Blood vessels Pathology (GOMEZ) Flashcards
(96 cards)
1
Q
Congential aneurysm (Berry aneursym)
A
seen in 2% of autopsies
most involve circle of Willis
saccular type aneurysm arising in an artery with a developmental wall abnormality – weak area of vessel wall
berry aneurysm -> presents with headaches or sudden death
2
Q
arteriovenous fistulas
A
rare abnormal communications between arteries and veins
most congenital; some produced (rupture of an arterial aneurysm into adjacent vein, injuries that pierce walls of artery and vein, or inflammatory necrosis of adjacent vessels)
short-circuit blood and cause heart to pump additional volume (high-output cardiac failure can ensue)
Both can rupture, especially critical in brain
3
Q
fibromuscular dysplasia
A
focal irregular medial and intimal
hyperplasia with thickening of walls of medium and large muscular
arteries which occurs more commonly in young women (more later)
4
Q
HTN
A
systolic > 140 mm Hg
2014 Evidence Based Guidelines suggest > 150/90 mm Hg for those > 60 years.
diastolic > 90 mm Hg
Prehypertension
Systolic 120-139 mm Hg
diastolic 80-89 mm Hg
Systolic blood pressure is more important than diastolic blood pressure as a determinant of cardiovascular risk
5
Q
systolic >220 mm Hg or diastolic >120 mm Hg with no evidence of target organ damage
A
hypertensive urgency
6
Q
Hypertensive emergency
A
Accelerated hypertension- significant increase in B. P. associated with target organ damage (flame-shaped hemorrhages or exudates of fundus, renal failure, headache, angina, etc.)
Malignant hypertension- as above + papilledema (swelling of optic disc)
7
Q
Secondary HTN?
A
Renal
glomerulopathies, CRD, polycystic, renal artery stenosis, renal vasculitis
Endocrine adrenocortical hyperfunction (Cushing's, primary aldosteronism, adrenal hyperplasia, licorice ingestion)
Cardiovascular
Neurologic -
8
Q
endothelin
A
causes vasoconstriction
9
Q
Liddle syndrome
A
beta or gamma subunit of ENaC
•Mutations in renal epithelial Na channel protein → leads to increased sodium reabsorption –> HTN
moderately severe salt sensitive hypertension due to
Increased distal tubular reabsorption of Na+ with aldosterone stimulation
10
Q
11-Beta hydroxylase deficiency
A
(enzyme that influences aldosterone synthesis) leading to increased aldosterone production
leads to HTN
11
Q
hardening of arteries
A
arteriosclerosis
12
Q
in muscular arteries of >50 y. o. with no vessel lumen narrowing (can ossify). Hardening of the media. Blood still passes through
A
monckeberg medial calcific sclerosis
13
Q
arterioLOsclerosis
A
Hyaline arteriolosclerosis –common Protein deposition (hyalinized) Seen in : aging diabetes mellitus benign nephrosclerosis (hypertension)
Hyperplastic arteriolosclerosis Cell death (onion-skinning) \+/-necrotizing arteriolitis Seen in : malignant hypertension
14
Q
atherosclerotic plaques
A
Cause decreased flow (obstruction)
myocardial infarction, cerebral infarction, aortic aneurysms, peripheral vascular disease (gangrene), mesenteric occlusion, sudden cardiac death, chronic ischemic heart disease, and ischemic encephalopathy
Can disrupt and precipitate thrombi (obstruction)
Can shed emboli
Can encroach on media and weaken the vessel wall
aneurysms and ruptures
***Turbulent flow and low shear stress areas are prone to atherosclerosis
Laminar flow induces endothelial genes for products that protect against atherosclerosis (superoxide dismutase)
Turbulent flow causes endothelial trauma and dysfunction increased risk for developing atherosclerotic plaque
15
Q
nonmodifiable risk factors for atherosclerosis
A
genetic abnormalities
family history
increasing age
male gender
16
Q
modifiable risk factors for atherosclerosis
A
Hyperlipidemia HTN BP > 169/95, increased risk of IHD Cigarette smoking Diabetes Inflammation
2 risk factors lead to 4x risk
3 lead to 7x risk
17
Q
metabolic syndrome
A
Obesity, dyslipidemia, hypertension, and insulin resistance (can also have hypercoagulability and inflammatory state)***
18
Q
statins
A
inhibit HMG-CoA reductase
promote synthesis of LDL receptors
19
Q
acyl-CoA (ACAT)
A
favors esterification and storage of excess cholesterol
20
Q
estrogens effect on cholesterol
A
increase HDL and decrease LDL
replacement therapy does NOT decrease risk for heart attacks in post menopausal women
21
Q
exercise and alcohol
A
increase HDL (good)
22
Q
obesity and smoking
A
decrease HDL (among other things)
23
Q
familial hypercholesterolemia
A
Mutations in the LDL receptor gene
Impair the intracellular transport and catabolism of LDL
Also impair the transport of IDL (plasma IDL is converted into LDL)
Causes elevated LDL cholesterol in the plasma
Oxidized LDL receptors take over (scavenger receptor pathway)
Amount catabolized by scavenger receptor pathway is directly related to the plasma cholesterol level
Monocytes, macrophages, smooth muscle and endothelial cells have receptors for chemically modified (e.g., acetylated or oxidized) LDLs
Cholesterol in macrophages contributes to atherosclerosis and xanthoma formation
Oxidized LDL is cytotoxic to endothelial and smooth muscle cells
24
Q
most common LDL receptor mutation?
