Biomedical subjects

F J Neumann

Publications and source records attributed to F J Neumann.

At least 91 records · Page 5Linked to original sources

PubMed1997

Flow resistance of individual neutrophils in coronary artery disease: decreased pore transit times in acute myocardial infarction.

OBJECTIVE: To investigate single neutrophil flow resistance in coronary artery disease, including myocardial infarction before initiation of reperfusion therapy. DESIGN: Neutrophil flow resistance was measured in 93 subjects in five groups: (group 1) 28 patients within 12 hours after the onset of myocardial infarction, before reperfusion therapy; (group 2) 18 with unstable angina; (group 3) 13 with stable angina; (group 4) 13 age matched patients without coronary disease, and (group 5) 21 healthy volunteers. MAIN PARAMETERS: Single neutrophil transit times through 8 microns oligopore filters determined with a modified cell transit analyser. RESULTS: Leucocyte count (10(9)/l) was increased in coronary disease, especially in myocardial infarction and unstable angina (mean and 95% confidence intervals for groups 1 to 5: 12.6 (11.0 to 14.2), 11.3 (8.5 to 14.1), 8.5 (7.4 to 9.6), 8.0 (6.0 to 10.0), 7.0 (6.1 to 7.9)). Polymorphonuclear granulocyte (PMN) flow resistance correlated negatively with white blood cell (WBC) count and was significantly decreased in coronary artery disease (CAD), especially in myocardial infarction; mean transit times (ms) for groups 1 to 5 were: 13.6 (11.8 to 15.4), 16.9 (13.9 to 19.0), 16.9 (12.8 to 21.0), 22.0 (19.6 to 24.4), and 18.6 (15.7 to 21.5). CONCLUSION: Neutrophil flow resistance was decreased in CAD, especially in myocardial infarction before reperfusion therapy. In contrast to previous findings in reperfused myocardial infarction, the present study showed that stiffened PMNs were not yet present in the circulating blood pool. Thus a pharmacological approach aimed at suppressing leucocyte activation before or during reperfusion therapy may be feasible.

Acute Disease↗

PubMed1997

Dysregulation of monocytic nuclear factor-kappa B by oxidized low-density lipoprotein.

Nuclear factor-kappa B (NF-kappa B)/Rel transcription factors may be involved in atherosclerosis, as is suggested by the presence of activated NF-kappa B in human atherosclerotic lesions. The aim of the present study was to investigate the effects of oxidized LDL (oxLDL) on the NF-kappa B system in human THP-1 monocytic cells as well as adherent monocytes. Our results demonstrate that short-term incubation of these cells with oxLDL activated p50/p65 containing NF-kappa B dimers and induced the expression of the target gene IL-8. This activation of NF-kappa B was inhibited by the antioxidant and H2O2 scavenger pyrrolidine dithiocarbamate and the proteasome inhibitor PSI. The oxLDL-induced NF-kappa B activation was accompanied by an initial depletion of I kappa B-alpha followed by a slight transient increase in the level of this inhibitor protein. In contrast, long-term treatment with oxLDL prevented the lipopolysaccharide-induced depletion of I kappa B-alpha, accompanied by an inhibition of both NF-kappa B activation and the expression of tumor necrosis factor-alpha and interleukin-1 beta genes. These observations provide additional evidence that oxLDL is a potent modulator of gene expression and suggest that (dys)regulation of NF-kappa B/Rel is likely to play an important role in atherogenesis.

Antioxidants↗

PubMed1997

Effect of human recombinant interleukin-6 and interleukin-8 on monocyte procoagulant activity.

