The document provides information on the diagnosis and types of acute myocardial infarction (AMI). It discusses coronary atherosclerosis as a chronic disease that progresses over decades. Acute coronary syndrome (ACS) refers to the spectrum of clinically manifest coronary artery disease from unstable angina to AMI. The criteria for diagnosing AMI include elevated cardiac biomarkers and evidence of myocardial ischemia. The document outlines 5 types of AMI and provides details on interpreting electrocardiograms and cardiac biomarkers in AMI.

2. The Diagnosis of Acute Myocardial Infarction
SFK House Staff July 2009

3. Coronary Atherosclerosis: A Chronic Disease
*
0 – 20 yrs 20 – 40 yrs 40 – 60 + yrs
† ∞

4. Coronary Atherosclerosis: A Chronic Disease

5. Coronary Atherosclerosis: A Chronic Disease
*
0 – 20 yrs 20 – 40 yrs 40 – 60 + yrs
† ∞

6. Nomenclature of ACS
The spectrum of clinically manifest Coronary Artery Disease
from UA to AMI is referred to as ACS.
Antman et al. Acute myocardial infarction. In: Braunwald EB, ed. Heart disease: a textbook of
cardiovascular medicine. Philadelphia, PA: WB Saunders, 1997.

7. Criteria for Acute Myocardial Infarction
Laboratory evidence of myocardial necrosis with clinical myocardial ischemia.
Any one of the following criteria meets the diagnosis for myocardial infarction:
• Detection of rise and/or fall of biomarkers (preferably troponin) with at least one
value above the 99th percentile of the upper reference limit (URL) together with
myocardial ischemia with at least one of the following:
• Symptoms of ischemia;
• New ischemic ST-T changes or new LBBB;
• New pathological Q waves;
• New loss of viable myocardium or regional wall motion abnormality
by imaging techniques.
• Sudden unexpected death from cardiac arrest.
• For PCI patients, new elevations of biomarkers greater than 3x 99th percentile
URL. A subtype related to stent thrombosis is recognized.
• For CABG patients, new elevations of biomarkers greater than 5x 99th percentile
URL plus new pathological Q waves or new LBBB, or angiographically documented
new graft or native coronary artery occlusion, or imaging of new loss of viable
myocardium.
Thygesen, et al. J. Am. Coll. Cardiol. 2007;50;2173-2195

8. Types of Myocardial Infarction
Type 1: Spontaneous myocardial infarction related to ischemia due to a primary
coronary event such as plaque erosion and/or rupture, fissuring, or dissection
Type 2: Myocardial infarction secondary to ischemia due to either increased oxygen
demand or decreased supply, e.g. coronary artery spasm, coronary embolism,
anemia, arrhythmias, hypertension, or hypotension
Type 3: Sudden unexpected cardiac death, including cardiac arrest, often with
symptoms of myocardial ischemia, but death occurring before blood samples could be
obtained or before the appearance of cardiac biomarkers in the blood
Type 4a: Myocardial infarction associated with PCI
Type 4b: Myocardial infarction associated with stent thrombosis as documented by
angiography or at autopsy
Type 5: Myocardial infarction associated with CABG
Thygesen , et al. J. Am. Coll. Cardiol. 2007;50;2173-2195

9. “Ischemic” Symptoms
• Not all chest pain is cardiac
• Not all cardiac pain is coronary insufficiency
• Not all coronary insufficiency is atherosclerosis
• Not all coronary occlusion is thrombosis
• Not all ACS requires immediate coronary
angiography / reperfusion
• 10-15% of myocardial infarctions are
asymptomatic

10. "False-Positive" Cardiac Catheterization Laboratory Activation Among
Patients With Suspected ST-Segment Elevation Myocardial Infarction
D Larson, K Menssen, S Sharkey, et al. JAMA. 2007;298(23):2754-2760
1345 Patients over 3.5 Years
1048 Transferred from 30 non-PCI hospitals
297 Presented initially to PCI hospital
10 Excluded
5 Died
5 Angiography cancelled
1335 Underwent angiography
187 Had no culprit CAD

11. Biomarkers in Acute Myocardial Infarction
Cardiac troponin-no reperfusion
100 Cardiac troponin-reperfusion
CKMB-no reperfusion
Multiples of the URL
50 CKMB-reperfusion
20
Troponin-I Normal = ≤ 0.09 ng/ml
10 CK-MB Fraction ULN = ≤6 ng/ml
5
2 URL = Upper Reference Limit
99%tile of Reference Control Group
1
0 1 2 3 4 5 6 7 8
Days After Onset of Myocardial Infarction
Alpert et al. J Am Coll Cardiol 2000;36:959.
Wu et al. Clin Chem 1999;45:1104.