A
class II - problem with transport
receptor protein transport from the endoplasmic reticulum to the Golgi apparatus is impaired due to abnormal protein folding
25
autosomal dominant heterozygotes in familial hypercholesterolemia
Heterozygotes 2-3x elevation of plasma cholesterol levels- don’t see xanthoma
26
autosomal dominant homozygotes
5x elevation of plasma cholesterol levels
Develop severe atherosclerosis, mitral valve stenosis corneal arcus and xanthomas
Die from complications as children or young adults
27
elevated homocyteine
(low folate and/or vitamin B intake, homocystinuria) associated with premature vascular disease
If you lower homocysteine it doesn’t lower risk
risk factor for atherosclerosis
28
lipoprotein A
(apolipoprotein B-100 portion of LDL linked to apolipoprotein A) associated with a higher risk of coronary and cerebrovascular disease. Can’t decrease this abnormal lipoprotein – but can control cholesterol levels in diet
29
BP systolic, cholesterol, HDL, Diabetes, Cigarettes, LVH by ECG (by the time you have this it means you’ve most likely had HTN for a long time)
what are these
risk factors for atherosclerosis
30
elevated plasminogen activator inhibitor 1
strong predictor of RISK for major atherosclerotic events
31
CRP
Acute-phase reactant synthesized primarily by the liver
Has roles in opsonizing bacteria and activating complement
Atherosclerosis - involved in endothelial adhesion of WBCs and thrombosis
Strongly and independently predicts the risk of myocardial infarction, stroke, peripheral arterial disease, and sudden cardiac death
No evidence that lowering CRP reduces cardiovascular risk,
Smoking cessation, weight loss, statins and exercise all reduce CRP
32
what infections MAY contribute to atherosclerosis
Chlamydia pneumoniae, herpesvirus, and cytomegalovirus
33
aspirin ?
inhibits cox 1 at low doses--> anti-clot
34
Celebrex (Celecoxib)
Cox 2 inhibitor (NSAID)
believed to ↓ endothelium-derived prostacyclin without inhibiting platelet-derived thromboxane A2 → prothrombotic state
35
aneurysm
Localized abnormal dilation of a blood vessel or the wall of the heart
Most important causes of aortic aneurysms are
atherosclerosis (abdominal aorta) – weaken the wall
Worst atherosclerosis down in abdomen area
hypertension via medial cystic degeneration (thoracic aorta)
Other causes: Marfan syndrome, Loeys-Dietz syndrome, Ehlers-Danlos syndrome, scurvy, trauma (traumatic aneurysms or arteriovenous aneurysms), congenital defects (berry aneurysms), syphilis and vasculitides
36
mycotic aneurysm
infections!
from embolization of a septic embolus (infective endocarditis)
from extension of an adjacent suppurative process - appendicitis
from circulating organisms infecting the arterial wall
Mycotic abdominal aortic aneurysms - atherosclerotic AAAs that have become infected (particularly in Salmonella gastroenteritis)
37
true aneurysm
– bounded by arterial wall component or myocardium
Saccular aneurysm – appears rounded, bubble
Fusiform aneurysm – involves long segment of artery and is not rounded
38
false aneurysm
(pseudoaneurysm) = hematoma secondary to transmural rupture
39
AAA
Usually below the renal arteries
Involvement of renal arteries can lead to renal complications
M>F, smokers and age >50 years
Inflammatory abdominal aortic aneurysm (5-10%) - rich in lymphocytes, plasma cells and macrophages, often giant cells (cause is uncertain and occur at younger age)
Consequences ?
