Treatment options for post-catheterisation femoral pseudoaneurysm closure

Background: Femoral artery pseudoaneurysm (FAP) complicates from 1% to 9% of all coronary angiography procedures and contributes to extended hospitalisation as well as patient discomfort.Aim: To compare three main methods of FAP closure which are used nowadays.Methods: Seventy-five subjects (38 females, 37 males, mean age 60.8±10.4 years) with post-catheterisation FAP were studied. The results of three methods of FAP closure - surgical, local compression and thrombin injection, were compared.Results: Between September 2000 and July 2001, fourteen patients developed FAP; in 9 (64%) patients FAP was closed with repeated prolonged compression whereas the remaining 5 (36%) patients required surgical closure of compression-resistant FAP. We observed that FAPs with longer neck (>10 mm) and primary signs of partial spontaneous coagulation were more prone to self-closure as compared to FAPs with short neck and no signs of perimural coagulation (p=0.01). Since July 2001, we introduced ultrasound-guided thrombin injection into FAP sack. The protocol included attempt of closing FAP with probe compression and compression dressing put overnight, and, if unsuccessful, followed by a quick injection of 2 ml of thrombin solution (400-3200 U), guided by ultrasound. During this period, we identified 61 patients with FAP. Out of this group, 5 (8.2%) subjects were referred for surgery without any attempt of thrombin-injection, in 16 (26.2%) patients FAP was closed with probe compression and dressing put overnight, and in the remaining 40 (65.6%) subjects ultrasound-guided thrombin-injection was performed. Thrombin injection into FAP sack caused closure of its cavity and neck in all patients, however, five patients required additional thrombin injection during the same session, and 2 (5.0%) patients - during the next procedure. No peri-procedural complications were observed. The duration of hospital stay shortened from a mean of 26.6±14.5 days in surgically treated patients to 7.9±6.7 in those in whom FAPs were closed with compression, and to 4.6±2.6 days in those treated with thrombin (

Artykuł oryginalnyZwężenie tętnicy szyjnej wewnętrznej u chorych z degeneracyjną stenozą zastawki aortalnej

Background: In patients with severe degenerative aortic stenosis (DAS) the operative mortality risk is 3% for isolated aortic valve replacement (AVR), but it significantly increases in patients with concomitant coronary artery disease (CAD) and internal carotid artery stenosis (ICAS). Aim: To assess the frequency of ICAS ł50% and factors determining its occurrence in patients with severe calcified DAS referred for AVR. Methods: The study included 104 patients (67 men), aged 63.4±8.4 years, with symptomatic moderate-to-severe DAS (aortic valve areaWstęp: Zwężenie tętnicy szyjnej wewnętrznej (ICAS) u chorych poddawanych operacji wymiany zastawki aortalnej (AVR), niekiedy połączonej z operacją pomostowania aortalno-wieńcowego (CABG), istotnie zwiększa ryzyko okołozabiegowego udaru mózgu. Cel:Celem pracy było określenie częstości występowania ICAS ł50% u chorych kwalifikowanych do AVR z powodu zaawansowanej degeneracyjnej stenozy zastawki aortalnej (DAS). Metodyka: Badaniem objęto 104 chorych (67 mężczyzn) w średnim wieku 63,4±8,4 roku (zakres 47–80 lat) z symptomatyczną zaawansowaną DAS (powierzchnia zastawki aortalne

RAGE and HMGB1 Expression in Orbital Tissue Microenvironment in Graves’ Ophthalmopathy

Graves’ ophthalmopathy (GO) is a chronic autoimmune inflammatory disorder involving orbital tissues. A receptor for advanced glycation end products (RAGE) and its ligand high mobility group box 1 (HMGB1) protein trigger inflammation and cell proliferation and are involved in the pathogenesis of various chronic inflammatory diseases. This study was aimed to evaluate RAGE and HMGB1 expression in GO to determine its potential clinical significance. To the best of our knowledge, this is the first study showing RAGE and HMGB1 expression in orbital tissue using immunohistochemistry. Sections of orbital adipose tissue obtained from patients diagnosed with GO (23 patients; 36 orbits) and normal controls (NC) (15 patients; 15 orbits) were analyzed by immunohistochemistry for RAGE and HMGB1 expression. Expression profiles were then correlated with clinical data of the study group. RAGE and HMGB1 expression were elevated in GO patients in comparison with NC (p=0.001 and p=0.02, respectively). We observed a correlation between RAGE expression and occurrence of dysthyroid optic neuropathy (DON) (p=0.05) and levels of TSH Receptor Antibodies (TRAb) (p=0.01). Overexpression of RAGE and HMGB1 might be associated with GO pathogenesis. In addition, RAGE and HMGB1 proteins may be considered as promising therapeutic targets, but this requires further research

RAGE and HMGB1 Expression in Orbital Tissue Microenvironment in Graves’ Ophthalmopathy

Graves' ophthalmopathy (GO) is a chronic autoimmune inflammatory disorder involving orbital tissues. A receptor for advanced glycation end products (RAGE) and its ligand high mobility group box 1 (HMGB1) protein trigger inflammation and cell proliferation and are involved in the pathogenesis of various chronic inflammatory diseases. This study was aimed to evaluate RAGE and HMGB1 expression in GO to determine its potential clinical significance. To the best of our knowledge, this is the first study showing RAGE and HMGB1 expression in orbital tissue using immunohistochemistry. Sections of orbital adipose tissue obtained from patients diagnosed with GO (23 patients; 36 orbits) and normal controls (NC) (15 patients; 15 orbits) were analyzed by immunohistochemistry for RAGE and HMGB1 expression. Expression profiles were then correlated with clinical data of the study group. RAGE and HMGB1 expression were elevated in GO patients in comparison with NC (p = 0.001 and p = 0.02, respectively). We observed a correlation between RAGE expression and occurrence of dysthyroid optic neuropathy (DON) (p = 0.05) and levels of TSH Receptor Antibodies (TRAb) (p = 0.01). Overexpression of RAGE and HMGB1 might be associated with GO pathogenesis. In addition, RAGE and HMGB1 proteins may be considered as promising therapeutic targets, but this requires further research