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Diseases of BLOOD VESSELS

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COMPONENTS Intima, Media, Adventitia, M>A or A>M

ENDOTHELIUM

INTERNAL ELASTIC LAMINA ECM: Elastin (~aging) S/D, collagen,

mucopolysaccharides

Smooth Muscle

Connective Tissue

Fat

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1) Blockage

(preceded by

narrowing)

2) Rupture

Preceded by

weakening)

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TOPICS Vascular wall

responses

Congenital

Anomalies

Atherosclerosis

Arteriosclerosis Hypertension

Aneurysms

Vasculitides

Raynaud

phenomenon

Veins

Lymphatics

Tumors Interventions

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DEFINITIONS ARTERIO-sclerosis

ATHERO-sclerosis

Aneurysm

Dissection

Thrombus

Hypertension

Vasculitis/Vasculitides, infectious/NON-infectious (often-autoimmune)

Varicosity

DVT/Thrombo-phlebitis/Phlebo-thrombosis

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DEFINITIONS Lymphangitis

Lymphedema

Angioma/Hemangioma (generic)

Lymphangioma

Angiosarcoma (generic)

Lymphangiosarcoma

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NON-Specific Vascular Wall

Response to Injury

Endothelial activation

Smooth Muscle cell roles

Development, Growth,

Remodeling

Intimal thickening

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ENDOTHELIAL CELLS Recall Jeckyl/Hyde concept: maintain hemostasis/cause

thrombosis

Maintenance of Permeability Barrier

Elaboration of Anticoagulant, Antithrombotic, FibrinolyticRegulators J: Prostacyclin, Thrombomodulin, Heparin, Plasminogen

Elaboration of Prothrombotic Molecules H:vWF, TF,Plasminogen activator inhibitor

Extracellular Matrix Production (collagen, proteoglycans)

Modulation of Blood Flow and Vascular Reactivity

Vasoconstrictors: endothelin, ACE Vasodilators: NO, Prostacyclin

Regulation of Inflammation and Immunity

Regulation of Cell Growth

Oxidation of LDL

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ENDOTHELIAL CELL

ACTIVATORS Cytokines, GFs

Bacterial Products

Hemodynamic Forces Lipid Products

Viruses

Complement

Hypoxia

Cigarette smoke

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VASCULAR SMOOTH MUSCLE

Vasoconstriction

Vasodilatation

Make ECM:

Collagen

Elastin

Proteoglycans

Regulated by:

PROMOTORS: PDGF, endothelin, thrombin,

FGF, etc.

INHIBITORS: Heparan SO4, NO, TGF-

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Vessel Growth

& Remodeling The sum total of all the factors and

processes involved in tissue injury

and the bodys ability to growvessels, develop new pathways,

and re-perfuse areas in response

to tissue and/or blood vesselinjury.

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CONGENITAL ANOMALIES Arteriovenous fistulas

Also called ArterioVenous Malformation

(AVM)

Common factor is abnormal communication

between high pressure arteries and lowpressure veins

Usually congenital (malformation), but can

be acquired by trauma or inflammation

Most often described in the brain as an AVM

Often asymptomatic or with hemorrhage or

pressure effects

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ARTERIO-SCLEROSIS

GENERIC term for ANYTHINGwhich HARDENS arteries

Atherosclerosis (99%)

Mnckeberg medial calcific

sclerosis (1%)

Arteriolosclerosis, involving smallarteries and arterioles, generally

regarded as NOT strictly being part

of atherosclerosis, but more relatedto hypertension and/or diabetes

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ATHEROSCLEROSIS

(classical) Etiology/Risk Factors

Pathogenesis

Morphology

Clinical Expression

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ATHEROSCLEROSIS

(ala Robbins) *Natural History

*Epidemiology

*Risk Factors

*Pathogenesis

*Other Factors

*Effects

*Prevention

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*NATURALHISTORY

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1) FATTY

STREAK

(non-

palpable,

but a

visible

YELLOW

streak)

2) ATHEROMA

(plaque)

(palpable)

3) THROMBUS

(non-

functional,

symptomatic)

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MORPHOLOGIC CONCEPTS

Macrophages (really monocytes) infiltrate

Intimal Thickening Lipid Accumulation Streak Atheroma Smooth Muscle Hyperplasia and Migration Fibrosis Calcification Aneurysm*