Rupture into the peritoneum or retroperitoneal tissues (fatal in > 50%)
Risk of rupture per year: size 6.0 cm (25%) [5cm or greater usually surgically repaired]
Obstruction of a vessel leading to ischemic tissue injury
Embolism from atheroma or mural thrombus
Impingement on an adjacent structure, such as compression of a ureter or erosion of vertebrae
Presentation as an abdominal mass (often palpably pulsating) that simulates a tumor
40
syphilitic (luetic) aneurysm
Obliterative endarteritis in tertiary stage of syphilis (lues) involves vasa vasorum (arterioles) of the thoracic aorta
Syphilitic aortitis - obliterative endarteritis of vasa (vessels are inflamed and the lumen is obliterative) → ischemic injury of the media → loss of the medial elastic fibers and muscle cells
Can lead to aneurysmal dilation that can include the aortic annulus leading to aortic valve incompetence
Can involve coronary ostia
41
aortic dissection
Dissection of blood between planes of the media
May or may not occur with an aneurysm
> 90% occur in men 40-60 with hypertension
Arteriolosclerosis → smooth muscle cell loss
In younger people may be connective tissue disorder (Marfan, Ehlers-Danlos, Vit. C deficiency)
Can be iatrogenic (arterial cannulation)
Rarely occurs during or following pregnancy
Occasionally 2ry to vasa vasorum rupture
Anti-HTN therapy!!
42
clinical presentation of aortic dissection
common cause of death?
types?
Sudden onset of excruciating pain, usually involves anterior chest, radiating to the back, and moving downward as the
dissection progresses
Most common cause of death is rupture into the body cavities
Retrograde dissection into the aortic root → aortic valvular apparatus dysfunction with aortic insufficiency
Can dissect into neck arteries, or coronary, renal, mesenteric, or iliac arteries, and compression of spinal arteries may cause transverse myelitis
Aggressive treatment of HTN may halt dissection
Occasionally the dissection can rupture back into vessel lumen causing a duel lumen vessel
Type A--> ascending aorta - worse
Type B--> after take-off of great vessels
43
Marfan syndrome
Loss of function mutation of fibrillin (1 per 5,000)
Heterozygotes have clinical symptoms
> 500 mutations of FBN1 gene (15q21) for fibrillin 1
Mutant fibrillin 1 prevents the assembly of normal microfibrils
75% of cases are familial (autosomal dominant pattern); rest are sporadic
Once incorrectly thought to be a dominant negative mutation!!!
With ↓fibrillin-1 there is ↑TGF-β activity and serum levels
Fibrillin 1 is involved in forming a complex that binds and inactivates TBF-β
TGF-β involved in embryonic development, cell growth and apoptosis
TGF-β enhances collagen production and extracellular matrix (ECM) remodeling
leads to overgrowth of bones and myxomatous changes in mitral valves
Mutations in the TGF-β receptors give rise to a similar syndrome called Loeys-Dietz syndrome (type 2 = Marfan syndrome, type II)
44
clinical presentation of Marfans
Skeleton: Slender with abnormally long legs, arms, and fingers (arachnodactyly); high-arched palate; hyperextensibility of joints; spinal deformities (kyphoscoliosis); pectus excavatum or pigeon-breast
Eyes: Bilateral dislocation (subluxation) of lens from weakness suspensory ligaments (ciliary zonules holding lens are made up exclusively of fibrillin)
Cardiovascular system: Aneurysmal dilation and aortic dissection; dilation of the aortic valve ring (aortic incompetence); mitral and tricuspid valve floppy valve syndrome giving rise to congestive cardiac failure
Death from aortic rupture may occur at any age and is the most common cause of death (less commonly, cardiac failure is the terminal event)
45
```
Fever
Weight loss
Myalgia
Arthralgia
Malaise
Fatigue
```
nonspecific symptoms with vasculitis
46
Granulomatous inflammation; also frequently involves the temporal artery. Usually occurs in patients older than age 50 and is associated with polymyalgia rheumatica***
large vessel vasculitis
Giant cell (temporal arteritis)
47
Granulomatous inflammation usually occurring in patients younger than age 50. Hard to feel pulse
Takayasu arteritis
48
Necrotizing inflammation typically involving renal arteries but sparing pulmonary vessels. Palpable purpura
polyarteritis nodosa
medium-vessel vasculitis
49
Arteritis with mucocutaneous lymph node syndrome; usually occurs in children. Coronary arteries can be involved with aneurysm formation and/or thrombosis +/- antiendothelial and smooth muscle antibodies
