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
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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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