Myocardial Infarction Pathology

1. Myocardial Infarction
Dr. Sobia Khalid

4. Myocardial infarction
A heart attack or acute myocardial infarction (MI) occurs when one of the arteries
that supplies the heart muscle becomes blocked. Blockage may be caused by
spasm of the artery or by atherosclerosis with acute clot formation. The blockage
results in damaged tissue and a permanent loss of contraction of this portion of the
heart muscle.

5. • Myocardial infarction (MI) is the irreversible
necrosis of heart muscle secondary to prolonged
ischemia. This usually results from an imbalance
of oxygen supply and demand.

6. CLASSIFICATION
1. Transmural: :(Q –wave infarction) : most
infartcts are transmural involve the full
thickness of ventricular wall in the
distribution of single coronary artery.
These infracts are caused by
• atherosclerosis,
• acute plaque changes
• less commonly thromboemboli or
vasospasm.

7. 2. Subendocardial: these infarcts involve inner one
third to one half of ventricular wall as subendo
cardial zone is less perfused area of myocardial
zone. The infarcts are caused by
• hypoperfusion of myocardium and not by
coronary occlusion. These occur in hypotensive
shock, and by typical ECG findings these are so
called non Q wave infarction.

8. PATHOGENESIS:

9. Occlusion is typically seen in the proximal 2 cm of the
left anterior descending and left circumflex arteries
and in the proximal and distal thirds of the right
coronary artery.
o Rupture of the lipid-rich atheromatous plaque,
intraplaque hemorrhage, andintraluminal thrombus
are three pathological hallmarks most commonly
recognized in the infarct-related coronary artery at
the site of acutemyocardial infarction.
o Role of the platelet-derived mediators (e.g. TXA2,
serotonin, ADP, & PDGF that promote thrombosis
and vasoconstriction occur.

10. o Diminished availability of those natural
endogenous substances that inhibitplatelet
aggregation, such as EDRF, tissue plasminogen
activator, and PGI2.
o Vasospasm is stimulated by mediators release
from platelets.
o Tissue factor activates the coagulation pathway.
o Thrombus occlude the lumen of vessel.
o Ischemia without detection of coronary
thrombosis due to vaculitis

13. These serial sections of a coronary artery demonstrate grossly the
appearance of lumenal narrowing with atherosclerosis.

14. • Grossly :Before 6 to 12 hours: No visible lesion is
seen.
• By 18 to 24 hours: Infarct area becomes pale to
cyanotic & swollen.
• In the first week: The infarct area becomes
progressively more sharply defined, yellow and
softened.
• By the 7to 10 days, circumference of the infarct
area becomes hyperemic, and progressively
expands.
• By the 6 weeks, fibrous scar is well established.

15. myocardial infarction
(2) of the tip of the
anterior wall of
the heart (an
apical infarct)
after occlusion (1)
of a branch of the
left coronary
artery(LCA, right
coronar

16. Ohr 2hr
24hr

17. This is an acute myocardial infarction in the septum. After several days,
there is a yellowish center with necrosis and inflammation surrounded
by a hyperemic border.

18. This is an acute myocardial infarction of the anterior left ventricular free wall and
septum in cross section. Note that the infarction is nearly transmural. There is a
yellowish center with necrosis and inflammation surrounded by a hyperemic borde

19. When the infarction is 3 to 5 days old, the necrosis and inflammation are most
extensive, and the myocardium is the softest, so that transmural infarctions may
be complicated by rupture. A papillary muscle may rupture as well to produce
sudden valvular insufficiency. Rupture through the septum results in a left-to-right
shunt and right heart failure.

20. Remote myocardial infarction (weeks to years)

21. Time from Onset Gross Morphologic Finding
18 - 24 Hours Pallor of myocardium
24 - 72 Hours Pallor with some hyperemia
3 - 7 Days
Hyperemic border with central
yellowing
10 - 21 Days
Maximally yellow and soft
with vascular margins
7 weeks White fibrosis
Gross morphologic changes evolve over time as follows:

22. This is normal myocardium. There are cross striations and central nuclei. Pale pink
intercalated disks are also present.

23. Microscopic features:
• Within 1 hour of ischemic injury, there is
intercellular edema and “wavy fibers” may be
present at the periphery of the infarct. These
are noncontrctile dead fibers, stretched by the
adjacent viable contracting myocytes.
• In 12 to 72 hours, there is infiltration of
neutrophils with progressive coagulative
necrosis of myocytes. Dead myocytes become
hypereosinophilic with loss of nuclei.
•

25. This is an early acute myocardial infarction. (<iday) Note the
prominent pink contraction bands.

26. 1-2 daysThis is an early acute myocardial infarction. There is increasing loss of
cross striations, and some contraction bands are also seen, and the nuclei are
undergoing karyolysis. Some neutrophils are beginning to infiltrate the
myocardium.

27. 1-2days This is an acute myocardial infarction. There is loss of cross
striations, and the nuclei are not present. There is extensive hemorrhage
here at the border of the infarction, which accounts for the grossly
apparent hyperemic border.

28. 3-4 days This is an acute myocardial infarction of several days'
duration. There is a more extensive neutrophilic infiltrate along
with the prominent necrosis and hemorrhage.

29. • Between 3 and 7 days after onset, dead myocytes begin to
disintegrate and are removed by macrophages and enzyme
proteolysis. There is proliferation of fibroblasts with formation
of granulation tissue, which progressively replaces necrotic
tissue.
• After 6 weeks, healing is complete by fibrosis.
• Contraction band necrosis: Contraction band necrosis,
characterized by hypereosinophilic transverse bands of
precipitated myofibrils in dead myocytes is usually seen at the
edge of an infarct or with reperfusion (e.g. with thrombolytic
therapy).
• Reperfusion of an infarct: Reperfusion of an infarct is also
associated with more hemorrhage, less acute inflammation, less
limitation of the acute inflammation to the periphery in the first
few days, reactive stromal cells, more macrophage infiltration
earlier and a more patchy distribution of necrosis, especially
around the periphery.

