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Christoph Bode

Publications and source records attributed to Christoph Bode.

72 records · Page 4Linked to original sources
PubMed2003

Arteriogenesis in hypoperfused rat brain.

Experimental and clinical studies have provided evidence for spontaneous and therapeutically induced arteriogenesis after occlusion of major peripheral or cardiac vessels. Such evidence is lacking for the cerebrovascular system. In halothane-anesthetized rats, different degrees of brain hypoperfusion were induced by one- to four-vessel occlusion, that is, one or both common carotid arteries in combination with or without bilateral vertebral artery occlusion. The flow decline was monitored by laser Doppler flowmetry, the residual hemodynamic reserve by testing flow reactivity to ventilation with 6% CO(2) and arteriogenesis by intravascular latex infusion and immunohistochemistry of vascular proliferation and monocyte adhesion. The optimum condition for induction of arteriogenesis was three-vessel (one carotid plus both vertebral arteries) occlusion, which led to reduction of blood flow to about 50% and complete suppression of CO(2) reactivity, but no histologic injury. One week after three-vessel occlusion, the ipsilateral posterior cerebral artery significantly enlarged by 39%, and after 3 weeks by 72%, paralleled by the partial return of CO(2) reactivity and the appearance of immunohistochemical markers of arteriogenesis. Three-vessel occlusion is a reliable model for the induction of arteriogenesis in the adult brain and is a new approach for exploring the potentials of arteriogenesis for the prevention of progressing brain ischemia.

Animals↗
PubMed2003

BMPER, a novel endothelial cell precursor-derived protein, antagonizes bone morphogenetic protein signaling and endothelial cell differentiation.

The development of endothelial cell precursors is essential for vasculogenesis. We screened for differentially expressed transcripts in endothelial cell precursors in developing mouse embryoid bodies. We cloned a complete cDNA encoding a protein that contains an amino-terminal signal peptide, five cysteine-rich domains, a von Willebrand D domain, and a trypsin inhibitor domain. We termed this protein BMPER (bone morphogenetic protein [BMP]-binding endothelial cell precursor-derived regulator). BMPER is specifically expressed in flk-1-positive cells and parallels the time course of flk-1 induction in these cells. In situ hybridization in mouse embryos demonstrates dorsal midline staining and staining of the aorto-gonadal-mesonephric region, which is known to host vascular precursor cells. BMPER is a secreted protein that directly interacts with BMP2, BMP4, and BMP6 and antagonizes BMP4-dependent Smad5 activation. In Xenopus embryos, ventral injection of BMPER mRNA results in axis duplication and downregulation of the expression of Xvent-1 (downstream target of Smad signaling). In an embryoid body differentiation assay, BMP4-dependent differentiation of endothelial cells in embryoid bodies is also antagonized by BMPER. Taken together, our data indicate that BMPER is a novel BMP-binding protein that is expressed by endothelial cell precursors, has BMP-antagonizing activity, and may play a role in endothelial cell differentiation by modulating local BMP activity.

Amino Acid Sequence↗
PubMed2003

Design of the START-trial: STimulation of ARTeriogenesis using subcutaneous application of GM-CSF as a new treatment for peripheral vascular disease. A randomized, double-blind, placebo-controlled trial.

Peripheral arterial disease (PAD) affects a large percentage of the elderly population. Standard invasive treatment, apart from risk factor modulation, consists of bypass surgery or percutaneous transluminal angioplasty. However, symptomatic recurrence rates are high for both procedures and a substantial part of the patient population with PAD is not a candidate for invasive revascularization due to complexity of the lesion and/or co-morbidity. Therapeutic arteriogenesis has been proposed as an alternative treatment option. The present paper describes the design of the START-trial. This trial aims to determine the potential of the pro-arteriogenic substance granulocyte/macrophage colony stimulating factor (GM-CSF) to increase maximal walking distance in patients with intermittent claudication. A double-blinded, randomized, placebo-controlled study will be performed in 40 patients with peripheral obstructive arterial disease Rutherford grade I, category 2 or 3, that are candidates for bypass surgery or percutaneous transluminal angioplasty. Based on pharmacokinetic and toxicologic studies, a dose of 10 microg/kg will be used. Patients will be treated for a period of 14 days on each consecutive day, with the last injection applied on day 12. The primary endpoint will be the change in walking distance from day 0 to day 14 as assessed by an exercise treadmill test. Secondary endpoints will be the ankle-brachial index at rest and after exercise, the pain-free walking distance and cutaneous microcirculatory alterations as assessed by laser Doppler fluxmetry. Iliac flow reserve and conductance will be measured by magnetic resonance imaging.

