{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,3]],"date-time":"2026-05-03T22:44:21Z","timestamp":1777848261611,"version":"3.51.4"},"reference-count":15,"publisher":"SAGE Publications","issue":"5","license":[{"start":{"date-parts":[[2016,7,10]],"date-time":"2016-07-10T00:00:00Z","timestamp":1468108800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Endovasc Ther"],"published-print":{"date-parts":[[2016,10]]},"abstract":"<jats:p>Purpose: To prospectively investigate the associations of serum cholinesterase (CHE) levels with ischemic outcomes after angioplasty and stenting for lower limb peripheral artery disease (PAD). Methods: A prospective cohort study enrolled 108 patients with Rutherford category 2\u20133 ischemia who had successful primary unilateral angioplasty and self-expanding bare metal stent implantation for superficial femoral artery (SFA) stenosis. The primary endpoint was a composite of nonfatal myocardial infarction, nonfatal stroke or transient ischemic attack, cardiovascular death, or &gt;80% target lesion restenosis within 2 years after peripheral angioplasty. Target lesion restenosis (restenosis endpoint) and the composite of the aforementioned atherothrombotic events (atherothrombotic endpoint) within 2-year follow-up were defined as secondary endpoints. Results: CHE levels were not available in 4 patients due to technical problems and 4 patients were lost to follow-up. The remaining 100 patients (median age 65 years; 62 men) met the minimum sample size requirement for statistical analysis. Median CHE levels were significantly lower in patients who subsequently experienced the primary endpoint compared with patients without ischemic events [7.1 (IQR 6.3\u20138.1) vs 8 (IQR 7\u20139.3) kU\/L, p=0.007]. A CHE level &lt;8.3 kU\/L was identified as the best cutoff value to predict the primary endpoint, providing an 82.1% sensitivity and 44.3% specificity. The primary endpoint occurred significantly more often in patients with low CHE &lt;8.3 kU\/L than in patients with higher CHE levels (32 vs 7 patients, p=0.01). In multivariable Cox regression analysis, low CHE was associated with a 2.6-fold increased risk (95% CI 1.1 to 5.9, p=0.03) of the primary endpoint. Moreover, patients who suffered the secondary restenosis endpoint had significantly lower median CHE levels than patients without restenosis [7.1 (IQR 6.3\u20138.2) vs 7.9 (IQR 7\u20138.9) kU\/L, p=0.02], and restenosis occurred more frequently in patients with low CHE compared with those with higher CHE levels (27 vs 7 patients, p=0.04). Conclusion: Low CHE is associated with an increased risk of long-term adverse ischemic events following SFA angioplasty with stent implantation for PAD.<\/jats:p>","DOI":"10.1177\/1526602816655521","type":"journal-article","created":{"date-parts":[[2016,6,22]],"date-time":"2016-06-22T15:33:50Z","timestamp":1466609630000},"page":"738-743","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":10,"title":["Serum Cholinesterase Levels Are Associated With 2-Year Ischemic Outcomes After Angioplasty and Stenting for Peripheral Artery Disease"],"prefix":"10.1177","volume":"23","author":[{"given":"Thomas","family":"Gremmel","sequence":"first","affiliation":[{"name":"Division of Angiology, Department of Internal Medicine II, Medical University of Vienna, Austria"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Patricia P.","family":"Wadowski","sequence":"additional","affiliation":[{"name":"Division of Angiology, Department of Internal Medicine II, Medical University of Vienna, Austria"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Markus","family":"Mueller","sequence":"additional","affiliation":[{"name":"Division of Angiology, Department of Internal Medicine II, Medical University of Vienna, Austria"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christoph W.","family":"Kopp","sequence":"additional","affiliation":[{"name":"Division of Angiology, Department of Internal Medicine II, Medical University of Vienna, Austria"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Renate","family":"Koppensteiner","sequence":"additional","affiliation":[{"name":"Division of Angiology, Department of Internal Medicine II, Medical University of Vienna, Austria"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Simon","family":"Panzer","sequence":"additional","affiliation":[{"name":"Department of Blood Group Serology and Transfusion Medicine, Medical University of Vienna, Austria"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2016,7,10]]},"reference":[{"key":"bibr1-1526602816655521","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.106.666388"},{"key":"bibr2-1526602816655521","doi-asserted-by":"publisher","DOI":"10.1016\/j.amjcard.2008.01.021"},{"key":"bibr3-1526602816655521","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa043012"},{"key":"bibr4-1526602816655521","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199910283411804"},{"key":"bibr5-1526602816655521","doi-asserted-by":"publisher","DOI":"10.1016\/j.ahj.2005.09.012"},{"key":"bibr6-1526602816655521","doi-asserted-by":"publisher","DOI":"10.1093\/eurheartj\/ehn269"},{"key":"bibr7-1526602816655521","doi-asserted-by":"publisher","DOI":"10.1038\/35067589"},{"key":"bibr8-1526602816655521","doi-asserted-by":"publisher","DOI":"10.2119\/molmed.2013.00139"},{"key":"bibr9-1526602816655521","doi-asserted-by":"publisher","DOI":"10.1093\/eurheartj\/ehp553"},{"key":"bibr10-1526602816655521","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2007.11.077"},{"key":"bibr11-1526602816655521","first-page":"381","volume":"21","author":"den Blaauwen DH","year":"1983","journal-title":"J Clin Chem Clin Biochem"},{"key":"bibr12-1526602816655521","doi-asserted-by":"publisher","DOI":"10.1093\/eurheartj\/ehs164"},{"key":"bibr13-1526602816655521","doi-asserted-by":"publisher","DOI":"10.2119\/molmed.2010.00015"},{"key":"bibr14-1526602816655521","doi-asserted-by":"publisher","DOI":"10.1016\/j.atherosclerosis.2008.12.022"},{"key":"bibr15-1526602816655521","doi-asserted-by":"publisher","DOI":"10.1177\/152660280100800509"}],"container-title":["Journal of Endovascular Therapy"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/journals.sagepub.com\/doi\/pdf\/10.1177\/1526602816655521","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/journals.sagepub.com\/doi\/full-xml\/10.1177\/1526602816655521","content-type":"application\/xml","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/journals.sagepub.com\/doi\/pdf\/10.1177\/1526602816655521","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T21:31:44Z","timestamp":1777498304000},"score":1,"resource":{"primary":{"URL":"https:\/\/journals.sagepub.com\/doi\/10.1177\/1526602816655521"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2016,7,10]]},"references-count":15,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2016,10]]}},"alternative-id":["10.1177\/1526602816655521"],"URL":"https:\/\/doi.org\/10.1177\/1526602816655521","relation":{},"ISSN":["1526-6028","1545-1550"],"issn-type":[{"value":"1526-6028","type":"print"},{"value":"1545-1550","type":"electronic"}],"subject":[],"published":{"date-parts":[[2016,7,10]]}}}