CARDIOVASCULAR DISORDERS

BLOOD VESSELS

SLIDE DIAGNOSIS CHARACTERISTICS

Thrombosis Virchow’s Triad
1. Endothelial injury
2. Stasis or turbulent blood flow
3. Hypercoagulability of blood

• Intact endothelium has antithrombotic properties, mediated by mediators

secreted by the endothelial cells that inhibit platelets such as Prostacyclin &
Nitric Oxide
• Would lead to platelet activation & the formation of a clot

Complete Obstruction by Thrombus

• During endothelial injury, accumulation of LDL occurs in the blood vessel &
platelets & inflammatory cells such as macrophages are also attracted at the
site of injury
o Macrophages develop into foam cells due to the ingestion of lipids
• Cells within the atheromatous plaque then release factors that stimulate the
proliferation of smooth muscle cells, extracellular matrix & other inflammatory
cells – leads to the formation of fibrous cap

Lines of Zahn: blood clot with alternating layers of light & dark areas that corresponds
to red blood cells alternating with fibrin deposits
Cholesterol Crystals: needle-shaped crystals
Monckeberg Medial Sclerosis: refers to calcification of tunica media of the artery

With canalization
• Thrombus can either propagate, embolize, dissolute, organize, or recanalize
• Recanalization may permit vascular flow

Organization & Recanalization: process where the thrombus is remodeled & eventually
may be incorporated within the vessel wall d/t the proliferation of endothelial cells,
smooth muscle cells, & fibroblasts
Necrotizing Vasculitis Vasculitis: inflammation of the blood vessels
Perivasculitis: presence of inflammatory cells surrounding the blood vessels composed
mostly of neutrophils
Any type of blood vessel can be affected, signs & symptoms would depend on the
underlying cause (infectious or non-infectious)
Can be immune-mediated which can be secondary to
• Deposition of immune complexes
• Presence of anti-neutrophil cytoplasmic antibodies (ANCA)
• Anti-endothelial cell antibodies
• Autoreactive T cells

Temporal Arteritis Also known as Giant Cell Arteritis

• Inflammatory diseases of the arteries are classified based on the etiologic agent
involved, caliber & location of the vessel affected, and type of microscopic
change observed
• Type of large vessel vasculitis syndrome
• Common after the age of 70

Characteristics
• Pain in the distribution of the temporal artery
• Localized tenderness

Pathogenesis
• T-cell mediated immune response to an unknown vessel wall antigen
• Cytokine induced inflammation
• Presence of anti-endothelial cell antibodies

Lymphohistiocytic: lymphocyte & macrophages

• Inflammation is usually found surrounding areas of a cellular collapsed elastic
lamellae

Diagnostic hallmark: Transmural Inflammation

• Changes in temporal arteries are often segmental thus a negative biopsy does
not rule out the diagnosis
Cystic Medial Necrosis Updated nomenclature: Cystic Medial Degeneration

• Characterized by an accumulation of basophilic ground substance in the tunica

media with cyst-like lesions
• Occurs in Marfan Syndrome & Secondary to hypertension
• Hypertension results in the constriction of the vasa vasorum which leads to
ischemia of the tunica media
o Ischemia of the tunica intima leads to weakening of the vessel wall
d/t smooth muscle cell loss, elastic fiber loss, & increased synthesis
of non-collagenous ECM
• This condition can eventually lead to weakening of the aortic wall & can
predispose to aortic dissection & aortic aneurysm

Aortic Dissection Dissection: splitting apart of the medial smooth muscle caused by an infiltration of
luminal blood under arterial pressure
Major risk factor: Hypertension
Site of Initiation: Tunica Intima which dissects into the media

• Narrowing or occlusion of the true lumen in the blood vessel

• Dissection plane may extend to and through the adventitial connective
tissue resulting in a vascular degeneration
Aortic Dissection Dissection: splitting apart of the medial smooth muscle caused by an infiltration of
luminal blood under arterial pressure
Major risk factor: Hypertension
Site of Initiation: Tunica Intima which dissects into the media

• Narrowing or occlusion of the true lumen in the blood vessel

• Dissection plane may extend to and through the adventitial connective
tissue resulting in a vascular degeneration

MI: 48 HOURS Tissue/Organ: Heart

Pathogenesis: Coronary Artery Occlusion
MI or commonly known as Heart Attack is an ischemic disease that results in Cardiac
Necrosis

• Majority are d/t reduced blood flow secondary to a ruptures coronary

atheromatous plaque
• Can also occur secondary to vasospasm if the coronaries or obstruction from an
embolus
• Necrosis of cardiac tissue would lead to the infiltration by inflammatory cells
mostly neutrophils

Presence of
1. Coagulative necrosis – Histologic feature
2. Intense eosinophilia
3. Waviness of the myocytes

Nuclear changes
1. Pyknosis
2. Karyorrhexis
3. Karyolysis
4. Contraction band necrosis – dark areas in cytoplasm common in
reperfusion injuries
5. Neutrophilic Infiltration
 MI: 4 DAYS Features:
1. Coagulative necrotic changes
2. Intense eosinophilia of the myocytes
3. Loss of the nucleus: cells are already necrotic