Arterial Occlusive Diseases↗
PubMed2003

Use of GPIIb/IIIa inhibitors in cardiovascular medicine.

The GPIIb/IIIa inhibitors were the first clinically used anti-integrin therapeutics. They opened the gate to a rapidly developing area of anti-integrin targeting as a therapeutic approach to many diseases. The use of GPIIb/IIIa inhibitors in interventional cardiology is widespread and still increasing, as is the number of percutaneous coronary interventions. There seems to be a class effect of GPIIb/IIIa inhibitors in percutaneous coronary intervention, but there are major differences in the pharmacokinetics and pharmacodynamics of these agents. Currently clinically approved for parenteral use are the Fab fragment abciximab (ReoPro, Lilly) and the small-molecule GPIIb/IIIa inhibitors eptifibatide (Integrilin, Millennium/Schering-Plough) and tirofiban (Aggrastat, Merck). This review focuses on the different pharmacological properties of these agents and summarizes present and future therapeutic use of GPIIb/IIIa inhibitors in cardiovascular and other vascular diseases.

Cardiovascular Diseases↗
PubMed2003

Increased glycolysis as protective adaptation of energy depleted, degenerating human hibernating myocardium.

In the current study on human hibernating myocardium (HHM), we tested the hypothesis that increased glycolysis might exert a positive effect during a supply-demand balance situation by augmentation of myocardial energy formation. In 14 patients HHM was preoperatively detected by clinical methods and validated by the recovery of contractile function three months following revascularization. During open-heart surgery, transmural biopsies were removed from the hibernating areas and analyzed using biochemical and morphologic methods. Metabolite contents were normalized for the degree of fibrosis (control: 9.8 +/- 0.5%, HHM 28.1 +/- 3.0%; p < 0.05), providing values for cardiomyocytes only. In energy depleted HHM, severe intracellular degeneration, glycogen accumulation and myocyte loss were found. Elevated lactate levels (2.22 +/- 0.26 vs. 25.38 +/- 3.53 micromol/wet wt, p < 0.001) were indicative of an increased anaerobic glycolytic flux. In conclusion the presence of abundant intracellular glycogen and an increased anaerobic glycolysis in HHM is indicative of a protective adaptation of this myocardium, which might balance energy deficit and may limit structural damage.

Adaptation, Physiological↗
PubMed2003

Independence of growth factor induced plasminogen activator inhibitor type-1 (PAI-1) expression from the 4G/5G polymorphism of the PAI-1 gene.

Increased PAI-1 expression has been implicated in accelerating atherogenesis. Increases under some conditions are modulated by growth factors. Genetic factors such as the 4G/5G polymorphism in the promoter of the PAI-1 gene play a role under certain circumstances. The present study was designed to delineate for the first time interactions between growth factors and the 4G/5G polymorphism with respect to PAI-1 expression in human arterial smooth muscle cells (HASMC). HASMC were genotyped and exposed to growth factors. PAI-1 gene and protein expression were induced consistently by TGF-beta (up to 4.0-fold), PDGF (2.1-fold), TNF-alpha (1.7-fold), and thrombin (2.3-fold). Results were similar regardless of which genotype (4G/4G [n=9], 4G/5G [n=13], and 5G/5G [n=7]) was present. The induction of increased PAI-1 expression in human arterial smooth muscle cells by growth factors implicated in accelerated atherogenesis is independent of the PAI-1 4G/5G polymorphism. Accordingly, modulation of PAI-1 expression is likely to be influenced predominantly by environmental factors acting on, rather than genetic factors intrinsic to the PAI-1 promoter.

