Atherosclerosis

Question 1

Atherosclerosis

Answer 1

It is the lipid laden deposits in the large and medium sized arteries in the tunica intima

Question 2

Where do you see atherosclerosis

Answer 2

Thoracic and abdominal aorta, coronary arteries, peripheral arteries and carotid arteries

Interestingly internal mammary (thoracic) artery is protected from it

Question 3

Pathogenesis

Answer 3

1. Chronic endothelial cell injury
2. Accumulation of LDLs
3. Modification of lesional lipoproteins by oxidation
4. Adhesion and migration of blood monocytes into the lesion, transformation into foam cells
5. Adhesion of platelets
6. Release of cytokines and growth factors, movement of smooth muscle into the intima
7. Smooth muscle cells proliferate and produce extracellular matrix
8. Enhanced accumulation of lipids

Question 4

What is a C reactive protein a measure of in terms of atherosclerosis

Answer 4

It is a measure of vascular inflammation.

It is only a marker of vascular disease and does not play a direct role in vascular inflammation

Question 5

Natural history of atherosclerosis

Answer 5

It can be divided into 2 phases, pre clinical and clinical phase

1. Preclinical starts with blood vessels that have lesion prone areas, accelerating risk factors can cause fibrofatty plaque deposition in these regions.

This leads to the formation of vulnerable plaque that mediates the clinical phase. It is important to know that the vulnerable plaque is still in the preclinical phase

2. So 3 things can happen to a vulnerable plaque leasion: there can be progressive plaque formation which can lead to occlusion of the vessel and cause ischemia downstream, there can be ANEURYSM due to MURAL THROMBOSIS or EMBOLIZATION which can lead to rupture of the wall of the vessel and finally there can be OCCLUSION by THROMBOSIS

Question 6

Details of the AHA classifications

Answer 6

1. Early on there can be plaque formation which is asymptomatic
2. Plaque formation can be occluded by thrombosis which can cause an acute MI, unstable Angina or sudden cardiac death
3. If it doesnt get occluded by a thrombosis the plaque can continue to grow causing Angina pectroris

Question 7

Risks of A by coronoary angiography

Answer 7

The progression and risks of A are often underestimated by coronary angiography.

It is important to know why since the lumen narrowing is a late phenomena and angiography can check for the thickening of the vessel

Question 8

Where are occlusions and aneurysms common

Answer 8

In the coronory artery occlusions are common whereas in the aorta aneurysms are common. Usually aneurysms are not seen in the coronary artery

Question 9

What is the difference between stable and vulnerable plaque

Answer 9

Stable plaque has a small lipid core with a thick fibrous core whereas a vulnerable plaque has a small fibrous layer and a thick lipid core.

The stable plaque has a narrow lumen but it has a better clinical prognosis as the thin fibrous cap on the vulnerable plaque is the one that gets damaged and causes rupture of the plaque

Question 10

Grading of a plaque

Answer 10

Depends on the lumen

Question 11

How do you image plaques

Answer 11

1. Angioplasty can only assess the lumen of a vessel
2. Ultrasound can be used to assess for the lipid content, data received from the ultrasound is used to develop a virtual histology of the wall of the vessel, it can also look for the calcification
3. Optical Coherence Tomogrpahy is good for checking for the lipid content in a vessel, short is OTC

Question 12

Patients with MI, how does thier vessels look like with angiogrpahy

Answer 12

Patients who have had acute MI, the plaques that rupture leading to atherosclerosis are not the ones that show stenosis in angiography

In other words, the tightest stenosis usually are less likely to cause MI

Question 13

Mechanisms by which inflammation can lead to occlusion

Answer 13

Question 14

Pathogenesis of thrombosis

Answer 14

It is called the virchow’s triad:

1. Increased coagubility of the blood
2. Alteration in the blood flow, causing turbulent flow, it is called rheology
3. There can be injury to endothelium, which can be chronic or acute

Question 15

How does rheology explain the location of plaque formation in the peripheral areas such as the carotids

Answer 15

At the site of bifrication of the carotids (division) there are sites of lower shear stress due to turbulent flow which can cause increased endothelial injury at the sites and this is most often the place where plaques form.

This only explains some of the places where plaque formaiton occur most frequently, it doesnt explain why in some places the plaque doesnt form

Question 16

What are some of the things that are common in aorta

Answer 16

1. Occlusion is rare, due to its size
2. Plaque formation is common, embolizations is common that can travel to the periphery and causes for example gangerene

These are usually silent manifestation

Question 17

Answer 17

Lines of Zanes, thrombosis, healing, thrombosis, healing

Question 18

How do you check for atherosclerotic embolism

Answer 18

If you see cholestrol crystals in the center of the lumen of the vessel then they probably came from upstream, cholestrol clefts dont form in the center of the lumen, they form at the edges but they can get dislodged and travel downstream

Question 19

Aortic aneurysm

Answer 19

1. These usually form at the abdomen and they do pulsate
2. Risk of rupture is directly related to the size of the vessel, usually 5 cm of a diameter is a good cut off when intervention is required
3. Operative risk is low if they dont rupture

Question 20

Claudification

Answer 20

Plaque progression in the peripheral arteries can lead to cramping pain in the peripheral parts of the body during exertion due to occlusion of the vessel. This phenomena is called claudification

Question 21

Answer 21

This is something that can be seen in the test and it is important to know that these kind of lesions are not a plaque progression problems but embolism problem and can be a marker for aortic embolism

Question 22

Answer 22

These are not cholestrol clefts but this is Recanalization where after oclusion of the vessel small vessels form within the artery to deliver blood, these vessels form by angiogenesis