30. 2-3 wks Toward the end of the first week, healing of the infarction
becomes more prominent, with capillaries, fibroblasts, and macrophages
filled with hemosiderin. The granulation tissue seen here is most prominent
from 2 to 3 weeks following onset of infarction.

31. weeks –years After a couple of weeks, healing is well under way, and there
is more extensive collagen deposition.

32. wks –yrs The remote myocardial infarction is evidenced by a
collagenous scar seen here in a subendocardial location.

33. Symptoms of a possible heart attack include chest pain and pain that radiates
down the shoulder and arm. Some people (the elderly, people with diabetes, and
women) may have little or no chest pain. Or, they may experience unusual
symptoms (shortness of breath, fatigue, weakness).
Women are more likely than men to have symptoms of nausea, vomiting, back or
jaw pain, and shortness of breath with chest pain.

34. • Clinical features: Chest pain- 20-30%
does not cause chest pain, common in
patients with diabetes mellitus,
hypertension, & in elderly patients.
• 2. Nausea, diaphoresis and dyspnea.

35. • Fate of the patient: hospitalized patients
(where angiography, echocardiography
and perfusion scintigraphy are available)
usual fate are:
• i) About 25 % of patients dye of
cardiogenic shock or fatal arrythmia.
• ii) Patients who survive the acute phase
may develop:

36. • Congestive heart failure
• - Cardiac arrythmia
• - Left ventricular failure with pulmonary edema.
• - Rupture of ventricular wall, interventricular
septum and papillary muscle
• - Thromboembolism.
• iii) 10-20% patients recover with no
complication.
• iv) Early restoration of blood flow by
thrombolysis or balloon angioplasty provides
better prognosis.
•

37. Screening and Diagnosis
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38. • DIAGNOSIS:
• It is based on
• Symptoms
• electrocardiographic change
• serum elevation of myocardial enzymes
(creatine kinase-MB isoenzyme) or other
proteins (troponin I, troponin T or myoglobin),
that leak out of dead cells.

39. • The classic ECG findings: ST segment
elevation, followed by T wave inversion and Q
waves, are associated with transmural
infarction. ST segment depression and T wave
inversion are associated with subendocardial
infarction.

43. • Complications: It depends on the size , location
duration of the lesion.
With in minutes to 3 days of onset:
1. Arrythmias :75-95% i) ventricular fibrillation ; ii)
block of A-V bundles and its branches causing
acute heart failure.
2. Cardiogenic shock 10-15%(usually in large
infarct) causing acute heart failure.
3. Thrombotic complication- 15-40% mural
thrombus over infarct area or Atrial thrombus,
causing embolism to brain, kidney etc.
4. Rupture of heart.

44. • 3-14 days:
Large infarct: There is softening of dead muscle
(myomalacia cordis) leading to rupture &
death.
Site of rupture is ventricular wall, papillary
muscle & interventricular septum.
5. Acute fibrinous or hemorrhagic pericarditis -
over infarct area.
After weeks or months:
6. Chronic heart failure
7. Cardiac aneurysm, which may rupture
producing hemopericardium and death.

45. Myocardial Rupture
Myocardial aneurysm with
thrombosis inside.

46. Rupture (at the arrow) into the pericardial sac can produce a life-
threatening cardiac tamponade, as seen here. The septum may also
rupture.

47. Rupture of papillary muscle…..mitral incompetence.

48. Left ventricular aneurysm
containing mural thrombus
A complication of infarction is aneurysm
formation, which is the bulge seen here in
the left ventricular wall. Note the very thin
white wall of the aneurysm toward the apex.

49. The myocytes here are hypertrophied, marked by the large, dark nuclei, and
there is interstitial fibrosis. This is an example of cardiomyopathy. In this case,
long-standing, severe occlusive atherosclerosis led to "ischemic" cardiomyopathy.

50. • 6- Dressler’s syndrome
• Is complication of transmural MI
• -an autoimmune disorder resulting from
damage of the myocardium
• -antibodies developed against protein release
from necrotic myocardial cells
• -autoimmune pericarditis, pericardial friction
rub and pleurisy.

51. R/ Revascularization procedures

52. 1) Stenting
• a stent is introduced into a blood vessel on a balloon
catheter and advanced into the blocked area of the
artery
• the balloon is then inflated and causes the stent to
expand until it fits the inner wall of the vessel,
conforming to contours as needed
• the balloon is then deflated and drawn back
•The stent stays in place permanently, holding the
vessel open and improving the flow of blood.

53. 2) Angioplasty
• a balloon catheter is passed through the guiding catheter to the
area near the narrowing. A guide wire inside the balloon catheter is
then advanced through the artery until the tip is beyond the
narrowing.
• the angioplasty catheter is moved over the guide wire until the
balloon is within the narrowed segment.
• balloon is inflated, compressing the plaque against the artery wall
• once plaque has been compressed and the artery has been
sufficiently opened, the balloon catheter will be deflated and
removed.

54. 3) Bypass surgery
• healthy blood vessel is removed from leg, arm or chest
• blood vessel is used to create new blood flow path in
your heart
• the “bypass graft” enables blood to reach your heart
by flowing
around (bypassing) the
blocked portion of the
diseased artery. The
increased blood flow
reduces angina and
the risk of heart attack.

55. •Get regular medical checkups.
•Control your blood pressure.
•Check your cholesterol.
•Don’t smoke.
•Exercise regularly.
•Maintain a healthy weight.
•Eat a heart-healthy diet.
•Manage stress.