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Biomedical subjects

E Pilger

Publications and source records attributed to E Pilger.

At least 37 records · Page 2Linked to original sources
PubMed2001

Oxidative stress during peripheral angioplasty. Implication for late restenosis?

BACKGROUND: Percutaneous transluminal angioplasty (PTA) is routine treatment for patients with peripheral arterial disease (PAD). The procedure induces local generation of reactive oxygen species (ROS), such as H2O2. Since these have been shown to stimulate vascular smooth muscle cell growth (VSMCG), we investigated peroxide levels in patients with PAD during PTA and related these results to late clinical outcome. METHODS: Thirty patients (17 male, 13 female, 20 Fontain stage II, 10 Fontaine stage IV, median age 68 years) undergoing PTA of a 2-6 cm stenosis of the femoral or popliteal artery were included. The procedure was performed successfully in all patients. At follow-up six months thereafter restenosis was evaluated by duplex sonography. Total peroxide concentrations were determined in plasma drawn before, 6, 24 and 48 hours after the procedure by the Operoxide activityO assay, which is based on the reaction of horseradish peroxidase with plasma peroxides, using tetramethylbenzidine as the chromogenic substrate. RESULTS: The median peroxide level before angioplasty was 280 mmol/L (range 47-549). Levels were higher in patients with advanced disease, in smokers and in patients with diabetes. In response to angioplasty, peroxide levels increased within 48 hours (p<0.001). Six months after the procedure, restenosis was observed in 10/30 (33 percent) of patients. Clinical outcome was not dependent upon baseline or postinterventional peroxide levels. CONCLUSIONS: Elevated peroxide levels are seen in patients with advanced arteriosclerotic disease and in those with diabetes, but are not predictive for late restenosis.

Aged↗
PubMed2001

The PlA1/A2 polymorphism of platelet glycoprotein IIIa is not associated with deep venous thrombosis.

BACKGROUND: Platelet glycoprotein (GP) IIb/IIIa, a fibrinogen and von Willebrand factor binding membrane receptor, has an important role in platelet aggregation. A common leucine33-proline polymorphism (PlA1/A2) of the gene encoding the GP IIIa subunit is associated with platelet reactivity and has been proposed as a risk factor for atherothrombotic disease. The aim of this study was to investigate the role of this polymorphism for deep venous thrombosis (DVT). METHODS: We performed a case-control study including 206 patients with documented DVT and a sex- and age-matched group of 310 control subjects. GP IIIa genotypes were determined by restriction fragment analysis of amplimers containing the polymorphic site. RESULTS: A1/A1, A1/A2 and A2/A2 genotypes were found in 67.0, 31.6 and 1.5 percent of patients and 72.3, 25.8 and 1.9 percent of controls (p=0.35), PlA2 allele frequencies were 0.17 in patients and 0.15 in controls (p=0.92). Odds ratio of the PlA2 allele for DVT was 1.21 (95 percent CI 0.85-1.71, p=0.29) and remained insignificant after adjustment for factor V Leiden and prothrombin 20210A genotypes (1.22, 95 percent CI 0.86-1.75, p=0.27). CONCLUSIONS: Our data suggest that the PlA1/A2 polymorphism of GP IIIa is not associated with DVT.

Adult↗
PubMed2000

Prothrombin G20210A, factor V Leiden, and factor XIII Val34Leu: common mutations of blood coagulation factors and deep vein thrombosis in Austria.

Mutations in the gene for prothrombin (F2 20210A) and factor V (F5 1691A, factor V Leiden) are established risk factors for deep venous thrombosis (DVT). Recently, a mutation in the gene for factor XIII (F13 100T) leading to a Valine-Leucine exchange at amino acid position 34 has been reported to be protective against DVT. To analyze the role of these mutations for DVT in Austria, we analyzed their prevalence in 154 patients with documented DVT and 308 sex- and age-matched control subjects. Allele frequencies of F2 20210A, F5 1691A, and F13 100T were 0.018, 0.039, and 0.274 among controls, and 0.045, 0.120, and 0.211 among patients, respectively. Odds ratios for DVT associated with F2 20210A, F5 1691A, and F13 100T alleles were 2.5 (95% CI: 1.1-5.7), 3.4 (95% CI: 1.9-5.8), and 0.7 (95% CI: 0.5-1.0). We conclude that F2 20210A, F5 1691A, and F13 100T are common mutations in the Austrian population. F2 20210A and F5 1691 increase the risk for DVT, whereas F13 100T is associated with a decreased risk for DVT. Routinely, analysis of these mutations may help to analyze the individual risk for DVT.

