cardiovascular histology

99
HISTOLOGY AND PATHOLOGY

Upload: jess-little

Post on 02-Jul-2015

196 views

Category:

Health & Medicine


1 download

DESCRIPTION

Review

TRANSCRIPT

Page 1: Cardiovascular Histology

HISTOLOGY AND

PATHOLOGY

Page 2: Cardiovascular Histology

BLOOD VESSELS

Page 3: Cardiovascular Histology
Page 4: Cardiovascular Histology

Functional Roles of Blood Vessels

• Elastic arteries (e.g. aorta) = conducting vessels

• Muscular arteries (medium-sized arteries) = distributing vessels

• Arterioles = resistance vessels

• Capillaries = exchange vessels

• Veins = capacitance (reservoirs)

Page 5: Cardiovascular Histology
Page 6: Cardiovascular Histology

Image Explanation

• This TEM image shows a continuous capillary, such as are found in muscle cells, general connective tissues and the central nervous system (CNS). This is a continuous (somatic) capillary because of its round shape, its continous endothelium (no fenestrations or discontinuities) and because of the many small vesicles in its thin cytoplasm.

• Capillaries are exchange vessels, where glucose, oxygen and CO2 are exchanged with the tissues of the body. Hence, "Exchange vessel" (answer "C") is the correct answer. The term conducting vessel usually refers to the large elastic arteries while distributing vessels usually refers to the medium-sized muscular arteries. Veins are capacitance/reservoir vessels where a great deal of the blood in the body is located at any one time.

Page 7: Cardiovascular Histology

Fenestrated Capillary

Page 8: Cardiovascular Histology

Endothelial Cell

SMC

Page 9: Cardiovascular Histology

4 Building Blocks

• Cellular

• Endothelial cells

• Smooth Muscle cells

• ECM

• Collagen

• Elastin

Page 10: Cardiovascular Histology

Endothelial Cells

• Endothelial cells are made of simple squamous epithelium, and line

all blood and lymphatic vessels.

• They are connected by tight junctions, adherens junctions, or gap

junctions.

• Their principal functions include: secretion of molecules (to regulate

vascular SM cells); exchange of: gases, H2O, nutrients, proteins,

WBCs; inhibition of coagulation; angiogenesis; inflammatory process.

• They are damaged in DM and in atherosclerosis.

Page 11: Cardiovascular Histology

Smooth Muscle Cells

• Vascular smooth muscle cells are small, mononucleated, spindle-

shaped cells with no banding pattern, no myofibrils, and no

sarcomeres

• The sarcoplasmic reticulum is continuous with (and basically identical

to) the smooth ER; there are no T tubules

• They are connected to other vascular smooth muscle cells or

endothelial cells by gap junctions

Page 12: Cardiovascular Histology
Page 13: Cardiovascular Histology
Page 14: Cardiovascular Histology

Comparison of the Three Types of Muscle

Features Skeletal (Striated) Cardiac (Striated) Smooth

Myofilaments Yes Yes Yes

Myofibrils Yes Yes No

Sarcomeres Yes Yes No

Anchoring of actin Z disks Z disks; fascia adherens junctions Dense bodies

NucleiMultinucleated (hundreds):

peripherally locatedOne (sometimes two): centrally located One: centrally located

Sarcoplasmic Reticulum Yes Yes Yes

T-tubules Yes: small, involved in triad formation Yes: large, involved in diad formation None

Cell-Cell JunctionsNone (connective tissue used to

mechanic couple)

Intercalated disks (gap; adherens;

desmosome)Gap junctions; adherens

Contraction Voluntary Involuntary Involuntary

Calcium BindingTroponin C

(actin-based regulation)

Troponin C

(actin-based regulation)

Calmodulin

(myosin-based regulation)

Regeneration Limited; via satellite cells None Yes

Mitosis No No Yes (mitosis)

