X

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Georg Thieme Verlag KG  (11)
  • Schillinger, Martin  (11)
  • 1
    Online Resource
    Online Resource
    E-Selectin and restenosis after femoropopliteal angioplasty: prognostic impact of the Ser128Arg genotype and plasma levels
    Georg Thieme Verlag KG ; 2004
    In:  Thrombosis and Haemostasis Vol. 91, No. 01 ( 2004), p. 171-179
    Details
    In: Thrombosis and Haemostasis, Georg Thieme Verlag KG, Vol. 91, No. 01 ( 2004), p. 171-179
    Abstract: Perivascular inflammation plays a key role in the development of restenosis after percutaneous transluminal angioplasty (PTA).The adherence of leucocytes to the activated endothelium, an essential feature in the restenotic process, is mediated by the cellular adhesion molecule E-Selectin. A DNA polymorphism in the regulator region of E-Selectin at codon 561 (Ser128Arg) is suggested to modulate the molecule’s physiological effects. Therefore, we investigated the association between the E-Selectin Ser128Arg genotype, E-Selectin plasma levels and restenosis after femoropopliteal PTA. We prospectively studied 175 consecutive patients with peripheral artery disease and intermittent claudication (n=126) or critical limb ischemia (n=49) who underwent primary successful femoropopliteal balloon angioplasty. E-Selectin Ser128Arg genotype and baseline E-Selectin plasma levels were determined and patients were followed up for median 12 months (IQR 11 to 14, total range 6 to 24) for the occurrence of postangioplasty restenosis (≥50%). E-Selectin plasma levels in homozygous Arg128Arg and heterozygous Ser128Arg patients were significantly higher compared to wildtype Ser128Ser patients (p=0.041). Patency rates for wildtype Ser128Ser, heterozygous Ser128Arg and homozygous Ser128Ser patients were 57%, 44% and 50% at 6 months, and 46%, 40% and 17%, at 12 months, respectively (Log Rank p=0.31). Patency rates for increasing tertiles of E-Selectin were 61%, 58% and 37% at 6 months, and 54%, 45% and 30% at 12 months, respectively (Log Rank p=0.020). Patients with an E-Selectin plasma level above 44.9 mg/dL (third tertile) had an 1.9-fold increased adjusted risk for restenosis (95% CI 1.09 to 3.30). E-Selectin plasma levels are modulated by the E-Selectin Ser128Arg genotype, and predict the risk for restenosis after PTA in patients with PAD. A direct association of the Ser128Arg polymorphism with late postangioplasty failure could not be demonstrated.
    Type of Medium: Online Resource
    ISSN: 0340-6245 , 2567-689X
    URL: Article
    DOI: 10.1160/TH03-06-0402
    Language: English
    Publisher: Georg Thieme Verlag KG
    Publication Date: 2004
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 2
    Online Resource
    Online Resource
    The impact of selectins on mortality in stable carotid atherosclerosis
    Georg Thieme Verlag KG ; 2015
    In:  Thrombosis and Haemostasis Vol. 114, No. 09 ( 2015), p. 632-638
    Details
    In: Thrombosis and Haemostasis, Georg Thieme Verlag KG, Vol. 114, No. 09 ( 2015), p. 632-638
    Abstract: Cellular adhesion molecules also known as selectins promote recruitment of inflammatory cells into the arterial wall where they interact with lipid particles leading subsequently to plaque formation. The intercellular adhesion molecule-1 (ICAM-1), the vascular cell adhesion molecule-1 (VCAM-1) and the endothelial-leukocyte adhesion molecule 1 (ELAM-1) also known as E-selectin mediate the attachment of leukocytes and have been implicated in the destabilisation of atherosclerotic plaques. Therefore, we hypothesised that plasma selectin levels are associated with adverse clinical outcome. We prospectively studied 855 patients with sonographically confirmed carotid atherosclerosis. During a median follow-up of 6.2 years, corresponding to 5,551 overall person-years, 275 patients (26 %) died. We detected a significant association between cardiovascular mortality and ICAM-1 (adjusted hazard ratio [HR]: 3.43, 95 % confidence interval [CI] 2.00–5.88, p 〈 0.001) as well as VCAM-1 (adjusted HR: 2.51, 95 % CI 1.45–4.34, p=0.001) when comparing the fourth with the first quartile. Comparable results were obtained for all-cause mortality. In contrast, we could not detect a significant association between E-selectin and all-cause or cardiovascular mortality. We identified the selectins ICAM-1 and VCAM-1 as strong and independent predictors of all-cause and cardiovascular mortality in patients with stable carotid atherosclerosis. These molecules are elevated in states of endothelial activation and might assist to monitor anti-atherosclerotic therapy and select those patients with carotid atherosclerosis, who are at higher risk for cardiovascular events.
