Inflammation and Arterial Injury Flashcards

1
Q

What is the main concern with drug-eluting stents (DES) in relation to late stent thrombosis?

A

DES can elicit a chronic inflammatory response even after the drug has fully eluted

This reaction is generally localized and hypothesized to be associated with an increased risk of very late stent thrombosis.

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2
Q

What is a significant difference between ticagrelor and clopidogrel?

A

Ticagrelor is a more potent platelet P2Y12 receptor antagonist than clopidogrel

In the PLATO trial, cardiovascular events were decreased with ticagrelor compared to clopidogrel among patients with ACS.

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3
Q

What does the figure demonstrate regarding vasoconstriction with different stent types?

A

Significantly more proximal and distal vasoconstriction with PES and SES vs. BMS

This suggests a chronic inflammatory response to permanent polymer.

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4
Q

What is the main outcome of the seminal meta-analysis of randomized controlled trials regarding CoCr EES?

A

Dramatically reduced rates of definite stent thrombosis at all time points compared to BMS

No other tested DES had lower definite stent thrombosis than BMS at 2-year follow-up.

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5
Q

What role do polymers play in drug-eluting stents (DES)?

A

Polymers modulate the elution characteristics of the drug on DES

They do not have an independent positive effect on neoatherosclerosis or in-stent restenosis rates.

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6
Q

What are the phases of the healing response after coronary stenting?

A

Phase I: de-endothelialization, Phase II: release of growth factors, Phase III: migration of smooth muscle cells and re-endothelialization

This process involves acute inflammatory cells and chronic inflammatory cells.

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7
Q

How do Paclitaxel and Sirolimus affect neointimal hyperplasia?

A

They decrease the amount of neointimal hyperplasia compared to BMS

However, the underlying polymer has no favorable effect on the healing process.

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8
Q

What are the factors that may increase inflammation and restenosis after stenting?

A

(a) certain polymers/drugs, (b) stent strut thickness, (c) medial injury or lipid core penetration

Deployment of stents in fibrous plaque can reduce inflammation.

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9
Q

What adverse effects can high-dose Paclitaxel have?

A

Augmented inflammatory response compared to polymer alone

Adverse events related to chronic inflammation and delayed healing were noted with the QuaDS QP-2 stent.

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10
Q

What is the primary systemic marker of inflammation studied in relation to PCI?

A

CRP (C-reactive protein)

The magnitude of pre-and post-PCI levels of CRP has been associated with adverse events after stenting.

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11
Q

What has been observed regarding the rates of stent thrombosis in newer generation metallic DES?

A

Progressively decreasing rates of both early and late stent thrombosis compared to early-generation counterparts

This is attributed to thinner struts and better materials.

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12
Q

True or False: Late acquired incomplete stent apposition is more common after BMS than DES.

A

False

Incomplete stent apposition is more common after DES.

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13
Q

What cytokine is primarily responsible for stimulating CRP production?

A

IL-6

IL-6 is produced by macrophages and is the main hepatic stimulus for CRP production.

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14
Q

Fill in the blank: The major cause of DES thrombosis is _______.

A

early cessation of DAPT

Rare hypersensitivity reactions can also occur post-implantation.

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15
Q

What is the impact of statin therapy prior to PCI?

A

Statin therapy seems to have the most benefit among patients with the highest level of pre-PCI inflammation

Atorvastatin, clopidogrel, and abciximab may blunt the inflammatory response after PCI.

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16
Q

What does flow-mediated dilation of the brachial artery reflect?

A

Systemic endothelial dysfunction

Abnormal endothelial function can be seen over 6 months after DES placement.

17
Q

What is the relationship between systemic cytokine rise and restenosis in the DES era?

A

No difference in systemic cytokine rise has been confirmed between DES and BMS

Local drug delivery likely suppresses inflammation and smooth muscle cell migration despite similar systemic responses.

18
Q

What occurs during cardiogenic shock according to newer evidence?

A

A systemic inflammatory response leading to nitric oxide synthase overproduction

This results in inappropriate vasodilation and refractory hypotension.

19
Q

What medications may blunt the inflammatory response after PCI?

A

Atorvastatin, clopidogrel, and abciximab

These medications may have a beneficial impact on PCI by reducing inflammation.

20
Q

What effect did abciximab have on CRP and IL-6 levels after PCI in the EPIC trial?

A

Blunted the rise of CRP and IL-6

This effect was observed in a subset of patients.

21
Q

How does clopidogrel affect patients with high CRP levels undergoing PCI?

A

Attenuates the increased risk associated with PCI

This suggests a protective role in high-risk patients.

22
Q

In which patients does statin therapy prior to PCI seem to have the most benefit?

A

Patients with the highest level of pre-PCI inflammation

This indicates that inflammation may influence the effectiveness of statins.

23
Q

Do systemic medications clearly impact long-term healing such as stent restenosis?

A

No

However, local applications of statin drugs may be promising for inflammation and smooth muscle cell migration.

24
Q

What factors have been proposed for increased stent thrombosis rates with bioresorbable scaffolds?

A

Thicker strut sizes, poorer radial strength, visualized intraluminal masses

These may represent early thrombi or late malapposed struts.

25
Q

What has been observed in follow-up studies from the ABSORB trials regarding bioabsorbable vascular scaffolds?

A

No residual struts seen at 5 years

Dilation improved but did not return completely to normal compared to adjacent undiseased segments.

26
Q

What did intravascular imaging reveal over areas of prior bioabsorbable vascular scaffolds?

A

Thick capped neointima

This finding indicates potential changes in the vascular structure post-implantation.

27
Q

What is the effect of GP IIb/IIIa inhibitors on platelet aggregation?

A

Decrease platelet aggregation and periprocedural myonecrosis

This is an important aspect of their function in PCI.

28
Q

What does the EPIC trial suggest about abciximab compared to heparin alone?

A

Decreased the rise of CRP and IL-6

This highlights its potential anti-inflammatory effects.

29
Q

What is the significance of the TARGET trial regarding tirofiban?

A

Inferiority of tirofiban compared to abciximab

This may relate to inadequate dosing and lack of anti-inflammatory effects.

30
Q

Have GP IIb/IIIa inhibitors been shown to prevent intimal hyperplasia and in-stent restenosis?

A

No

This raises questions about their long-term efficacy in preventing these conditions.