Distinctive FeaturesLong, Cylindrical shaped cells, many

peripheral nuclei

Small, branched cells, intercalated

disks, one central nucleus

Small fusiform cells, no striations,

one nucleus,

no banding pattern

Page 15: Cardiovascular Histology

Biomechanical Properties

• Smooth muscle cells regulate the diameter of vessels (important for

shunting during shock, etc.) and resist expansion

• Elastic laminae add elasticity to vessels, which allows temporary

expansion of high pressure vessels during systole and their elastic

recoil during diastole

• Collagen fibers resist stretching and prevent over-expansion of

vessels

Page 16: Cardiovascular Histology

3 layers of Blood Vessel

• Tunica intima - longitudinal

• Single layer of squamous cells

• Subendothelial loose connective tissue, with smooth muscle cells

• Arteries only - tunica intima is often separated from the tunica

media by an internal elastic lamina

• Primary site of structural changes associated with atherosclerosis

• Tunica media - circular

• SMCs interspersed w/ elastic sheets and Type III collagen

• Arteries only - an external elastic lamina between the tunica media

and tunica externa

• Tunica externa (tunica adventitia) - longitudinal

• Fibroblasts, Type I collagen, and elastic fibers

• May contain blood vessels (vasovasorum), lymphatics, or nerves

Page 17: Cardiovascular Histology
Page 18: Cardiovascular Histology
Page 19: Cardiovascular Histology

Marfan’s Syndrome and Aneurysms

• People with Marfan's Syndrome have defects in elastic

fibers and elastic sheets often due to defect in FBN1

leading to insufficient functional fibrillin, one part of elastic

microfibrils (http://ghr.nlm.nih.gov/gene/FBN1)

• Since the tunica media in large arteries has a thick elastic

layer, people with Marfan's often have defects in their

large arteries that may result in aortic aneurysms

Page 20: Cardiovascular Histology

Medium Arteries and Veins

• Medium (muscular) arteries have an external elastic

lamina between the tunica media and the tunica externa

and arteries have an internal elastic lamina between the

tunica intima and the tunica media

• Medium veins do not have elastic layers or as much

circular muscle, this allows them to stretch (and stay

stretched) which is vital to their function as reservoirs.

Medium veins also have valves to prevent backflow of

blood

Page 21: Cardiovascular Histology
Page 22: Cardiovascular Histology
Page 23: Cardiovascular Histology

Aorta

Page 24: Cardiovascular Histology
Page 25: Cardiovascular Histology

Arterioles and Capillaries

• Arterioles have an endothelium surrounded by 1 to 6 layers of smooth

muscle and may have an internal elastic lamina, a feature not found

in veins

• Capillaries have a small lumen diameter, usually only big enough to fit

a single RBC

• No smooth muscle cells

• Endothelium surrounded by basal lamina and occasional pericytes, which likely

have a function in regulating blood flow and may differentiate into endothelial cells or

smooth muscle cells

Page 26: Cardiovascular Histology
Page 27: Cardiovascular Histology
Page 28: Cardiovascular Histology

3 Types of Capillaries

• Continuous capillaries • Continuous sheet of endothelium joined by tight junctions; under endothelium

is continuous basal lamina

• Water, O2, CO2, and small hydrophilic molecules can diffuse across the endothelium

• Glucose and ions use membrane transporters and cytosolic diffusion, proteins use transcytosis

• Found in muscle, brain, and connective tissue

• Fenestrated capillaries• Endothelium has 60-80 nm pores; under the endothelium is a continuous basal

lamina

• Pores allow passage of macromolecules and small molecules

• Found in intestines and renal glomeruli

• Discontinuous capillaries (sinusoidal capillaries) • Allow the slow circulation of blood

• Discontinuous endothelium and discontinuous basal lamina, which allows the free exchange of all blood components except RBCs

• Found in the liver lobules, bone marrow, splenic red pulp, and some endocrine glands (anterior pituitary and adrenal cortex)

Page 29: Cardiovascular Histology

Continuous: Skeletal muscle, skin,

lung, and brain

Fenestrated capillaries: Exocrine

glands, renal glomeruli, and intestinal

mucosa

Discontinuous capillaries: Liver,

spleen, and bone marrow

Page 30: Cardiovascular Histology

Lymphatic vessels

• Lymphatic capillaries are blind-ended and composed of loosely joined

endothelial cells

• Very thin walls

• Lack tight junctions

• No RBCs

• Valves

• Do not have a complete basal lamina

• Bundles of anchoring filaments provide some structural support

• Lymph often has a granular appearance after fixation

• Wbc’s might be present, but no PMNs

• Larger lymphatic vessels have smooth muscle cells

Page 31: Cardiovascular Histology
Page 32: Cardiovascular Histology

Vasculogenesis and Angiogenesis

• Vasculogenesis is de novo formation of blood vessels

• Endothelial cell precursors (called angioblasts) coalesce into loose

chords of cells

• The cells then differentiate into endothelia and form the tubes that

make up the primary vascular network

• Angiogenesis is when new blood vessels sprout from pre-

existing vasculature

• During development this is used to develop vascular patterns

• It is also a repair mechanism and is sometimes a response to

blocked vessels

• Solid tumors need a blood supply to continue to grow, so

angiogenesis is also seen in tumors

Page 33: Cardiovascular Histology

In the Vena Cava, the adventitia layer is

the thickest and smooth muscle can be

seen in all three layers.

