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Nonatherosclerotic Arterial Syndromes Amjad AlMahameed, MD, MPH, FACP Division of Cardiology Beth Israel Deaconess Medic PowerPoint Presentation
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Nonatherosclerotic Arterial Syndromes Amjad AlMahameed, MD, MPH, FACP Division of Cardiology Beth Israel Deaconess Medical Center. Occlusive Arterial Disease. 90% atherosclerotic. 10% Non-atherosclerotic. Vasculitidis, FMD, Thromboangiitis Obliterans, Thoracic Outlet Syndrome,

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slide1

Nonatherosclerotic Arterial Syndromes

Amjad AlMahameed, MD, MPH, FACP

Division of Cardiology

Beth Israel Deaconess Medical Center

slide2

Occlusive Arterial Disease

90% atherosclerotic

10% Non-atherosclerotic

Vasculitidis, FMD,

Thromboangiitis Obliterans,

Thoracic Outlet Syndrome,

Vasospastic Disorders,

Other

temporal arteritis
Evidence of temporal arteritis: A painting by Jan Van Eyck (c. 1385–1440), entitled “The Virgin” with Canon Van der Paele, 1436.Notice the prominent arteries on the temples of the bishopTemporal Arteritis

.

slide4

Normal medium-sized artery

Vessel affected by giant cell arteritis

The inflammatory cells appear as dark blue dots. The giant cells are circled.

GCA: TA/Takayasu’s

slide5

Arteries Commonly Affected by TA

Temporal Artery

Ophthalmic

Artery

Facial

Artery

Carotid

Artery

Central Retinal Artery Occlusion

slide8

Types of Involvement in Takayasu’s Arteritis

Classical

Takayasu’s

Pulmonary

Arteries

Descending

Aorta

Asc. & Desc.

Aorta

slide10

16 y/o Female with Takayasu.

Right and left renal art stenosis and SMA not present

slide12

(A) MRA patient with active TA at diagnosis. There is complete occlusion of the left SCA at its origin (arrow) with numerous collaterals evident and an ostial stenosis of the left common carotid artery. (B) MRA image from the same patient in remission. No significant progression of the lesions found on the baseline MRA is seen.

Andrews, J et al. Ann Rheum Dis 2004;63:995-1000

slide13

(A) [18F]FDG-PET scan of patient with active TA at diagnosis. Note the markedly abnormal uptake of [18F]FDG in the aortic arch and carotid arteries (arrows). (B) [18F]FDG-PET scan of the same patient in remission after treatment with prednisolone and intravenous cyclophosphamide. Note almost complete resolution of abnormal [18F]FDG uptake in these areas.

Andrews, J et al. Ann Rheum Dis 2004;63:995-1000

Copyright ©2004 BMJ Publishing Group Ltd.

polyarteritis nodosa
Polyarteritis Nodosa
  • More common in adult males
  • Spares the arterioles, capillaries, venules and glomeruli
  • Associated with hepatitis B antigenemia
  • Kidney (most frequently affected): 85%
  • Multiple intrarenal aneurysms
  • Aneurysms may thrombose and disappear
  • Appear in new locations
slide15
PAN

GCA

prominent eosinophilic "fibrinoid" necrosis involving the intima and media. In contrast to GCA, there is no granulomatosis inflammation. Notice also how the lumen has been occluded by granulation tissue.

polyarteritis nodosa presentation

Polyarteritis nodosa

Low index of

suspicion is

necessary

Headache

Arthralgias

&

Myalgias

Stroke

Myocardial

Ischemia

Mesenteric

Ischemia

Nephritis &

renal failure

  • No hematuria
  • 30% positive
  • for hepatitis B
  • surface antigen

Liver

damage

Digital

ischemia or

Gangrene

p-ANCA titers often

are found but are not

diagnostic

Neuropathy

Polyarteritis Nodosa: Presentation
  • Abdominal pain
  • Systemic hypertension
  • Anorexia and weight loss
  • Abdominal distention
  • Hematemesis, melena
  • Jaundice
  • Painless hematuria
  • Peripheral neuropathy
  • Tender subcutaneous nodules
  • Gangrene of fingers and toes

HTN

slide17

Polyarteritis Nodosa

Micro “Berry” aneurysms

slide19

Tender, hyperpigmented, firm subcutaneous nodules with a background of livedo reticularis common in cutaneous PAN

Nonspecific, firm, tender subcutaneous nodules without livedo reticularis and/or systemic involvement

Tender erythematous nodules with central "punched out" ulcerations common in cutaneous PAN

buerger s disease
Buerger’s Disease

Buerger’s Thromboangiitis Obliterans

Pathology Specimen shows

INFLAMMED/SCARRED

NEUROVASCULAR BUNDLE

slide22
The histopathological findings vary according to the duration of the disease. The findings are most likely to be diagnostic in the acute phase of the disease
  • The hallmark of the acute-phase lesion is an occlusive, highly cellular, inflammatory thrombus, with less inflammation in the walls of the blood vessels. Polymorphonuclear leukocytes, microabscesses, and multinucleated giant cells may be present
slide24

Self mutilation by smoking – this patient had

all four limbs amputated for a Buerger’s type

of arteritis. His cigarette holder was made out

of a coat hanger by one of his friends on the

ward

slide27

example of how to perform the Allen’s test on the hands is shown in figure 2 and 3.

Collateralization around areas of occlusion (corkscrew collaterals)

Allen’s test Source

classify the fmd subtype
Classify the FMD Subtype

Medial Fibroplasia

Intimal Fibroplasia