Adolescent↗
PubMed2000

C242T polymorphism of the p22 phox gene is not associated with peripheral arterial occlusive disease.

Formation of reactive oxygen metabolites is vital for the microbicidal activity of phagocytes. As an unwanted side effect, these metabolites may contribute to oxidative stress in the vasculature and thus lead to arteriosclerosis. p22 phox, a component of the NADH/NADPH oxidase in phagocytes and vascular smooth muscle cells, is essential for production of reactive oxygen metabolites. Recently, a C/T polymorphism at position 242 of the p22 phox gene has been associated with coronary artery disease (CAD), suggesting a protective effect of the 242 T allele on the vasculature. In the present study, we analysed the relation of this polymorphism to peripheral arterial occlusive disease (PAOD). C242T polymorphism was determined by restriction fragment polymorphism (RFLP) analysis in 324 patients with documented PAOD and 295 control subjects without any known arterial disease. p22 phox 242 T allele frequencies and genotype distributions were not significantly different between patients and controls; the adjusted relative risk associated with the 242 T allele was 1.14 (95% CI 0.84-1.54, P=0.39), assuming an additive effect of the T allele. C242T polymorphism was not associated with the age of patients at the onset of the disease. Our data indicate that C242T polymorphism of the p22 phox gene is not associated with PAOD.

Aged↗
PubMed2000

Pulmonary embolism and intracardiac thrombi--individual therapeutic procedures.

Mobile right heart thrombus is a severe but rare presentation of thromboembolic disease and usually coexists with an already massive pulmonary embolism (PE). But looking at the literature there is no clear consensus on therapeutic management. We therefore tried to find possible therapeutic guidelines and to evaluate an optimal diagnostic procedure looking at three patients who presented at our department with mobile right heart thrombus in the last year. The first patient with a small (diameter = 1 cm) thrombus in the right ventricle and peripheral pulmonary embolism underwent successful thrombolytic therapy without any complications. Patients II and III showed large intracardiac masses, in patient III extending into the superior vena cava, with central PE. These two patients underwent pulmonary arteriotomy. The diagnostic line in each case was transthoracal echocardiography followed by a helix lung CT scan. Only patients with small intracardiac thrombi and thrombotic masses in the peripheral pulmonary arteries but with hemodynamically significant PE should be treated with thrombolytic agents.

Coronary Thrombosis↗
PubMed2000

Osteomyelitis of the spine and abscess formation in the left thigh after stent-graft implantation in the superficial femoral artery.

PURPOSE: To present a rare case of abscess formation around a covered stent in the superficial femoral artery. METHODS AND RESULTS: Two weeks after balloon dilation of a left superficial femoral artery (SFA) occlusion, during which a Hemobahn covered stent had been placed to treat dissection, a 77-year-old nondiabetic male developed intolerable pain and swelling of his left thigh. An abscess had formed around the stent, which was patent; intravenous antibiotic therapy quelled the symptoms, and the patient discontinued his oral antibiotic regimen weeks after discharge. General septicemia ensued. Acute lower limb ischemia and excruciating back pain prompted readmission. The SFA stent-graft occlusion required femoropopliteal bypass; the abscess and spondylodiskitis that had developed in the T12 and L1 vertebrae responded to intravenous antibiotics. The patient is without signs of infection at 6 months. CONCLUSIONS: Local and systemic infections associated with intraluminal prostheses are rare, and prophylactic antibiotic therapy is not commonly employed. Balloon- or device-induced arterial injury may expose the arterial wall to bacterial colonization, suggesting that patients receiving lengthy stents or experiencing arterial injury during angioplasty should receive antibiotics as a precautionary measure.