Page 34: Cardiovascular Histology

CARDIAC MUSCLE

Page 35: Cardiovascular Histology
Page 36: Cardiovascular Histology

Layers of the Heart

• Epicardium: includes the serous pericardium, which is mesothelium,

and connective tissue and adipose tissue containing blood vessels

and nerves

• Myocardium: cardiac muscle tissue and delicate connective tissue

• Endocardium: endothelium and underlying connective tissue (can

contain some smooth muscle).

• Subendocardium: Fibrous skeleton (dense connective tissue),

Conducting System: Purkinje Fibers (in ventricles)

Page 37: Cardiovascular Histology
Page 38: Cardiovascular Histology

Purkinje Fibers

• Purkinje fibers are located in the subendocardium:

• lower density of myofibrils

• larger in size the myocytes

• They often show clear areas where myofibrils are lacking and are

replaced by glycogen.

• DO contain intercalated disks & myofibrils

• less organized than cardiac myocytes and have greater number of

gap junctions (rapidly conduct APs throughout cell)

Page 39: Cardiovascular Histology

Lumen of Ventricle

Endocardium

Purkinje Fibers (LX) –(Modified cardiac muscle fibers)

Myocardium(Cardiac Myocytes)

Page 40: Cardiovascular Histology

3 Types of Muscle

Skeletal Muscle Cardiac

Muscle

Smooth Muscle

Page 41: Cardiovascular Histology

Features Skeletal Cardiac Smooth

Myofilaments

(thick & thin)Yes Yes Yes

Sarcomeres Yes Yes No

Myofibrils Yes Yes No

NucleiMultinucleated:

peripherally located

One: centrally

locatedOne: centrally located

Sarcoplasmic

ReticulumYes Yes Yes

T-tubules Yes Yes None

Cell-Cell

JunctionsNone Intercalated disks Gap junctions

Contraction Voluntary Involuntary Involuntary

Calcium Binding

Troponin C

(actin-based

regulation)

Troponin C

(actin-based

regulation)

Calmodulin

(myosin-based

regulation)

Regeneration Yes, via satellite cells None Yes

Distinctive

Features

Long, Cylindrical

shaped, many

peripheral nuclei

Branched cells,

intercalated disks, 1-

2 nuclei

Fusiform cells, no

striations, one nucleus

Page 42: Cardiovascular Histology

Cardiac Muscle Contraction

• Action potential opens L type calcium channel in plasma membrane of t tubule

• Trigger calcium enters the cell through channel

• Trigger calcium induces the opening of calcium channel (ryanodine receptors, RYR) in the membrane of the terminal cisternae of the sarcoplasmic reticulum (SR)

• Calcium in the lumen of the SR flows down its concentration gradient into the cytosol of muscle cell, increasing cytoplasmic Ca++ concentration

• When there is Ca, the Ca binds to the TnC subunit of the troponin complex. This binding induces a conformational change that moves the entire troponin complex. This move causes the tropomyosin to shift deeper into the helical groove of the actin, revealing the myosin binding site

• Myosin binds and undergoes the conformational cycle/power stroke to induce the sliding of the actin (thin filaments) relative to myosin (thick filaments).

Page 43: Cardiovascular Histology

Sarcomere

Page 44: Cardiovascular Histology
Page 45: Cardiovascular Histology
Page 46: Cardiovascular Histology

Calcium Antiporter

• Cardiac muscles must remove calcium in order to relax.

• In addition to SERCA, cardiac myocytes have a sodium/calcium

antiporter (sodium-calcium exchanger) in the plasma membrane that

extrudes calcium from the cell against a calcium concentration

gradient by using the energy of sodium flowing down its concentration

gradient across the plasma membrane.

• In addition, there is a calcium ATPase enzyme in the plasma

membrane that also contributes to removing calcium from the cell.

Page 47: Cardiovascular Histology

Cardiac Action Potential

• It has a long plateau phase and long refractory period so no chance

for tetany.