12. Elevated Troponin Without Overt Ischemic Heart Disease
Cardiac contusion or other trauma, including surgery, ablation, pacing, etc.
Congestive heart failure—acute and chronic
Aortic dissection
Aortic valve disease
Hypertrophic cardiomyopathy
Tachy- or bradyarrhythmias, or heart block
Takotsubo stress cardiomyopathy (Apical ballooning syndrome)
Rhabdomyolysis with cardiac injury
Pulmonary embolism, severe pulmonary hypertension
Renal failure
Acute neurological disease, including stroke or subarachnoid hemorrhage
Infiltrative diseases, e.g. amyloidosis, hemochromatosis, sarcoidosis,
scleroderma, neoplasia
Inflammatory diseases, e.g. myocarditis, endocarditis or pericarditis
Drug toxicity or toxins
Critically ill patients, especially with respiratory failure or sepsis
Burns, especially if affecting 30% of body surface area
Extreme exertion
Modified from Jaffe et al. (4) and French and White (5).

13. ECG Manifestations of Acute Myocardial Ischemia
(in Absence of LVH and LBBB)
ST elevation
New ST elevation at the J-point in two contiguous leads >0.2 mV in men or
>0.15 mV in women in leads V2–V3, or >0.1 mV in other leads
ST depression and T-wave changes
New horizontal or down-sloping ST depression >0.05 mV in two contiguous
leads; or T inversion >0.1 mV in two contiguous leads with prominent
R-wave or R/S ratio ≥1

14. QRS Changes Associated With Myocardial Infarction
Any Q-wave ≥0.02 sec or QS complex in “anterior leads” V2 -- V3
Q-wave ≥0.03 sec and ≥0.1 mV deep or QS complex in any two leads
of a contiguous lead group:
“lateral leads” I, aVL,V6
“anterolateral leads” V2–V6
“inferior leads” II, III, aVF
R-wave ≥0.04 sec in “posterior leads” V1–V2 and R/S ≥1 with a
concordant positive T-wave (in the absence of a conduction defect)

15. ECG Pitfalls in Diagnosing Myocardial Infarction
False positives
Benign early repolarization
LBBB
Pre-excitation
Brugada syndrome
Pericarditis, myocarditis
Pulmonary embolism
Subarachnoid hemorrhage
Metabolic disturbances such as hyperkalemia
Failure to recognize normal limits for J-point displacement
Lead transposition or misplacement
Cholecystitis
Takotsubo stress cardiomyopathy
False negatives
Prior myocardial infarction with Q-waves and/or persistent ST elevation
Paced rhythm
LBBB
Thygesen et al. JACC Vol. 50, No. 22, 2007

16. 1 sec (25 mm / sec)
200 msec
40 msec

17. 1 sec (25 mm / sec)
200 msec
40 msec
1 mv
0.1 mv or “1 mm”

18. 1 sec (25 mm / sec)
200 msec
40 msec
0 300 150 100 75 60 50
BPM
1 mV (10 mm / mV)
0.1 mv or “1 mm”

19. ?Ant-STEMI ?LVH ?HyperK+ ?LBBB ?WNL ?Pericarditis
? Takotsubo ?RBBB+STEMI ?Brugada ?Pul Embolism

20. Normal
Normal
(Early
Repolari-
zation)
Normal
(Repolari-
zation
Variant)

21. ?Ant-STEMI ?LVH ?HyperK+ ?WNL ?LBBB ?Pericarditis
?Takotsubo ?RBBB+STEMI ?Brugada ?Pul Embolism

22. I
tis
I EM
BB
i K+ EM ST da
H
rd r T + ga
LV
B a pe t-S
L ric Hy n BBB Bru
e A

23. Pulmonary
Embolism
DC Cardio-
version

26. RZ: 54 Latin-American male in ED (NOT SFK)

27. DR: 71 y male with chest pain in the Cardiac Procedures Unit

29. VP 32 y South Asian male surgical resident sought ED evaluation for chest
pain and extreme fatigue. No significant past history. FH positive for
premature CAD. CK and troponin-I elevated.

30. VP 32 y South Asian male surgical resident sought ED evaluation for chest
pain and extreme fatigue. No significant past history.
FH positive for premature CAD. CK and troponin-I elevated. Onset of pain
after running a marathon, without training. Left AMA after overnight
observation and IV hydration.

36. AR 96 y female with acute onset epigastric and substernal pain, nausea, onset
3:30 PM. In ED 6:54 PM, no history of coronary disease, +HTN, +PAF. Systolic
murmur Ao valve. Trop-I 15.54 ng/ml, echocardiogram LVH, mild AS,
inferoapical akinesis. CCL 7:20 PM.