• Macrophages will start to phagocytose the necrotic myocytes

MI: 8-10 DAYS Granulation Tissue Formation: important slide feature aside from coagulative necrosis
1. Connective tissue deposition
2. Angiogenesis – very important feature
3. Infiltration by inflammatory cells

• Necrotic myocytes degraded by macrophages

• Resorption of dead myocytes
• No collagen deposition
MI: 1 MONTH Collagen tissue deposition already & will correspond to areas previously occupied by
necrotic cardiac myocytes

Other features
1. Collagen deposition admixed with angiogenesis
2. No infiltration of inflammatory cells
3. Hemosiderin cells
4. Granulation tissue
5. Angiogenesis

MI: 6 MONTHS Repair is complete by collagen deposition

Presence of Dense Collagenous Scar

Absence of
1. Granulation tissue
2. Cognitive necrosis
3. Inflammatory cells
Acute Fibrinous Pericarditis Most common form of acute pericarditis may be d/t
1. Myocardial infarction
2. Uremia
3. Radiation therapy
4. Infection
5. Malignancy
6. Trauma

• Fibrinous Exudate: occurs when there is a large vascular leak or a pro-coagulant

stimulus
• Type of inflammation is characteristic in the lining of the body cavity such as the
pericardium
• Increase in vascular permeability will cause Fibrinogen to leak out from the
blood vessels and be deposited in the extracellular space as Fibrin
• Normally, the pericardium is smooth & filled with fluid to minimize friction
o Fibrinous pericarditis: coarse granular appearance
• Fibrin has eosinophilic amorphous appearance and is admixed with blood cells
and inflammatory cells
• If fibrin is not removed: growth of Fibroblasts which will cause thickening of the
pericardium
• Presence of retrosternal chest pain and pericardial friction rub

Complications
1. Cardiac tamponade
2. Progression to constrictive pericarditis
Constrictive Pericarditis Tissue/Organ: Pericardium/Heart

• Caused by the growth of Fibroblasts which lead to fibrous thickening and

formation of adhesions
• Will lead to the obliteration of the pericardial space and the restriction of
movement of the heart thus impairing its function

Prolonged pericarditis: result in persistent accumulation of fluid which may form a

thick coating that surrounds the myocardium causing constrictive pericarditis
Multinucleated Giant Cells d/t chronic inflammation
 Bacterial Endocarditis • Infection of the cardiac valves or endocardium which leads to the formation of
Vegetations (hallmark)
• Manifest as fever, chills, & murmurs

Acute Infective Endocarditis

o Commonly caused by Staphylococcus aureus
o Usually affects normal heart valves
o Common among intravenous drug users

Subacute Infective Endocarditis

o Caused by organisms with a lower virulence factor such as Streptococcus
viridans
o Common in previously damaged heart valve

Most commonly affected

1. Aortic Valve
2. Mitral Valve

Presence of Bacterial Plaque – healed endocarditis will no longer show vegetations

grossly or histologically

Dx: Duke’s Criteria

Complications
1. Glomerulonephritis
2. Arrhythmia
3. Sepsis
Amyloidosis Primary: Multiple Myeloma
Secondary: Systemic Inflammatory Process
Stain: Congo Red

• Presence of extracellular deposition of fibrillar proteins d/t misfolded proteins

• Has an eosinophilic appearance and is acellular: leads to Pressure Atrophy of the
cardiac fibers
• Important cause of Restrictive Cardiomyopathy
o Decreased ventricular compliance
o Impaired ventricular diastolic filling

Hypertrophic Cardiomyopathy • Most commonly d/t mutations in genes that encode sarcomere proteins
• Leads to defective energy transfer from the mitochondria into the sarcomeres
• Left ventricle is non-compliant which leads to Reduced Stroke Volume
• Presence of asymmetric septal hypertrophy

Characterized by
1. Myocardial hypertrophy
2. Poorly compliant left ventricle
3. Particular outflow obstruction

Architecture
1. Disorganized
2. Myocytes are arranged at perpendicular and oblique to each other
3. Some have y-shaped branching and side-to-side junctions
 Cardiac Myxoma Most common primary tumor of the heart
Arise from Primitive Mesenchymal Stem Cells

• Can be sporadic or genetic

• Majority are located in the left atrium wherein they are grossly soft polypoid and
lobulated, often attached by a stock to the septum near the foramen ovale
• Ball Valve Effect – leads to obstruction in the blood flow within the heart

Microscopically: presence of round stellate or polygonal cells surrounded by an

abundant loose stroma rich in mucopolysaccharides
Tx: Surgery

Chronic Passive Congestion, Lung Tissue/Organ: Lung

Most common cause: Congestive Heart Failure

• Can also arise in Chronic Venous Obstruction

• Feature of capillary rupture: thickening of the interstitium d/t fibrosis

Hemosiderin-Laden Macrophages/Heart Failure Cells

• Phagocytosed extravasated RBCs by tissue macrophages
• Heme component of hemoglobin is catabolized
• Deposition of iron in the cytoplasm of the phagocytic cells