• The action potential spreads throughout the plasma membrane and

into the T‐tubules. The action potential opens the voltage‐gated

L‐type calcium channels (also called dihydropyridine receptors)

located in the plasma membrane of the T‐tubules (very close to the

terminal cisternae of the sarcoplasmic reticulum).

Page 48: Cardiovascular Histology

Beta Adrenergic Control• β-adrenergic receptors in the plasma membrane of the cardiac myocytes are

activated by norepinephrine released from sympathetic nerve terminals in the heart or epinephrine in the blood (derived from the adrenal medulla).

• Activation of the β-adrenergic receptor (a 7 pass G protein-coupled membrane receptor) results in activation of the enzyme adenylate cyclase (AC) and an increase in the concentration of cAMP in the cytosol. The cAMP activates the cAMP-dependent protein kinase (PKA) which phosphorylates a number of proteins in the cardiac myocyte.

• Activation of protein kinase A (PKA) results in phosphorylation of several proteins, including the voltage gated L-type Ca++ channels and a protein called phospholamban (PLB) which regulates SERCA (the calcium pump in the the sarcoplasmic reticulum membrane). Phosphorylation of the L-type Ca++ channels causes more trigger calcium to enter the cell with each action potential.

• Phosphorylation of phospholamban stimulates the activity of SERCA and thus increases the rate of removal of calcium from the cytosol and the extent of calcium accumulation in the SR between each action potential. Thus the sarcoplasmic reticulum (SR) can release more calcium during the next depolarization of the cell resulting in an increase in the force of contraction

Page 49: Cardiovascular Histology
Page 50: Cardiovascular Histology

ATHEROSCLEROSIS

Page 51: Cardiovascular Histology

ATHEROSCLEROSIS

Page 52: Cardiovascular Histology

Progression of Atherosclerosis

Page 53: Cardiovascular Histology

Name the Complications

Page 54: Cardiovascular Histology

Atheroembolism will show cholesterol

plaques

Page 55: Cardiovascular Histology

ISCHEMIC HEART

DISEASE

Page 56: Cardiovascular Histology

12 Hours Post MI

Page 57: Cardiovascular Histology

3-5 Days Post MI

Page 58: Cardiovascular Histology

6-10 Days Post MI

Page 59: Cardiovascular Histology

Chronic Ischemic Heart Disease

Page 60: Cardiovascular Histology

Ventricular Wall Rupture

Page 61: Cardiovascular Histology

Papillary Muscle Dysfunction

Page 62: Cardiovascular Histology

Pericarditis

Page 63: Cardiovascular Histology

Mural Thrombus

Page 64: Cardiovascular Histology

Ventricular Aneurysm

Page 65: Cardiovascular Histology

VALVULAR DISEASE

Page 66: Cardiovascular Histology

Calcific Degenerative Disease

• Heaped up calcific masses on the outer side of the aortic cusps at

insertion site, protruding in the aortic sinuses.

• Valvular orifice is narrowed.

• Generally not associated with commissural fusion (in trileaflet valves)

and free edges not involved.

• Secondary concentric left ventricular hypertrophy.

Page 67: Cardiovascular Histology

Acute Rheumatic Carditis

• Inflammation of the endocardium results in fibrinoid necrosis within

the cusps or along the tendinous cords.

• Overlying these necrotic foci are small (1- to 2-mm) vegetations,

called verrucae, along the lines of closure.

Page 68: Cardiovascular Histology

Aschoff Bodies

• Distinctive lesions occur in the heart, called Aschoff bodies, which

consist of foci of lymphocytes (primarily T cells), occasional plasma

cells, and plump activated macrophages.

• These macrophages (Anitschkow cells) have abundant cytoplasm

and central round-to ovoid nuclei in which the chromatin forms a

slender, wavy ribbon (“caterpillar cells”), and may become

multinucleated.

Page 69: Cardiovascular Histology

Chronic Rheumatic Heart Disease

• Thickened, fibrotic and calcified leaflets with commissural fusion.

• Thickening and fusion of the tendinous cords

Page 70: Cardiovascular Histology

Mitral Valve Prolapse

• Interchordal ballooning (hooding) of the mitral leaflets

• Leaflets are enlarged, redundant, thick, and rubbery

• Chordae may be elongated, thinned, or even ruptured, and the

annulus may be dilated

Page 71: Cardiovascular Histology

MVP Microscopy

• Thickening of the spongiosa layer with deposition of mucoid

(myxomatous) material

• Attenuation of the collagenous fibrosa layer of the valve

Page 72: Cardiovascular Histology

Endocarditis

• RHD: Small, warty vegetations along the lines of closure of the valve leaflets.

