This document provides information about atherosclerosis, including its definition, locations where it commonly occurs, complications that can arise, risk factors, pathogenesis, and histological features. It defines atherosclerosis as a hardening and loss of elasticity of arterial walls. The most common sites are the abdominal aorta, iliac arteries, coronary arteries, and carotid arteries. Complications include myocardial infarction, stroke, aneurysm formation, and gangrene. Major risk factors include hyperlipidemia, hypertension, smoking, and diabetes. The pathogenesis involves response to endothelial injury from various insults, resulting in inflammation and deposition of lipids in the arterial wall.

1. Faculty of Medicine
Pathology of
Cardiovascular System
KING
ABDULAZIZ
UNIVERSITYITY
RABIGH BRANCH
Dr. Imrana Tanvir

2. Atherosclerosis
(ATH)
KING
ABDULAZIZ
UNIVERSITYITY
RABIGH BRANCH
Dr. Imrana Tanvir

3. Learning ObjectivesLearning Objectives
 Define atherosclerosis, arteriosclerosis, fatty
streaks, and fibrous atheromatous plaques, and
identify the most common sites of
atherosclerosis.
 List the vessels most commonly affected by
atherosclerosis, and describe the vessel
changes that occur with atherosclerosis and
possible complication.
 Describe possible mechanisms involved in the
development of atherosclerosis.
Pathology of
Cardiovascular System
Dr. Mohamad Nidal Khabaz
KING
ABDULAZIZ
UNIVERSITYITY
RABIGH BRANCH

4. Atherosclerosis (ATH)Atherosclerosis (ATH)
 Hardening of arteries (Hardening of arteries (Thickening and loss of elasticityThickening and loss of elasticity ofof
arterial walls).arterial walls).
 Systemic disease at multiple sites affects vital organs, inSystemic disease at multiple sites affects vital organs, in
which ATH is revealed atwhich ATH is revealed at::
 Elastic arteries, Large arteries,Elastic arteries, Large arteries, Medium sized arteries.Medium sized arteries.
 It is common worldwide, almost everyone in U.S is subject toIt is common worldwide, almost everyone in U.S is subject to
ATH if they live long enough. Accounting for about 50% of allATH if they live long enough. Accounting for about 50% of all
deaths in West.deaths in West.
 The characteristic lesion of ATH is calledThe characteristic lesion of ATH is called AtheromaAtheroma

5. AtheromaAtheroma ((fibrofatty plaques)fibrofatty plaques)
 Atheroma is focalAtheroma is focal lesion oflesion of intimaintima, that is characterized by, that is characterized by
intimal deposition of lipids,intimal deposition of lipids, intruding into the lumen (0.3 tointruding into the lumen (0.3 to
1.5 cm in diameter),1.5 cm in diameter),
 Atheroma leads toAtheroma leads to iintimal thickening, scarring, andntimal thickening, scarring, and
reducing the lumen sizereducing the lumen size ccausing stenosis, which ends withausing stenosis, which ends with
ischemia and infarction.ischemia and infarction.
 GrosslyGrossly: Atheroma consist of lipid core covered by a firm: Atheroma consist of lipid core covered by a firm
white fibrous cap, and havewhite fibrous cap, and have threethree main components:main components:
 Cells: includingCells: including SMCs, macrophages, leukocytesSMCs, macrophages, leukocytes
 Extracellular matrix, includingExtracellular matrix, including collagen, elastic fibers,collagen, elastic fibers,
and proteoglycansand proteoglycans
 Intracellular and extracellularIntracellular and extracellular lipidlipid..
 Around the lesions, there is neovascularization.Around the lesions, there is neovascularization.

6. Foam cells are large lipid-laden cells that derive predominantlyFoam cells are large lipid-laden cells that derive predominantly
from blood monocytes (tissue macrophages), but SMCs canfrom blood monocytes (tissue macrophages), but SMCs can
also absorb lipid to become foam cells.also absorb lipid to become foam cells.
Two type of atheromatous plaquesTwo type of atheromatous plaques
Soft plaquesSoft plaques (abundant lipid).(abundant lipid).
Solid or fibrous plaquesSolid or fibrous plaques (SMCs and fibrous tissue).(SMCs and fibrous tissue).

