PULMONARY THROMBOEMBOLISM FOLLOWING RADIOFREQUENCY ABLATION OF THE ATRIOVENTRICULAR NODE IN A PATIENT HETEROZYGOUS FOR THE FACTOR V LEIDEN AND THE MTHFR C677T MUTATIONS
Pešut DP1,2*, Raljević SV2, Kontić MDj2, Božić DZ2, Buha IB2, Stević RS1,3
*Corresponding Author: Dragica P. Pešut, School of Medicine University of Belgrade; Clinical Centre of Serbia, Institute of Lung Diseases and Tuberculosis, Research and Epidemiology Department, 11000 Belgrade, Visegradska 26/20, Serbia; Tel.: +381-11-361-5561; Fax: +381-11-268-1591; E-mail: dragica. pesut@gmail.com
page: 51

INTRODUCTION

Pulmonary thromboembolism (PTE) is a worldwide problem, particularly in people with known risk factors. The multifactorial nature of PTE necessitates identification of predisposing genetic and environmental risk factors in the patients [1]. Virchow’s classic triad of risk-stasis, venous injury, and hypercoagulability- reflects the influence of genetic and environmental risk factors and their interactions [2]. Factor V (FV), Leiden, prothrombin mutation G20210A, deficiency in protein C, protein S, or antithrombin, hyperhomocysteinemia and plasminogen/ fibrinolysis disorders are the most common genetic risk factors for thrombophilia [3]. Factor V Leiden, which causes resistance to activated protein C, is the most common and is caused by a single point mutation (ARG506 to GLN) in the FV gene [4]. This is only found in Caucasians, the prevalence varying between countries. It is associated with a 5-10-fold increased risk of thrombosis and is found in 20.0-60.0% of Caucasian patients with thrombosis [4] and is present in approximately 5.0% of the general population of European origin [2]. We here report on PTE as a rare major complication of a surgical procedure performed on a patient treated for arrhythmia.



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