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Progressive
Pathology of CAD:
Coronaries -> atherosclerosis -> narrowing of the lumen due to fibrotic
plaques and atheromas
Plaques may be covered with fibrinous clots in an acute occlusion
Granulation tissue of the plaque and thrombi in older lesions may
reestablish blood flow via recanalization
Wall contains calcium and cholesterol deposits
1/28/09 Pathology wk1
Myocardial Infarction:
Rapid, sudden occlusion of
a coronary artery
Causes:
• Thrombosis of a coronary
artery (80-90%)
• Ulceration of an
embolized
atherosclerotic plaque
• Prolonged vasospasm
1/28/09 Pathology wk1
Types of MI’s
Transmural Subendocardial
Transmural:
Subendocardial or Intramural:
• Most common
• Infarction usually concentric
• All 3 layers of the heart involved
around the subendocardial
• Free wall of the left ventricle and/or
interventricular septum usually
layer of the left ventricle
involved • Q waves are absent
• New Q-waves develop
1/28/09 Pathology wk1
Subacute Myocardial Infarct-
Wavy, eosinophilic myocytes Granulation Tissue and Histology of MI:
with contraction bands Macrophages (over 1 week)
Microscopic changes precede
macroscopic changes
• Myocardial Rupture
• Left Ventricular Aneurysm
• Mural Thrombus
Ventricular Aneurysm
W/ Mural Thrombus
Ventricular Aneurysm With Infarcted
Myocardial Wall
1/28/09 Pathology wk1
Mural Thrombus
• Endocardium damaged/disrupted
• Blood coagulates in contact with the necrotic
endocardium/exposed myocardium -> thrombus
attached to the wall
• Complications:
– Impede blood flow
– Weakens ventricular
contractions
– May detach giving rise
to emboli -> cerebral
Infarcts
Note: PMN’s Have segmented Nuclei, they are granulomas (Innate immunity)
4 Stages of MI-Microscopic Findings
• Days 3-7: The infarcted area becomes
infiltrated with macrophages, which persist in
the lesion for about a week that phagocytize
and remove necrotic debris and myocytes.
Subacute Myocardial Infarct- Granulation Tissue
and Macrophages (over 1 week)
4 Stages of MI-Microscopic Findings
• Days 7-28 : Toward the end of the first week,
the infarct is invaded with granulation tissue
composed of small blood vessels
(angiogenesis), myofibroblasts and
fibroblasts depositing collagenous matrix.
Macrophages replace the PMN’s and
phagocytized the necrotic debris. (these are
subacute findings in an MI)
Subacute Myocardial Infarct with Collagen and
Angiogenesis (Granulation Tissue)
4 Stages of MI-Microscopic Findings
• Months: Ultimately, the necrotic myocardium
is replaced by white fibrous scarring between
islands of myocytes.
Old, Remote Infarct with White,
Myocardial Fibrous Scarring
4 Stages of MI-Gross Findings
The infarcted area cannot be definitively
identified during the first 1-2 days. There may
be some pallor of the infarcted area.
1-7 days : After the occlusion, the infarct
becomes yellow.
Acute Myocardial Infarct-Soft Yellow and
Hemorrhagic Tissue
4 Stages of MI-Gross Findings
• 7-28 days :After the occlusion, the infarct
becomes pallor and is surrounded by a
hemorrhagic rim, and the infarcted
myocardium is soft as a result of action of
hydrolytic enzymes released from the
neutrophils.
Acute Myocardial Infarction-
Granulation Tissue (Pallor
surrounded by Red rim)
• Months: White-tan fibrosis predominates
within an older or chronic infarct.
Old Myocardial Infarct
Pericarditis
Pericarditis
• Inflammation of the visceral or parietal pericardial
layers
• Most often associated with myocarditis,
tuberculosis
Causes of Pericarditis:
• Bacteria, viruses, fungi (rarely)
• Severe autoimmune diseases (SLE)
• Rheumatic Heart Disease
• Chronic renal failure -> metabolic waste products in
the blood (uremia)
• Trauma, radiation injury, and open-heart surgery
1/28/09 Pathology wk1
Pathology of Pericarditis
Exudation of fluid into the pericardial sac
– Clear yellow with serous pericarditis (viral infections)
– Purulent with bacterial infections
– Serofibrinous exudate associated with more severe damage
(Rheumatic fever)
Bacterial
(Suppurative) Serous
Panarteritis with
granulomatous
inflammation
– Infiltrates of neuts,
lymphs, and giant
cells
• Claudication
• Painful
ulceration of
the digits
Pulmonary edema
Right Heart Failure
• Etiology:
– Most common cause is left
heart failure
– If isolated: cor pulmonale
• Pathology:
– Backward failure -> congestion
of the venous system
Centrilobular passive congestion of – Hepatomegaly: chronic passive
the liver (Nutmeg liver) congestion of the liver
(“Nutmeg liver”)
– Splenomegaly
– Ascites (fluid within the
abdomen)
– Peripheral edema
• Ankle
• Sacrum
– JVD
Pitting ankle (petal) edema – Pleural effusions