Interleukin (IL)-6 and IL-8 are important regulators of inflammatory responses in myocardial infarction. Induction of monocyte procoagulant activity (PCA) by these cytokines could present a mechanism that links inflammatory responses to thrombotic events. We therefore investigated the effect of IL-6 and IL-8 on monocyte tissue factor (TF) expression. Recombinant human IL-6 and IL-8 caused a time- and dose-dependent increase in PCA (recalcification time) of monocytic U937 cells and of mononuclear leukocytes. Using blocking anti-TF monoclonal antibodies and factor VII-deficient control plasma, this PCA was shown to be TF dependent. Compared with unstimulated cells, mononuclear cell PCA increased by 4.5-fold to 17 +/- 2 mU/5x10(5) cells after exposure to 100 ng/L IL-6 for 4 hours and by 6.6-fold to 27 +/- 4 mU/5x10(5) cells after exposure to IL-8 under the same conditions. Northern blot analysis showed an increase in TF mRNA after stimulation with IL-6 or IL-8 for 2 hours, and after 4 hours an increase in cellular TF protein content was found by immunoassay. Flow cytometry demonstrated that IL-6 and IL-8 induced an increase in TF surface expression on monocytes. Thus, IL-6 and IL-8 induce monocyte PCA by increasing mRNA, protein content, and surface expression of TF.

Blood Coagulation Factors↗

PubMed1996

Increased neutrophil-platelet adhesion in patients with unstable angina.

BACKGROUND: Neutrophil-platelet adhesion may occur as a consequence of platelet activation. The role of this heterotypic adhesion in ischemic disorders is poorly understood thus far. METHODS AND RESULTS: Systemic venous blood samples were taken from 25 patients with stable angina pectoris and 25 patients with unstable angina pectoris. Neutrophil activation and neutrophil-platelet adhesion were evaluated by two-color flow cytometry. Patients with unstable angina showed a significant increase in neutrophil-platelet adhesion compared with patients with stable angina (mean +/- SEM, 132.1 +/- 20.5 versus 29.8 +/- 4.7 anti-glycoprotein IIb/IIIa mean fluorescence intensity, P = .0001). Systemic neutrophil activation was found in patients with unstable angina compared with those with stable angina assessed by cell surface CD11b expression and shedding of L-selectin (115.6 +/- 10.3 versus 74.0 +/- 6.3 anti-CD11b mean fluorescence intensity, P = .002; 49.8 +/- 6.0 versus 72.1 +/- 4.0 anti-L-selectin mean fluorescence intensity, P = .006). Markers of neutrophil activation were related to the extent of neutrophil-platelet adhesion (CD11b: r = .5, P = .0005; L-selectin: r = .42, P = .012). In vitro studies revealed that binding of purified platelet membranes to control neutrophils caused a dose-dependent increase in CD11b surface expression, a decrease in surface L-selectin, and the release of superoxide anions. CONCLUSIONS: Thus, this study demonstrates that increased neutrophil-platelet adhesion may contribute to neutrophil activation in unstable angina.

Aged↗

PubMed1996

Platelet function and platelet-leukocyte adhesion in symptomatic coronary heart disease. Effects of intravenous magnesium.

Spontaneous P-selectin surface expression on platelets and platelet-leukocyte adhesion was increased in patients with symptomatic coronary heart disease (n = 12) compared to normal controls (n = 10) (p < 0.05). ADP-induced P-selectin expression and platelet-leukocyte adhesion was also enhanced in the patient group (p < 0.05). Administration of intravenous Mg2+ significantly reduced both platelet surface expression of P-selectin and platelet-leukocyte adhesion ex vivo (p < 0.02). The effect of extracellular Mg2+ was evaluated in in vitro experiments. Both in whole blood and in isolated neutrophil suspension Mg2+ inhibited platelet adhesion to neutrophils dose dependently with half maximal effects at 4 mM. Moreover, Mg2+ inhibited adhesion of isolated platelet membranes to neutrophils. We conclude that platelet function is altered in symptomatic coronary heart disease and can be modulated by administration of intravenous Mg2+.

Adenosine Diphosphate↗

PubMed1996

Platelet activation and coronary stent implantation. Effect of antithrombotic therapy.