    Type of Medium: Online Resource
    ISSN: 0340-6245 , 2567-689X
    URL: Article
    DOI: 10.1160/TH14-12-1014
    Language: English
    Publisher: Georg Thieme Verlag KG
    Publication Date: 2015
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 3
    Online Resource
    Online Resource
    Serum albumin predicts cardiac adverse events in patients with advanced atherosclerosis – interrelation with traditional cardiovascular risk factors
    Georg Thieme Verlag KG ; 2004
    In:  Thrombosis and Haemostasis Vol. 91, No. 03 ( 2004), p. 610-618
    Details
    In: Thrombosis and Haemostasis, Georg Thieme Verlag KG, Vol. 91, No. 03 ( 2004), p. 610-618
    Abstract: Low serum albumin is a powerful predictor of cardiovascular adverse events in healthy subjects and patients with subclinical atherosclerosis. We investigated the association between serum albumin, traditional cardiovascular risk factors, markers of inflammation and cardiovascular outcome in 515 patients with advanced atherosclerosis and severe peripheral artery disease. Cardiovascular risk profile, serum albumin, serum amyloid A (SAA) and fibrinogen were obtained at baseline, and patients were followed for median 21 months (interquartile range 12 to 25) for the occurrence of major adverse cardiac events (MACE: myocardial infarction, percutaneous coronary interventions, coronary artery bypass graft, and death). We observed 135 MACE in 109 patients (21%). Cumulative event-free survival rates at 6, 12, and 24 months were 95%, 91%, and 80%, respectively. Low albumin predicted MACE independently of SAA and fibrinogen. Adjusted hazard ratios for the occurrence of MACE, any death, and the composite of death and MI according to increasing quartiles of albumin were 2.40, 1.14 and 1.09 (p 〈 0.001), 2.94, 1.34 and 1.11 (p=0.003) and 3.63, 1.86 and 1.29 (p 〈 0.001), respectively, as compared to the highest quartile. Considering albumin in conjunction with traditional cardiovascular risk factors (smoking, hyperlipidemia, hypertension and diabetes), we found that low albumin predicted MACE only in patients with a low risk profile (less than 3 risk factors) (p 〈 0.001), whereas low albumin was not associated with MACE in patients with three or more risk factors (p=0.66). We conclude that low serum albumin is associated with cardiovascular outcome of patients with advanced atherosclerosis adding to the prognostic information of other inflammatory markers, and may be particularly useful for risk prediction in patients with few traditional risk factors.