7. Fate Of AtheromaFate Of Atheroma
 Plaques change and progressively enlarge throughPlaques change and progressively enlarge through
 Cell death and degeneration,Cell death and degeneration,
 Synthesis and degradation of extracellular matrix,Synthesis and degradation of extracellular matrix,
 Organization of thrombus.Organization of thrombus.
 Atheroma often undergo calcification.Atheroma often undergo calcification.
 ComplicationComplication: rupture (ulceration or erosion), hemorrhage,: rupture (ulceration or erosion), hemorrhage,
thrombosis, aneurysmal dilationthrombosis, aneurysmal dilation

8.  Large BV :Large BV :
 Abdominal aortaAbdominal aorta
 IliacIliac
 In descending orderIn descending order
 CoronaryCoronary
 PoplitealPopliteal
 CarotidCarotid
 Circle of Willis.Circle of Willis.
 Vessels of the upperVessels of the upper
extremities are usuallyextremities are usually
spared,spared,
 The severity of AS in oneThe severity of AS in one
artery does not predict itsartery does not predict its
severity in anotherseverity in another

9. Atherosclerosis: ComplicationsAtherosclerosis: Complications
 Major consequencesMajor consequences
 Coronary arteries: IHD (Coronary arteries: IHD (myocardial infarctionmyocardial infarction))
 Cerebrovascular system: Cerebral infarction (Cerebrovascular system: Cerebral infarction (strokestroke))
 Aorta:Aorta: Hypertension and aneurysmHypertension and aneurysm formationformation
 Peripheral vascular systemPeripheral vascular system
 Decreased perfusion to extremities causingDecreased perfusion to extremities causing
gangrene of the legs (gangrene of the legs (coagulative necrosiscoagulative necrosis))
 More consequences (diminished arterial perfusion)More consequences (diminished arterial perfusion)
 Mesenteric occlusion, Sudden cardiac death, ChronicMesenteric occlusion, Sudden cardiac death, Chronic
IHD, Ischemic encephalopathyIHD, Ischemic encephalopathy

11. Atherosclerosis:Atherosclerosis: Fatty streaksFatty streaks
 Fatty streaks, (composed ofFatty streaks, (composed of foam cellsfoam cells), are not), are not
significantly raised and thus do not cause any disturbancesignificantly raised and thus do not cause any disturbance
in blood flow.in blood flow.
 They begin as multiple yellow, flat spots (They begin as multiple yellow, flat spots (fatty dotsfatty dots) less) less
than 1 mm, then combine into elongated streaks.than 1 mm, then combine into elongated streaks.
 Fatty streaks appear in the aortas of children regardless ofFatty streaks appear in the aortas of children regardless of
geography, race, sex, or environment.geography, race, sex, or environment.
 Coronary fatty streaks begin to form in adolescence.Coronary fatty streaks begin to form in adolescence.
 The relationship of fatty streaks to atherosclerotic plaquesThe relationship of fatty streaks to atherosclerotic plaques
is uncertain.is uncertain.

12. Gross views of atherosclerosis in the aorta.Gross views of atherosclerosis in the aorta.
A. Mild atherosclerosis composed of fibrous plaques,A. Mild atherosclerosis composed of fibrous plaques,
one of which is denoted by the arrow.one of which is denoted by the arrow.
B. Severe disease with diffuse, complicated lesions.B. Severe disease with diffuse, complicated lesions.

13. Morphologic typesMorphologic types
Fatty dotsFatty dots Atheroma Plaques ComplicatedAtheroma Plaques Complicated

14. Histologic features of atheromatous plaqueHistologic features of atheromatous plaque
in the coronary artery.in the coronary artery.

15. Histologic features ofHistologic features of
atheromatous plaque in theatheromatous plaque in the
coronary artery.coronary artery.
The plaque shown in A, stainedThe plaque shown in A, stained
forfor elastin (black)elastin (black) demonstratingdemonstrating
that the internal and externalthat the internal and external
elastic membranes areelastic membranes are
destroyed and the media of thedestroyed and the media of the
artery is thinned under the mostartery is thinned under the most
advanced plaque (arrow).advanced plaque (arrow).

