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Home Pathology
Myocardial Infarction Made Easy
October 19, 2011 | 9:37 am | Pathology | No Comment
The 4 Ischemic Heart Diseases caused due to imbalance between supply and demand of
the heart for oxygenated blood are:
1. Acute Myocardial Infarction (MI)
2. Angina Pectoris
3. Chronic Ischemic Heart Disease (IHD)
4. Sudden Cardiac Death
Myocardial Infarction (MI) Commonly known as a heart attack, is an anemic infarct with
coagulative necrosis of a large area of the myocardium due to occlusion of one of the three
main trunks of the coronary arteries.
Types:
Basis of Difference Transmural Infarct Subendocardial Infarct
Definition Full-thickness, solid Inner 1/3rd to 1/2nd, patchy (mosaic
infarct)
Frequency More frequent (95%) Less frequent
Distribution Specific area of coronary supply Circumferential
Pathogenesis Absolute persisten ischemia as
a result of stenosis of one main
trunk of coronary artery
Worsening of temporary relative
ischemia as a result of stenosis of
one or more main trunk of coronary
Who wrote this article?
This entry was
posted by Sulav
Shrestha on
October 19, 2011 at
9:37 am and filed
under Pathology
category.
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! Infarction ! Myocardial ! Coronary Artery ! Mnemonic
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8/1/14 6:17 PM Myocardial Infarction Made Easy | Medchrome
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arteries
Coronary thrmobosis Common Rare
Risk Factors:
1. Age: Increased
2. Sex: Male
3. Other Predisposing factors of atherosclerosis (Predisposing factors and Pathogenesis of
Atherosclerosis)
Pathogenesis:
A) Coronary Artery Occlusion:
Mechanisms:
1. Coronary Atherosclerosis:
Distribution: Left Anterior Descending (LAD) CA> Right Coronary Artery (RCA)> Left
Circumflex (LCX) CA
Process:
Atherosclerotic Plaque Disruption (rupture/fissuring, erosion/ulceration, hemorrhage i.e.
complicated atherosclerosis) leading to exposure of subendothelial collagen and
necrosis of plaque. Plaques having more foam cells, extracellular lipid, inflammatory
cells, less smooth muscle cells and thin fibrous cap are the vulnerable plaques.
Activated macrophages and T-lymphocytes localized at the site of plaque rupture are
thought to release metalloproteases and cytokines which weaken the fibrous cap.
Sequence of process of hemostasis:
Adhesion, aggregation and activation of platelets and release of aggregators
including TXA2 (Thromboxane A2), serotonin, etc.
Vasospasm
Extrinsic pathway of coagulation cascade activated to form thrombus
Complete occlusion of coronary vessel lumen
2. Non-atherosclerotic Vasospasm
3. Emboli: Left sided mural thrombus, Endocarditis, Paradoxical emboli
4. Unexplained: Amyloid, Hemoglobinopathies
B) Myocardial Response:
Loss of critical blood supply to myocardium
Decreased aerobic glycolysis and Increased anaerobic glycolysis
Decreased ATP and Increased Lactate accumulation
Loss of contractility
Acute Heart Failure
Microvascular injury leading to Coagulative necrosis
Feature Time
Onset of ATP depletion Seconds
Loss of contractility < 2 min
ATP Depletion
50% of normal
10% of normal
10 min
40 min
Irreversible cell injury 20-40 min
Microvascular injury >1 hour
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1. Anterior wall infarcts: Occlusion of Left Anterior Descending (LAD) Coronary artery
2. Posterior wall infarcts: Occlusion of Right Coronary artery
3. Lateral wall infarcts: Occlusion of Left Circumflex (LCX) Coronary artery
Gross Features by Time from Onset:
Acute Infarction: Pale infarction with cyanotic areas of hemorrhages and yellow border
(Correlate with Microscopic changes of Coagulative necrosis and Acute inflammatory
changes)
12-24 hours: Pallor
24-72 hours: Pallor, sometimes hyperemia; yellowing at periphery (due to neutrophilic
infiltration)
Subacute Infarction: Central yellow softening with hyperemic border (Correlate with
Microscopic features of phagocytosis and healing)
3-7 days: Hyperemic border; central yellow-brown softening
1-3 weeks: Maximally yellow and soft with depressed red-brown hyperemic margins
(due to growth of granulation tissue)
Old Infarction: Fibrosis
6 weeks: Mature Grey white fibrous scar and compensatory hypertrophy of the rest of
the myocardium
8/1/14 6:17 PM Myocardial Infarction Made Easy | Medchrome
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Acute: Pale areas of infarction and Old: White fibrous scar
Early infarcts (3 to 6 hours old) can be detected by histochemical staining for dehydrogenases
(LDH) using Triphenyl tetrazolium chloride (TTC) which stains red color to normal heart
muscle while the infarcted area fails to stain due to lack of dehydrogenases.
Microscopic features by Time from Onset:
Acute Infarction: Caogulative necrosis with loss of striations and Acute Inflammatory reaction
1/2 to 4 hours: Waviness of fibers at border
4-12 hours: Beginning coagulation necrosis; edema; focal hemorrhage, beginning
neutrophilic infiltration
12-24 hours: Continuing coagulation necrosis with loss of cross striations; pyknotic
nucleus; myocyte contraction bands
1 -3 days: Coagulation necrosis completes with loss of nucleus and striations;
neutrophilic infiltrate
Subacute: Appearance of macrophages, phagocytosis and Healing reaction
3-7 days: Disintegration of myofibers and phagocytosis by macrophages
1-3 weeks: Completion of phagocytosis; prominent granulation tissue with
neuvascularization and fibrovascular reaction
Old: Fibrosis
6 weeks: Mature fibrous scar
Electron microscopy:
1. Reversible phase (0-1/2 hours): Glycogen depeltion; mitochondrial swelling and
relaxation of myofibrils
2. Irreversible phase (>1/2 hours): Sarcolemmal disruption, Mitochondrial amorphous
densities
Reperfusion Injury:
Reperfusion after ischemia overloads the tissue surrounding the necrotic area with calcium.
This produces a continuous spasm leading to necrosis with contraction bands.
Complications:
1. Arrhythmias and Conduction defects with possible sudden cardiac death
2. Cardiogenic shock
3. Mural thrombosis with possible embolization
4. Myocardial rupture leading to cardiac tamponade and arrest
5. Infarct extension or re-infarction
6. Fibrinous pericarditis
7. Papillary muscle necrosis with possible valvular insufficiency
8. Congestive Heart Failure
9. Myocardial aneurysm resulting from ventricular akinesis
Mnemonic: HEART PASs away during MI
H: Heart Failure
E: Embolism following Mural thrombus formation
A: Arrhythmia which may lead to Sudden cardiac death
R: Re-infarction
T: Tamponade following Myocardial rupture
P: Pericarditis and Dresslers syndrome; Papillary muscle necrosis
A: Aneurysm (Ventricular) resulting from Akinesis
Ss: Shock (Cardiogenic)
8/1/14 6:17 PM Myocardial Infarction Made Easy | Medchrome
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Cardiac markers:


Clinical Features, Diagnosis and Treatment of Myocardial Infarction
Tags: MI, myocardial infarction
17 Like Like
Last updated: October 19, 2011
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