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Ischemic Heart Disease
Acute Myocardial Infarction
Cora Uram-Tuculescu, MD
Department of Pathology, VCUHS
[email protected]
Infarct modification by reperfusion
Case 1
1. What changes do you observe in
the heart?
2. What is the most likely diagnosis
and what was the likely cause?
3. What histologic features would
you expect in a section of the
grossly abnormal myocardium?
4. Describe the likely
pathophysiology leading to
death in this case.
5. Describe the sequence of
histologic changes that occurs in
the myocardium as a result of
acute occlusion of flow in a
coronary artery.
Case 1
Case 1- Acute myocardial infarction with rupture
What changes do you observe in
the heart?
Case 1
What changes do you observe in
the heart?
The myocardium of the anterior
left ventricular wall is diffusely
yellow in appearance in contrast
to the normal red myocardium
adjacent to it.
Case 1
What is the most likely diagnosis
and what was the likely cause?
Case 1
What is the most likely diagnosis
and what was the likely cause?
Acute transmural MI. The probe
demonstrates rupture of the wall.
Most likely cause is coronary
artery atherosclerosis with
occlusive thrombus over a
ruptured plaque.
Case 1
Describe the likely
pathophysiology leading to death
in this case.
Case 1
Describe the likely
pathophysiology leading to death
in this case.
Acute rupture of the ventricular
wall would result in accumulation
of blood in the pericardial sac
(hemopericardium). This would
prevent the heart from filling
normally in diastole (tamponade).
Case 1
Describe the sequence of
histologic changes that occurs in
the myocardium as a result of
acute occlusion of flow in a
coronary artery.
Case 1
Temporal sequence of early biochemical findings and progression of necrosis after onset of severe myocardial
ischemia.
A, Early changes include loss of adenosine triphosphate (ATP) and accumulation of lactate.
B, For approximately 30 minutes after the onset of even the most severe ischemia, myocardial injury is potentially
reversible.
Thereafter, progressive loss of viability occurs that is complete by 6 to 12 hours. The benefits of reperfusion are
greatest when it is achieved early, and are progressively lost when reperfusion is delayed.
(Modified with permission from Antman E: Acute myocardial infarction. In Braunwald E, et al [eds]: Heart Disease: A Textbook of Cardiovascular Medicine, 6th ed. Philadelphia,
WB Saunders, 2001, pp 1114-1231.)
The temporal evolution of the morphologic changes in acute MI and subsequent healing
Time
Gross features
Light microscopy
EM
0-1/2 hrs
None
None
Relaxation of myofibrils
Glycogen loss
Mitochondrial swelling
½-4 hrs
None
Usually none; variable waviness of fibers at border
Sarcolemmal disruption
Mitochondrial
amorphous densities
4-12 hrs
Dark mottling (occasional)
Early coagulation necrosis; edema; hemorrhage
12-24 hrs
Dark mottling
Ongoing coagulation necrosis; pyknosis of nuclei; myocyte
hypereosinophilia; marginal contraction band necrosis
1-3 days
Mottling with yellow-tan infarct center
Coagulation necrosis, with loss of nuclei and striations; brisk interstitial
infiltrate of neutrophils
3-7 days
Hyperemic border; central yellow-tan
softening
Beginning disintegration of dead myofibers, with dying neutrophils;
early phagocytosis of dead cells by macrophages at infarct border
7-10 days
Maximally yellow-tan and soft, with
depressed red-tan margins
Well developed phagocytosis of dead cells; granulation tissue at
margins
10-14 days
Red-gray depressed infarct borders
Well- established granulation tissue with new blood vessels and
collagen deposition
2-8 wks
Gray-white scar, progressive from
border toward core of infarct
Increased collagen deposition, with decreased cellularity
>2 month
Scarring complete
Dense collagenous scar
Progression of myocardial necrosis after coronary artery occlusion. Necrosis begins in a small zone of the
myocardium beneath the endocardial surface in the center of the ischemic zone. The area that depends
on the occluded vessel for perfusion is the “at risk” myocardium (shaded).
Case 2
1. Describe the gross pathologic
changes? What is the most likely
diagnosis?
2. What is the pathogenesis of these
changes? What portion of the
ventricle is most often affected by
the change you see in the image?
3. What histologic appearance would
you expect in a section of the
abnormal area?
4. How is this change in the heart
related to the patient’s neurological
process?
5. What other complications can
result from this pathologic change?
Case 2
Case 2- Left ventricular aneurysm
Case 2
Describe the gross pathologic changes?
What is the most likely diagnosis?
Case 2
Describe the gross pathologic changes?
What is the most likely diagnosis?
A portion of the left ventricular wall is
white rather than red in color, and
thinner than the adjacent normal
myocardium.
What is the pathogenesis of these
changes? What portion of the ventricle
is most often affected by the change
you see in the image?
Case 2
What is the pathogenesis of these
changes? What portion of the ventricle is
most often affected by the change you see
in the image?
During acute transmural infarction, the
zone of infarcted myocardium can
undergo expansion, stretching and
thinning because of traction by adjacent
viable myocardium. When infarcted area
heals with scar tissue, the thinned zone
becomes permanent and is referred to as
an aneurysm.
The anterior LV wall and the apex are
most commonly affected.
Case 2
Case 2
What histologic appearance would you
expect in a section of the abnormal
area?
Case 2
What histologic appearance would you
expect in a section of the abnormal
area?
Dense collagenous scar tissue.
Myocardium surrounding the scar likely
would be hypertrophic, as a
compensatory response.
Case 2
How is this change in the heart related
to the patient’s neurological process?
Case 2
How is this change in the heart related
to the patient’s neurological process?
The endocardium overlying the
aneurysmal myocardium often is the
site of mural thrombus formation.
Endothelial damage may predispose to
this, as well as the hemodynamic
changes (relative stasis) in this area of
the ventricle. A mural thrombus may
have dislodged and embolized into the
systemic circulation and lodged in a
cerebral artery (ischemic infarct).
Case 2
What other complications can result
from this pathologic change?
Case 2
What other complications can result
from this pathologic change?
Arrhythmias may occur if the scar
tissue prevents normal conduction of
impulse. Heart failure may occur
depending on the size of the scarred
area of myocardium. Rupture is NOT
likely since the thinned ventricular wall
is composed of dense fibrous scar
tissue.
Key Concepts
The vast majority of ischemic heart disease is due to coronary artery
atherosclerosis; vasospasm, vasculitis, or embolism are less common
causes.
 Cardiac ischemia results from a mismatch in coronary supply and
myocardial demand, and presents as different, albeit overlapping
syndromes
Acute myocardial infarction typically results from acute thrombosis after
plaque disruption; most occur in plaques that did not previously exhibit
critical stenosis.
Key Concepts
Myocardial ischemia leads to loss of function within 1 to 2 minutes, but
causes necrosis only after 20 to 40 minutes.
Myocardial infarction is diagnosed based on symptoms, EKG changes,
and measurement of serum CK-MB and troponins.
Gross and histologic changes of infarction require hours to days to
develop.
 Infarction can be modified by therapeutic intervention (e.g.,
thrombolysis or stenting), which salvages myocardium at risk, but
potentially induces reperfusion-related injury.
 Complications of infarction include: ventricular rupture, papillary
muscle rupture, aneurysm formation, mural thrombus, arrhythmia,
pericarditis, and CHF.