16. Histologic features ofHistologic features of
atheromatous plaque in theatheromatous plaque in the
coronary artery.coronary artery.
The junction of the fibrous cap andThe junction of the fibrous cap and
core showing scatteredcore showing scattered
inflammatory cells,inflammatory cells, calcificationcalcification
(broad arrow),(broad arrow), andand
neovascularization (small arrows)neovascularization (small arrows)

17. Atherosclerosis:Atherosclerosis:
Risk FactorsRisk Factors
 Non-modifiable risk factors (Constitutional)Non-modifiable risk factors (Constitutional)
 Age, Sex, GeneticsAge, Sex, Genetics
 Modifiable risk factors (Major)Modifiable risk factors (Major)
 Hyperlipidemia, Hypertension, Smoking, DiabetesHyperlipidemia, Hypertension, Smoking, Diabetes
 Modifiable risk factors (Other)Modifiable risk factors (Other)
 Diet (obesity), life style (stress), personal habits (lack ofDiet (obesity), life style (stress), personal habits (lack of
regular exercise)regular exercise)

18. AtherosclerosisAtherosclerosis
Constitutional Risk FactorsConstitutional Risk Factors
 AgeAge: it is clinically evident after middle age, between ages: it is clinically evident after middle age, between ages
40-60 increases the incidence of MI 5 fold.40-60 increases the incidence of MI 5 fold.
 SexSex: men > premenopausal women, but men = women by: men > premenopausal women, but men = women by
77thth
-8-8thth
decades (decades (↓↓ postmenopausal estrogen).postmenopausal estrogen).
 GeneticsGenetics: familial predisposition (polygenic): familial predisposition (polygenic)
 Well-defined hereditary genetic derangement inWell-defined hereditary genetic derangement in
lipoprotein metabolism (familial hypercholesterolemia)lipoprotein metabolism (familial hypercholesterolemia)
 Familial clustering of other risk factors: hypertension orFamilial clustering of other risk factors: hypertension or
diabetesdiabetes

19. Atherosclerosis: Major Risk FactorsAtherosclerosis: Major Risk Factors
Hyperlipidemia (HypercholesterolemiaHyperlipidemia (Hypercholesterolemia))
 LDL increases the risk of ATH.LDL increases the risk of ATH.
 HDL has a protective effect (negative risk factor)HDL has a protective effect (negative risk factor)..
 It mobilizesIt mobilizes the cholesterol from tissues to liver,the cholesterol from tissues to liver,
 It is iIt is increased by exercise and ethanol usencreased by exercise and ethanol use
 High dietary intakeHigh dietary intake
 ssBad fatsBad fats: cholesterol and saturated fats (egg yolk,: cholesterol and saturated fats (egg yolk,
animal fats, and butter)animal fats, and butter)
 Good fatsGood fats such as omega-3 fatty acids (fish oils),such as omega-3 fatty acids (fish oils),
unsaturated fats)unsaturated fats)
 Low ratio of saturated to polyunsaturated fats lowersLow ratio of saturated to polyunsaturated fats lowers
risk.risk.

20. Atherosclerosis: Major Risk FactorsAtherosclerosis: Major Risk Factors
HypertensionHypertension
 Hypertension: Men ages 45-62 with (Hypertension: Men ages 45-62 with (BP 169/95)BP 169/95) →↑→↑ X 5X 5
of IHD than men with (BP 140/90).of IHD than men with (BP 140/90).
 Cigarette smokingCigarette smoking increases the incidence and severity ofincreases the incidence and severity of
ATH in M &F and dATH in M &F and deecreasescreases HDLHDL
 1 pack +/day for years1 pack +/day for years→↑→↑ X2-3 of death rate from IHDX2-3 of death rate from IHD
 Diabetes mellitusDiabetes mellitus
 Induces hypercholesterolemiaInduces hypercholesterolemia
 MI (X 2)MI (X 2)
 strokestroke
 gangrene (X100- 150gangrene (X100- 150))

21. Atherosclerosis: Other Risk FactorsAtherosclerosis: Other Risk Factors
 Decrease physical activityDecrease physical activity (lack of regular exercise)(lack of regular exercise)
 Life style (competitive, stressful with tLife style (competitive, stressful with type A personality)ype A personality)
 Obesity (decrease HDL)Obesity (decrease HDL)
 Multiple risk factors have multiplicative effect.Multiple risk factors have multiplicative effect.
 ATH may develop in absence of known risk factor.ATH may develop in absence of known risk factor.