Thrombosis

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FATTY

STREAKS

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PLAQUE

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MILD ADVANCED

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ADVANCED FEATURES

RUPTURE

ULCERATION

EROSION ATHEROEMBOLI

HEMORRHAGE

THROMBOSIS

ANEURYSM

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FUN THINGS TO FIND:

Lumen, Fibrous cap (fibrous plaque), Lipid core,External Elastic Membrane thinning/destruction,

Calcification, Neovascularization

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*EPIDEMIOLOGY

& RISK FACTORS

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Epid./RiskFactors

Related to development of nation

US highest

50-70% DECREASE 19632000. Why?awareness, dietary restrictions

AGE

SEX, M>F until menopause, estrogen

protection

GENETICS (multigenic)

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MAJORfactors

Hyperlipidemia

Hypertension

Cigarette Smoking

Diabetes Milletus

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Risk Factors for Atherosclerosis

Major MinorNON-modif iable Modif iable

Increasing age Obesity

Male gender Physical inactivity

Family history Stress ("type A" personality)

Genetic abnormalities Postmenopausal estrogen deficiency

High carbohydrate intake

Modif iable

Hyperlipidemia Alcohol

Hypertension Lipoprotein Lp(a)

Cigarette smoking Hardened (trans)unsaturated fat intake

Diabetes Chlamydia pneumoniae

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MAJORfactors

Hyperlipidemia

Hypertension

Cigarette Smoking

Diabetes Milletus

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HYPERLIPIDEMIA Chiefly CHOLESTEROL,

LDL>>>>HDL

HDL mobilizes cholesterol FROMatheromas to liver

LOW CHOLESTEROL diet is GOOD

UNSATURATED fatty acids GOOD

Omega-3 fatty acids GOOD

Exercise GOOD

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Foamy MACROPHAGES

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CHOLESTEROL* CLEFTS

*Really cholesterol esters

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HYPERTENSION HYPERTENSION causes

ATHEROSCLEROSIS. Why?

ATHEROSCLEROSIS causesHYPERTENSION. Why?

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CIGARETTES What more needs to be said?

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DIABETES If there was one disease

which I could challenge youto, as a dare, to PROVE tome that was NOT EXACTLY

THE SAME asatherosclerosis, it would beDIABETES! Any takers?

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NON major factors

Homocysteinuria/homocysteinemia, relatedto low B6 and folate intake

Coagulation defects

Lipoprotein Lp(a), independent ofcholesterol. Lp(a) is an altered form of LDL

Inadequate exercise, Type A personality,

obesity (independent of diabetes) Protective effect of moderate alcohol?

Medical LIE, sponsored by the booze

industry and alcoholic physicians!

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PATHOGENESIS

atherosclerosis is a chronic

in f lammatory response of

the arterial wal l ini t iated byinjury to the endothelium

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PATHOGENESIS SAGA

Chronic endothelial injury LDL, Cholesterol in arterial WALL OXIDATION of lipoproteins Monocytes migrate endothelium* Platelet adhesion and activation Migration of SMOOTH MUSCLE from media to

intima to activate macrophages (foam cells) Proliferation of SMOOTH MUSCLE and ECM Accumulation of lipids in cells and ECM

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M i FOUR STARS f

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Main FOUR STARS of

PATHOGENESIS SAGA

1) Endothelial Injury 2) Inflammation

3) Lipids

4) Smooth Muscle Cells, SMCs

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Other Pathogenesis

Considerations Oligoclonality of cells in

plaque

Chlamydia, CMV as

endothelial injurers

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PREVENTION PRINCIPLES

Know what is preventable

Know what is MAJOR (vs. minor)

Know PRIMARY vs. SECONDARY

principles Understand atherosclerosis begins in

CHILDHOOD

Risk factors in CHILDREN predict theADULT profile

Understand SEX, ETHNIC differences

C th l i

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Can atherosclerosis

be REVERSED?

?

NON ATHEROSCLEROSIS

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NON ATHEROSCLEROSIS

VASCULAR DISEASES

HYPERTENSION

ANEURYSMSVASCULITIDES

VEIN DISORDERS NEOPLASMS

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HYPERTENSION

ESSENTIAL 95%

SECONDARY 5%

SECONDARY

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SECONDARY Renal Acute glomerulonephritis

Chronic renal disease

Polycystic disease

Renal artery stenosis

Renal artery fibromuscular dysplasia

Renal vasculitis

Renin-producing tumors

Endocrine Adrenocortical hyperfunction

(Cushing syndrome, primary aldosteronism, congenital adrenal hyperplasia, licorice ingestion)

Exogenous hormones (glucocorticoids, estrogen [including pregnancy-induced and oralcontraceptives], sympathomimetics and tyramine-containing foods, monoamine oxidaseinhibitors)

Pheochromocytoma, acromegaly, HYPO-thyroidism (myxedema), HYPER-thyroidism

pregnancy-induced

Cardiovascular: Coarctation of aorta, polyarteritis nodosa (or other vasculitis) Increased intravascular volume

MISC: Increased cardiac output, Rigidity of the aorta, neurologic, Psychogenic,Increased intracranial pressure, sleep apnea, acute stress, including, surgery

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DEFINITION 140/90

SUSTAINED diastolic >90

SUSTAINED systolic >140

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BP = CO x PR

ALL Hypertension

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E.F.

R i A i t i Ald t

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ReninAngiotensinAldosteroneAXIS (RAAS)

If the perfusion of thejuxtaglomerularapparatus in the kidneys decreases, then the

juxtaglomerular cells release the enzymerenin.

Renin cleaves an inactive peptide calledangiotensinogen, converting it intoangiotensin I.

Angiotensin I is then converted to angiotensinII by angiotensin-converting enzyme (ACE),which is found mainly in lungcapillaries.

Angiotensin II is the major bioactive product ofthe renin-angiotensin system. Angiotensin IIacts as an endocrine, autocrine/ paracrine, and

intracrine hormone.

http://en.wikipedia.org/wiki/Juxtaglomerular_apparatushttp://en.wikipedia.org/wiki/Juxtaglomerular_apparatushttp://en.wikipedia.org/wiki/Kidneyhttp://en.wikipedia.org/wiki/Enzymehttp://en.wikipedia.org/wiki/Reninhttp://en.wikipedia.org/wiki/Peptidehttp://en.wikipedia.org/wiki/Angiotensinogenhttp://en.wikipedia.org/wiki/Angiotensinhttp://en.wikipedia.org/wiki/Angiotensinhttp://en.wikipedia.org/wiki/Angiotensinhttp://en.wikipedia.org/wiki/Angiotensin-converting_enzymehttp://en.wikipedia.org/wiki/Lunghttp://en.wikipedia.org/wiki/Capillarieshttp://en.wikipedia.org/wiki/Endocrine_systemhttp://en.wikipedia.org/wiki/Autocrine_signallinghttp://en.wikipedia.org/wiki/Paracrine_signallinghttp://en.wikipedia.org/wiki/Intracrinehttp://en.wikipedia.org/wiki/Intracrinehttp://en.wikipedia.org/wiki/Paracrine_signallinghttp://en.wikipedia.org/wiki/Autocrine_signallinghttp://en.wikipedia.org/wiki/Endocrine_systemhttp://en.wikipedia.org/wiki/Capillarieshttp://en.wikipedia.org/wiki/Lunghttp://en.wikipedia.org/wiki/Angiotensin-converting_enzymehttp://en.wikipedia.org/wiki/Angiotensin-converting_enzymehttp://en.wikipedia.org/wiki/Angiotensin-converting_enzymehttp://en.wikipedia.org/wiki/Angiotensinhttp://en.wikipedia.org/wiki/Angiotensinhttp://en.wikipedia.org/wiki/Angiotensinhttp://en.wikipedia.org/wiki/Angiotensinogenhttp://en.wikipedia.org/wiki/Peptidehttp://en.wikipedia.org/wiki/Reninhttp://en.wikipedia.org/wiki/Enzymehttp://en.wikipedia.org/wiki/Kidneyhttp://en.wikipedia.org/wiki/Juxtaglomerular_apparatushttp://en.wikipedia.org/wiki/Juxtaglomerular_apparatus

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GENETIC

ACQUIRED

HISTOPATHOLOGY of

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HISTOPATHOLOGY of

ESSENTIAL HYPERTENSION

HYALINE = BENIGN HTN. HYPERPLASTIC = MALIGNANT HTN. SYS>200

1) ONION SKIN 2) FIBRINOID NECR.

GENETIC

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GENETICvs.

