Skip to Main Content

++

Chapter 60. Stent Thrombosis

++
++
++

After percutaneous coronary intervention (PCI) with a drug-eluting stent (DES), what is the incidence of acute and subacute stent thrombosis?

++
++
++

A. Similar to incidence after bare metal stent (BMS)

++
++

B. Higher than incidence after BMS

++
++

C. Lower than incidence after BMS

++
++

D. Higher for first-generation DES than for BMS but lower for second-generation DES than for BMS

+
++

The correct answer is A

++

Early stent thrombosis (ST) is predominantly dictated by procedural considerations (proper deployment and expansion and lack of residual dissection) and adherence to dual antiplatelet therapy and much less by stent type. With proper technique, all devices have a 0.5% to 0.7% rate of early ST.

++
++
++

Contributors to late and very late DES thrombosis include which of the following?

++
++
++

A. Delayed healing and incomplete endothelialization of stent struts

++
++

B. Chronic inflammation related to polymer-releasing drug

++
++

C. Neoatherosclerosis

++
++

D. All of the above

+
++

The correct answer is D

++

Late and very late ST is a complex process involving the interaction between a diseased, nonhealing endothelium (because of the antiproliferative drug), chronic inflammation from the polymer delivering the drug, and even ensuing stent strut fracture. More recently, neoatherosclerosis was added to the list of contributors. It describes a process of accelerated atherosclerosis occurring in the stented segment and leading to plaque rupture similar to that observed in spontaneous myocardial infarction.

++
++
++

In ADAPT-DES, high platelet reactivity after PCI, defined as platelet reactivity units (PRU) >208:

++
++
++

A. Was an independent predictor of mortality at 2 years

++
++

B. Was an independent predictor of definite ST at 2 years

++
++

C. Was an independent predictor of death or ST at 2 years

++
++

D. None of the above

+
++

The correct answer is B

++

ST, definite in particular, is the quintessential platelet-derived adverse event. Thus, it is logical that insufficient platelet inhibition, as measured by high residual platelet reactivity (HPR), will be associated with and predictive of ST. The association of HPR with death is complicated by the higher risk of bleeding in patients without HPR, which may counteract the effect of lack of ST on mortality.

++
++
++

In the Dual Antiplatelet Therapy (DAPT) study, powered for ST as an ...

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.