22. Atherosclerosis: Other Risk FactorsAtherosclerosis: Other Risk Factors
(Cont…)(Cont…)
 HyperhomocystenemiaHyperhomocystenemia: homocysteine increases platelet: homocysteine increases platelet
adhesion and coagulation abnormalities, resulting inadhesion and coagulation abnormalities, resulting in
increased arterial and venous clots, leading to strokes andincreased arterial and venous clots, leading to strokes and
heart attacksheart attacks
 Can be caused by low intake of Folic acid, vitamin BCan be caused by low intake of Folic acid, vitamin B

23. Atherosclerosis – PathogenesisAtherosclerosis – Pathogenesis
The Response to Endothelium Injury HypothesisThe Response to Endothelium Injury Hypothesis
1.1. ATH is considered to be a chronic inflammatory responseATH is considered to be a chronic inflammatory response
of the arterial wall initiated byof the arterial wall initiated by injury to the endotheliuminjury to the endothelium
(focal areas of chronic endothelial injury (slight), because of(focal areas of chronic endothelial injury (slight), because of
 derivatives of cigarette smoke,derivatives of cigarette smoke,
 homocysteine,homocysteine,
 viruses and other infectious agents,viruses and other infectious agents,
 hyperlipidemiahyperlipidemia

24. Atherosclerosis – PathogenesisAtherosclerosis – Pathogenesis
The Response to Endothelium Injury HypothesisThe Response to Endothelium Injury Hypothesis
2. Result in endothelial dysfunction that causes2. Result in endothelial dysfunction that causes
 ↑↑endothelial permeability,endothelial permeability,
 enhanced leukocyte adhesionenhanced leukocyte adhesion
 alteration in expression of EC gene products (ICAM-1) &alteration in expression of EC gene products (ICAM-1) &
(VCAM-1) that mediate adhesion of circulating(VCAM-1) that mediate adhesion of circulating
monocytes, lymphocytes and platelets. (thromboticmonocytes, lymphocytes and platelets. (thrombotic
potential)potential)

25. Atherosclerosis – PathogenesisAtherosclerosis – Pathogenesis
The Response to Endothelium Injury HypothesisThe Response to Endothelium Injury Hypothesis
3.Depositions of lipoproteins in the vessel wall, mainly LDL3.Depositions of lipoproteins in the vessel wall, mainly LDL
with its high cholesterol content. Then modification ofwith its high cholesterol content. Then modification of
lesional lipoproteins by oxidation.lesional lipoproteins by oxidation.
4.Adhesion of blood monocytes (and other leukocytes) to the4.Adhesion of blood monocytes (and other leukocytes) to the
endothelium, followed by their migration into the intima andendothelium, followed by their migration into the intima and
their transformation into macrophages and foam cells.their transformation into macrophages and foam cells.
5.Adhesion of platelets.5.Adhesion of platelets.

26. Atherosclerosis – PathogenesisAtherosclerosis – Pathogenesis
The Response to Endothelium Injury HypothesisThe Response to Endothelium Injury Hypothesis
6. Release of factors from activated platelets and6. Release of factors from activated platelets and
macrophages that cause migration of SMCs from media intomacrophages that cause migration of SMCs from media into
the intima.the intima.
7. Proliferation of SMCs in the intima, and elaboration of7. Proliferation of SMCs in the intima, and elaboration of
extracellular matrix, leading to accumulation of collagen andextracellular matrix, leading to accumulation of collagen and
proteoglycans.proteoglycans.
8. Enhanced accumulation of lipids both within cells8. Enhanced accumulation of lipids both within cells
(macrophages and SMCs) and extracellularly.(macrophages and SMCs) and extracellularly.

27. Atherosclerosis - PathogenesisAtherosclerosis - Pathogenesis
The Role of Endothelial InjuryThe Role of Endothelial Injury
 Determinants of endothelial alterationsDeterminants of endothelial alterations
 Homodynamic disturbancesHomodynamic disturbances
 Effects of hypercholesterolemiaEffects of hypercholesterolemia
 Tendency for plaques to occur at ostia of exiting vessels,Tendency for plaques to occur at ostia of exiting vessels,
branch points and along the posterior wall of thebranch points and along the posterior wall of the
abdominal aorta (where there are disturbed flowabdominal aorta (where there are disturbed flow
patterns).patterns).

