Lec 27 Diseases of the Aorta Flashcards
What is a true aneurysm vs false aneurysm?
true = dilatation of all 3 layers of aorta [>50% increase in diameter]
false = rupture through intimal and medial layers contained by adventitia or perivascular thrombus/clot
What is fusiform vs saccular aneurysm? which is more common?
fusiform = more comm, symmetrical on both side saccular = localized just one side
What is primary pathogenesis of ascending thoracic aortic aneurysm?
cystic medial necrosis/degeneration = degeneration and fragmention of elastic fibers
normal media components replaced with acellular stuff [collagen/mucoid material]
What are some etiologies of cystic medial necrosis causing ascending aortic aneurysm?
- occurs with aging due to hypertension
- or w/ disorders that affect connective tissue
- – Marfan
- – Loeys-Dietz syndrome
- – Ehlers-Danlos syndrome
- or bicuspid aortic valve
What causes marfan?
missense mutation in fibrillin gene –> impaired formation of elastin
What causes loeys dietz?
autosomal dom. mutation in TFG-B receptors
What causes ehler-danlos syndrome?
mutation in collagen
What is pathogenesis of anuerysms of descending thoracic and abdominal aorta?
usually due to atherosclerosis
What are some risk factors for descending aorta aneurysm?
- smoking
- dyslipidemia
- men
- HTN
- age [older]
== atherosclerotic risk factors
What is most common location of aortic aneurysm?
abdominal aorta
Besides the most common cystic medial necrosis and atherosclerosis, what are some other possible etiologies of aortic aneurysm?
- post-stenotic
- infection of arterial wall
- vasculitis [giant cell arteritis/takayasu arteritis]
What is natural history of aortic aneurysms?
expand by avg 1-4 mm/year
What are predictors of rate of abdominal aortic expansion?
- initial size [bigger size = faster expansion]
- active smoking
- hypertension
At what diameter abdominal aortic aneurysm should you call surgery? what about in marfans pt?
at 5.5 cm for normal pt; 5 cm for marfans
What are most common complications of abdominal aortic aneurysm?
- death
- rupture
- dissection
What is normal clinical presentation of aortic anuerysm?
- usually asymptomatic
- if thoracic –> may have cough/ dyspnea/ dysphagia from compression neighboring struct
- if ascending –> may have aortic regrug and symptoms of CHF
- if abdominal –> may have ab or back pain or nonspecific GI symptoms
How is aortic aneurysm normally discovered?
pt has chest or ab radiograph for some other reason and see dilation of vessel
How do you diagnose aortic aneurysm?
- chest or abdominal radiograph –> widened mediastinum
What is treatment for aortic aneurysm?
- reduce risk factors:
- – BBlockers to lower BP
- – smoking cessation
- once diagnosed monitor by image every 6-12 mo
When do you refer aortic aneurysm for repair?
based on side
>5.5 cm for abdominal aortic aneurysm OR
growth rate > 1 cm/yr
What is surgical treatment for aortic aneurysm?
- open surgical repair OR PCI: transfermoral stent graph repair
What is aortic dissection?
blood from vessel lumen passes through tear in intima into medial layer and spreads along the artery = forms a false lumen
What is acute intramural hematoma?
variant of aoritc dissection = hemorrhage in wall of aorta without evidence of intimal tear
What is a penetrating atherosclerotic ulcer?
erosion of plaque into aortic wall
What is an aortic rupture?
may be a complication of aortic dissection, intramural hematoma, penetrating atherosclerotic ulcer or from trauma
What is Stanford type A aortic dissection vs type B?
type A = involves ascending aorta [can also involve descending]
type B = involves descending aorta and DOES NOT involve ascending
What are the 2 postulated mech of aortic dissection?
- circumfrerential or transverse tear in intimal layer of the vessel –> blood enters media –> propagates along plane of muscle layer
OR
- rupture of vaa vasorum –> hemorrhages into the media –> forms hematoma in arterial wall –> tears through intima into vessel lumen
Who most commonly gets aortic dissection?
men in 60s-70s
What are risk factors for aortic dissection?
- hypertension
- smoking
- use of cocaine or stimulants
- connective tissue disease [marfans, ehlers danlos etc]
- congenital structural abnormality [coartcation of the aorta, abnormal aortic valve]
- inflammatory disease
- can be brought on by weight lifting/trauma
What part of aorta most commonly dissects?
- ascending thoracic aorta = 65%
- descending thoracic aorta = 20%
What is clinical presentation of aortic dissection?
sudden severe tearing pain
radiating to back
unequal BP in arms
How do you diagnose aortic dissection?
CT or echo
CXR shows mediastinal widening
How do you treat aortic dissection?
immediately need treatment
if typa A = ascending –> get to cardiac surgeon
if type B = descending –> manage medically; if symptoms worsen get surgeon
medically = reduce systolic BP by beta-blocker and nitroprusside [force reduction and vasodilation respectively]
What are complications of aortic dissection?
step1
- aortic rupture –> pericardial tamponade
- occlusion of aortic branches –> stroke, MI, renal failure
- distortion of aortic annulus –> aortic valve regurgitation
- death
What is the definition of peripheral artery disease?
flow-limiting lesion in artery that provides blood supply to limbs = noncoronary artery syndrome
What is the most common cause of peripheral artery disease?
atherosclerosis
What are risk factors for atherosclerotic PAD?
same as those for CAD –> smoking, diabetes, dyslipidemia, HTN, atherosclerosis, age
~40% of pts with PAD have concurrent CAD
What is pathogenesis of PAD?
- diseased peripheral vasculature –> impaired response to vasodilating substances, reduction in amount of endogenous vasodilation
- changes in muscle struct/function due to chronic ischemia –> denervation, muscle fiber dropout –> muscle atrophy
What is clinical presentation of peripheral artery disease?
- claudication [with walking]
- pain at rest [in severe PAD]
- ulceration
- infection
- skin necrosis
loss of pulses, muscle atrophy
How do you differentiate ischemic ulcers from venous ulcers?
ischemic ulcer: frequently in injury-prone areas like tips of toes, lateral ankle
venous ulcer: reddish-brown discoloration and varicose veins, usually more proximal/medial
What is risk equivalent with PAD?
patient with PAD has same risk of cardiac event as a patient who previously had an MI
What is normal ankle brachial index [ABI]?
normal > 0.90; usually 1 or a little higher
abnormal < 0.9
borderline 0.91-0.99
normal 1-1.4
non-compressible > 1.4
How do you calculate ABI?
- Use Doppler to locate arteries
- Take systolic pressure in brachial arteries; use the higher value
- Take systolic pressure in both ankles at posterior tibial (PT) and dorsalis pedis (DP) arteries
- Use higher value (PT or DP) for each ankle
- Calculate right and left ABIs: higher ankle over higher brachial value
- Use lower ABI for diagnostic purposes
What does it mean if ABI > 1.4?
non-compressible artery = also a disease state maybe calcification, rigid vessels
What is treatment for peripheral arterial disease?
- antiplatelet therapy
- risk factor modification
- increase ischemic capacity by doing exercise
- cilostazol to improve exercise capacity
meds to prevent MI
What interventional treatment for PAD?
percutaneous revascularization or surgical revascularization by stent or bypass respectively
