Atherosclerosis/Atherogenesis

Question 1

Atherosclerosis pathogensis

Answer 1

Chronic inflammation of intima of arteries - lymphocytes are involved

Endothelial cell dysfunction leads to intimal macrophage and LDL accumulation

Leads to foam cells and fatty streaks

Smooth muscle cell migration from media and bone marrow

Involves PDGF and FGF leads to proliferaiton and ECM deposition

Leads to fibrous plaque nad complex atheromas

Question 2

Growth mechanisms

Answer 2

In first 4 stages - growth mainly by lipid accumulation…then accelerated smooth muscle and collagen increase (starts in 4th decade)…lastly, thrombosis and hematoma

Complicated lesion is what causes acute events

Question 3

Sites of coronary plaques

Answer 3

Early on - proximal LADA

Overtime, moves more distal

Question 4

Vulnerable coronary artery atherosceltrotic plaque

Answer 4

At risk for acute rupture with atherothrombosis

Inflammation 
Thin fibrous cap
Large necrotic core
Neoangiogenesis
Expansive outward remoedling (over 1.1)
Spotty calcifications

Question 5

Risk factors

Answer 5

Systolic BP
Cholesterol
Low HDL
Diabetes
Cigarettes
LVH by ECG

Question 6

Complications

Answer 6

Thrombosis
Plaque rupture
Hemorrhage
Wall weakeneing
Calcification

MI, cerebral infarct, gangrene of extremities, abdominal aortic aneurysm

Question 7

PAD

Answer 7

Limb/Lower extremity

Foot claudication, sichemia, gangrene

50% of amputations in diabetics

PAD plaque progression underlies the limb ishcemia with impending gangrene…with inc CV morbidity and mortality at other sites

Diabetes combines accelerated atheroscelrosis with MV arterioloscelorsis

Question 8

Ednovascular therapy

Bypass surgery

Answer 8

DEB or stent of femoral-popliteal artery aims to avoid neo-intimal restonosis

Paclitaxel (DEB) or nitinol (DES)

Try to replace/revascularize segments

Question 9

La Place’s Law

Answer 9

Wall tension=P*R

Aneurym formation increases wall tension which causes further dilation

When tensile limit is reached, dissection or rupture may occur

Dissection CAN occur without aneurysms

Question 10

Def of aneurysm

Answer 10

Permanent localized arterial dilation of more than 50% of normal

May cause pain which is sign of leaking, dissection or imminent rupture

Question 11

AAA risk factor and anatomy

Answer 11

Male>age
SMoking, HTN, Abdominal adiposity

Occurs below the renal arteries

Absent vasa vasora in the abdominal aorta

Question 12

Atherosclerosis of pulm artery

Answer 12

Chronic pulm HTN (could be secondary to COPD)

Question 13

Saphenous vein coronary bypass grafts

Answer 13

Vein will become arterialized

The veins develop a neo-intima and has all the complications of atherosclerosis

Question 14

Percutaneous trnasluminal angioplasty

Answer 14

Site of isolated coronary is distended with inflatable catheter

Worry about thrombiosis or neointima grwoth

Risk of immediate acute thombotic occlusion and stent restenosis from neointima or neoatherosclerosis formaiton

Question 15

What is neointima

Answer 15

New layer of inner vessel wall lining known to form inside vein and inside gortex tube grafts

New mesenchymal cells and ECM resembling native intima

May migrate from smooht muscle via disruptid internal elastic layer and or from circulating stem cells from bone marrow

Reparative collagen which differs from normal

Thombogenic which can acutely lead to in-stent rhombosis

May develop all features of native atherosclerosis

Question 16

Tx of peripheral femoral poplitwal artery stenosis

Answer 16

Balloon angioplasty wit hintimal tx of taxol or nitinol with drug eluted stent

Cellular migration from medial layer via disrupted internal elastic layer is pathology in this setting

in PVD< DM contributes ot post-int arterial restenosis