ENVIRONMENTAL GENETIC UN-CONTROLLABLE ENVIRONMENTAL CONTROLLABLE

STRESS

OBESITY

SMOKING

PHYSICAL ACTIVITY

NaCl INTAKE

ANEURYSMS

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ANEURYSMS TRUE vs. FALSE

ATHEROSCLEROTIC NON-ATHEROSCLEROTIC

CONGENITAL

LUETIC (SYPHILITIC)

TRAUMATIC

MYCOTIC (MIS-leading term)

2 to VASCULITIS

SACCULAR (i.e., Berry) vs. FUSIFORM

DISSECTION vs. NON-DISSECTION

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ANEURYSMS

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ANEURYSMS 2 CAUSES:

1) ATHEROSCLEROSIS 2) CYSTIC MEDIAL DEGENERATION (NECROSIS), can be familial

NORMAL elastic fibers DISRUPTED, FRAGMENTED elastic fibers

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Most abdominal aortic aneurysms (AAA) occur between

the renal arteries and the bifurcation of the aorta

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(sequelae)RUPTURE

OBSTRUCTION

EMBOLISM

COMPRESSION

URETER SPINE

MASS EFFECT

THORACIC

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THORACICANEURYSMS

Encroachment

Respiratory difficulties

Hoarseness?Dysphagia

Cough

PainAortic valve dilatation

Rupture

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DISSECTION

ANEURYSMS

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ANEURYSMS

(luetic)Chiefly thoracic

Follows an AORTITIS

PLASMA CELLS predominate

VASCULITIDES

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VASCULITIDES

TEMPORAL GIANT CELL ARTERITIS TAKAYASU ARTERITIS

POLY (PERI) ARTERITIS NODOSA

KAWASAKI DISEASE

WEGENERs GRANULOMATOSIS

THROMBOANGI(i)TIS OBLITERANS(BUERGER[s] DISEASE)

OTHER

INFECTIOUS

VASCULITIDES

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VASCULITIDES

Chiefly arterial Infectious (5%) vs. Non-infectious (95%)

NON-infectious are generally AUTO-

IMMUNE. Why? Persistent findings:

Immune complexes

ANTI-NEUTROPHIL ABs (Wegeners, Temporal)

ANTI-ENDOTHELIAL CELL ABs (Kawasaki)

Often DRUG related (Hypersensitivity, e.g.),especially small blood vessels.

TEMPORAL ARTERITIS

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TEMPORAL ARTERITIS

aka, Giant Cell Arteritis, GCA ADULTS Mainly arteries of the head and

temporal arteries are the most visibly,palpably, and surgically accessible

BLINDNESS most feared sequelae

GRANULOMATOUS WALLinflammation diagnostic

OFTEN associated with marked ESRelevation to be then known asPOLYMYALGIA RHEUMATICA

Anti-NEUTROPHIL ABs often POSITIVE

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TEMPORAL ARTERITIS

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TEMPORAL ARTERITIShttp://www.path.

uiowa.edu/cgi-bin-

pub/vs/fpx_gen.

cgi?slide=623&vi

ewer=java&view

=0&lay=iowa

S S

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TAKAYASU ARTERITIS

Involves aortic arch and other heavilly

elastic arteries, i.e., chief thoracicaorta branches, most commonly young

Asian women

FEMALES

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POLY-(Peri-) ARTERITIS

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NODOSA (PAN)

ANY MEDIUM or SMALL artery OFTEN visceral arteries

Infarcts, aneurysms, ischemia

CLASSICAL AUTOIMMUNE disease SEGMENTAL, TRANSMURAL,

NECROTIZING (fibrinoid) inflammation

Sometimes anti-neutrophil antibodies,especially in the smaller vessel diseases

One of the CLASSICAL systemic auto-

immune diseases, like SLE, RA, or SS

http://www

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.path.uiow

a.edu/cgi-

bin-

pub/vs/fpx

_gen.cgi?s

lide=584&

viewer=jav

a&view=0

&lay=iowa

KAWASAKI DISEASE

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KAWASAKI DISEASE

CHILDREN

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HYPERSENSITIVITY VASCULITIS

LEUKOCYTOCLASTIC VASCULITIS

SMALL VESSELS OF ALL TYPES,e.g., capillaries and veins too

FRAGMENTED NEUTROPHILS aka, LEUKOCYTOCLASIA

aka, NUCLEAR DUST

Most are ALLERGIC reactions toallergens like penicillin or strep

DERMATOLOGISTs DISEASE

http://ww

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http://ww

w.path.ui

owa.edu/

cgi-bin-

pub/vs/fpx_gen.cg

i?slide=6

34&view

er=java&

view=0&l

ay=iowa

WEGENER GRANULOMATOSIS

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WEGENER GRANULOMATOSIS

M>F, often in 40s

ACUTE NECROTIZING GRANULOMAS OF

UPPER an LOWER respiratory tract

NECROTIZING GRANULOMATOUSVASCULITIS of SMALL vessels of ALL types

Often renal involvement, crescentic

glomerulonephritis

ANTI-NEUTROPHIL-CYTOPLASMIC-ABs

usually present

necrosis

granulomas

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necrosisgranulomas

necrosis

granulomas

necrosis

granulomas

necrosisgranulomas

necrosisgranulomas

necrosis

granulomas

necrosis

granulomas

necrosisgranulomas

granulomas

necrosis

granulomas

necrosis

granulomasnecrosis

granulomas

THROMBOANGIITIS OBLITERANS

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THROMBOANGIITIS OBLITERANS

BUERGER(s) Disease

100% caused by cigarette smoking

MEN>>>F, 30s, 40s

Often arteries are 100% obliterated,

hence the name obliterans

EXTREMITIES most often involved

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http://www.path.uio

wa.edu/cgi-bin-

pub/vs/fpx_gen.cgi

?slide=704&viewer=java&view=0&lay

=iowa

OTHER VASCULITIDES

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OTHER VASCULITIDES

SLE

RHEUMATOID ARTHRITIS

INFECTIOUS ARTERITIDES

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INFECTIOUS ARTERITIDES

ASPERGILLIS

MUCORMYCOSIS

MYCOTIC ANEURYSMS aregenerally MISNOMERS

NON ATHEROSCLEROSIS

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VASCULAR DISEASES HYPERTENSION

ANEURYSMS

VASCULITIDES

VEIN DISORDERS

NEOPLASMS

FINAL TOPICS

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FINAL TOPICS Raynaud Phenomenon

Veins and Lymphatics Varicosities

Thrombophlebitis/Phlebothrombosis

SVC/IVC syndromes Lymphangitis

Lymphedema

Tumors: Benign, Intermediate(Borderline), Malignant

Vascular Interventions: Angioplasty,Stents, Grafts

R d Ph

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Raynaud Phenomenon PRIMARY: (formerly Raynaud DISEASE)

Digital PALLORCYANOSISHYPEREMIA (WHITE) (BLUE) (RED) Vasoconstriction usually triggered by COLD, emotion

Can be tip of nose, not only digits Self Limited, Gangrene UN-common

Arteries often do NOT show diagnostic pathology

SECONDARY: (formerly Raynaud Phenomen.)

Atherosclerosos

SLE

Buerger Disease

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WHITE

BLUE

RED

Varicose Veins

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Varicose Veins 20% of population, F>M

Related to increased venous pressure, age, valvedysfunction

Superficial veins of lower extremities most

common PATH: 1) DILATED, 2) TORTUOUS, 3) ELONGATED,

4) SCARRED (phlebosclerosis), 5) CALCIFICATIONS,

6) NON-UNIFORM SMOOTH MUSCLE

Conceptually like varices or hemorrhoids

Phlebosclerosis is what your pathologist will

call it

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THROMBOPHLEBITIS

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THROMBOPHLEBITIS

90% DEEP veins of the legs IDENTICAL to PHLEBOTHROMBOSIS

Factors: CHF, Neoplasia (esp. GI, panc.

Lung adenocarcinomasmigratorythrombophlebitis), pregnancy, obesity,post-op, immobilization, or any of theparts of Virchows triangle

Sequelae: PE most feared

Symptoms: edema, cyanosis, heat, pain,tenderness, but usually..NONE!!!