Adult↗
PubMed2002

Modulation of collateral artery growth in a porcine hindlimb ligation model using MCP-1.

For an appropriate extrapolation to patients with peripheral arterial obstructive disease, we tested the efficacy of monocyte chemoattractant protein 1 (MCP-1) treatment in a porcine hindlimb ligation model. In 40 minipigs, a femoral artery ligation was performed. Control animals were examined immediately after ligation (n = 4) or after 2 wk of intra-arterial infusion of PBS (n = 11). A second group of animals was evaluated after intra-arterial infusion of 2.0 microg/h of MCP-1 for 48 h (followed by 12 days of PBS; n = 13) or 2 wk continuously (n = 12). In the terminal experiment after 2 wk, resting flow to the leg and peripheral arterial pressures were assessed without vasodilatation. Subsequently, vascular conductance was determined by using a pump-driven extracorporal circulation during maximal vasodilatation. The results showed that resting blood flow to the hindlimb was 53% of the normal after 2 wk of infusion of PBS, compared with 81% in both MCP-1 treatment groups (P < 0.05). Collateral conductance was 645 +/- 346 ml x min(-1) x mmHg(-1) after 2 wk of infusion with PBS, compared with 1,070 +/- 530 and 1,158 +/- 535 ml x min(-1) x mmHg(-1) after 48 h and 2 wk treatment with MCP-1, respectively (P < 0.05). Modulation of the process of arteriogenesis is feasible in this large animal model via intra-arterial infusion of the Cys-Cys-chemokine MCP-1.

Angiography↗
PubMed2002

Mortality at 1 year with combination platelet glycoprotein IIb/IIIa inhibition and reduced-dose fibrinolytic therapy vs conventional fibrinolytic therapy for acute myocardial infarction: GUSTO V randomized trial.

CONTEXT: Among patients with acute myocardial infarction, combination reperfusion therapy with a platelet glycoprotein IIb/IIIa receptor inhibitor (abciximab) and a half dose of a plasminogen activator (reteplase) did not significantly reduce mortality at 30 days compared with a full dose of reteplase. Rates of nonfatal ischemic complications were significantly diminished. OBJECTIVE: To determine if the beneficial effects of abciximab and reteplase (combination therapy) on early nonfatal complications would translate into a reduction in the risk of death by 1 year. DESIGN, SETTING, AND PATIENTS: One-year follow-up of a randomized controlled trial (Global Use of Strategies To Open Coronary Arteries [GUSTO] V). Of 16 588 patients who had been treated in 820 community and referral hospitals in 20 countries between July 1999 and February 2001, mortality data were available for 16 453 (99.2%). INTERVENTION: Patients were randomly assigned to receive (intravenously) a standard dose of reteplase (two 10-U boluses, 30 minutes apart) or the combination of a standard dose of abciximab (0.25 mg/kg bolus, 0.125 microg/kg per minute infusion [maximum 10 micro g/min for 12 hours]) and a half dose of reteplase (two 5-U boluses, 30 minutes apart). MAIN OUTCOME MEASURE: One-year all-cause mortality rates. RESULTS: All-cause mortality at 1 year occurred in 692 (8.38%) of 8260 patients in the reteplase group and 698 (8.38%) of the 8328 patients in the combination therapy group (hazard ratio [HR], 1.00; 95% confidence interval [CI], 0.90-1.11; P>.99). Reinfarction within the first 7 days occurred in 3.5% of patients in the reteplase group and 2.3% of patients in the combination therapy group, and was significantly associated with 1-year mortality (22.6% in patients with reinfarction vs 8.0% in patients without reinfarction; HR, 3.08; 95% CI, 2.53-3.75; P<.001). However, treatment assignment did not significantly influence time of mortality regardless of reinfarction status. CONCLUSION: Combination therapy (abciximab and reteplase) did not reduce mortality over 1 year compared with fibrinolytic therapy with reteplase alone.