• IE: Large, irregular masses on the valve cusps that can extend onto the chordae

• NBTE: Small, bland vegetations, usually attached at the line of closure.

• LSE: Small or medium-sized vegetations on either or both sides of the valve

Page 73: Cardiovascular Histology

Infective Endocarditis

Page 74: Cardiovascular Histology

NBTE

Page 75: Cardiovascular Histology

Libman Sachs Endocarditis

Page 76: Cardiovascular Histology

Carcinoid Heart Disease

• Firm plaquelike endocardial fibrous thickenings on the inside surfaces

of the cardiac chambers and the tricuspid and pulmonary valves

Page 77: Cardiovascular Histology

Carcinoid Microscopy

• Intimal proliferation composed predominantly of smooth muscle cells

and sparse collagen fibers embedded in an acid mucopolysaccharide-

rich matrix material. Elastic fibers are not present in the plaques.

Page 78: Cardiovascular Histology

CARDIOMYOPATHY

Page 79: Cardiovascular Histology

Dilated Cardiomyopathy

Page 80: Cardiovascular Histology

Hypertrophic Cardiomyopathy

Page 81: Cardiovascular Histology

Restrictive Cardiomyopathy

Page 82: Cardiovascular Histology

Restrictive Cardiomyopathy

Amyloidosis, Sarcoidosis, Hemochromatosis, Glycogen Storage Disease

Page 83: Cardiovascular Histology

Myocarditis

Lymphocytic infiltrate is most common. (A below)

Hypersensitivity myocarditis will show eosinophils. (B below)

Chagas disease shows trypanosomes in mycocytes. (C below)

Page 84: Cardiovascular Histology

PERICARDITIS

Page 85: Cardiovascular Histology

Acute Pericarditis

A. Fibrinous

B. Hemorrhagic

C. Suppurative

Page 86: Cardiovascular Histology

Chronic Pericarditis

Page 87: Cardiovascular Histology

AORTIC PATHOLOGY

Page 88: Cardiovascular Histology

A. Abdominal Aortic Aneurysm

B. Thoracic Aortic Aneurysm

C. Aortic Dissection

Page 89: Cardiovascular Histology

CARDIAC TUMORS

Page 90: Cardiovascular Histology

Benign Cardiac Tumors

• Myxomas are the most common primary cardiac tumor.

• Occur in middle aged patients, more common in women

• Patients may have peripheral embolization of the tumor, obstruction of

an AV valve, or sx of a systemic disease (fever, malaise, etc).

• Typically pedunculated masses located in the LA

• T1-weighted images show a mass with intermediate signal intensity

similar to myocardium. However, this signal may be variable due to

calcifications that are hypointense or hemorrhage that is hyperintense

to myocardium. Myxomas typically enhance heterogeneously.

• Lipomas are the second most common primary cardiac tumor

• Have a high intensity on T1-weighted images that darkens on fat

suppressed sequences.

Page 91: Cardiovascular Histology

Myxoma

• Clinicopathologic:• Most common primary cardiac tumor.

• 90% in atria, 80% on left side. LEFT ATRIUM

• Mean age is 50. ADULTS

• Clinical manifestations:• “Ball-valve” obstruction of “wrecking-ball” destruction of valve.

• Tumor embolization.

• Systemic symptoms due to cytokine production.

• Gross Morphology:• Often at site of fossa ovalis.

• 1-10 cm in size.

• May be sessile or pendunculated, hard or gelatinous texture.

• Microscopic Appearance:• Stellate myoxoma cells embedded in myxomatous mucopolysaccharides substance.

• Prominent vessels, hemorrhage and inflammation common.

Page 92: Cardiovascular Histology

Lipoma

• Pathogenesis: • Benign tumors composed of mature fat cells

• Adults

• Most often occur in left ventricle, right atrium or atrial septum.

• Clinical manifestations:• Typically asymptomatic; incidental finding on imaging.

• May cause ball-valve obstruction or arrhythmias

• Gross Morphology:• May occur in the subendocardium (bulge into the chamber), myocardium (wall

thickening), or subepicardium (bulge into pericardial space).

• Cut section show yellow, glistening, adipose tissue.

• Microscopic Appearance:• Mature adiopose tissue with entrapped myocardium.

Page 93: Cardiovascular Histology

Papillary Fibroelastoma

• Pathogenesis:• Benign tumor of adult.

