{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,26]],"date-time":"2026-02-26T01:18:39Z","timestamp":1772068719981,"version":"3.50.1"},"reference-count":38,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2010,10,29]],"date-time":"2010-10-29T00:00:00Z","timestamp":1288310400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cardiovasc electrophysiol"],"published-print":{"date-parts":[[2010,11]]},"abstract":"<jats:p> <jats:bold>The P\u2010Selectin Gene Polymorphism Val168Met.<\/jats:bold>\u2002<jats:italic>Aims:<\/jats:italic> Ventricular fibrillation (VF) in the setting of acute myocardial infarction (AMI) is the leading cause of sudden cardiac death (SCD). Family history of SCD is described as risk factor for primary VF during acute AMI. Genetic factors may be associated with primary VF. We examined polymorphisms in genes related to the activation and adhesion of blood platelets in patients with and without VF in the setting of AMI and among healthy controls.<\/jats:p><jats:p> <jats:italic>Methods:<\/jats:italic> Two hundred and forty patients with a history of AMI and 475 healthy controls were studied. Seventy\u2010three patients (30%) had primary VF during AMI. By using PCR techniques with sequence\u2010specific primers (PCR\u2010SSP), we genotyped 5 single nucleotide polymorphisms (SNPs) in P\u2010selectin (<jats:italic>SELP<\/jats:italic>) (V168M, S290N, N592D, V599L, T715P), 2 SNPs (M62I, S273F) in P\u2010selectin glycoprotein ligand\u20101 (<jats:italic>SELPLG<\/jats:italic>), 5 SNPs in <jats:italic>CD40LG<\/jats:italic> (\u22123459A&gt;G, \u2212122A&gt;C, \u2212123A&gt;C, 148T&gt;C, intr4\u201313T&gt;C), the H558R SNP in <jats:italic>SCN5A<\/jats:italic>, and rs2106261 in <jats:italic>ZFHX3<\/jats:italic>. In addition, length polymorphisms in <jats:italic>SELPLG<\/jats:italic> (36bp\u2010tandem repeat) and <jats:italic>CD40LG<\/jats:italic> (CA\u2010repeat) were genotyped by PCR methods. Results were evaluated by 2\u2010sided <jats:italic>t<\/jats:italic>\u2010tests, chi\u2010square tests, and logistic regression analysis.<\/jats:p><jats:p> <jats:italic>Results:<\/jats:italic> None of the gene polymorphisms showed significant differences between AMI patients and healthy controls. Among patients with a history of VF, however, the <jats:italic>SELP<\/jats:italic> 168M variant showed a significantly higher prevalence (14\/73 patients; 19.2%) as compared with patients without VF (13\/167 patients; 7.8%; P &lt; 0.01). This association remained significant in a logistic regression analysis after adjustment for age and gender (P = 0.013; odds ratio 2.8; 95% confidence interval 1.2\u20136.3).<\/jats:p><jats:p> <jats:italic>Conclusions:<\/jats:italic> This is the first description of an association of the <jats:italic>SELP<\/jats:italic> gene variant 168M with primary VF during acute MI. This variant may be a candidate polymorphism for evaluating the susceptibility for VF in the setting of acute MI. <jats:italic>(J Cardiovasc Electrophysiol, Vol. 21, pp. 1260\u20101265, November 2010)<\/jats:italic><\/jats:p>","DOI":"10.1111\/j.1540-8167.2010.01833.x","type":"journal-article","created":{"date-parts":[[2010,6,25]],"date-time":"2010-06-25T15:32:06Z","timestamp":1277479926000},"page":"1260-1265","source":"Crossref","is-referenced-by-count":12,"title":["The P\u2010Selectin Gene Polymorphism Val168Met: A Novel Risk Marker for the Occurrence of Primary Ventricular Fibrillation During Acute Myocardial Infarction"],"prefix":"10.1111","volume":"21","author":[{"given":"ELIF","family":"ELMAS","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"PETER","family":"BUGERT","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"TATJANA","family":"POPP","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"SIEGFRIED","family":"LANG","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"CHRISTEL","family":"WEISS","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"MICHAEL","family":"BEHNES","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"MARTIN","family":"BORGGREFE","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"THORSTEN","family":"K\u00c4LSCH","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2010,10,29]]},"reference":[{"key":"e_1_2_6_2_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1540-8167.2008.01419.x"},{"key":"e_1_2_6_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2006.07.010"},{"key":"e_1_2_6_4_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.103.20.2447"},{"key":"e_1_2_6_5_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.103.19.2361"},{"key":"e_1_2_6_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/0735-1097(91)90805-J"},{"key":"e_1_2_6_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ijcard.2005.03.047"},{"key":"e_1_2_6_8_2","doi-asserted-by":"publisher","DOI":"10.1002\/clc.4960290408"},{"key":"e_1_2_6_9_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.90.1.139"},{"key":"e_1_2_6_10_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9149(83)80103-9"},{"key":"e_1_2_6_11_2","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/28.8.1263"},{"key":"e_1_2_6_12_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.102.17.2045"},{"key":"e_1_2_6_13_2","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-199512010-00030"},{"key":"e_1_2_6_14_2","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/7.8.1277"},{"key":"e_1_2_6_15_2","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/11.17.2015"},{"key":"e_1_2_6_16_2","doi-asserted-by":"publisher","DOI":"10.1515\/CCLM.2004.202"},{"key":"e_1_2_6_17_2","doi-asserted-by":"publisher","DOI":"10.1136\/heart.84.5.548"},{"key":"e_1_2_6_18_2","doi-asserted-by":"publisher","DOI":"10.1161\/hq1001.097022"},{"key":"e_1_2_6_19_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V97.10.3306"},{"key":"e_1_2_6_20_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2141.2001.03151.x"},{"key":"e_1_2_6_21_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1529-8817.2003.00053.x"},{"key":"e_1_2_6_22_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.hrthm.2004.07.013"},{"key":"e_1_2_6_23_2","doi-asserted-by":"publisher","DOI":"10.1038\/ng.416"},{"key":"e_1_2_6_24_2","doi-asserted-by":"publisher","DOI":"10.1007\/s00109-003-0459-2"},{"key":"e_1_2_6_25_2","doi-asserted-by":"crossref","first-page":"573","DOI":"10.1160\/TH06-12-0730","article-title":"The risk for thromboembolic disease in lupus anticoagulant patients due to pathways involving P\u2010selectin and CD154","volume":"97","author":"Bugert P","year":"2007","journal-title":"Thromb Haemost"},{"key":"e_1_2_6_26_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI200316879"},{"key":"e_1_2_6_27_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.27.16160"},{"key":"e_1_2_6_28_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000129773.70647.94"},{"key":"e_1_2_6_29_2","doi-asserted-by":"publisher","DOI":"10.1097\/00001721-199710000-00002"},{"key":"e_1_2_6_30_2","first-page":"515","article-title":"Soluble form of P\u2010selectin in patients with acute myocardial infarction","volume":"5","author":"Ikeda H","year":"1994","journal-title":"Coron Artery Dis"},{"key":"e_1_2_6_31_2","first-page":"952","article-title":"Increase in the adhesion molecule P\u2010selectin in endothelium overlying atherosclerotic plaques. 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