BACKGROUND: Platelet activation and surface expression of adhesive glycoproteins play a key role in ischemic thrombotic complications after coronary intervention. The purpose of this case-control study was to evaluate the effects of two different antithrombotic regimens on platelet function after coronary Palmaz-Schatz stent implantation. METHODS AND RESULTS: The study group consisted of 46 "low-risk" patients who were treated with ticlopidine (250 mg BID) and aspirin (100 mg BID) after stenting. The control group was derived from a cohort of 151 patients receiving conventional anticoagulation therapy, including phenprocoumon (target international normalized ratio, 3.5), heparin (activated partial thromboplastin time, 80 to 120 seconds), and aspirin (100 mg BID) after stenting. Criteria for matching were indication for stenting, target vessel, balloon size, inflation pressure, and number of inserted stents. Matches were obtained for 38 patients. Platelet function was evaluated before and daily for 12 days after stenting in venous blood samples with immunologic activation markers. Patients receiving anticoagulation therapy showed a significantly increased surface exposure of LIBS1 (activated fibrinogen receptor; P < .05) and CD62P (P-selectin; P < .001) above prestent values, peaking days 3 to 6 after stenting. In contrast, in patients receiving ticlopidine, expression of LIBS1 decreased (P < .01) and expression of CD62P remained basically unchanged after stenting. Platelet count significantly decreased after stenting in patients treated by anticoagulation (day 3; P < .01), whereas no significant changes were found in the ticlopidine group. CONCLUSIONS: Significant platelet activation occurs in patients receiving anticoagulation therapy after stenting, while platelet deactivation is found in patients treated with combined antiplatelet therapy. This may contribute to a lowering of the incidence of subacute stent thrombosis.

Adult↗

PubMed1996

A randomized comparison of antiplatelet and anticoagulant therapy after the placement of coronary-artery stents.

BACKGROUND: The clinical benefit of coronary-artery stenting performed in conjunction with coronary angioplasty is limited by the risk of thrombotic occlusion of the stent as well as hemorrhagic and vascular complications of intensive anticoagulation. We compared antiplatelet therapy with conventional anticoagulant therapy with respect to clinical outcomes 30 days after coronary-artery stenting. METHODS: After successful placement of Palmaz-Schatz coronary-artery stents, 257 patients were randomly assigned to receive antiplatelet therapy (ticlopidine plus aspirin) and 260 to receive anticoagulant therapy (intravenous heparin, phenprocoumon, and aspirin). The primary cardiac end point was a composite measure reflecting death from cardiac causes or the occurrence of myocardial infarction, aortocoronary bypass surgery, or repeat angioplasty. The primary noncardiac end point comprised death from noncardiac causes, cerebrovascular accident, severe hemorrhage, and peripheral vascular events. RESULTS: Of the patients assigned to antiplatelet therapy, 1.6 percent reached a primary cardiac end point, as did 6.2 percent of those assigned to anticoagulant therapy (relative risk, 0.25; 95 percent confidence interval, 0.06 to 0.77). With antiplatelet therapy, there was an 82 percent lower risk of myocardial infarction than in the anticoagulant-therapy group, and a 78 percent lower need for repeat interventions. Occlusion of the stented vessel occurred in 0.8 percent of the antiplatelet-therapy group and in 5.4 percent of the anticoagulant-therapy group (relative risk, 0.14; 95 percent confidence interval, 0.02 to 0.62). A primary noncardiac end point was reached by 1.2 percent of the antiplatelet-therapy group and 12.3 percent of the anticoagulant-therapy group (relative risk, 0.09; 95 percent confidence interval, 0.02 to 0.31). Hemorrhagic complications occurred only in the anticoagulant-therapy group (in 6.5 percent). An 87 percent reduction in the risk of peripheral vascular events was observed with antiplatelet therapy. CONCLUSIONS: As compared with conventional anticoagulant therapy, combined antiplatelet therapy after the placement of coronary-artery stents reduces the incidence of both cardiac events and hemorrhagic and vascular complications.

Aged↗

PubMed1996

Neutrophil and platelet activation at balloon-injured coronary artery plaque in patients undergoing angioplasty.

