Myocardial
Infarction (MI)
Epidemiology:
- Women at
reproductive age are remarkably protected
Common sites:
Gross features:
- most are transmural
- common
distributions:
- (LAD) anterior wall of LV near apex, anterior ventricular
septum, apex circumferentially
- (RCA)
inferior/posterior wall of LV, posterior septum,
inferior/posterior RV in some
- (circumflex) lateral
wall of LV except at apex
- right ventricle
can be involved in posterior MIs
- isolated
right-sided MI in only 1-3%
- some are subendocardial, limited to inner half of ventricular
wall
- aborted MI
- prolonged low
blood pressure (shock) cirumferential subendocardial MIs
- 0-4h none
- 4-12h pallor, occasionally
dark mottling
- 12-24h pallor,
hyperemia sometimes, yellowing at periphery
- 1-3d mottling
with yellow-tan infarct centre
- 3-7d hyperemic
border, central yellow-tan softening
- 7-10d maximally
yellow-tan and soft, with depressed red-tan margins
- 10-14d red-gray
depressed infarct borders
- 2-8wk gray-white
scar, progressive from border towards core of infarct
- >2mo scarring
complete
- coronary arteries:
- atherosclerotic
lesion with associated thrombus
- hemorrhage within
an atherosclerotic lesion
- in 10%, no significant
lesion is identified
- vasospasm
as in cocaine abuse
- vasculitis
- hemoglobinopathies
- amyloid
deposition in vascular walls
- repurfusion changes (usually therapy-induced)
Histologic features:
- 0-30min none
- 0.5-4h:
- usually none
- variable
waviness of fibres at border
- 4-12h:
- coagulation
necrosis beginning
- edema
- hemorrhage
- 12-24h:
- coagulation
necrosis
- pyknosis of nuclei
- myocyte hypereosinophilia
- marginal
contraction band necrosis
- beginning neutrophilic infiltrate
- 1-3d:
- coagulation
necrosis with loss of nuclei and striations
- interstitial
infiltrate of neutrophils
- 3-7d:
- disintegration
of dead myofibres beginning
- early phagocytosis of dead cells by macrophages at infarct
border
- dying neutrophils
- 7-10d:
- phagocytosis well established
- fibrovascular granulation tissue beginning at
margins
- 10-14d:
- granulation
tissue well established
- new blood
vessels and collagen deposition
- 2-8wk:
- collagen
deposition increased
- decreased cellularity
- >2mo:
- myocytolysis at viable margin of infarct and
immediately subendocardial:
- large vacuolar
spaces within cells
- repurfusion changes (usually therapy-induced):
- contraction-band
necrosis intensely eosinophilic transverse
bands in myocytes
- acute plaque
changes in coronary arteries:
- rupture /
fissuring with resulting thrombus formation
- often at
junction of plaque with uninvolved arterial segment
- erosion /
ulceration with resulting thrombus formation
- hemorrhage into atheroma, expanding its volume
-
Immunophenotype:
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Marker:
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Sensitivity:
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Specificity:
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Molecular features:
Other features:
- EM:
- 0-30min:
- relaxation
of myofibrils
- glycogen
loss
- mitochondrial
swelling
- 0.5-4h:
- sarcolemmal disruption
- mitochondrial
amorphous densities
- troponin-I and troponin-T:
- rise
at 2-4h
- peak
at 48h
- elevated
for 7-10d
- virtually
100% sensitive
- complications
following MI:
- contractile
dysfunction with left heart failure
- arrhythmias
(often cause of sudden death) (more common with posterior MIs)
- myocardial
rupture
- rupture
of the free wall with tamponade (usually
fatal) (lateral wall most common)
- rupture
of the septum leading to left to right shunt
- papillary
muscle rupture leading to severe mitral
regurgitation
- pericarditis
- right
ventricular dysfunction
- infarct
extension
- mural
thrombus and thromboembolism
- ventricular
aneurysm
- false
aneurysm covered only by pericardium
- true
aneurysm bounded by scarred myocardium
- papillary
muscle dysfunction with mitral regurg
- in cocaine abuse,
vasospasm perhaps associated with platelet aggregation can cause MI
- irreversible
myocardial damage (necrosis) begins at 20-40 minutes of severe ischemia
(usually at least 2-4h occurs)
References: