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Helmut Rumpold

Publications and source records attributed to Helmut Rumpold.

16 recordsLinked to original sources
PubMed2005

Prognostic impact of fibrinogen in carotid atherosclerosis: nonspecific indicator of inflammation or independent predictor of disease progression?

BACKGROUND: Fibrinogen is a key factor in the coagulation cascade, it exhibits proinflammatory properties, and it is suggested to play a pivotal role in atherogenesis. We investigated whether fibrinogen predicts future progression of carotid atherosclerosis, analyzing whether fibrinogen levels add to the prognostic information of other inflammatory parameters. METHODS: We prospectively studied 1268 consecutive patients without recent (12 months) symptoms from cerebrovascular disease. Patients underwent serial ultrasound investigations in 6- to 9-month intervals, categorizing carotid arteries as 0% to 29%, 30% to 49%, 50% to 69%, 70% to 89%, or 90% to 99% stenosed, or occluded. Fibrinogen levels were determined at baseline and follow-up. The risk for progressive carotid atherosclerosis according to fibrinogen levels was calculated, adjusting for traditional risk factors and other inflammatory parameters (C-reactive protein and serum amyloid A). RESULTS: Progression of carotid atherosclerosis was found in 117 of 1268 patients (9.2%) after a median of 8 months (range 6 to 18). Adjusted hazard ratios for atherosclerosis progression with increasing quartiles of baseline fibrinogen were 1.83 (P=0.037), 2.09 (P=0.008), and 2.45 (P=0.002), respectively, compared with the lowest quartile. Fibrinogen at follow-up also was associated with progressive disease (P=0.004). However, additionally adjusting for other inflammatory parameters diminished these associations to a nonsignificant level. CONCLUSIONS: Elevated fibrinogen, reflecting the level of inflammatory activity, is associated with progression of carotid atherosclerosis, as it was demonstrated previously for other inflammatory parameters. However, this association seems to be nonspecifically related to the extent of the inflammatory process in atherosclerotic disease rather than to specific properties of fibrinogen.

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PubMed2005

Inflammation and Carotid Artery--Risk for Atherosclerosis Study (ICARAS).

BACKGROUND: Compelling evidence suggests that inflammation is fundamentally involved in the pathogenesis of atherosclerosis; however, temporal correlation between inflammation and morphological features of atherosclerosis progression has not been demonstrated unequivocally. METHODS AND RESULTS: We prospectively studied 1268 consecutive patients who were initially asymptomatic with respect to carotid artery disease. Patients underwent serial carotid ultrasound investigations at baseline and after a follow-up interval of a median of 7.5 months (range 6 to 9 months), with measurement of carotid flow velocities and categorization of carotid arteries as 0% to 29%, 30% to 49%, 50% to 69%, 70% to 89%, or 90% to 99% stenosed or occluded. High-sensitivity C-reactive protein (hs-CRP) and serum amyloid A (SAA) were measured at baseline and follow-up. Progression of carotid atherosclerosis was found in 103 (8.1%) of 1268 patients. Hs-CRP and SAA, respectively, at baseline (P=0.004 and P=0.014) and follow-up (P<0.001 and P<0.001) and the change from baseline to follow-up (P<0.001 and P<0.001) were significantly associated with progressive atherosclerosis. Adjusted ORs (95% CI) for atherosclerosis progression with increasing quintiles of baseline hs-CRP were 1.65 (0.71 to 3.84), 1.87 (0.8 to 4.37), 3.32 (1.49 to 7.39), and 3.65 (1.65 to 8.08), and with increasing quintiles of baseline SAA, they were 0.86 (0.38 to 1.92), 0.99 (0.49 to 1.99), 1.72 (0.91 to 3.28), and 2.28 (1.24 to 4.20), respectively, compared with the lowest quintiles. CONCLUSIONS: These findings supply evidence for a close temporal correlation between inflammation and morphological features of rapidly progressive carotid atherosclerosis, which suggests that elevation or increase of the inflammatory biomarkers hs-CRP and SAA identifies the presence of active atherosclerotic disease.

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PubMed2005

Cerebrospinal fluid neurone-specific enolase in mitochondrial encephalomyopathies.

Whether cerebrospinal fluid (CSF) neurone-specific enolase (NSE) contributes to the diagnosis of mitochondrial encephalomyopathies (MEMs) is unknown. Aim of the present study was thus to assess the validity of CSF-NSE in the diagnosis of MEM. CSF-NSE was determined in 24 controls, aged 28-88 years; and 23 MEM patients, aged 47-81 years. In controls, CSF-NSE was independent of sex (p = 0.849) and age (p = 0.346). Twenty-one MEM patients had clinical CNS involvement and two CNS abnormalities on imaging investigations exclusively. CSF cells were increased in 7, CSF protein in 17, CSF glucose in 1, and CSF lactate in 2 MEM patients. The upper reference limit of CSF-NSE was 14.66 ng/mL. CSF-NSE was elevated in 6 (26%) MEM patients. CSF-NSE was increased in a single MEM patient with subclinical CNS involvement. This study shows that CSF-NSE is elevated in only one quarter of the MEM patients. Determination of CSF-NSE appears to be of minor importance for the assessment of clinical or subclinical CNS involvement in MEM.

Adult↗
PubMed2004

Statin therapy improves cardiovascular outcome of patients with peripheral artery disease.

AIMS: We sought to examine the interrelationship between statin use, inflammation, and outcome of high-risk patients with advanced atherosclerosis. METHODS AND RESULTS: We prospectively studied 515 patients with severe peripheral artery disease (median age 70 years, 296 males). The cardiovascular risk profile and laboratory parameters of inflammation (high-sensitivity C-reactive protein [hs-CRP], serum amyloid A [SAA], fibrinogen, serum albumin, neutrophil counts) were obtained, and patients were followed for a median of 21 months (interquartile range 12-25) for the occurrence of myocardial infarction (MI) and death. We observed 19 MIs (5 fatal and 14 nonfatal) and 65 deaths. Cumulative survival and event-free survival rates (freedom from death and MI) at 6, 12, and 24 months were 97%, 95%, and 89%, and 96%, 93% and 87%, respectively. Patients receiving statin therapy (n=269, 52%) had a lower level of inflammation (hs-CRP p<0.001, SAA p=0.001, fibrinogen p=0.007, albumin p<0.001, neutrophils p=0.049) and better survival (adjusted hazard ratio [HR] 0.52, p=0.022) and event-free survival rates (adjusted HR 0.48, p=0.004) than patients not treated with statins. However, patients with low inflammatory activity (hs-CRP < or =0.42 mg/dl) had no significant benefit from statin therapy (p=0.74 for survival; p=0.83 for event-free survival), whereas in patients with high hs-CRP (>0.42 mg/dl) statin therapy was associated with a significantly reduced risk for mortality (adjusted HR 0.58, p=0.046) and the composite of myocardial infarction and death (adjusted HR 0.46, p=0.016). CONCLUSION: Statin therapy is associated with a substantially improved intermediate-term survival of patients with severe peripheral artery disease and a high inflammatory activity, whereas in patients with low hs-CRP no survival benefit was observed.

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PubMed2004

Microarrayed allergens for IgE profiling.

Diagnosis of type I allergy is based on anamnesis, provocation testing, and serological determination of total and specific IgE. Currently, in vivo and in vitro diagnostic tests employ allergen extracts prepared from various allergen sources (e.g., pollen, mites, animal dander, moulds, foods, venoms, etc.). The application of recombinant DNA technology to the field of allergen characterization has allowed to reveal the molecular nature of the most common allergens. To date a continuously increasing number of allergen sequences has become available and panels of recombinant allergens-assembling the epitope complexity of natural allergens sources-can be produced. The use of recombinant allergens instead of crude, natural extracts for allergy diagnosis allows us to determine the individual IgE reactivity profile of each patient. To enable a comprehensive analysis of the patient's IgE binding pattern to a large number of individual allergens, a new type of serological test is required. In this paper, we applied microarray technology to create a multi-allergen test system, based on microarrayed recombinant allergens.

Allergens↗
PubMed2004

Endovascular brachytherapy: effect on acute inflammatory response after percutaneous femoropopliteal arterial interventions.

PURPOSE: To investigate whether endovascular brachytherapy diminishes vascular inflammation in response to femoropopliteal percutaneous transluminal angioplasty (PTA) or stent implantation in two double-blind randomized-controlled trials. MATERIALS AND METHODS: Forty-seven consecutive patients from two double-blind randomized-controlled trials were studied. Patients either underwent femoropopliteal PTA with endovascular gamma irradiation (n = 8) or placebo irradiation (n = 7) or underwent PTA and stent implantation with brachytherapy (n = 15) or placebo irradiation (n = 17). High-sensitivity C-reactive protein (CRP), serum amyloid A (SAA), and fibrinogen levels were measured at baseline and 8, 24, and 48 hours after the intervention. The change of acute phase parameters from baseline to 48 hours after intervention indicated the extent of the inflammatory response and was compared between patients undergoing brachytherapy and those undergoing placebo irradiation. Fisher exact test was used for comparison of categorical data, and nonparametric statistical methods were applied for analysis of continuous data (Mann-Whitney U tests for unpaired data and Friedman analysis for repetitive measurements). RESULTS: Median patient age was 70 years (interquartile range, 56-74 years); 33 (70%) patients were men and 14 (30%) were women. Clinical characteristics and baseline values of acute phase parameters were similar between groups. A statistically significant increase in CRP, SAA, and fibrinogen values was observed after PTA and stent implantation, both in the patients who underwent brachytherapy and in those who underwent placebo irradiation. Compared with placebo irradiation, however, brachytherapy did not significantly reduce any acute phase parameter from baseline to 8, 24, or 48 hours after the intervention (P >.05 for all comparisons). CONCLUSION: Endovascular brachytherapy did not diminish early vascular inflammation in response to PTA or stent implantation and even induced a trend toward an increased inflammatory response.

Acute-Phase Reaction↗
PubMed2003

Joint effects of C-reactive protein and glycated hemoglobin in predicting future cardiovascular events of patients with advanced atherosclerosis.

BACKGROUND: C-reactive protein (CRP) and glycohemoglobin (HbA1c) are established risk factors for the development of cardiovascular disease. We investigated the joint effects of these parameters on cardiovascular outcome of patients with advanced atherosclerosis. METHODS AND RESULTS: We studied 454 patients with advanced atherosclerosis (median age, 69 years; 264 male). Cardiovascular risk profile, high-sensitivity CRP (hs-CRP), and HbA1c were obtained at baseline, and patients were followed for a median of 21 months (interquartile range, 13 to 26) for the occurrence of major adverse cardiovascular events (MACE) (myocardial infarction, percutaneous coronary interventions, coronary artery bypass graft, carotid revascularization, stroke, and death). We observed 166 MACE in 128 patients (28%). Cumulative event-free survival rates at 6, 12, and 24 months were 91%, 85%, and 73%, respectively. Adjusted hazard ratios for the occurrence of MACE according to increasing quartiles of hs-CRP and HbA1c were 1.35 (P=0.31), 1.90 (P=0.026) and 2.13 (P=0.007), and 1.40 (P=0.26), 1.81 (P=0.059), and 2.36 (P=0.023), respectively, compared with the lowest quartiles. Considering both parameters jointly, we found that patients with hs-CRP >0.44 mg/dL and HbA1c >6.2% (upper quartiles) were at highest risk for MACE, with each parameter adding to the prognostic information of the other. CONCLUSIONS: Inflammation, indicated by hs-CRP, and hyperglycemia, indicated by HbA1c, jointly contribute to the cardiovascular risk of patients with advanced atherosclerosis. Patients with both hs-CRP and HbA1c in the upper quartiles (>0.44 mg/dL and >6.2%, respectively) are at particularly high risk for poor cardiovascular outcome.

Aged↗
PubMed2003

Endovascular revascularization below the knee: 6-month results and predictive value of C-reactive protein level.

PURPOSE: To determine the association between pre- and postintervention serum C-reactive protein (CRP) levels and 6-month restenosis after endovascular treatment of atherosclerotic lesions in arteries below the knee. MATERIALS AND METHODS: Eighty-nine patients with peripheral arterial disease underwent primary successful percutaneous transluminal angioplasty (PTA) of the distal popliteal, anterior tibial, posterior tibial, and fibular arteries. Six-month patency was evaluated with the ankle brachial index (ABI) and color-coded duplex ultrasonography (US). The association between restenosis and preintervention and 48-hour postintervention CRP levels was assessed with multiple logistic regression analysis. RESULTS: ABI improved from a preintervention median of 0.54 to a postintervention median of 0.75 (P <.001). The primary technical success rate was 94% (100 of 106). In 50 patients, a suboptimal technical result was achieved with 30%-40% residual stenosis at the dilated segment. The median ABI at 6 months was 0.65, and it was inversely correlated with preintervention (r = -0.27, P =.009) and 48-hour postintervention (r = -0.40, P <.001) CRP levels. With duplex US at 6 months, restenosis (> or =50%) occurred in 36 patients. Patients with a preintervention CRP level of 0.23-0.92 mg/dL (2.3-9.2 mg/L) had a 3.7-fold increased adjusted risk for restenosis (P =.05); patients with a preintervention CRP level greater than 0.92 mg/dL (9.2 mg/L) had a 4.7-fold increased adjusted risk (P =.03). Postintervention CRP values greater than 2.42 mg/dL (24.2 mg/L) were associated with a 10.7-fold adjusted risk for restenosis (P =.002). Suboptimal PTA result was the only other parameter associated with an increased risk for restenosis (odds ratio, 3.7; P =.03). CONCLUSION: Pre- and postintervention CRP levels were associated with restenosis after PTA of the distal popliteal and tibioperoneal arteries, which indicates that inflammation plays a crucial role in the pathophysiology of this process.

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PubMed2003

Acute-phase response after stent implantation in the carotid artery: association with 6-month in-stent restenosis.

PURPOSE: To determine the prognostic importance of periintervention serum levels of acute-phase reactants in 6-month restenosis after stent implantation in the carotid artery. MATERIALS AND METHODS: One hundred eight consecutive patients with 70% or greater stenosis of the internal carotid artery (ICA) according to the North American Symptomatic Carotid Endarterectomy Trial criteria underwent successful stent implantation in the ICA in a prospective cohort study. Six-month patency was evaluated at color-coded duplex ultrasonography. The association between in-stent restenosis (> or =50%, North American Symptomatic Carotid Endarterectomy Trial criterion) and C-reactive protein (CRP) and serum amyloid A levels at baseline and at 24 and 48 hours after intervention was assessed. RESULTS: Restenosis was found in 15 (14%) patients within 6 months. CRP level at 48 hours, exemplary for the postintervention acute-phase response, was significantly (P =.01) associated with 6-month restenosis by using multiple logistic regression analysis. Recurrent stenosis after prior stent implantation in the carotid artery (odds ratio, 9.2; 95% CI: 1.6, 53.2; P =.01) and residual stenosis of 10%-30% after stent implantation (odds ratio, 9.7; 95% CI: 1.6, 59.3; P =.01) were independent clinical predictors of restenosis. CONCLUSION: Extent of vascular inflammatory response after stent implantation in the carotid artery measured with acute-phase reactants is associated with 6-month patency. Recurrent stenosis after prior stent implantation and initial suboptimal technical result seem to be clinically relevant predictors of postangioplasty outcome.

Acute-Phase Proteins↗
PubMed2003

Interleukin-1 cluster combined genotype and restenosis after balloon angioplasty.

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 (> or = 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.

Aged↗
PubMed2002

Inflammatory response to stent implantation: differences in femoropopliteal, iliac, and carotid arteries.

PURPOSE: To investigate the postintervention course of serum acute-phase reactants after stent implantation in the femoropopliteal, iliac, and carotid arteries. MATERIALS AND METHODS: This prospective cohort study included 274 consecutive patients who underwent stent implantation in the femoropopliteal (n = 95), iliac (n = 70), and carotid (n = 109) arteries. C-reactive protein (CRP), serum amyloid A (SAA), and fibrinogen levels were measured at baseline and at 48 hours after intervention. Polynomial logistic regression analysis was applied to assess the independent association of the course of acute-phase reactants and the site of stent implantation. RESULTS: Stent implantation in the femoropopliteal artery was associated with a higher postintervention increase in CRP (P =.01), SAA (P =.04), and fibrinogen (P =.01) values compared with values with iliac artery stent implantation, with adjustment for age, sex, fluoroscopy duration, contrast agent dose, complication occurrence, stenosis grade, total vessel occlusion, and stent cumulative length. No significant difference in the postintervention course of CRP (P =.9) and SAA (P =.1) levels was determined for stents implanted in the carotid artery compared with those implanted in the iliac artery; however, a higher increase in fibrinogen levels (P =.04) was noted. CONCLUSION: Stent implantation in the muscular femoropopliteal artery was associated with a more extensive vascular inflammatory response than was stent implantation in the elastic iliac and carotid arteries, independent of lesion morphology and interventional factors.

Aged↗
PubMed2002

Vascular inflammation and percutaneous transluminal angioplasty of the femoropopliteal artery: association with restenosis.

PURPOSE: To determine the association of pre- and postprocedural serum levels of C-reactive protein (CRP), serum amyloid A (SAA), and fibrinogen at 6-month evaluation of restenosis after percutaneous transluminal angioplasty (PTA) of the femoropopliteal artery. MATERIALS AND METHODS: In a prospective cohort study, 172 consecutive patients with peripheral artery disease of Fontaine stage IIa, IIb, or III who underwent successful PTA of the superficial femoral and popliteal arteries were included. Patency at 6 months was evaluated by using oscillography, ankle-brachial index, and color-coded duplex ultrasonography. The association of restenosis and CRP, SAA, and fibrinogen levels at baseline, 24 hours, and 48 hours after intervention was assessed by means of multivariate analysis with adjustment for known risk factors for restenosis. RESULTS: Restenosis was found in 56 patients (33%) within 6 months. CRP values at baseline (adjusted odds ratio, 2.2; 95% CI: 1.1, 4.2) and 48 hours after intervention (adjusted odds ratio, 2.3; 95% CI: 1.6, 3.1) were independently associated with 6-month restenosis. SAA and fibrinogen values at any time interval were not significantly associated with patency in the multivariate models. CONCLUSION: The extent of vascular inflammation as measured by means of acute-phase reactants before and after PTA of the femoropopliteal artery is associated with 6-month restenosis. Baseline and 48-hour CRP levels were independent predictors of postangioplasty outcome.

Acute-Phase Proteins↗
PubMed2002

Balloon angioplasty and stent implantation induce a vascular inflammatory reaction.

PURPOSE: To investigate whether peripheral balloon angioplasty with and without stent implantation independently causes an inflammatory vascular response measured by serum acute-phase reactants. METHODS: This was a prospective cohort study enrolled 388 consecutive patients (218 men; median age 70 years, interquartile range 59-76) with peripheral artery disease undergoing balloon angioplasty (n = 187), stent implantation (n = 140), and diagnostic angiography (control group, n = 61). C-reactive protein (CRP) measured by standard and high-sensitivity assays, serum amyloid A (SAA), fibrinogen, and white blood cell (WBC) count were obtained at baseline and at 8, 24, and 48 hours postintervention. Polynomial logistic regression analysis was used to assess the independent association of acute-phase reactants and the interventional group. RESULTS: CRP levels measured by both standard and the high-sensitivity assays significantly increased after balloon angioplasty (standard CRP, p = 0.02; high-sensitivity CRP, p = 0.02) and stent implantation (standard CRP, p = 0.004; high-sensitivity CRP, p = 0.008) compared to the control group adjusting for age, sex, duration of fluoroscopy, volume of contrast, and periprocedural complications. SAA values differed only between the stent group and controls (p = 0.05). Fibrinogen and WBCs were not different among the 3 interventional groups. CONCLUSIONS: Balloon injury and stent implantation induce a vascular inflammatory response at the dilated vessel segment measurable by serum acute-phase parameters. The standard CRP assay is adequate to quantify acute-phase response in these patients.

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PubMed2002

Heme oxygenase-1 genotype is a vascular anti-inflammatory factor following balloon angioplasty.

PURPOSE: To investigate the association of the heme oxygenase-1 (HO-1) genotype, which has potent anti-inflammatory capability, and the inflammatory response induced by balloon angioplasty. METHODS: Three hundred seventeen patients (188 men; median age 70 years, range 57-77) undergoing femoropopliteal balloon angioplasty (n=150) or stenting (n=61) were evaluated for upregulation of the HO-1 genotype; 106 patients undergoing lower limb angiography served as controls. The acute phase reactants C-reactive protein (CRP), serum amyloid A (SAA), and fibrinogen were measured 24 and 48 hours postintervention and compared to baseline values. An association of the relative increase (Delta, %) of these inflammatory markers with short (<25) (GT)(n) dinucleotide repeats in the HO-1 gene promoter was assessed. RESULTS: The HO-1 genotype was significantly associated with Delta CRP(24) (p<0.0001), Delta CRP(48) (p<0.0001), Delta SAA(24) (p=0.02), and Delta SAA(48) (p=0.006) after balloon angioplasty; Delta fibrinogen showed no association. Patients with a higher Delta CRP(48) after balloon angioplasty exhibited significantly reduced odds for the presence of short (<25) (GT)(n) repeats. The adjusted odds reduction in the multivariate model was 80% (p=0.002) in the third quartile of Delta CRP(48) values and 90% (p=0.001) in the fourth quartile. No association of HO-1 genotype and inflammatory response was found 24 and 48 hours after stenting (p=0.3, p=0.5) or angiography (p=0.2, p=0.6). CONCLUSIONS: The HO-1 promoter genotype is independently associated with the inflammatory response seen after balloon angioplasty. Short alleles (<25 GT repeats) seem to be an intrinsic vascular anti-inflammatory factor.

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PubMed2002

Fibrinogen predicts restenosis after endovascular treatment of the iliac arteries.

OBJECTIVE: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.

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