28. Atherosclerosis - PathogenesisAtherosclerosis - Pathogenesis
The Role of LipidsThe Role of Lipids
 Evidence linkingEvidence linking hypercholestrolemiahypercholestrolemia & ATH& ATH
 Increased LDL cholesterol levels,Increased LDL cholesterol levels,
decreased HDL cholesterol levels, anddecreased HDL cholesterol levels, and
increased levels of the abnormal Lp(a)increased levels of the abnormal Lp(a)
 Lipids in atheromas (plaques) are plasma-Lipids in atheromas (plaques) are plasma-
derived cholesterol and cholesterol esters.derived cholesterol and cholesterol esters.
 Relationship between increased LDL levelRelationship between increased LDL level
and the severity of ATHand the severity of ATH

29. Atherosclerosis - PathogenesisAtherosclerosis - Pathogenesis
The Role of Lipids ( Cont…)The Role of Lipids ( Cont…)
 Genetic or acquired conditions result inGenetic or acquired conditions result in
hypercholesterolemia.hypercholesterolemia.
 familial hypercholesterolemiafamilial hypercholesterolemia
 diabetes mellitusdiabetes mellitus
 hypothyroidismhypothyroidism
 nephrotic syndromenephrotic syndrome
 alcoholismalcoholism
 Lowering levels of serum cholesterol by diet or drugLowering levels of serum cholesterol by diet or drug
slows the rate of progression of ATH, and causesslows the rate of progression of ATH, and causes
regression of plaques.regression of plaques.

30. Atherosclerosis - PathogenesisAtherosclerosis - Pathogenesis
The Role of Lipids (mechanisms)The Role of Lipids (mechanisms)
 Hyperlipidemia,Hyperlipidemia, may directly impair EC function throughmay directly impair EC function through
increased production ofincreased production of oxygen free radicalsoxygen free radicals ((inin
macrophages or EC)macrophages or EC) thatthat deactivate nitric oxidedeactivate nitric oxide (the major(the major
endothelial-relaxing factor).endothelial-relaxing factor).
 Free radicalsFree radicals induce chemical changes of lipid in the arterialinduce chemical changes of lipid in the arterial
wall by oxidizing LDL, leading to:wall by oxidizing LDL, leading to:
 Accumulation ofAccumulation of lipoproteinslipoproteins ((mainly LDL or oxidizedmainly LDL or oxidized
LDLLDL) in intima at sites of increased endothelial) in intima at sites of increased endothelial
permeability.permeability.

33. Atherosclerosis - PathogenesisAtherosclerosis - Pathogenesis
The Role of Lipids (mechanisms)The Role of Lipids (mechanisms)
 Role of oxidized LDL in atherogenesisRole of oxidized LDL in atherogenesis
 Oxidized LDL is ingested through small intestinesOxidized LDL is ingested through small intestines
 cavenger receptor of macrophages thus forming foam cells.cavenger receptor of macrophages thus forming foam cells.
 Increases monocytes accumulation in lesion (adhesion)Increases monocytes accumulation in lesion (adhesion)
 Stimulates release of GF & cytokinesStimulates release of GF & cytokines
 Oxidized LDL is cytotoxic to ECs and SMCsOxidized LDL is cytotoxic to ECs and SMCs
 Oxidized LDL can induce endothelial cell dysfunctionOxidized LDL can induce endothelial cell dysfunction

34. The Role ofThe Role of
Monocytes, Macrophages and PlateletsMonocytes, Macrophages and Platelets
 Adhesion of monocytes to ECs, then migration into the intima,Adhesion of monocytes to ECs, then migration into the intima,
followed by transformation into macrophages which engulffollowed by transformation into macrophages which engulf
lipoproteins largely oxidized LDL to become foam cells.lipoproteins largely oxidized LDL to become foam cells.
 MacrophagesMacrophages produceproduce IL-1 & TNFIL-1 & TNF which increase adhesionwhich increase adhesion
of leukocytesof leukocytes
 MacrophagesMacrophages produceproduce toxic O2 speciestoxic O2 species
 MacrophagesMacrophages elaborate GF that contribute inelaborate GF that contribute in SMCSMC
proliferation.proliferation.
 Adhesion of plateletsAdhesion of platelets
 Release of factors from activated platelets and macrophagesRelease of factors from activated platelets and macrophages
that cause migration of SMCs from media into thethat cause migration of SMCs from media into the intima.intima.

35. Atherosclerosis - PathogenesisAtherosclerosis - Pathogenesis
The Role of Smooth Muscle Cell ProliferationThe Role of Smooth Muscle Cell Proliferation
 Proliferation of SMCs in the intima and elaboration of ECM,Proliferation of SMCs in the intima and elaboration of ECM,
leading to accumulation of collagen and proteoglycans.leading to accumulation of collagen and proteoglycans.
 Convert fatty streak into a mature fibrofatty atheroma andConvert fatty streak into a mature fibrofatty atheroma and
contribute to the progression of ATH.contribute to the progression of ATH.
 Enhanced accumulation of lipids both within cellsEnhanced accumulation of lipids both within cells
(macrophages and SMCs) and extracellularly.(macrophages and SMCs) and extracellularly.

36. AneurysmsAneurysms
Abnormal dilations of blood vessel orAbnormal dilations of blood vessel or
the heartthe heart..

37. AneurysmsAneurysms
 Develop where there is marked weakening of the wallDevelop where there is marked weakening of the wall
(congenital, infections, trauma, systemic diseases).(congenital, infections, trauma, systemic diseases).
 True aneurysmsTrue aneurysms (Atherosclerotic, syphilitic, congenital(Atherosclerotic, syphilitic, congenital
vascular aneurysms and the left ventricular aneurysm)vascular aneurysms and the left ventricular aneurysm)
are of two shapes: Fusiform and Saccular.are of two shapes: Fusiform and Saccular.
 False aneurysmFalse aneurysm is a tear in the vascular wall leading tois a tear in the vascular wall leading to
an extravascular hematoma that freely communicatesan extravascular hematoma that freely communicates
with the intravascular space (pulsating hematoma).with the intravascular space (pulsating hematoma).
 Aortic dissection (dissecting hematoma), patients withAortic dissection (dissecting hematoma), patients with
hypertension or with abnormality of connective tissuehypertension or with abnormality of connective tissue
that affects the aorta (Marfan syndrome).that affects the aorta (Marfan syndrome).
 ComplicationsComplications: Thrombosis, Embolism, Rupture: Thrombosis, Embolism, Rupture

38. Proximal aortic dissectionProximal aortic dissection
demonstrating a small, obliquedemonstrating a small, oblique
intimal tear (demarcated by theintimal tear (demarcated by the
probe), allowing blood to enterprobe), allowing blood to enter
the media, creating anthe media, creating an
intramural hematoma (narrowintramural hematoma (narrow
arrows).arrows).
Note that the intimal tear hasNote that the intimal tear has
occurred in a region largelyoccurred in a region largely
free from atheroscleroticfree from atherosclerotic
plaque, and that propagation ofplaque, and that propagation of
the intramural hematoma isthe intramural hematoma is
arrested at a site more distallyarrested at a site more distally
where atherosclerosis beginswhere atherosclerosis begins
(broad arrow).(broad arrow).

39. Abdominal Aortic Aneurysm (AAA)Abdominal Aortic Aneurysm (AAA)
CausesCauses
 Atherosclerosis causes arterial wall thinning through medialAtherosclerosis causes arterial wall thinning through medial
destruction.destruction.
 Cystic medial degenerationCystic medial degeneration of the arterial mediaof the arterial media
 Focal loss of elastic and muscle fibers in the aortic mediaFocal loss of elastic and muscle fibers in the aortic media
and replacement by cystic spaces filled with myxoidand replacement by cystic spaces filled with myxoid
material (hypertension, Marfan’s syndrome)material (hypertension, Marfan’s syndrome)
 Common site is abdominal aorta below the renal arteriesCommon site is abdominal aorta below the renal arteries
and above the bifurcation of the aorta. But the common iliacand above the bifurcation of the aorta. But the common iliac
arteries, the arch, and descending parts of the thoracic aortaarteries, the arch, and descending parts of the thoracic aorta
can be involved.can be involved.
 AAAs areAAAs are saccular or fusiformsaccular or fusiform, and thrombus frequently fills, and thrombus frequently fills
at least part of the dilated segment .at least part of the dilated segment .