OBJECTIVES: This study sought to investigate changes in the expression of activation-dependent adhesion receptors on neutrophils and platelets after exposure to the balloon-injured coronary artery plaque. BACKGROUND: Activation of blood cells at the balloon-injured coronary artery plaque may contribute to abrupt vessel closure and late restenosis after percutaneous transluminal coronary angioplasty. METHODS: In 30 patients undergoing elective coronary angioplasty, blood specimens were obtained through the balloon catheter proximal to the plaque before dilation and distal to the plaque after dilation. Simultaneous blood samples obtained through the guiding catheter served as control samples. Total surface expression of the inducible fibrinogen receptor (CD41) and surface expression of the activated fibrinogen receptor (LIBS1) on platelets as well as Mac-1 (CD11b) and L-selectin (CD62L) surface expression on neutrophils were assessed by flow cytometry. RESULTS: After exposure to the dilated coronary artery plaque, surface expression of LIBS1 on platelets increased by 40.5 +/- 11.0 mean (+/-SE) fluorescence (p=0.001) and that of CD11b on neutrophils increased by 20.1 +/- 4.4 mean fluorescence (p=0.018). Concomitantly, anti-CD62L binding on neutrophils decreased by 6.6 +/- 2.4 mean fluorescence (p=0.022). In contrast, surface expression of the adhesion receptors did not change significantly between the coronary ostium and the prestenotic coronary segment. CONCLUSIONS: The results of this study demonstrate neutrophil and platelet activation at the balloon-injured coronary artery plaque. This cellular activation may serve as a target for pharmacologic interventions to improve the outcome of coronary angioplasty.

Adult↗

PubMed1996

Platelet function in acute myocardial infarction treated with direct angioplasty.

BACKGROUND: In acute myocardial infarction (AMI), platelets play a key role in thrombotic processes that limit the patency of the recanalized, infarct-related coronary artery and contribute to reperfusion injury. Platelet function in the course of AMI treated by direct percutaneous transluminal coronary angioplasty (PTCA) has not been evaluated. METHODS AND RESULTS: In 15 patients with anterior AMI, peripheral venous blood samples were obtained before and 4, 8, 24, and 48 hours after recanalization of the occluded artery by PTCA. Fifteen patients who had stable coronary heart disease and were undergoing elective balloon angioplasty served as control subjects. Fibrinogen receptor function and surface expression of P-selectin on platelets were determined by flow cytometry. In addition, we evaluated generation of platelet-derived microparticles and the effect of systemic plasma from patients with AMI on normal platelet function and on platelet adhesion to human endothelial cells in culture. We found fibrinogen receptor activity and P-selectin expression on circulating platelets 8 hours after direct PTCA are decreased (P < .01). This coincided with a decrease in peripheral platelet count (P < .05) and an increase in generation of microparticles (P < .002). Twenty-four to 48 hours after PTCA, fibrinogen receptor activity and P-selectin expression increased again. Systemic plasma obtained before and after direct PTCA sensitized normal platelets to hyperaggregate in vitro (P < .001) and stimulated platelet adhesion to endothelial cells in culture (P < .01). None of the changes found in AMI were detectable in the control group. CONCLUSIONS: After transient apparent deactivation of circulating platelet, probably caused by sequestration of hyperactive platelets, the level of platelet activation increases in patients with AMI treated by direct PTCA. These findings underscore the need for novel antiplatelet strategies in AMI.

Adult↗

PubMed1996

Prospective evaluation of hemostatic predictors of subacute stent thrombosis after coronary Palmaz-Schatz stenting.

OBJECTIVES: This study sought to investigate hemostatic predictors of subacute occlusive coronary stent thrombosis. BACKGROUND: Better hemostatic monitoring may improve antithrombotic therapy after stenting. METHODS: In 140 consecutive patients undergoing Palmaz-Schatz stent implantation for suboptimal angioplasty results, we obtained serial blood samples immediately before and daily for 12 days after stenting. We prospectively tested the hypothesis that subacute stent thrombosis was more frequent if the surface expression of the inducible fibrinogen receptor on platelets (flow cytometry) or the concentration of plasma fibrinogen or that of the prothrombin fragments F1 + 2 before stent implantation exceeded the 75th percentile of the entire study cohort. RESULTS: All five stent occlusions encountered during the study occurred in patients with platelet fibrinogen receptor expression above the 75th percentile. Thus, the rate of stent occlusion differed significantly between the groups defined by platelet fibrinogen receptor expression (14.3% vs. 0%, p = 0.0008). In both the group with fibrinogen concentration and that with F1 + 2 concentration above the 75th percentile, three stent occlusions occurred. Between the groups defined by these variables, the rate of stent occlusion did not differ significantly (8.6% vs. 1.9%, p = 0.10). Logistic regression analysis, including angiographic and hemostatic variables, confirmed platelet fibrinogen receptor expression as an independent predictor of stent occlusion (p = 0.020). Stent occlusion could not be predicted by the time course of any of the hemostatic variables. CONCLUSIONS: Platelet fibrinogen receptor expression is an independent predictor of subacute stent occlusion. However, fibrinogen and F1 + 2 concentrations do not show a strong relation to the risk of stent occlusion.

Adult↗

PubMed1996

Coronary Palmaz-Schatz stent implantation in acute myocardial infarction.

OBJECTIVE: To investigate the feasibility of coronary stenting in acute myocardial infarction. DESIGN: Prospective observational study. PATIENTS: 80 patients undergoing direct balloon angioplasty for acute myocardial infarction who had coronary Palmaz-Schatz stents implanted during a 3 year study period. Indications for stenting were abrupt reocclusion, large dissection with threatened reocclusion, and failure to achieve brisk flow of contrast by angioplasty alone. INTERVENTIONS: After stenting, 50 patients were treated by conventional anticoagulation and 30 patients received antiplatelet therapy with aspirin and ticlopidine. MAIN OUTCOME MEASURES: Death and subacute reocclusion within two weeks. RESULTS: Coronary stenting fully restored vessel patency in 79 patients (98.8%). 10 of 14 patients with symptoms of Killip class IV on admission were discharged from hospital alive. Three of the 66 patients with symptoms of Killip classes I-III died in hospital. Repeat angiography in 59 of these patients, showed 3 symptomatic and 2 silent reocclusions (reocclusion rate 8.5%). No stent thromboses were detected in patients treated with ticlopidine. CONCLUSIONS: Coronary stenting is a safe and effective treatment for complicated direct balloon angioplasty in acute myocardial infarction. In patients with symptoms of Killip classes I to III the risk of subacute reocclusion is comparable to that of bail-out stenting after elective balloon angioplasty.

Adult↗

PubMed1996

Changes in membrane glycoproteins of circulating platelets after coronary stent implantation.

OBJECTIVES: To evaluate platelet function in patients with coronary stents. DESIGN: A non-randomised control trial in 30 patients who had immediate implantation of Palmaz-Schatz coronary stents because of a suboptimal angioplasty result. All patients received a standardised anticoagulation regimen including intravenous heparin (activated partial thromboplastin time (APTT) 80 to 120 s), oral vitamin K antagonist (target international normalised ratio (INR) of 3.5), and 100 mg aspirin twice daily. Platelet surface expression of glycoprotein IIb-IIIa, activated fibrinogen receptor, and P-selectin as well as binding of von Willebrand factor and fibrinogen were determined by flow cytometry in peripheral venous blood samples collected before the intervention and then daily for 4 days after it. The results were compared with those in 30 patients undergoing elective coronary balloon angioplasty. SETTING: University hospital. RESULTS: After coronary stenting surface expression of the activated fibrinogen receptor significantly increased, peaking at day 2 (P < 0.001). Similar results were found for von Willebrand factor binding and P-selectin surface expression, with a maximum at day 2 to 4 after stenting (von Willebrand factor, P < 0.001; P-selectin, P < 0.001). The changes in platelet membrane glycoproteins coincided with a significant drop in peripheral platelet count after stent placement (P < 0.01). No significant change in fibrinogen receptor activity, von Willebrand factor binding, P-selectin surface expression, or platelet count was seen in the control group. CONCLUSIONS: The present study shows that current anticoagulation treatment is inefficient in suppressing platelet activation in patients with coronary stents and, therefore, might not be the best treatment for reducing the incidence of subacute stent thrombosis.

Adult↗

PubMed1996

Intravascular ultrasound-guided emergency coronary Palmaz-Schatz stent placement without post-procedural systemic anticoagulation.

OBJECTIVE: To test the efficacy of intravascular ultrasound (IVUS)-guided stent placement and to determine the clinical outcome during the first 30 days in those patients who were treated with antiplatelet therapy rather than anticoagulants because they met the IVUS criteria for optimal stent placement. DESIGN: Prospective observational study. PATIENTS: 126 patients with successful, non-elective Palmaz-Schatz stent placement. INTERVENTIONS: IVUS was performed to assess the attachment of stent struts, the coverage of the dissection, and the intrastent minimal lumen area. MAIN OUTCOME MEASURES: Intrastent lumen area, clinical outcome during the first 30 days. RESULTS: In all patients IVUS showed complete apposition and coverage of the dissection. In 23 patients (18%) the IVUS lumen area criterion was achieved. In 75 patients, further balloon dilatation was performed and in 41 IVUS criteria were finally fulfilled. The minimal intrastent lumen area increased from a mean (SD) of 6.81 (1.15) mm2 to 9.56 (2.61) mm2 (P < or = 0.01) between the first and final IVUS investigations. 64 patients (51%) who met the IVUS criteria were treated with aspirin (100 mg) and ticlopidine (250 mg) twice a day. During the first 30 days none of the following events occurred: death, myocardial infarction, repeat intervention, aortocoronary bypass surgery, and subacute stent thrombosis. CONCLUSION: The additional information provided by IVUS examination helped the operator to decide whether further dilatation was needed after a coronary stent had been placed. For patients who met the IVUS criteria for optimal stent placement, antiplatelet therapy was associated with an excellent clinical outcome during the first 30 days.

Angioplasty, Balloon, Coronary↗

PubMed1996

Agglutination of isolated platelet membranes.

Platelet membrane glycoproteins play a central role in platelet aggregation and thus in primary hemostasis. To investigate mechanisms of platelet-platelet interaction in the absence of cellular activation events, we studied immunological and functional aspects of isolated platelet membranes. Platelet membranes contained significant amounts of the inducible fibrinogen receptor, glycoprotein (GP) IIb-IIIa, which exposes conformation-dependent LIBS1 and PMI-1 epitopes in response to fibrinogen-mimetic peptides GRGDSP and HHLG-GAKQAGDV. In the presence of soluble fibrinogen, membrane-coated latex beads showed Ca(2+)-dependent agglutination that could be partially inhibited by GRGDSP but not by the biologically inactive peptide GRGESP. Thrombospondin enhanced agglutination of membrane-coated beads, which could be inhibited by polyvalent anti-thrombospondin Fab fragments and anti-thrombospondin monoclonal antibody MA-II. Mg2+ inhibited both GPIIb-IIIa- and thrombospondin-mediated agglutination of membranes in a dose-dependent manner. The results of the present study indicate that isolated platelet membranes are a useful tool to study regulation of GPIIb-IIIa- and thrombospondin-mediated platelet-platelet interaction.

Agglutination↗

PubMed1995

Cardiac release of cytokines and inflammatory responses in acute myocardial infarction.

BACKGROUND: In animal models of myocardial infarction (MI), inflammatory responses compromise microcirculation during reperfusion and restrict functional recovery. To investigate cardiac inflammatory responses in patients with acute MI, we examined the cardiac release of cytokines, the expression on neutrophils of the beta 2-integrin Mac-1 (CD11b/CD18) and L-selectin (CD62L), and the cardiac release of thrombomodulin as a marker of endothelial injury. METHODS AND RESULTS: In 12 patients with acute anterior MI, blood samples were obtained from the coronary sinus and from the aorta immediately before and after recanalization of the coronary occlusion by balloon angioplasty. Twelve patients undergoing elective balloon angioplasty served as control subjects. Plasma concentrations of interleukin (IL)-1 beta, IL-6, IL-8, tumor necrosis factor-alpha, and thrombomodulin were determined by immunoassay, and surface expression of CD11b and CD62L was assessed by flow cytometry. Differences in coronary sinus and arterial blood were found in IL-6 before (median, 6.3 ng/L, P = .01) and after (13.4 ng/L, P = .002) recanalization and in IL-8 after recanalization (10.7 ng/L, P = .02). The cardiac release of both cytokines significantly (P < or = .03) increased with reperfusion. Cytokine release after reperfusion was associated with significant transcardiac gradients in surface expression on neutrophils of CD11b (10.1 mean channel of fluorescence intensity [mean fl], P = .01) and CD62L (-87 mean fl, P = .007) and with a thrombomodulin release (4.5 micrograms/L, P = .004). Transcardiac gradients in IL-1 beta and tumor necrosis factor-alpha were not found. None of the changes found in MI were detectable in the control group. CONCLUSIONS: As evidence of cardiac inflammatory responses in reperfused acute MI, the study demonstrates cardiac neutrophil activation with signs of endothelial injury and a release of the proinflammatory cytokines IL-8 and IL-6. These findings may assist in the design of pharmacological interventions aimed at reducing microvascular reperfusion injury.