    Type of Medium: Online Resource
    ISSN: 0340-6245 , 2567-689X
    URL: Article
    DOI: 10.1160/TH03-08-0504
    Language: English
    Publisher: Georg Thieme Verlag KG
    Publication Date: 2004
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 4
    Online Resource
    Online Resource
    Interleukin-1 cluster combined genotype and restenosis after balloon angioplasty
    Georg Thieme Verlag KG ; 2003
    In:  Thrombosis and Haemostasis Vol. 90, No. 09 ( 2003), p. 491-500
    Details
    In: Thrombosis and Haemostasis, Georg Thieme Verlag KG, Vol. 90, No. 09 ( 2003), p. 491-500
    Abstract: The interleukin-1 system is fundamentally involved in the pathogenesis of restenosis after percutaneous transluminal angioplasty (PTA). In order to further define the clinical impact of genetic variation in this potent proinflammatory pathway we investigated the joint effects of two single nucleotide polymorphisms in the interleukin-1 beta gene [IL-1B(–511) and IL-1B(+3954)] and a variable number tandem repeat polymorphism in intron 2 of the interleukin 1 receptor antagonist gene (IL-1RN VNTR) on postintervention inflammation and occurrence of restenosis in 183 consecutive patients who underwent successful femoropopliteal PTA. C-reactive protein (CRP) and serum amyloid A (SAA) were determined pre- and 48 hours postintervention. Patients were followed up to 12 months for the occurrence of postangioplasty restenosis (≥50 %). When analyzed separately, none of the polymorphisms was associated either with inflammation or restenosis. However, when the IL-1B (–511) and the IL-1RN VNTR genotypes were combined, a highly significant relationship was observed: Non-carriers of the two repeat allele of the IL-1RN VNTR (IL-1RN*2) who were heterozygous and homozygous for the IL-1B (–511)T allele exhibited a gradually increased inflammatory response and a higher restenosis risk. In contrast, carriers of the IL-1RN*2 and the IL-1B (–511)T allele showed a significantly better outcome. This remarkable gene dose-dependent association emphasizes the advantage of considering combinations of genetic markers rather that isolated polymorphisms in the analysis of multifactorial vascular disease.
    Type of Medium: Online Resource
    ISSN: 0340-6245 , 2567-689X
    URL: Article
    DOI: 10.1160/TH03-01-0064
    Language: English
    Publisher: Georg Thieme Verlag KG
    Publication Date: 2003
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 5
    Online Resource
    Online Resource
    The effect of p22-PHOX (CYBA) polymorphisms on premature coronary artery disease (≤ 40 years of age)
    Georg Thieme Verlag KG ; 2011
    In:  Thrombosis and Haemostasis Vol. 105, No. 03 ( 2011), p. 529-534
    Details
    In: Thrombosis and Haemostasis, Georg Thieme Verlag KG, Vol. 105, No. 03 ( 2011), p. 529-534
    Abstract: Acute myocardial infarction at a young age is associated with high morbidity and long-term mortality. The NADPH oxidase system as a main source of reactive oxygen species in vascular cells has been implicated in development and progression of coronary artery disease (CAD). In our study, we investigated the effect of polymorphisms in the p22-PHOX (CYBA) gene on CAD in young patients (≤ 40 years). We prospectively recruited 302 subjects into our multi-centre case control study, including 102 young myocardial infarction patients (≤ 40 years) from two high-volume cardiac catheterisation hospitals and frequency-matched them on age, gender, and center to 200 hospital controls in an approximate 2:1 ratio per case patient. The homozygote c.-930A 〉 G promoter polymorphism was significantly more prevalent in the controls than in the infarction patients. In the adjusted logistic regression analysis, we detected a protective effect of the c.-930A 〉 G promoter polymorphism against premature myocardial infarction. Using a logadditive/per-allele model, we detected an unadjusted odds ratio (OR) of 0.63 (95% confidence interval [CI] 0.45–0.9, p-value 0.011). In the adjusted model the association was more pronounced with an OR of 0.5 (95% CI 0.3–0.81, p-value 0.005). The C242T polymorphism and the 640A 〉 G polymorphism did not differ significantly between the study groups. Furthermore we could not detect a significant effect for these polymorphisms in the logistic regression analysis. The present study suggests a protective association between the c.-930A 〉 G promoter polymorphism in the p22-PHOX (CYBA) gene and the development of myocardial infarction in young individuals (≤ 40 years).
