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Resistance to activated protein C and FV Leiden mutation in patients with a history of acute myocardial infarction or primary hypertension
Affiliation:1. Cardiology Department, 2nd Reg BTC, Haemost Laboratory, “Laikon” General Hospital, Medical School, University of Athens, Athens, Greece;1. Department of Clinical Chemistry, Albert Ludwigs-University, Freiburg, 79106;, Germany;2. Department of Paediatrics, Albert Ludwigs-University, Freiburg, 79106;, Germany;1. Service de médecine interne, CHU, hôpital Général, 3, rue du faubourg Raines, 21033 Dijon cedex, France;2. service de rhumatologie, CHU, hôpital Général, 3, rue du faubourg Raines, 21033 Dijon cedex, France;3. laboratoire de biochimie, hôpital d''enfants, 2, boulevard Maréchal de Lattre-de-Tassigny, 21033 Dijon cedex, France;1. Service d''hématologie biologique, CHU, BP 632, 97261 Fort-de-France, Martinique France;2. service des urgences, CHU, BP 632, 97261 Fort-de-France, Martinique France;1. Service d’Hématologie, Hôpital Pellegrin, Bordeaux, France;2. Chromogenix AB, Mölndal, Sweden.
Abstract:This study was designed to investigate both resistance to activated protein C (APC-R) and the factor FV Q506 mutation incidence in patients with a history of acute myocardial infarction (AMI) and patients with primary hypertension (PH), a high-risk group for arterial thrombosis. Eighty patients with a history of AMI (group A), 160 patients with a history of PH (group B), and 124 age-matched controls without arterial disease (group C) were studied. APC-R was determined using the Coatest APC Resistance Kit of Chromagenix, Sweden. The prevalence of the FV Q506 mutation was estimated by DNA analysis (Bertina method). The prevalence of the FV Q506 mutation was 20%, 13.75%, and 8% in groups A, B, and C, respectively (A v C P = .0466). The prevalence of APC-R was 47.5% in group A v 13% in group C (P < .0001) and 36.25% in group B v 13% in group C (P < .0001). The response to activated protein C expressed as mean value ± SD was 2.05 ± 0.33 in group A v 2.56 ± 0.46 in group C (P < .05) and 2 ± 0.22 in group B v 2.56 ± 0.46 in group C (P < .05). These findings suggest that patients with a history of AMI or PH have a significantly increased incidence of both APC-R and FV Q506 mutation compared with the control group. These findings support the hypothesis that these anticoagulant defects may be risk factors for arterial thrombosis.
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