Abciximab↗
PubMed2002

The GP IIb/IIIa inhibitor abciximab (c7E3) inhibits the binding of various ligands to the leukocyte integrin Mac-1 (CD11b/CD18, alphaMbeta2).

Cross-reactivity with integrins other than glycoprotein IIb/IIIa (GP IIb/IIIa) is discussed as a potential reason for the overall clinical benefits of the GP IIb/IIIa-blocking antibody-fragment abciximab. We evaluated whether abciximab binds to the leukocyte integrin Mac-1, whether it inhibits binding of the distinct ligands and thereby may modulate inflammation, cell proliferation and coagulation. Binding of fluorescence-labelled abciximab to phorbolmyristate acetate-stimulated monocytes and to a monocytic cell line (THP-1) could be detected in flow cytometry. The binding of fibrinogen, the inactivated complement factor 3b (iC3b), and the coagulation factor X to Mac-1 could be inhibited by abciximab (10 microg/ml) in vitro. As a functional consequence, the conversion of factor X to factor Xa mediated by Mac-1, as detected by the chromogenic substrate SZ-2222, was impaired by abciximab. Adhesion of THP-1 cells to immobilized intercellular adhesion molecule 1 (ICAM-1) and to fibrinogen was reduced significantly by abciximab. Fibrinogen-mediated cell aggregation was also impaired. In conclusion, we describe binding of abciximab to Mac-1 on stimulated monocytes. Thereby, abciximab inhibits binding of the ligands fibrinogen, ICAM-1, iC3b and factor X. Furthermore, we demonstrated that Mac-1-dependent conversion from factor X to factor Xa is impaired by abciximab, arguing for the direct modulation of the coagulation cascade by abciximab. Overall, the inhibition of Mac-1 could provide additional clinical benefits of abciximab beyond the well-described blockade of GP IIb/IIIa.

Abciximab↗
PubMed2002

Severe energy deprivation of human hibernating myocardium as possible common pathomechanism of contractile dysfunction, structural degeneration and cell death.

OBJECTIVES: We tested the hypothesis that severe alterations in myocardial energy metabolism play an important role in the pathophysiology of human hibernating myocardium (HHM). BACKGROUND: It is well established that a disturbed myocardial energy metabolism results in impairments of contractile performance, structure and viability. All of these are important characteristics of HHM. METHODS: In 16 patients with documented coronary artery disease and impaired left ventricular function, HHM was preoperatively detected by thallium-201 scintigraphy, radionuclide ventriculography and low-dose dobutamine echocardiography. These regions were validated as HHM by their recovery of contractile function three months following revascularization. During open-heart surgery, transmural biopsies were removed from the hibernating areas and analyzed both biochemically and morphologically. These findings were compared to normal human myocardium. All metabolite contents given were normalized for the degree of fibrosis (control: 9.8 +/- 0.5%; HHM: 28.1 +/- 3.0%; p < 0.05), providing myocellular contents. RESULTS: In HHM, decreased contents (micromol/g wet weight) in adenosine triphosphate (ATP) (control: 4.17 +/- 0.26; HHM: 1.72 +/- 0.25; p < 0.001), creatine phosphate (5.67 +/- 0.70 vs. 0.84 +/- 0.13; p < 0.001) and creatine (27.6 +/- 3.19 vs. 11.2 +/- 1.56; p < 0.0001) were found, but contents in lactate (2.22 +/- 0.26 vs. 25.38 +/- 3.53; p < 0.001), purine bases (0.58 +/- 0.09 vs. 1.26 +/- 0.13; p < 0.001) and protons (pH units: 7.199 +/- 0.01 vs. 6.59 +/- 0.07; p < 0.001) were increased. Levels in adenosine diphosphate, adenosine monophosphate and inorganic phosphate remained unchanged. Energy depletion in HHM was reflected by decreases in the free energy of ATP hydrolysis and in energy charge. CONCLUSIONS: These data confirm our hypothesis that HHM is energy-depleted myocardium, exhibiting signs of chronic reduction in resting blood flow and a downregulation of energy turnover. The alterations in energy metabolism observed may become operative in triggering and maintaining contractile dysfunction, continuous tissue degeneration and cardiomyocyte loss.