Abscess↗
PubMed2000

Factor II G20210A and factor V G1691A gene mutations and peripheral arterial occlusive disease.

BACKGROUND: G to A mutations at positions 20210 of the prothrombin gene (F2) and 1691 of the factor V gene (F5) are established risk factors for venous thrombosis. Several factors associated with coagulation and/or fibrinolysis have been associated with arterial occlusive disease, but the role of F2 20210A and F5 1691A for arterial occlusive disease remains unclear. OBJECTIVE: To investigate if F2 20210A and F5 1691A are associated with peripheral arterial occlusive disease (PAOD). METHODS AND RESULTS: We analyzed the prevalence of F2 20210A and F5 1691A alleles in 336 patients with documented PAOD at Fontaine stage II-IV and 300 controls without vascular disease. Allele frequencies in patients and controls were 0.013 and 0.022 for F2 20210A, and 0.042 and 0.045 for F5 1691, respectively, both differences being not statistically significant. CONCLUSION: Our data suggest that mutations F2 G20210A and F5 G1691A are not associated with PAOD.

Aged↗
PubMed1999

Changes in the fibrinolytic system in patients with peripheral arterial occlusive disease undergoing percutaneous transluminal angioplasty.

We have investigated fibrinolytic parameters in 33 patients with peripheral arterial occlusive disease (PAOD) before and 6, 24, and 48 hours after percutaneous transluminal angioplasty (PTA) as well as in 35 gender-matched healthy controls, whose mean age was not significantly different from the mean age of the patients. PAOD patients had significantly higher plasma levels of t-PA antigen (12.0+/-4.9 vs. 9.2+/-5.5 ng/ml), PAI-1 antigen (34.8+/-22.1 vs. 27.2+/-23.6 ng/ml), PAI-1 activity (10.0+/-6.5 vs. 8.0+/-8.0 U/ml), PCI (188.2+/-55.6 vs. 134.1+/-75.5% as compared with normal human plasma), and fibrinogen (420.2+/-92.6 vs. 261.9+/-32.7 mg/dl) as compared with controls. After angioplasty, fibrinolytic parameters and fibrinogen levels increased, reaching higher than preintervention levels 24 and 48 hours after the intervention. Six months after initially successful PTA, restenosis was demonstrated in 14 out of 33 patients (42%). Patients with late restenosis had significantly higher levels of PAI-1 activity 24 and 48 hours after PTA, as compared with patients with late patency (24 hours: 16.1+/-8.0 vs. 10.0+/-7.4; 48 hours: 16.5+/-7.9 vs. 12.0+/-7.0; p<0.05 for both time points). The results suggest that impaired fibrinolysis early after PTA might be a cause or marker of a disturbed repair process of vascular injury, leading to restenosis.

Aged↗
PubMed1998

[Protection against myocardial ischemia by nisoldipine--an experimental study with valinomycin K-sensitive microelectrodes].

It has been shown that dihydropyridines exert a cardioprotective effect during experimental ischemia. This effect is reflected in a reduced K-efflux from the ischemic tissue. Recently we have shown that ischemic K-efflux is largely mediated by ATP-dependent K-channels. Using K-selective microelectrodes we studied the effect of nisoldipine on K-efflux during simulated ischemia (guinea pig papillary muscle immersed in paraffin oil; normal Tyrode solution, HEPES buffered, 100% O2-equilibrated, 37 degrees C). While ischemic K-efflux was Ca-dependent in stimulated preparations, it was independent of extracellular Ca in resting preparations. Our results show that nisoldipine leads to an inhibition of ischemic K-efflux during simulated ischemia. In resting preparations this inhibition is not a direct Ca-antagonistic effect, since withdrawal of extracellular Ca does not inhibit ischemic K-efflux but nisoldipine does. We suggest a direct effect of nisoldipine on the KATP channel which is mainly responsible for ischemic K-loss.

Animals↗