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Flashcards in CVD 2 Deck (17):
1

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

low grade with most MI caused by <50% sentosish

2

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

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

3

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

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

4

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

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

5

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

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)

6

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

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)

7

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

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

8

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

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

9

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

triggering event, rupture, thrombosis and paradoxical vasoconstriction

10

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

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

11

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

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

12

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

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

13

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

thrombosis

14

1. When does CAD begin?

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

15

1. What is usually the intial presentation of CAD?

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

16

1. What is the "reasonable approach" to addressing CVD.

early and aggressive risk factor management

17

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

thin cap, large lipid core, increased inflammatory activity