SVC SYNDROME

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SVC SYNDROME

Usually from bronchogenic CAor mediastinal lymphoma

DUSKY CYANOSIS of:Head

Neck

Arms

IVC SYNDROME

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IVC SYNDROME

Secondary to: NEOPLASMS (external compression)

ASCENDING THROMBOSIS from

FEMORALS, ILIACS

AAA, Gravid uterus

Bilateral leg edema

Massive proteinuria if renal veinsinvolved (like nephrotic syndrome)

LYMPHANGITIS

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LYMPHANGITIS From regional infections Group-A beta-hemolytic strep most

common

Lymphatics dilated, filled with WBCs Cellulitis usually present too

Lymphadenitis also usually follows

If lymph nodes cannot filter (process)antigens enoughsepticemia

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LYMPHEDEMA

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LYMPHEDEMA

Lymphatic channels blocked orscarred or absent:

Post surgical

Post radiationFilaria

Congenital

Tumoral (peau dorange- breast)

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CHYLE

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CHYLE CHYLOUS ASCITES

CHYLOTHORAX

CHYLOPERICARDIUM

Vascular TUMORS

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Vascular TUMORS

BENIGN (NEVER metastasize, in factsome are not even TRUE neoplasms,

but hamartomas)

INTERMEDIATE (rarely metastasize)

MALIGNANT (FREQUENT and EARLYmetastases, like any other sarcomalung)

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BENIGN---------------------------------------MALIGNANTRare mitosis--------------------------Common mitosisMild, rare atypia------------Frequent, severe atypiaNO mets----------------------------Early, frequent mets

via BLOODSTREAM

HEMANGIOMA

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HEMANGIOMA Often a generic term for ANY benign blood

vessel tumor

CAPILLARY (small vascular spaces)

Also called juvenile, often called birth marks Usually regress with age

CAVERNOUS (LARGE vascularspaces) Also called adult

Usually do NOT regress

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PYOGENIC GRANULOMA

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PYOGENIC GRANULOMA

ORAL CAVITY MOST COMMON

Histology like capillary

hemangioma

Regress

Indistinguishable from normal

granulation tissue

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LYMPHANGIOMA

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LYMPHANGIOMA Small 1-2 mm

90% Head and neck region in kids

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GLOMUS TUMOR

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GLOMANGIOMA

1 cm

Most commonly under nail

Painful

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MISC. BENIGN TUMORS

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-ectasias, telangiectasias

Nevus Flammeus, aka, port wine stain----

Spiders (spider telangiectasias), ass. W.

pregnancy, cirrhosis------------------------- Osler-Weber-Rendu Disease (Hereditary

Hemorrhagic Telangiectasia)------------- Bacillary Angiomatosis, in HIV patients,

caused by bacilli of Bartinella species

INTERMEDIATE (BORDERLINE)VASCULAR NEOPLASMS

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VASCULAR NEOPLASMS

Kaposi Sarcoma, KS 1) Classic European, described 1872, NON-HIV

2) African, pre-HIV, now HIV- and HIV+

3) Transplant associated, HIV-

4) AIDS KS, caused by HHV-8, aka KSHV

PATCH PLAQUENODULE HEMANGIOENDOTHELIOMA*

(HETEROGENEOUS GROUP OFNEOPLASMS)

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Diagnosis of vascular neoplasms may require

the use of endothelial cell markers such as

Factor VIII or CD-31, especially if clear cutvascular spaces are difficult to see, especially if

the tumor is UNDIFFERENTIATED enough to the

degree that endothelial lined spaces are NOT

clearly seen.

MALIGNANT VASCULAR

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TUMORS

ANGIOSARCOMA May not look vascular at all

Severe atypia

Frequent and often bizarre mitoses

Behave as any sarcoma might, i.e., early

pulmonary metastases

HEMANGIOPERICYTOMA* HETEROGENOUS group of disorders Most commonly arising in pelvic retroperitoneum

VASCULAR INTERVENTIONS

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VASCULAR INTERVENTIONS

ANGIOPLASTY

STENTS

GRAFTS

Autologous (saphenous v., internal

mammary a.)

Synthetic (Teflon)

ANGIOPLASTIES

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ANGIOPLASTIES Plaque fracture (crackling sound)

Dissection

Arterial dilatation initially Restenosis ~ 6 months

STENTS

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STENTS

Metallic mesh Permanently placed

Stays patent longer

than angioplasty OFTEN DRUG COATED

Goals:

Prevent thrombosis Prevent spasm

Delay RE-stenosis

GRAFTS

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GRAFTS 400,000 CABG grafts per year in USA Saphenous v. vs. Internal mammary a. (internal

thoracic a.)

50% patent after 10 years, for saphenous v. 90% patent after 10 years, for mammary a.

Endothelial and smooth muscle migration andproliferation are key factors for success