Aged↗
PubMed2002

Exogenous application of transforming growth factor beta 1 stimulates arteriogenesis in the peripheral circulation.

Increased expression of transforming growth factor beta1 (TGF-beta1) during collateral artery growth, as well as its numerous effects on monocytes/macrophages and the smooth muscle cell cycle and differentiation, suggest a modulating role for this growth factor during arteriogenesis. We studied the effects of exogenously applied TGF-beta1 on arteriogenesis as well as its interactions with monocytes, endothelial cells, and smooth muscle cells. In a New Zealand White (NZW) rabbit model of femoral artery ligation, increased expression of active TGF-beta1 was found around proliferating arteries in NZW rabbits. The exogenous application of TGF-beta1 led to an increase in both the number of visible collateral arteries as well as the conductance of the collateral circulation (4.0 +/- 0.5 ml/min/100 mmHg vs. 28.9 +/- 3.7 ml/min/100 mmHg, P<0.05). Fluorescence activated cell sorting analysis showed an increase in the expression of the MAC-1 receptor in both rabbit and human monocytes after treatment with TGF-beta1 (control: 91.2 +/- 4.2/482 +/- 21.7; TGF-beta1 200 ng/ml 193.9 +/- 6.7/ 675.5 +/- 25.7, P<0.05 for all differences). TGF-beta1 treated monocytes showed an increased endothelial adhesion and transmigration in transendothelial migration assays (5.75 +/- 0.63 x 10(5) vs. 10.11 +/- 0.04 x 10(5), P<0.05). TGF-beta1 had no direct pro-angiogenic effect on human umbilical vein endothelial cells in a spheroid model of angiogenesis and inhibited the angiogenic effects of vascular endothelial growth factor.

Animals↗
PubMed2002

Drug-eluting stent: the "magic bullet" for prevention of restenosis?

The need for repeat interventions after initially successful PTCA due to restenosis has been called the "Archilles heel" of a percutaneous revascularization procedure. The incidence of restenosis varies between 20-50 % depending on the stent material, the presence of risk factors, and the location of vascular disease. Some risk factors such as diabetes have been clearly identified, others are currently debated. After years of failures trying to reduces restenosis rates, locally administered antiproliferative means have been shown to successfully inhibit excessive cell growth in response to PTCA. Local radiotherapy of in-stent restenosis results in a reduction of recurrent stenosis versus a conventional PTCA procedure. However, long-term evaluation indicated that restenosis may only be delayed with radiation therapy. Moreover, the restenosis rates were reduced, but the restenotic process was not eliminated. Coronary stents eluting the anti-proliferative agent rapamycin have demonstrated for the first time, that restenosis rates of zero percent are achievable after percutaneous revascularization procedures. Thus, it is intriguing to believe that the elimination of restenosis may have become reality. The purpose of this review is to discuss, whether a stent eluting drugs should be considered as the "magic bullet" for prevention of restenosis after PTCA.

Angioplasty, Balloon, Coronary↗
PubMed2002

Effects of different thrombolytic treatment regimen with abciximab and tirofiban on platelet aggregation and platelet-leukocyte interactions: a subgroup analysis from the GUSTO V and FASTER trials.