    Type of Medium: Online Resource
    ISSN: 0340-6245 , 2567-689X
    URL: Article
    DOI: 10.1160/TH10-08-0529
    Language: English
    Publisher: Georg Thieme Verlag KG
    Publication Date: 2011
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 6
    Online Resource
    Online Resource
    Plasminogen activator inhibitor-1 and outcome after femoropopliteal angioplasty: analysis of genotype and plasma levels
    Georg Thieme Verlag KG ; 2003
    In:  Thrombosis and Haemostasis Vol. 90, No. 10 ( 2003), p. 717-723
    Details
    In: Thrombosis and Haemostasis, Georg Thieme Verlag KG, Vol. 90, No. 10 ( 2003), p. 717-723
    Abstract: Plasminogen activator inhibitor-1 (PAI-1) is suggested to be involved in the pathophysiology of early thrombosis and late restenosis after percutaneous transluminal angioplasty (PTA). The role of the PAI-1 promoter genotype in this context is indeterminate. We investigated the association of the (4G/5G) polymorphism at nucleotide position (–675) in the PAI-1 gene promoter, PAI-1 plasma levels, and postangioplasty outcome after femoropopliteal PTA. We studied 251 consecutive patients who underwent femoropopliteal PTA. In a subgroup of 86 patients PAI-1 plasma levels at baseline,8,24 and 48 hours postintervention were measured and correlated to the genotype. Patients were followed for early thrombosis and the late restenosis (≥50%) within 12 months. Multivariate Cox proportional hazards analysis was performed to assess the association between the PAI-1 genotype and PTA failure. Results show that the PAI-1 genotype was neither associated with PAI-1 plasma levels (p=0.40) nor the change of PAI-1 from baseline to 8 (p=0.39), 24 (p=0.86) and 48 hours (p=0.89). Three out of 35 homozygous (4G/4G) patients (9%) had early thrombotic reocclusions, compared to two out of 153 heterozygous (4G/5G) patients (1%) and none of the 63 homozygous (5G/5G) patients (p=0.007). Restenosis after median 5 months (interquartile range 3 to 9) was found in 117 patients (42%), without significant association between the PAI-1 genotype and late postangioplasty failure (Log Rank p=0.95). We can conclude that carriers of the 4G allele exhibited a higher frequency of early thrombotic reocclusions after percutaneous angioplasty. However, the PAI-1 gene promoter polymorphism (4G/5G) was not associated with PAI-1 plasma levels or late postangioplasty restenosis.
    Type of Medium: Online Resource
    ISSN: 0340-6245 , 2567-689X
    URL: Article
    DOI: 10.1160/TH03-03-0159
    Language: English
    Publisher: Georg Thieme Verlag KG
    Publication Date: 2003
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 7
    Online Resource
    Online Resource
    A microsatellite polymorphism in the heme oxygenase-1 gene promoter is associated with increased bilirubin and HDL levels but not with coronary artery disease
    Georg Thieme Verlag KG ; 2004
    In:  Thrombosis and Haemostasis Vol. 91, No. 01 ( 2004), p. 155-161
    Details
    In: Thrombosis and Haemostasis, Georg Thieme Verlag KG, Vol. 91, No. 01 ( 2004), p. 155-161
    Abstract: Heme oxygenase 1 (HO-1) is involved in the generation of the endogenous anti-oxidant bilirubin which exerts beneficial effects against arteriosclerosis. A (GT) repeat polymorphism in the HO-1 promoter region modulates HO-1 expression in response to oxidative stress. Recently, this polymorphism has been reported to protect from coronary artery disease in Orientals. We intended to confirm this observation in Caucasians. We studied 649 individuals with myocardial infarction (n=258), stable coronary artery disease (n=180) and controls without coronary artery disease (n=211). Carriers of short alleles ( 〈 25 repeats) had higher bilirubin levels (median 0.66 mg/dL, IQR 0.49 to 0.91) compared to non-carriers (median 0.61mg/dL, IQR 0.45 to 0.82; p=0.03) and a more favourable lipid profile (HDL median 47mg/dL, IQR 40 to 50 vs. median 45, IQR 37 to 55, p=0.01; triglycerides median 118mg/dL, IQR 87 to 174 vs. median 132, IQR 97 to 191, p=0.03). However, no significant differences of the genotype distribution were observed between the three groups in this Caucasian study population (p=0.94). Although potentially beneficial effects of the short HO-1 allele on lipid profile and serum bilirubin were observed, in contrast to Orientals, the HO-1 genotype was not associated with coronary artery disease in Caucasians.