40. Abdominal Aortic Aneurysm (AAA)Abdominal Aortic Aneurysm (AAA)
 Two variants:Two variants: InflammatoryInflammatory AAAs andAAAs and MycoticMycotic AAAsAAAs
 Males > 50 years old, (50% of patients are hypertensive).Males > 50 years old, (50% of patients are hypertensive).
 Complications: depend primarily on location and size:Complications: depend primarily on location and size:
 Rupture into the peritoneal cavity or retroperitonealRupture into the peritoneal cavity or retroperitoneal
tissues with massive hemorrhage.tissues with massive hemorrhage.
 Obstruction of a vessel, particularly of the iliac,Obstruction of a vessel, particularly of the iliac,
mesenteric, renal, or vertebral branches.mesenteric, renal, or vertebral branches.
 Embolism from atheroma or mural thrombus.Embolism from atheroma or mural thrombus.
 Pressure on an adjacent structure (ureter or vertebrae).Pressure on an adjacent structure (ureter or vertebrae).

41. Abdominal aortic aneurysm that ruptured.Abdominal aortic aneurysm that ruptured.

42. A. Cross-section of aortic media with markedA. Cross-section of aortic media with marked elastinelastin
fragmentationfragmentation and formation of areas devoid of elastin thatand formation of areas devoid of elastin that
resemble cystic spaces, from a patient with Marfan syndrome.resemble cystic spaces, from a patient with Marfan syndrome.
<cystic medial necrosis><cystic medial necrosis>
B. Normal aortic media, showing the regular layered pattern ofB. Normal aortic media, showing the regular layered pattern of
elastic tissue.elastic tissue.
In both A and B the tissue section is stained to highlightIn both A and B the tissue section is stained to highlight elastinelastin
as black.as black.

43. Aortic Dissection (DissectingAortic Dissection (Dissecting
Hematoma)Hematoma)
 Entry of blood into the arterial wall, through an intimal tear,Entry of blood into the arterial wall, through an intimal tear,
usually in the aortic arch, dissecting the media between theusually in the aortic arch, dissecting the media between the
middle and outer third, causing massive hemorrhage.middle and outer third, causing massive hemorrhage.
 Aortic dissection (dissecting hematoma), occurs inAortic dissection (dissecting hematoma), occurs in
patients with hypertension (90%) or with abnormality ofpatients with hypertension (90%) or with abnormality of
connective tissue that affects the aorta (Marfanconnective tissue that affects the aorta (Marfan
syndrome).syndrome).
 Dissection of the aorta or other branches (coronary) mayDissection of the aorta or other branches (coronary) may
occur during or after pregnancy (rare).occur during or after pregnancy (rare).

44. Histologic view of the dissection demonstratingHistologic view of the dissection demonstrating
an aortic intramural hematoma (asterisk). Aortican aortic intramural hematoma (asterisk). Aortic
elastic layers black and blood red in this section,elastic layers black and blood red in this section,
stained with Movat stain.stained with Movat stain.

45. Aortic Dissection (DissectingAortic Dissection (Dissecting
Hematoma)Hematoma)
 Sudden onset of severe pain, beginning in the anteriorSudden onset of severe pain, beginning in the anterior
chest, radiating to the back, and moving downward as thechest, radiating to the back, and moving downward as the
dissection progresses. (Not MI).dissection progresses. (Not MI).
 Aortic dissections are classified into two types:Aortic dissections are classified into two types:
 Proximal lesionsProximal lesions: more common (dangerous), involving: more common (dangerous), involving
the ascending aorta or both the ascending and thethe ascending aorta or both the ascending and the
descending aorta (called type A).descending aorta (called type A).
 Distal lesionsDistal lesions begin distal to the subclavian artery (calledbegin distal to the subclavian artery (called
type B)type B)

46. Aortic dissections
are classified into
two types: A and B.

47. Aortic Dissection (Dissecting Hematoma)Aortic Dissection (Dissecting Hematoma)
ComplicationComplication
 The most common cause of death isThe most common cause of death is rupturerupture of theof the
dissection outward into any of the three body cavitiesdissection outward into any of the three body cavities
(pericardial, pleural, or peritoneal).(pericardial, pleural, or peritoneal).
 Retrograde dissection into the aortic root can causeRetrograde dissection into the aortic root can cause
disruption of the aortic valve causing cardiac tamponade,disruption of the aortic valve causing cardiac tamponade,
aortic insufficiency, and myocardial infarction.aortic insufficiency, and myocardial infarction.
 Extension of the dissection into the great arteries of theExtension of the dissection into the great arteries of the
neck or into the coronary, renal, mesenteric, or iliac arteries,neck or into the coronary, renal, mesenteric, or iliac arteries,
causing critical vascular obstruction.causing critical vascular obstruction.