kawasaki disease
medium vessels
50
Granulomatous inflammation involving the respiratory tract and necrotizing vasculitis affecting small vessels, including glomerulonephritis. Associated with PR3-ANCAs (c-anca)
Wegener granulomatosis (Small-Vessel Vasculitis (Arterioles, Venules, Capillaries, and Occasionally Small Arteries)
51
Eosinophil-rich*** granulomatous inflammation involving the respiratory tract and necrotizing vasculitis affecting small vessels. Associated with asthma and blood eosinophilia. Associated with
MPO-ANCAs (p-anca)
Churg-strauss syndrome
52
Necrotizing small-vessel vasculitis with few or no immune deposits; necrotizing arteritis of small and medium-sized arteries can occur. Necrotizing glomerulonephritis and pulmonary capillaritis are common. Associated with MPO-ANCAs
microscopic polyangitis
53
MPO-ANCAs (p-ANCA),
, antineutrophil cytoplasmic antibodies, directed against myeloperoxidase
54
PR3-ANCAs (c-ANCA
antineutrophil cytoplasmic antibodies, directed against proteinase 3
55
Segmental, thrombosing, acute and chronic inflammation
of medium-sized and small arteries (tibial and radial), and extending to veins and nerves of the extremities
Previously occurred almost exclusively among heavy cigarette-smoking ***men, increasing in women
Begins before age 35 in most cases
Chronic ulcerations of the toes, feet, or fingers and gangrene
Secondary Raynaud phenomenon
Exercise induced instep claudication
Severe pain, even at rest (nerve involvement)
Rx- stop smoking (during early disease)
Thromboangiitis Obliterans (Buerger Disease)
56
Behcet disease
?
57
hypothermia?
Prolonged exposure to low ambient temperature
At about 90°F, loss of consciousness occurs, followed by bradycardia and atrial fibrillation at lower core temperatures
Direct effects: Physical disruptions and high salt concentrations within cells due to crystallization of the intra- and extracellular water
Indirect effects: Circulatory changes
Vasoconstriction and increased permeability (leading to edema)
Alcohol causes vasodilation lowering body temperature faster
58
Chilblain (perniones/perniosis)
Nonfreezing temperatures and damp conditions
| Chronic, recurrent vasculitis with red raised lesions
59
frostnip
Vasoconstriction involving nose, ears, hands, feet
60
immersion (trench) foot
Feet have been wet, but not freezing
May not heal, chronic pain, edema and blotchy discoloration
Often produces a superficial, moist, liquefaction gangrene
61
frostbite
Sudden sharp drops in temperature that are persistent
Vasoconstriction and increased viscosity of the blood
Hyperemia and edema, large, clear blisters, vesicles filled with hemorrhagic fluid to complete gangrene
62
Raynauds
Pallor or cyanosis of the digits of the hands or feet and, infrequently, tips of the nose or ears
Primary Raynaud phenomenon
Cold or emotion-induced vasoconstriction
Patients should undergo evaluation to rule out an underlying 2ry cause (approximately 10% of patients have secondary Raynaud phenomenon)
Late in the course intimal thickening can appear
Median age is 14 years, prevalence 3% - 5% of population
Secondary Raynaud phenomenon
Arterial insufficiency caused by various conditions
SLE, systemic sclerosis (scleroderma), atherosclerosis, or Buerger disease
63
varicose veins
Dilated, tortuous veins
increased intraluminal pressure and loss of vessel wall support
Valves imcompetent
venous stasis, congestion, edema, pain, and thrombosis
Prevalence 15-20% (10-20% ♂; 25-33% ♀)
Long periods of standing or long car or airplane rides lead to venous stasis and pedal edema (simple orthostatic edema) and contribute to varicosities
>50 years old, obese, and women (elevated venous pressure in pregnancy) are at risk
Can develop stasis dermatitis (brawny induration)
64
Usually neoplasm compresses or invades with cyanosis and dilation of the veins of the head, neck, and arms
If pulmonary vessels also compressed have respiratory distress
SVC syndrome
65
Neoplasm compresses or penetrates (renal, hepatic or adrenal cortex carcinomas) or a thrombus propagates upward with leg edema, distention of lower abdomen superficial collateral veins
With renal vein involvement massive proteinuria
IVC syndrome
66
- age 10 to 25 years, usually female, unknown cause with edema starting in the feet and slowly accumulating throughout life (extremity may swell to many times its normal size and the process may extend to the trunk)
lymphedema praecox
67
Milroy