    Type of Medium: Online Resource
    ISSN: 0340-6245 , 2567-689X
    URL: Article
    DOI: 10.1160/TH03-05-0291
    Language: English
    Publisher: Georg Thieme Verlag KG
    Publication Date: 2004
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 8
    Online Resource
    Online Resource
    High plasma heparin cofactor II activity protects from restenosis after femoropopliteal stenting
    Georg Thieme Verlag KG ; 2004
    In:  Thrombosis and Haemostasis Vol. 92, No. 11 ( 2004), p. 1108-1113
    Details
    In: Thrombosis and Haemostasis, Georg Thieme Verlag KG, Vol. 92, No. 11 ( 2004), p. 1108-1113
    Abstract: High heparin cofactor II (HCII) activity has recently been described to protect from coronary instent restenosis, presumably by inactivating thrombin in injured arteries. In this study, we investigated the association of HCII activity and restenosis after femoropopliteal stenting. We studied 63 consecutive patients with peripheral artery disease who underwent femoropopliteal stent implantation after initial failure of plain balloon angioplasty due to a significant residual stenosis ( 〉 30% lumen diameter reduction) or a flow limiting dissection. HCII activity was measured before stenting and patients were followed for median 10 months (interquartile range 6 to 17) for the occurrence of a first instent restenosis, defined as a 〉 50% lumen diameter reduction by color coded duplex sonography and confirmed by angiography. Cumulative freedom from restenosis at 6 and 12 months in patients with lower HCII activity (≤100%, lower tertile, n=20) was 84% and 35% as compared to 93% and 72% in patients with high HCII activity ( 〉 100%, middle and upper tertile, n=43; p=0.024 by Log Rank test). Adjusting for the material of the implanted stents (nitinol vs.Wallstents), patients with a high HCII activity had a 0.39-fold reduced risk for instent restenosis (95% CI 0.17 to 0.90, p=0.028), additional adjustment for diabetes mellitus, poor run-off, critical limb ischemia and cumulative length of the stented segment did not alter the observed effect. Higher activity of heparin cofactor II may exert a protective effect against instent restenosis also in the femoropopliteal vessel area, confirming a prior observation after coronary stenting.
    Type of Medium: Online Resource
    ISSN: 0340-6245 , 2567-689X
    URL: Article
    DOI: 10.1160/TH04-05-0311
    Language: English
    Publisher: Georg Thieme Verlag KG
    Publication Date: 2004
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 9
    Online Resource
    Online Resource
    Fibrinogen Predicts Restenosis after Endovascular Treatment of the Iliac Arteries
    Georg Thieme Verlag KG ; 2002
    In:  Thrombosis and Haemostasis Vol. 87, No. 06 ( 2002), p. 959-965
    Details
    In: Thrombosis and Haemostasis, Georg Thieme Verlag KG, Vol. 87, No. 06 ( 2002), p. 959-965
    Abstract: Fibrinogen is an acute phase protein as well as a component of the coagulation cascade. Vascular inflammation and disturbed coagulation are suggested to cause restenosis after percutaneous transluminal angioplasty (PTA). We investigated the prognostic impact of fibrinogen on restenosis after endovascular treatment of iliac artery occlusive disease. In a prospective cohort study 137 consecutive patients after iliac artery PTA (n = 74) and PTA plus selective stent implantation (n = 63) were included, 109 patients after lower limb angiography served as a control group. Patients were followed for 6 months with oscillography, ankle brachial index and duplex sonography for occurrence of restenosis. Fibrinogen and serum amyloid A (SAA), as a control parameter of inflammation, were obtained at baseline, 8, 24 and 48 h postintervention. PTA (adjusted OR 3.1, p = 0.05) and stenting (adjusted OR 13.3, p = 0.001) were independently associated with a higher postintervention increase of fibrinogen compared to angiography. Restenosis was found in 29 patients (21%). Patients with pre-intervention fibrinogen values in the third quartile (411-463 mg/dl) had a 6.2-fold increased adjusted risk for restenosis (p = 0.03), patients in the fourth quartile ( 〉 463 mg/dl) had a 8.9-fold increased adjusted risk (p = 0.007). Pre-intervention SAA values were also significantly associated with restenosis (p 〈 0.0001). Postintervention fibrinogen and SAA levels showed no association with outcome. Balloon angioplasty and stenting of the iliac arteries cause an elevation of postintervention fibrinogen levels independently of angiographic factors. A higher pre-procedure fibrinogen level, presumably a marker of inflammatory activity, indicates a higher risk for restenosis.
