Myocardial infarction occurs when a coronary artery becomes blocked, interrupting blood flow to heart muscle. This causes damage and permanent loss of contraction in that portion of the heart. Over time, the affected area evolves from pallor to yellowing to fibrosis as dead heart cells are removed and replaced by scar tissue. Microscopically, early signs include wavy fibers at the border and loss of striations within infarcted regions. Complications can include arrhythmias, heart failure, mural thrombi, rupture and aneurysm formation depending on the size and location of the infarct. Examination of autopsy specimens involves analysis of coronary arteries and dissection of the heart to identify infarct location, extent and healing stage

1. Myocardial Infarction
• Presenter : Dr Gopal G Hargi
» PG in dept of FM & T

2. • Acute Myocardial infarction is one of
the pathological condition caused by
prolonged ischemia where there is
irreversible necrosis of the myocardial
tissue

3. • IHD refers to a group of closely related syndromes
caused by imbalance between myocardial oxygen demand &
blood supply.
• Ischemia is the most common type of cell injury, (in
contrast to hypoxia ,the injury is faster)
• IHD - 90% due to atherosclerosis affecting coronary
arteries
• 10% other causes
• Most common cause of ischemia
Narrowing of coronaries by atherosclerosis

4. Depending on rate & severity of myocardial injury one of 4
syndromes may develop
1)Angina pectoris
2)MI
3)Sudden cardiac death
4)Chr IHD& CCF
Other less common sequele (non cardiac) due to atherosclerosis
• Perepheral vascular disease
• aneurysms
• Ischemic encephalopathy
• mesentric artery occlusion

5. Pathology of atherosclerosis: affects primarily
the intima of large & medium sized muscular
arteries and is characterized by endothelial
thickenings, fibro fatty plaques or atheromas.
(atheros-porridge –ref to soft lipid rich material in
the centre of atheroma.sclerosis- CT in plaque.
Common sites – Aorta/Coronaries/Cerebral vessels

6. • Clinical manifestation may develop at any age but
more common in older adults with peak incidence
after age of 60 yrs in men & 70 yrs in women
• Risk factors
• Major : constitutional: age/sex/genetics/familial &
race
acquired : ^ lipid/HT/DM/smoking
• Minor : Environmental/obesity/hormones/physical
inactivity / stress/alcohol/infections(cmv ,
herpes)

7. • Atherosclerosis formation – no of theories
• 1) insudation theory ( virchows ) :also called
response to injury theory.
cellular proliferation of intimal cells from imbibing
of lipids from blood.
2) Encrustation theory ( Rokitansky) : Atheroma
causes a form of encrustation on the arterial wall
from the components of blood to form thrombi (
platelets ,fibrin, leucocytes)
(currently reaction to injury& monoclonal theory
based on proliferation of SMC is accepted )

9. • The 4 key significant factors responsible are
• Arterial SMC
• Endothelial cells
• Blood Monocytes
• Hyperlipidemia
Reaction to injury is taken as the endothelial
injury followed by SMC proliferation so that early
lesion consists of SMC mainly .The lipoproteins enter
into the intima ,followed by lipid accumulation in
macrophages( foam cells)

10. • Earliest pathological lesions in atherosclerosis are
• 1)Intimal thickening-
• 2)Fatty streaks fore-runners in the evolution
• of atherosclerosis.
Fatty streaks : these lie under the endothelium
& composed of closely packed foam cells ,lipid
containing SMC & few lymphoid cells.
3) Atheromatous plaques: also called fibrous plaque ,
fibro fatty plaque & atheromas

13. • Complication:(fate of atheroma)
• covering endothelium remains intact but danger
to life is caused by luminal reduction from bulge
of enlarging plaque
• Fibroendothelial cap begins to breakdown under
pressure by central necrosing process & erosions
caused by blood flow
• May rupture into lumen leading to acute
obstruction causing death
• Contents of the plaque may get washed down
causing embolism

15. Changes
• Calcification
• Ulceration
• Thrombosis: plaque - internal necrosis - surface
eroded –fibrofatty content exposed
- nidus for thrombosis
• Hemorrhages : rupture of blood vessels in the
periphery
• aneurysm

16. • IHD - 90% due to atherosclerosis affecting coronary
arteries
• 10% other causes
Other causes ( non atherosclerotic )
• Vasospasm
• Stenosis of coronary ostia: syphilitic aortitis
• Arteritis: kawasaki disease/TB/polyarteritis
• Embolism: infective endocarditis
• Thrombotic disease: polycythemia vera , SSA , TTP
• Aneurysms: DAA into coronary artery
• Compression: tumour of heart
• Trauma: contusion to muocardium

