Balkan Journal of Medical Genetics

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

CASE REPORT

A 41-year-old Caucasian male, smoker (20 cigarettes daily for 20 years), was admitted 2 weeks after an episode of persistent sharp chest pain, fever and fatigue, which occurred soon after slow pathway radiofrequency ablation of the AV, performed because of arrhythmia. There was no family history of thrombosis but no investigation for family thrombophilia was performed. He was afebrile, with a heart rate of 80 beats·min-1, blood pressure 140/90 mmHg, and a respiratory rate of 18 breaths·min-1. Routine laboratory findings were within normal ranges. Arterial blood gas analysis showed hypoxemia with signs of hyperventilation – PaO2: 9.2 kPa (standard value 11.28-12.18 kPa), Pa- CO2: 4.5 kPa, saturated oxygen: 95%, pH: 7.47. An electrocardiogram gave normal results. Standard postero- anterior chest X-ray showed obtuse right costophrenic angle and laminar atelectasis in the right lower lung lobe (Figure 1). D-dimer level, measured by the immunoturbidometric method (Dade-Behring, Deerfield, IL, USA), was 261 μg·L-1 (normal <250 μg·L-1). A perfusion lung scan showed massive bilateral defects in middle and lower parts of the right lung and segmental defects in basal part of the left lung, which did not correlate with the changes in the chest X-ray (Figure 2). The ventilation scan was not available. Doppler ultrasonography of the lower limb veins gave negative results for deep venous thrombosis (DVT). Computed tomography showed a thrombotic mass (12 mm diameter) in the pulmonary artery. Echocardiography showed increased mean blood pressure in the right ventricle (27mmHg). Blood tests for antinuclear antibodies (ANA), antineutrophil cytoplasmic antibodies (ANCA) and antiphospholipid antibodies were negative and the level of anticardiolipin antibodies was not elevated. Sputum smear was negative for pathogenic agents including Mycobacteria. Hematological investigation revealed normal activities of protein C, protein S and antithrombin III. DNA analyses for FV Leiden, FII G20210A and MTHFR C677T mutations were performed by polymerase chain reaction (PCR) as previously described [5,6] at the Institute of Molecular Genetics and Bioengineering, Belgrade, Serbia. The PCR analyses for FV Leiden and MTHFR C677T were positive, and both indicated heterozygotes. Therapy started with intravenous heparin, followed by warfarin, keeping the international rate (INR) of prothrombin time in therapeutic range, i.e., INR = 2-3. The lifelong oral anticoagulant treatment was recommended. The patient’s clinical state gradually improved, disease outcome was favorable and computed tomography showed no thrombotic mass in the pulmonary artery after 3 months. During a 2-year follow-up, he had no new thrombotic episodes.

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