    Type of Medium: Online Resource
    ISSN: 0340-6245 , 2567-689X
    URL: Article
    DOI: 10.1055/s-0037-1613118
    Language: English
    Publisher: Georg Thieme Verlag KG
    Publication Date: 2002
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 10
    Online Resource
    Online Resource
    Interleukin-1 gene cluster variants and abdominal aortic aneurysms : A matched case control study
    Georg Thieme Verlag KG ; 2005
    In:  Thrombosis and Haemostasis Vol. 94, No. 09 ( 2005), p. 646-650
    Details
    In: Thrombosis and Haemostasis, Georg Thieme Verlag KG, Vol. 94, No. 09 ( 2005), p. 646-650
    Abstract: Inflammation is a key factor in the pathogenesis of abdominal aortic aneurysms (AAA). Interleukin 1 (IL-1), a fundamental regulator of the inflammatory cascade, has been shown to be involved in this process. Several functional polymorphisms in the IL-1 gene cluster are known. In this matched case-control study, we investigated a potential association between six genetic variants in IL-1 and IL-1 receptor antagonist (IL-1 RN) withAAA. We enrolled 405 individuals, 135 consecutive patients with AAA were individually age- and sex-matched to 270 patients with coronary artery disease (CAD). Traditional cardiovascular risk factors and IL-1 genotypes were determined, and the distribution of six single nucleotide polymorphisms were compared between patients and controls by multivariable conditional logistic regression analysis: IL-1A (-889) C 〉 T, IL-1A (+4845) G 〉 T, IL-1B (-511) C 〉 T, IL-1B (-31) C 〉 T, IL-1B (+3954) C 〉 T and IL-1RN (+2018) C 〉 T. IL-1A (-889) C 〉 T and IL-1A (+4845) G 〉 T (kappa 0.98, 95% CI 0.96 to 1.00), and IL-1B (-511) C 〉 T and IL-1B (-31) C 〉 T (kappa 0.98, 95% CI 0.96 to 1.00) were closely linked, therefore IL-1A (-889) C 〉 T and IL-1B (-31) C 〉 T were not considered for further analyses. None of the 4 remaining polymorphisms showed a significant association with AAA: IL-1RN (+2018) C 〉 T (p=0.061), IL-1B (+3954) C 〉 T (p=0.51), IL-1B (-511) C 〉 T (p=0.61) and IL-1A (+4845) G 〉 T (p=0.81). No significant first-degree interactions between the genetic variants andAAA were detected. In conclusion, these six genetic variants in the interleukin-1 gene cluster do not seem to play a clinically relevant role in the pathogenesis of AAA, although we cannot rule out the existence of higher degree gene-gene or gene-environment interactions.
    Type of Medium: Online Resource
    ISSN: 0340-6245 , 2567-689X
    URL: Article
    DOI: 10.1160/TH05-03-0203
    Language: English
    Publisher: Georg Thieme Verlag KG
    Publication Date: 2005
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
Nothing or not found what you are looking for? Please check your search query or use the Interlibrary Loan Search.
Close ⊗
This website uses cookies and the analysis tool Matomo. Further information can be found on the KOBV privacy pages