Myocardial Infarction
1. Acute Myocardial Infarction
A. Obstruction–> Thrombosis–> Occlusion
B. Ischemic injury prolonged–> Irreversible injury
2. Location and Size
A. Location and severity of obstruction
B. Size of vascular bed
C. O2 needs of myocardium
D. Collateral development
E. Coronary artery spasm
F. Tissue factors
G. Thrombotic and thrombolytic substances
3. Types of Infarction
A. Transmural
1) Acute coronary thrombosis
2) Localized zone of distribution
B. Subendothelial (non-transmural)
1) Coronaries narrowed but patent
2) Thrombotic occlusion–> thrombolysis
3) Increased oxygen demand and/or decreased oxygen delivery
4) Pulmonary embolism
5) Hypotension
6) Hypertension
7) Aortic stenosis
8) Anemia
9) Operative procedures
10) Cerebrovascular accident
4. Sites of Involvement
A. Most involve LV and interventricular septum
B. Up to 65% or IMI involve RV
C. Isolated RV in 3-5%
1) COPD
2) RVH
5. Pathology
Gross Changes
| Time | Changes |
| < 6 hours | No change |
| > 6 hours | Pale, bluish, edematous |
| 18-36 hours | Tan, reddish purple |
| >48 hours | Gray, yellow lines at periphery |
| 8-10 days | decreased wall thickness, coagulation necrosis |
| 2-3 months | Thin, form scar |
6. Coronary Artery Thrombosis
A. Coronary atherosclerosis
B. Vasospasm
C. Plaque rupture
D. Platelet actuation
7. Coronary Atherosclerosis
A. Acute occlusion =Rapidity of development/Collateral circulation
1) Transmural
2) Subendocardial
3) None
B. Vasospasm
1) Increased Thromboxane A2
C. Plaque rupture
1) Ulceration
2) Fissure formation
D. Platelet activation
1) Adhesion–> aggregates–> increase Thromboxane A2
2) Decreased Fibrinolytic activity
3) Decreased tissue plasminogen activator
8. Collateral Circulation
A. Coronary occlusive disease
B. Chronic hypoxia
1) COPD
2) Anemia
3) Cyanotic CHF
C. LVH
9. Pathophysiology
A. Systolic Function
B. Infarcted area
1) Dyssynchrony
2) Hypokinesis
3) Akenisis
4) Dyskinesis
C. Non-infarcted areas
1) Hyperkinesis
D. Manifestations
1) Decreased diastolic compliance
2) Decreased ejection fraction (>15%)
3) CHF (>25)
4) Cardiogenic shock (>40%)
10. Infarct Size Limitation
A. O2 supply (coronary perfusion pressure)
B. O2 demand (ventricular wall tension)
11. Complications
A. Hypotension
B. Arrhythmias
C. Congestive heart failure
D. Hypoxemia
E. Anemia
F. Infections
G. Hypertension
H. Cardiogenic shock
1) Pharmacologic
2) Mechanical
3) Surgical– VSD, MR, Ventricular rupture
12. Reperfusion of infarction
A. Increased systolic function
B. Increased diastolic function
C. Decreased mortality
13. Treatment
A. Coronary thrombolysis
B. Angioplasty
14. Coronary Thrombolysis
A. Agents
1) Streptokinase
2) Plasminogen streptokinase activation complex (APSAC)
3) Tissue-type plasminogen activator (tPA)
B. Indications
1) Impending or evolving MI
2) 3 hours of symptom onset
3) Heparin (bolus ==>infusion)
4) ASA
15. Contraindications
A. Recent trauma
B. Major surgery (6 weeks)
C. GI bleeding (3 months)
D. Bleeding diathesis
E. Chronic liver disease
F. Allergy to thrombolytics
G. Stroke with residual
H. TIA (6 months)
I. Cerebral hemorrhage
J. Pregnancy
16. Angioplasty
A. Indications
1) Thrombolytic contraindicated
2) Thrombolytic unsuccessful
3) Extensive ischemia
17. Summary
A. Atherosclerotic coronary artery disease
1) Stenosis
2) Thrombosis
3) Vasoconstriction
4) Plaque disruption
B. Segmental disease
C. Endocardium–> epicardium
D. Irreversible injury >15-20 minutes occlusion
1) Maximal damage 4-6 hours
2) Best salvage 1-2
E. Size depends on collateral
1) Morbidity and mortality
2) O2 supply/O2demand
F. RV infarct with inferior MI