the absence of myocardial infarction:
- Preexcitation syndromes
- Obstructive or dilated cardiomyopathy
- LBBB
- RBBB
- Left anterior fascicular block
- LVH
- RVH
- Myocarditis
- Acute cor pulmonale
- Hyperkalemia
Diseases That May be Confused with Acute MI
- Benign early repolarization (e.g. high take-off)
- Pericarditis
- LBBB
- Pulmonary embolism
- Myocarditis
- Brugada syndrome
- Preexcitation syndromes
- Subarachnoid hemorrhage
- Cholecystitis
- Electrolyte imbalance (hyperkalemia)
- Lead misplacements
- Different lead configurations (e.g. modified Mason-Likar lead configurations)
- Misevaluation of J point variations
Evaluation of Biomarkers
Myocardial cell death can be recognized by the appearance in the blood of different proteins released into the circulation from the damaged myocytes: myoglobin, cardiac troponin T (cTnT) and I (cTnI), CK (Creatine Kinase), LDH (Lactate Dehydrogenase), as well as many other enzyme markers of necrosis.[2]
Myocardial infarction is diagnosed when blood levels of sensitive and specific biomarkers such as cardiac troponins (T and I) or CK-MB are increased in the clinical setting of acute myocardial ischemia. [1]
Although elevations in these biomarkers reflect myocardial necrosis, they do not indicate its mechanism. Thus, an elevated value of cardiac troponin in the absence of clinical evidence of ischemia should prompt a search for other etiologies of myocardial necrosis. [1][3][4][5][6][7]
Pathologic diagnosis of MI
References
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 Thygesen K, Alpert JS, White HD; et al. (2007). "Universal definition of myocardial infarction". Circulation. 116 (22): 2634–53. doi:10.1161/CIRCULATIONAHA.107.187397. PMID 17951284. Unknown parameter
|month=ignored (help) - ↑ Jaffe AS, Ravkilde J, Roberts R; et al. (2000). "It's time for a change to a troponin standard". Circulation. 102 (11): 1216–20. PMID 10982533. Unknown parameter
|month=ignored (help) - ↑ Morrow DA, Cannon CP, Jesse RL; et al. (2007). "National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: Clinical characteristics and utilization of biochemical markers in acute coronary syndromes". Circulation. 115 (13): e356–75. doi:10.1161/CIRCULATIONAHA.107.182882. PMID 17384331. Unknown parameter
|month=ignored (help) - ↑ Jaffe AS, Babuin L, Apple FS (2006). "Biomarkers in acute cardiac disease: the present and the future". J. Am. Coll. Cardiol. 48 (1): 1–11. doi:10.1016/j.jacc.2006.02.056. PMID 16814641. Unknown parameter
|month=ignored (help) - ↑ Jaffe AS (2006). "Chasing troponin: how low can you go if you can see the rise?". J. Am. Coll. Cardiol. 48 (9): 1763–4. doi:10.1016/j.jacc.2006.08.006. PMID 17084246. Unknown parameter
|month=ignored (help) - ↑ Apple FS, Jesse RL, Newby LK, Wu AH, Christenson RH (2007). "National Academy of Clinical Biochemistry and IFCC Committee for Standardization of Markers of Cardiac Damage Laboratory Medicine Practice Guidelines: Analytical issues for biochemical markers of acute coronary syndromes". Circulation. 115 (13): e352–5. doi:10.1161/CIRCULATIONAHA.107.182881. PMID 17384332. Unknown parameter
|month=ignored (help) - ↑ Macrae AR, Kavsak PA, Lustig V; et al. (2006). "Assessing the requirement for the 6-hour interval between specimens in the American Heart Association Classification of Myocardial Infarction in Epidemiology and Clinical Research Studies". Clin. Chem. 52 (5): 812–8. doi:10.1373/clinchem.2005.059550. PMID 16556688. Unknown parameter
|month=ignored (help)