CVD 2

Question 1

3. Most myocardial infarctions are caused by (hi/low?) -grade stenoses.

Answer 1

low grade with most MI caused by <50% sentosish

Question 2

3. Is the severity of a lesion a good predictor of mortality?

Answer 2

no, lesion severity is a poor predictor of survival; comparable survival was noted with those of mild and severe CAD

Question 3

3. Describe the Glagov (hypothesis) of arterial remodeling.

Answer 3

exposure ot risk factors causes artery to undergo compensatory expansion of vessel to maintain the lumen, that atherosclerosis is primarily a disease of the vessel wall, not the lumen

Question 4

3. Describe angiogram ability to distinguish vessels effected with plaques.

Answer 4

because there is normally not a change in vessel diamter until very late in disease, angiogram does not capture the changes in vascular walls that are part of atheroma

Question 5

4. What is the difference between a stable plaque and an unstable plaque?

Answer 5

the size of the fibrous cap in relation to the size of the lipid core, the larger the cap, the smaller the lipid core, the more stable (there is no good clinical way to assess which plaques are stable)

Question 6

3. What is the cause and result of a plaque rupture?

Answer 6

cuased by a change in shear stress (ie. Physical exertion) which causes the fibrous cap to rupture and formation of a clot (sometimes with paradoxyl vasoconstrcition)

Question 7

4. Plaques formation is not homogenous, where are plaques likely to form?

Answer 7

at points of high turbulance (at ostia or in bifurcations), note the most likely area of the cap to rupture is the “shoulder region” of the cap

Question 8

3. List 3 factors that may trigger the conversion of a unstable clot into acute disease.

Answer 8

patient activity (physical), psychological stress, and circadian variation (sympathetic surge in AM/dehydration)

Question 9

3. Desribe the other events occuring with surrounding the rupture of a plaque.

Answer 9

triggering event, rupture, thrombosis and paradoxical vasoconstriction

Question 10

3. What do you know about the plaques in persons’ body based on observing a signal plaque?

Answer 10

people have multiple types of plaques, the more stable plaques that are observed, the greater the probability of vulnerable plaques

Question 11

4. How do inflammatory cells effect the integrity of a plaque’s fibrous cap?

Answer 11

inflammatory cells can send molecular messages to the SM (IFN gamma) that inibit its ability to synthesize new collagen and strengthen the fibrous cap as well as release proteolytic enzymes that degrade collagen and increasing TPA a potent procoagulant

Question 12

4. How could a clinician measure the inflammation within a patients systemic vessels?

Answer 12

CRP, an acute phase protein excreted liver, at constitutive levels can approximate the level of inflammation

Question 13

4. _____ can occur in macrophage-rick lesions that do not necessarily cause critical stenosis.

Answer 13

thrombosis

Question 14

1. When does CAD begin?

Answer 14

as early as during fetal development given the mother eats an atherogenic diet

Question 15

1. What is usually the intial presentation of CAD?

Answer 15

because CAD progresses sliently, as plaques build they are not expressed with symptoms, the initial presentation is usually MI or sudden death

Question 16

1. What is the “reasonable approach” to addressing CVD.

Answer 16

early and aggressive risk factor management

Question 17

3. Name the three key characteristics of an vulnerable plaque.

Answer 17

thin cap, large lipid core, increased inflammatory activity