(heredofamilial congenital lymphedema) have lymphatic agenesis or hypoplasia
68
most common vascular tumor usually skin, subcutaneous tissues, and mucous membranes, but can be in any organ with a vascular supply
lumina may be thrombosed, rupture of vessels causes scarring (hemosiderin pigment occasionally found)
Capillary hemangioma
69
"strawberry type" capillary hemangioma of the skin of newborns (1 in 200 births), grows rapidly in the first few months, and regresses by age 7 in 75% to 90%
juvenile hemangioma
70
cavernous hemangioma
Larger, less circumscribed, and
more frequently involves deep structures
than capillary hemangiomas
May be locally destructive
No tendency to regress
Intravascular thrombosis with associated dystrophic calcification
Hemangiomas of the brain threatening since cause pressure symptoms or rupture
71
hemangioblastoma
seen in Von-hippel lindau disease
72
```
polypoid capillary hemangioma
rapidly growing red nodule
skin or gingival or oral mucosae
bleeds easily and is often ulcerated
1/3 develop after trauma
edema and inflammatory infiltrate
(resemble exuberant granulation tissue)
```
pyogenic granuloma (lobular capillary hemangioma)
73
pyogenic granuloma that occurs in the gingiva of 1% of pregnant women (regresses after delivery)
granuloma gravidarum
74
in children in the neck or axilla and, rarely, retroperitoneum
massively dilated, cystic lymphatic spaces
cystic hygromas (lymphangioma colli) of the neck occur in Turner syndrome***
cavernous lymphangioma
| aka cystic hygroma
75
Benign often painful*** tumor
From modified cells of the glomus body
(arteriovenous anastomosis involved in thermoregulation)
Most commonly distal digit
Small slightly elevated, rounded, red-blue, firm nodules
minute foci of fresh hemorrhage if under the fingernails
Specialized glomus cells (modified smooth muscle cells on electron microscopy) arranged around vessels
Glomus Tumor (Glomangioma
76
Telangiectasia
- congenital anomaly or acquired permanent exaggeration of preformed vessels
composed of prominent capillaries, venules, and arterioles
77
Nevus Flammeus
birthmark
| most common form of ectasia (head and neck)
78
sturge weber syndrome
```
encephalotrigeminal angiomatosis)
uncommon congenital disorder
venous angiomatous masses in the leptomeninges
ipsilateral port-wine nevi with
trigeminal nerve distribution
often associated with mental retardation,
seizures, hemiplegia, and
radiopacities in the skull
```
79
port wine stain
may grow proportionately with child with no tendency to fade
80
spider telangiectasia
dilated subcutaneous arteries or arterioles about a
central core that blanches when pressure is applied
to its center.
usually face, neck, or upper chest
Most frequent in pregnant women and in cirrhosis (hyperestrinism)***
blanches with compression
81
Hereditary Hemorrhagic Telangiectasia (Osler-Weber-Rendu Disease) –
congenital malformations consisting of dilated capillaries and veins
Present at birth and distributed widely over the skin and mucous membranes of the oral cavity, lips, and respiratory, gastrointestinal, and urinary tracts
Autosomal dominant mutations
in TGF-β signaling pathway genes
82
Bacillary angiomatosis
Opportunistic infection of immunocompromised persons by gram-negative bacilli of the Bartonella family (first described in AIDS)
Skin, bone, brain, and other organs
Domestic cat is the reservoir of B. henselae and cat flea its vector (cause of cat-scratch disease)
Human body louse in infection due to B. quintana (cause of trench fever)
Closely related vascular lesion in liver and spleen called bacillary peliosis
Host tissue induction of hypoxia-inducible factor 1 (HIF-1α) leads to increased VEGF inducing vascularity
Rx- macrolide antibiotics (erythromycin)
83
stages of Kaposi Sarcoma
Patch stage- pink to purple solitary or multiple macules
Dilated angulated blood vessels and chronic inflammatory cells (lesions difficult to distinguish from granulation tissue)
Plaque stage- larger, violaceous dermal jagged vascular channels lined by plump spindle cells with occasional mitoses with RBC extravasation
Nodular stage – raised nodular lesions
often accompanied by involvement of lymph nodes and of viscera
sheets of spindle cells with mitotic figures and slit-like spaces that often contain rows of red cells
84
Older men of Eastern European (especially Ashkenazi Jews) or Mediterranean descent Multiple red to purple skin plaques or nodules, primarily on the arms or legs spreading proximal Viscera or mucosa becomes involved in approximately 10% of patients