• Typically occur on valves

• May occur on endocardial surface

• Clincial manifestations:• Often incidental finding.

• May break off and embolize.

• Aortic tumors may prolapse into coronary ostia.

• Gross Morphology: • Compared to sea anemone

• Distinctive cluster of yellow-white hairlike projections covering large portions of valvular surface

• Microscopic Appearance:• Narrow, elongated and branching papillary fronds composed of collagen.

• Lined by endothelium.

Page 94: Cardiovascular Histology

Rhabdomyoma

• Pathogenesis: • Most common cardiac tumor of CHILDREN

• Benign tumor of cardiac myocytes.

• Frequently associated with tuberous sclerosis

• Most commonly occur in ventricles; often multiple.

• Clinical manifestations:• May result in arrhythmias or chamber obstruction

• Natural history is regression.

• Gross Morphology:• Myocardial tumor that may bulge into ventricular chamber.

• Cut section shows tan-white homogenous solid tissue.

• Microscopic Appearance:• Enlarged, atypical myocytes with abundant cleared out cytoplasm (glycogen).

• Cytoplasm strands to connect nucleus to cell membrane (spider cells).

Page 95: Cardiovascular Histology

Cardiac Fibroma

• Pathogenesis: • Typically tumor of CHILDREN, most often in first year of life.

• Benign tumor of fibroblasts; may be locally infiltrative.

• Most often in ventricles (left>right) or ventricular septum.

• Clinical manifestations:• Heart failure, cyanosis, syncope or arrhythmias.

• Gross Morphology:• Myocardial tumor that may bulge into cardiac chamber.

• Nearly always solitary.

• Cut surface is firm, white with whorled appearance.

• Microscopic Appearance:• Bland spindle cell lesion with collagen production.

• May infiltrate into surrounding myocardium.

Page 96: Cardiovascular Histology

Malignant Cardiac Tumors

• Metastatic tumors are the most common tumors found in the heart. The most common cardiac metastases include lung, breast, melanoma, and lymphoma. • Metastases often induce a pericardial effusion.

• Angiosarcoma: the most common primary malignancy of the heart• Usually located in the right atrium.

• Characterized by heterogenous signal on T1-weighted images with areas of elevated signal representing hemorrhage.

• Angiosarcomas demonstrate hyperenhancement after the administration of gadolinium contrast agents.

• Other primary malignant tumors are liposarcoma, leiomyosarcoma, and lymphoma.

• Malignant tumors are more likely to be necrotic, have associated nearby edema, be vascular, demonstrate invasion into adjacent tissues, and have an inhomogeneous appearance.

Page 97: Cardiovascular Histology

Angiosarcoma

• Pathogenesis: • Most common malignant cardiac tumor of ADULTS.

• Usually in RIGHT ATRIUM

• Clinical manifestations:• Arrhythmias, heart block, CHF, angina, or infarction.

• Cardiac tamponade.

• Vast majority are metastatic at presentation.

• Highly aggressive tumor with poor response to therapy.

• Gross Morphology:• Large, infiltrating dark brown, necrotic mass.

• Infiltration of inferior vena cava or tricuspid valve common.

• Microscopic Appearance:• Highly atypical, malignant cells with enlarged nuclei, and prominent nucleloli

• Rudimentary vascular channels.

• Hemorrhage and necrosis.

Page 98: Cardiovascular Histology

Metastatic Tumors

• Direct consequences of tumor:• Pericardial and myocardial metastases

• (melanoma, carcinoma, leukemia/lymphoma).

• A cardiac mass is 40x more likely to be a metastasis than a primary tumor

• Large vessel obstruction

• Pulmonary tumor emboli.

• Indirect consequences of tumor• Nonbacterial thrombotic endocarditis (mucinous adenocarcinoma).

• Carcinoid heart disease (neuroendocrine carcinoma).

• Effect of tumor therapy• Chemotherapy

• (dilated cardiomyopathy).

• Radiotherapy

• (pericarditis, coronary artery disease, restrictive cardiomyopathy).

Page 99: Cardiovascular Histology

Myocarditis

• The most common cause of myocarditis is viral infection

• Coxsackievirus B.

• Inflamed myocardium hyperenhances on early gadolinium enhanced

T1 weighted images due to increased inflow of blood. T2 weighted

images will be bright due to edema.

• Delayed enhanced imaging will demonstrate enhancement in the mid-

myocardium, often in a patchy pattern.