Analysis of ADAPT-DES registry grades risk of stent thrombosis after PCI

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An analysis of data from the ADAPT-DES registry, published in JACC: Cardiovascular Interventions, indicates that rates of stent thrombosis after percutaneous coronary intervention (PCI) are highest among myocardial infarction (MI) patients, and lowest among those with stable ischaemic heart disease.

The study, authored by Katherine Chau (Columbia University Irving Medical Center/NewYork-Presbyterian Hospital, New York, USA) and colleagues, sought to determine the risk period for increased stent thrombosis after PCI in patients with acute coronary syndromes (ACS) and whether this increased risk is related to high platelet reactivity.

Writing in the study’s introduction, Chau and colleagues note that stent thrombosis is an infrequent but clinically important complication of PCI, associated with high rates of MI and death. Patients presenting with ACS have an increased risk for stent thrombosis after PCI with drug-eluting stents (DES) compared to patients presenting with stable ischaemic heart disease, they note. This is thought to be due, at least in part, to a more acute prothrombotic state, and previous studies have shown a correlation between high platelet reactivity and stent thrombosis.

Heightened platelet reactivity is frequently present in patients with ACS and in part underlies the rationale for the use of more potent antiplatelet therapies (and for a longer duration) in such patients, the study’s authors suggest. They acknowledge that current guidelines recommend dual-antiplatelet therapy (DAPT) with a potent P2Y12 receptor inhibitor and aspirin for one year post-PCI in patients presenting with ACS, noting that there is uncertainty whether the increase in the risk for stent thrombosis after PCI in patients presenting with ACS continues throughout this period.

Using data from the ADAPT-DES (Assessment of dual antiplatelet therapy with drug-eluting stents) registry, Chau and colleagues compared stent thrombosis rates during two-year follow-up post-PCI with drug-eluting stents among patients presenting with ACS—either MI or unstable angina—or stable ischaemic heart disease. Analysis was done at 30 days and one year post-PCI.

The analysis included data from a total of 8,582 patients (mean age: 63.6±10.9 years, 25.9% female), enrolled after successful drug-eluting stent placement between January 2008 and September 2010. Of these, 2,063 presented with MI, 2,370 with unstable angina, and 4,149 with stable ischaemic heart disease.

Ajay J Kirtane was a contributing author on the study

The study team reports that the incidence rate of high platelet reactivity was 48%, 43.3%, and 39.8%, in the respective groups (p<0.001), adding that within the first 30 days post-PCI, patients presenting with MI had an increased risk of stent thrombosis compared to patients with stable ischaemic heart disease (hazard ratio [HR]: 4.52; 95% confidence interval [CI]: 2.01‒10.14; p<0.001).

After 30 days, they add, relative stent thrombosis risks were progressively lower and no longer significant between groups (31 days to one year post-PCI: HR: 1.97; 95% CI: 0.80‒4.85; >one year post-PCI: HR: 0.89; 95% CI: 0.27‒2.92). The elevated stent thrombosis risk in patients with MI within 30 days was largely confined to those with high platelet reactivity  on clopidogrel (HR: 5.77; 95% CI: 2.13‒15.63; p<0.001).

The authors suggest that the present study is the first to look at the risk for stent thrombosis after PCI in different time periods as a function of high platelet reactivity and acuity of presentation. Key findings, they suggest, include the presence of a gradient of stent thrombosis risk during two-year follow-up after PCI, according to the initial acuity of clinical presentation.

The increased risk for stent thrombosis in patients with ACS, they add, was greatest in the first 30 days after PCI, and this increased risk for early stent thrombosis was largely confined to patients with increased high platelet reactivity on clopidogrel.

“The monotonic increase in stent thrombosis  risk from non-ACS [stable ischemic heart disease] to UA [unstable angina] to NSTEMI [non-ST-segment elevation MI] to STEMI [ST-segment elevation MI] in the present study is striking and is concordant with lower levels of platelet inhibition to clopidogrel along this continuum of risk,” Chau and colleagues write.

They go on to state: “In addition, the finding that the increased ST risk was evident primarily within the first 30 days after PCI is notable, further emphasising the therapeutic importance of higher potency P2Y12 inhibition in the subacute phase after PCI in ACS. The potential for safely reducing the intensity of DAPT beyond this initial high-risk period (as might be inferred from the present study) is consistent with recent reports.”

Furthermore, they add, data from trials enrolling patients at high bleeding risk have suggested that shorter durations—one or three months—of DAPT may be safe. The data, the study’s authors suggest, are mechanistically supportive of recent trends in de-escalating the duration or intensity of DAPT after 30 days, particularly in those without MI, but also support large-scale randomised trials examining the safety and effectiveness of this practice in MI.


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