42. 10275665: NC 25 year old male with abrupt onset of severe chest pain.
No substance abuse, no medications, no CV history. Cigarettes ½ ppd.
Chol 157 mg/dl, LDL-C 80 mg/dl. CK 81 IU/L, troponin-I 0.05 ng/ml.

43. 10275665: NC 25 year old male with abrupt onset of severe chest pain.
No substance abuse, no medications, no CV history. Cigarettes ½ ppd.
Chol 157 mg/dl, LDL-C 80 mg/dl. CK 81 IU/L, troponin-I 0.05 ng/ml.
Repeat CK 7668 IU/L, troponin-I >100 ng/ml. Echo LVEF 35% with apical clot.
Symptoms began while driving home from first-time skydiving.

48. 1-31-2006 0920 Hrs
34 y Asian F RN from UCSF. Presented to ED with acute onset severe chest pain 1 hr earlier. No CV history.
Rare migraine headaches, most recently 5 d earlier. No medications. No illicit drug use, trauma, tobacco or
alcohol. No hypertension, no diabetes, never obese, no FH atherosclerotic nor connective tissue vascular
disease. No nocturnal chest pain nor palpitation. G2 P2 3 ½ yr post-partum, LMP 2 wks ago, HCG negative, no
oral contraceptives.
Total choesterol 165 mg/dl, triglycerides 175 mg/dl, HDL-C 31 mg/dl, LDL-C 99 mg/dl.
Troponin I 0.04 ng/ml (nl 0.0-0.09), CK-MB fxn 2.9 (nl <7.8).

49. 1-31-2006 1356 Hrs
Chest pain resolved, rhythm and hemodynamics normal.
CK-MB index 5.9
CK-MB fxn 191.5 ng/ml
CK 3240 U/L
Trop I >22.8 ng/ml

55. DL 64y female hospital ward clerk with abrupt onset of chest pain and
dyspnea while rushing to meet son at airport. No CV disease history.
Maximum CK xxx IU/L, troponin-I 44.6 ng/ml. Cardiogenic shock required
IABP.

61. RC 83 y male in CV – ICU, immediately post-op from aorto-coronary bypass

63. RF 82 y female in ED with acute onset epigastric pain and nausea and
substernal chest pressure

72. JC 27 y male with no CV disease history presented to ED in RWC with acute
chest pain and shortness of breath. Substance abuse denied, toxicology studies
negative.

73. JC 27 y male with no CV disease history presented to ED in RWC with acute
chest pain and shortness of breath. Substance abuse denied, toxicology studies
negative. CK 1372 IU/L, troponin-I >50 ng/ml. Platelet count 1472 K/mm3.
Emergent transfer to the CCL. Follow-up ECG 30 minutes later:

79. NW 36 y male alcoholic fell unconscious at home, ambulance to ED,
intubated. CK 775 IU/L, troponin-I 0.14 ng/ml.

80. NW 36 y male alcoholic fell unconscious at home, ambulance to ED,
intubated. CK 775 IU/L, troponin-I 0.14 ng/ml.
Repeat ECG 9 minutes later:

87. 42 y Asian female on chemotherapy for metastatic breast carcinoma, acute
onset chest pain and dyspnea, troponin-I 1.11 ng/ml

88. 42 y Asian female on chemotherapy for metastatic breast carcinoma, acute
onset chest pain and dyspnea, troponin-I 1.11 ng/ml.
Echocardiography revealed large pericardial effusion due to carcinomatosis.

90. AG 81 y male with chest pain worse with inspiration, sternal tenderness,
elevated troponin-I.

91. AG 81 y male with chest pain worse with inspiration, sternal tenderness,
elevated troponin-I.
Brought to ED by EMT from MVA. X-ray diagnosis of sternal fracture.

92. RH: 56 y male in ED with chest pain

93. DG: 58 y male in ED with lightheadedness and near syncope

94. JS: 84 y male in CV - ICU

95. How to Avoid Misdiagnosis
• Talk to the patient, take a history
• Examine the patient
• Obtain and review original documents
• Do not believe everything in the
computer
• Consider the differential diagnosis
• Re-examine the patient
• Think

96. Questions to Ask Yourself
• Is my diagnosis correct?
• Is my treatment plan appropriate for
this diagnosis?
• Is my treatment plan appropriate for
this patient?
• Does my patient understand and
agree with the treatment plan?
• Do I need help?

98. Betelgeux Bellatrix
Great Nebula
Rigel
Saiph