Healio
Healio
July 01, 2016
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Low serum cholinesterase increases adverse ischemic event risk after angioplasty, stenting for PAD

Low levels of serum cholinesterase may be a risk factor for ischemic events in patients with peripheral artery disease undergoing endovascular intervention.

Researchers conducted a recent prospective cohort study of 108 patients (median age, 65 years; 62 men) with stenosis of the superficial femoral artery (SFA) and intermittent claudication designated as Rutherford category 2 or 3. All patients underwent successful primary unilateral angioplasty and bare-metal stent implantation for treatment of SFA stenosis from 2008 to 2010. Self-expanding BMS used included Absolute (Abbott Vascular), Astron Pulsar (Biotronik), Epic (Boston Scientific), Protégé Everflex (Medtronic/Covidien) and Smart (Cordis Corporation). Patients also received daily aspirin 100 mg and clopidogrel 75 mg for 3 months.

Blood was drawn from all patients 1 day after stenting and serum cholinesterase levels were evaluated. The median serum cholinesterase level was 7.5 kU/L (interquartile range: 6.7-8.6).

Overall, four patients were lost to follow-up and four patients did not have available serum cholinesterase levels.

The primary composite endpoint comprised nonfatal MI, nonfatal stroke/transient ischemic attack, CV death or > 80% target lesion restenosis within 2 years following peripheral angioplasty. The primary composite endpoint occurred in 39 of 100 patients, with two nonfatal MIs, three ischemic strokes/TIAs and 34 with > 80% restenosis (29 patients underwent target lesion revascularization), according to data published in the Journal of Endovascular Therapy.

The secondary endpoints of target lesion restenosis > 80% occurred in 34 patients and the first occurrence of nonfatal MI, nonfatal stroke/TIA or CV death occurred in seven patients within 2 years, including three nonfatal MIs, three nonfatal strokes/TIAs and one CV death.

The researchers observed no stent fractures during the 2-year follow-up.

Patients in whom the primary endpoint occurred had significantly lower median serum cholinesterase levels vs. those in whom the endpoint did not occur (7.1 kU/L vs. 8 kU/L; P = .007).

The researchers identified a serum cholinesterase level < 8.3 kU/L as the optimal cutoff value for predicting the primary endpoint. This cutoff level yielded a sensitivity of 82.1% and a specificity of 44.3%. Based on this cutoff value, 66 of 100 patients were classified as having low serum cholinesterase (< 8.3 kU/L). Those with low serum cholinesterase had a significantly higher incidence of the primary endpoint compared with those with higher levels (32 vs. seven patients; P = .01). Further, low serum cholinesterase was associated with a 2.6-fold increase risk for the primary endpoint.

The association between low serum cholinesterase and the primary endpoint persisted after adjustment for age, hypercholesterolemia and proton pump inhibitor use.

Patients with restenosis greater than 80% during 2 years had significantly lower median serum cholinesterase levels vs. patients with no restenosis (7.1 kU/L vs. 7.9 kU/L; P = .02). Additionally, the secondary restenosis endpoint was more prevalent in patients with low serum cholinesterase vs. those with higher levels (27 patients vs. seven patients; P = .04).

“Low [serum cholinesterase] is associated with an increased risk of long-term adverse ischemic events following SFA angioplasty with stent implantation for PAD,” the researchers wrote. “Adding [serum cholinesterase] to established risk factors for adverse outcomes in PAD may improve risk prediction and help to more specifically identify high-risk patients who benefit from intensified treatment regimens.” – by Jennifer Byrne
Disclosure: The researchers report no relevant financial disclosures.

Sources/Disclosures

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Source:

Gremmel T, et al. J Endovasc Ther. 2016;doi:10.1177/1526602816655521.