no HIV
Chronic (classic or european)
Resection of primary lesions and recurrences in early disease
Radiation for multiple lesions in a restricted area
Chemotherapy is used for extensive or disseminated disease
85
Young Bantu children of South Africa (same region involved by Burkitt lymphoma)
Extremely aggressive (~100% mortality in 3 years)
Localized or generalized lymphadenopathy
Skin lesions are sparse
no HIV
Lymphadenophatic (african or endemic)
chemo or radiotherapy
86
Months to few years post-organ transplant with high doses of immunosuppressive therapy
Aggressive
Lymph nodes, mucosa, and visceral organs in half of patients and organ or internal involvement is usually fatal
Skin lesions may be absent
no HIV
Transplant associated immunosuppression associated
Withdrawal or reduction of immunosuppression
Possibly chemotherapy or radiotherapy
87
Most common cancer in the United States in AIDS (2-3% of AIDS patients) ***
Lesions have no site of predilection, but involvement of lymph nodes and the gut and wide dissemination tend to occur early
Most patients eventually succumb to the opportunistic infectious complications of AIDS rather than the KS
HIV yes**
AIDS-associated KS
Antiretroviral therapy for HIV with HAART (highly active antiretroviral therapy) incidence has declined
Chemotherapy or radiotherapy Interferon alpha may be used
Angiogenesis inhibitors effective in limited cases
88
hemangioendothelioma
Histologic features and clinical behavior intermediate between hemangiomas and angiosarcomas
Epithelioid hemangioendothelioma
vascular tumor occurring around medium and large veins in the soft tissue of adults
inconspicuous well-defined vascular channels and tumor cells are plump and often cuboidal
most cured by excision but
40% recur
20% to 30% metastasize
15% die from metastases
89
Malignant and vary from differentiated (hemangiosarcoma) to anaplastic
More often in older adults, anywhere in the body
Most commonly skin, soft tissue, breast, and liver
Have local invasion and metastatic spread (5 year survival 30%)
Can be induced by radiation*** and may be associated with foreign material introduced into the body
Immunohistochemistry CD31, CD34, Factor VIII or vWF ***
CD31 and CD34 are adhesion molecules
angiosarcoma
90
cutaneous angiosarcoma
Small, often asymptomatic, red nodules
| Eventually become large, fleshy, pale, gray-white, with central softening, necrosis and hemorrhage
91
hepatic angiosarcoma
Associated with carcinogens [arsenic, Thorotrast and vinyl chloride***]
Many years between exposure and tumors
92
lymphangiosarcoma
Arise in chronic lymphedema (approximately 10 years following radical mastectomy)
93
Hemangiopericytoma
Believed to be derived from pericytes (myofibroblasts)
Some fibroblastic tumors previously incorrectly included in this category
Fleshy or spongy consistency
Slowly growing in pelvic retroperitoneum or lower extremities (especially thigh) of middle aged women
Thin-walled branching ("staghorn") vascular pattern
1/2 act benign and 1/2 malignant
Necrosis, high mitotic rate, and nuclear pleomorphism, associated with aggressive behavior
94
balloon angioplasty
Dilation of a stenosis of an artery by
a percutaneously inserted balloon
catheter (percutaneous transluminal
coronary angioplasty)
Cause plaque rupture, medial
dissection, and stretching of the
media ***
```
COMPLICATIONS
abrupt reclosure (extensive circumferential or longitudinal dissection, thrombosis)- occurs early after procedure
proliferative in-stent restenosis (intimal thickening in 30% to 50% of patients within the first 4 to 6 months)
```
95
vascular stents
Expandable tubes of metallic mesh
used in 90% of angioplasties
Limit elastic recoil and mechanically
prevent vascular spasm
Damage endothelium and stretch wall
Initially covered by platelet-fibrin coating
and later by endothelium-lined neointima
Early thrombosis (use platelet antagonists)
Late intimal thickening (use antiproliferative drugs, i.e. paclitaxel or rapamycin)
96
vascular grafts
Synthetic or autologous
Large-diameter (12 to 18 mm) Dacron grafts in high-flow locations such as the aorta
Small-diameter fabric grafts (up to 6 to 8 mm) perform less well (thrombotic occlusion)
Endothelialization of clinical grafts is unusual
neointima in a 12- to 15-mm zone near the anastomosis
pseudointima with thrombus or cells other than endothelial cells lining remainder of graft