17. • MI is the most feared consequence of CAD .Many die within
few hrs ,remaining suffer from effects of impaired cardiac
functions.
• According to WHO statistics ,globally ,MI is responsible for
nearly 32% & 27% of all the mortalities in males & females
respectively
• 13.5 million alive today with history of MI
• 5% of MI in people under 40 years , particularly with HTN
• In 48% of men and 33% of women who died suddenly of MI,
there were no previous symptoms

18. Acute MI is one of the pathological condition caused
by prolonged ischemia where there is irreversible
necrosis of the myocardial tissue due to
coronary blood flow myocardial demand,
hypertrophy
Risk factors
• HTN
• DM
• Cigarettes
• Dislipidemia with familial hypercholesteremia

19. • Depending upon site
• LV . LAD- 40-50% . LCCA- 15-20% . RCA- 30-40 %

22. • MI caused by ischemic injury .
• Types are
• 1)Full thickness or transmural(regional/focal) : chr
atherosclerosis
• 2)Subendocardial or laminar: thrombi absent (diffuse
stenosing coronary atherosclerosis & therefore no
plaque disruption or thrombosis.- hypoperfusion.
MI typically begins in subendocardial region
1) last area to be perfused
2) intra mural pressure- inflow of blood

23. • Age of infarct is difficult to establish because onset
of symptoms are often much later ( 1- 1.5hrs)than the
onset of the pathological lesions precipitated by the
occlusion
• Various methods of detection
• Histochemical method
• Flouroscent method
• Enzyme chemistry
• Immunohistochemical method

24. • Diagnosis
• Clinical features: sudden onset /pain /shock /
indigestion / oliguria /acute pul oedema
• ECG changes/ serum cardiac markers (troponin
• c,troponin t, CCK-MB ) / SGOT,PT

25. • 10%formol soln- non infarcted area-stain ,infarcted
• Haematoxylin –eosin stain – eosinophilia & oedema
• PAS- peripheral pink stain ,infarcted. Grey blue –
healthy
• Phosphotungstic acid haematoxylin- change in
striation pattern of MI fibres
• Histochemical –LDH activity of succin
dehydrogenase,malic dehydrogenase
• Floroscene test-normal-brown.infarcted-green

26. • 1cc thick slices ,across ventricles ,washed .The slices
dipped into 1% soln of 2:3:5 triphenyl tetrazolium
chloride .After this the slices are treated with 10%
formalin which fixes the stain .The brown stained
area indicates increased activity of dehydrogenase
enzyme and viable tissue .The necrosed tissue
appears pale. These detected tissues can be collected
for histological examination

27. 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.

28. Ohr 2hr
24hr

29. 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:

30. 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
• Electron microscopy shows reversible changes
(swelling of mitochondria & endoplasmic
reticulum and relaxation of myofibrils).
• Histochemically, there is loss of oxidative
enzyme & fall of glycogen.
• In 12 to 72 hours, there is infiltration of
neutrophils with progressive coagulative
necrosis of myocytes. Dead myocytes become
hypereosinophilic with loss of nuclei.
•

31. This is normal myocardium. There are cross striations and central nuclei

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

33. 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.

34. 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.

35. • 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, contracted
myofibrils 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, 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.

36. 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.

37. • Examination procedure for MI victims at autopsy
• Examination of Coronaries: angiography,inj of barium-
gelatin mix into coronary ostia.fix 24hrs. Wash –xray
• Perfusion –fixation . Intra aortic perfusion of 10%
formalin at a pressure of 100 mm of Hg
• Dissection
• Section tranversely at 3-5mm interval ,the RCA,LAD,CCX.
Diagonal,obtuse,marginal & PD arteries .Grade the
reduction of cross section area by atheroma as grade
1=25%, grade 2=26-50%,grade3=50-75%, grade4=76-
100%.
• Look for thrombus ,plaque & dissection.
• Section from sites of maximal narrowing

38. Cardiac dissection methods:
1. Inflow-outflow method
2. Short-axis method
3. Four chamber method
4. Long axis method
5.Base of heart method
6.Window method
7.Unrolling method
8.Partition method.
Useful for
demonstrating
cardiac pathology
Anatomic
teaching and
museum
specimen
demonstration
s/
preparations.
Considerab
le
Mutilation
of the
heart

39. 1-1.5c
cm

42. • Examination of myocardium
• Location/extent/distribution
• Inflow-outflow method

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. Complications
• Arrythmias
• CCF
• Mural thrombi & thromboemnbolism
• Rupture
• Cardiac aneurysms
• Pericarditis
• Cardiac Tamponade
• Post MI syndrome

46. Remote myocardial infarction (weeks to years)

47. Myocardial Rupture
Myocardial aneurysm with
thrombosis inside.

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

50. 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.

51. 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

52. 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.

53. Thank You