BACKGROUND: Due to considerably high rates of reocclusion under standard thrombolytic therapy GP IIb/IIIa inhibitors have been combined with thrombolytics to improve therapeutic outcomes. Potential reasons for arterial reocclusion may be increased platelet activation, interaction of platelets with other cell types such as leukocytes and inadequate drug dosing due to lack of ideal platelet monitoring. We compared combination therapy regimens consisting of GP IIb/IIIa inhibitors and thrombolytics with respect to platelet inhibition and platelet-leukocyte interactions. METHODS AND RESULTS: From the GUSTO V trial (standard rPA vs. reduced dose rPA and abciximab) and the FASTER trial (standard TNK-tPA vs. reduced dose TNK-tPA and tirofiban) 15 patients were monitored by platelet aggregometry, rapid platelet function assay (RPFA) and flow cytometry (FC). rPA alone (n = 5) caused initial increases in platelet aggregation. However, platelet aggregation was significantly (p < 0.05) and sufficiently (>80%) inhibited by abciximab/rPA (n = 5) and tirofiban/TNK-tPA (n = 5). The platelet inhibitory effect of tirofiban/TNK-tPA was more pronounced compared to abciximab/rPA with a significant difference after 2 h (p < 0.05). Tirofiban/TNK-tPA and abciximab/rPA caused decreases in platelet-leukocyte aggregates as well as in binding of specific antibodies to the platelet vitronectin receptor and P-selectin (p < 0.05, respect.). No differences among the treatment groups were seen with respect to antibody binding to MAC-1 and CD154/CD40 ligand. CONCLUSIONS: Taken together, GP IIb/IIIa inhibitors overcome the platelet activating effect of thrombolytics resulting in sufficient platelet inhibition. RPFA is a suitable monitoring tool to accurately assess platelet inhibition. Within the given combination treatment regimen tirofiban appears to be more effective compared to abciximab and to exert effects beyond the inhibition of GP IIb/IIIa.

Abciximab↗
PubMed2002

Hirudin in acute coronary syndromes.

Acute coronary syndromes are a major cause of morbidity and mortality in Western societies. The term describes a spectrum from unstable angina, the recently defined non-Q wave infarction (the Non ST-Elevation Myocardial Infarction [NSTEMI]), to acute transmural myocardial infarction. With regard to treatment, a series of recently published studies compared the specific direct thrombin inhibitor hirudin with standard unfractionated heparin. Initial small studies showed promising results and led to the initiation of large-scale clinical trials addressing patients with acute coronary syndromes. However, in these studies, an unacceptably high incidence of serious hemorrhagic complications prompted safety boards to stop trials. In those studies carried out according to the protocol, no significant clinical benefit of hirudin over standard heparin was proved. Here, hirudin has been shown to be equivalent to unfractionated heparin for the treatment of unstable coronary syndromes with or without ST elevation and as an adjunct to percutaneous coronary balloon angioplasty. Because of its narrow therapeutic window between clinical benefit and increased bleeding hazards, hirudin should be used cautiously. For patients with heparin-induced thrombocytopenia, hirudin is accepted as an important therapeutic alternative.

Angioplasty, Balloon↗
PubMed2002

Transmyocardial laser revascularization and left ventricular reduction surgery affect ventricular arrhythmias and heart rate variability.

BACKGROUND: Transmyocardial laser revascularization (TMLR) and left ventricular reduction by endoventricular patch plasty (LVR) are 2 new surgical procedures performed in patients with endstage coronary artery disease and left ventricular dilation/aneurysms, respectively. As these are performed in patients at high risk for sudden cardiac death and may interact with arrhythmogenesis, we assessed the influence of these procedures on incidence and severity of ventricular tachyarrhythmias and time-domain heart rate variability. METHODS: Preoperative and one week postoperative 24-hour Holter recordings were performed in 37 patients undergoing TMLR (n = 23, CO2-laser technique) or LVR (n = 14). RESULTS: TMLR patients received a mean of 27.2 +/- 9.2 laser channels. Postoperatively, the proportion of patients who underwent TMLR with spontaneous ventricular tachycardia (> or =4 repetitive ventricular beats) increased (0% vs 26%, P <.05), including one patient who died from documented ventricular fibrillation during monitoring. There was no correlation to the number and/or location of laser-induced channels or to perioperative CK levels. HRV parameters were not altered by TMLR. By contrast, LVR did not significantly influence ventricular tachyarrhythmia episodes but markedly depressed all major HRV parameters (SDNN 116.4 vs 61.8, RMSSD 35.2 vs 19.9, pNN50 14.5 vs 4.9, all P <.05). CONCLUSIONS: Early after TMLR, there is evidence of an increased incidence of spontaneous ventricular tachycardia enhancing the risk for sudden cardiac death, while HRV remains unaffected. By contrast, LVR resulted in a marked reduction in HRV still present one week postoperatively, while no effect was observed on incidence and/or severity of spontaneous ventricular tachyarrhythmias.

Aged↗
PubMedDate not supplied

Adhesion of monocytes to medical steel as used for vascular stents is mediated by the integrin receptor Mac-1 (CD11b/CD18; alphaM beta2) and can be inhibited by semiconductor coating.

Implantation of stents into stenosed arteries helps to restore normal blood flow in ischemic organs. However, limited biocompatibility of the applied medical steel can cause acute thrombosis and long-term restenosis. Adhesion of monocytes to stent metal may participate in those acute and long-term complications of stent placement. Based on described prominent electrochemical properties of the interaction between the monocyte integrin receptor Mac-1 and its various ligands, we hypothesized, that this receptor is a central mediator of monocyte adhesion to stent metal and that semiconductor coating of medical steel reduces monocyte adhesion. Adhesion of monocytes on L-316 stainless steel was directly evaluated by light microscopy. Mac-1 could be identified as mediator of monocyte adhesion, since cell adhesion could be blocked by anti-Mac-1-antibodies, including the cross-reacting anti-GPIIb/IIIa antibody fragment abciximab. To further prove the central role of Mac-1, two CHO cell lines were generated expressing recombinant Mac-1 either as wild type, resulting in a low affinity receptor, or mutant with a GFFKR deletion of the alpha(M) subunit, resulting in a high affinity receptor. Indeed, adhesion was specific for Mac-1 and dependent on the affinity state of this integrin. Finally, we could demonstrate that Mac-1-mediated adhesion of monocytes to stents can be significantly inhibited by silicon carbide coating of the stent metal. In conclusion, the integrin Mac-1 and its affinity state could be identified as major mediators of monocyte adhesion on medical steel. As therapeutic strategies, the blockade of Mac-1 by antibodies or silicon carbide coating of steel inhibits monocyte adhesion on stents.

Adhesiveness↗
PubMedDate not supplied

Computed tomography coronary angiography with 370-millisecond gantry rotation time: evaluation of the best image reconstruction interval.

OBJECTIVE: To evaluate the best reconstruction window for noninvasive coronary angiography when using a 16-detector row computed tomography (CT) scanner with a gantry rotation time of 370 milliseconds. METHODS: In a pilot study, 189 coronary artery segments of 21 patients with a mean heart rate of 65 beats per minute (bpm, maximum: 45-94 bpm) were investigated using a 16-detector row CT scanner. Raw data were reconstructed in 10% increments from 40% to 70% of the RR interval. Two experienced observers independently evaluated the image quality of the coronary arteries in a segmental fashion. A 5-point ranking scale was applied, with 1 being very poor (no evaluation possible); 2, poor; 3, moderate; 4, good; and 5, very good. RESULTS: In the mean of all patients, the best reconstruction window was found to be at 60% of the RR interval. In patients with higher heart rates, the best reconstruction window was found to be at an earlier stage of the R wave-to-R wave interval. CONCLUSIONS: Initial results show that good diagnostic image quality could be achieved for all evaluated segments of the coronary tree with image reconstructions at 60% of the R wave-to-R wave interval in patients with heart rates of 70 bpm or less. Using a 16-detector row CT scanner with a gantry rotation time of 370 milliseconds, the need for adapting the reconstruction window to each segment for the best image quality was overcome in those cases. In patients with heart rates faster than 70 bpm, reconstructions at an earlier stage within the cardiac cycle were necessary.

Adult↗