Adult↗

PubMed1995

Efficacy and safety of collagen implants for haemostasis of the vascular access site after coronary balloon angioplasty and coronary stent implantation. A randomized study.

A vascular haemostasis device has recently been introduced that allows percutaneous implantation of collagen plugs for haemostatic sealing of puncture sites even under full anticoagulation. This study assessed the incidence of access site complications after collagen plug implantation in patients with percutaneous coronary angioplasty (PTCA) or coronary stenting. Seventy-eight patients with coronary stenting and 231 patients with PTCA were included in a prospective randomized trial comparing collagen plug implantation to conventional haemostasis. Collagen plug implantation significantly reduced median manual compression times from 45 min (quartiles: 35 min, 51 min) to 5 min (4 min, 6 min) after stenting (P = 0.001) and from 27 min (20 min, 32 min) to 5 min (4 min, 6 min) after PTCA (P = 0.0001). After stenting, in 15 of the 37 patients with collagen implants, access site complications occurred (11 pseudoaneurysms, one arteriovenous fistula, three bleedings requiring blood transfusion, four local infections). The complication rate in the control group (17/41) was not significantly different (P = 0.88). After PTCA, three of the 114 control group patients suffered access site complications, while in the corresponding treatment group of 117 patients, complications occurred in 16 (seven pseudoaneurysms, one arteriovenous fistula, six infections, two femoral occlusions, one bleeding with nerve compression; P = 0.0049). In conclusion, the vascular haemostasis device allows rapid sealing of the vascular access site even under full anticoagulation. Its use after PTCA was however associated with increased access site complications, particularly infections, and even after coronary stenting, failed to reduce the incidence of access site complications.

Angioplasty, Balloon, Coronary↗

PubMed1995

Neutrophil hyper-reactivity after exercise-induced angina pectoris.

BACKGROUND: Previous studies have suggested an increased risk of myocardial infarction associated with physical exercise. Activated neutrophils may contribute to the triggering mechanisms. METHODS: Fifteen patients with stable angina pectoris underwent symptom-limited bicycle ergometry. In neutrophils obtained from serial blood samples, superoxide anion production (SOP) was determined by superoxide dismutase-inhibited reduction of cytochrome C and chemotactic mobility in the microchemotaxis chamber. The same ergometry was repeated after successful balloon angioplasty [percutaneous transluminal coronary angioplasty (PTCA)]. RESULTS: Rate-pressure products and systemic lactate concentrations were similar in both ergometries. Angina was induced in all exercise tests before PTCA, but in none after PTCA. Before the ergometries, systemic neutrophil counts, SOP and chemotactic mobility were essentially the same. Compared with baseline, exercise-induced angina immediately after the first ergometry was associated with an increase in neutrophil count by 0.8 +/- 0.1 nl-7 (P < 0.01), an increase in N-formyl-methionyl-leucyl-phenylalanine (FMLP)-stimulated SOP by 2.44 +/- 0.49 nmol/15 min/5000 cells (P < 0.01) and an increase in chemotaxis by 10.28 +/- 1.65 cells per vision field (P < 0.01). In the ergometry after PTCA this increase in SOP and in chemotaxis disappeared (0.26 +/- 0.39 nmol/15 min/5000 cells and 2.15 +/- 1.52 cells per vision field; NS), whereas the increase in neutrophil count was not significantly different from that in the ergometry before PTCA. CONCLUSION: This study reveals that neutrophil hyper-reactivity after exercise-induced angina can be attributed to myocardial ischaemia.

Aged↗

PubMed1994

Emergency coronary stenting for dissection during percutaneous transluminal coronary angioplasty: angiographic follow-up after stenting and after repeat angioplasty of the stented segment.

OBJECTIVES: The purpose of this study was to assess the angiographic results after emergency coronary stenting and after repeat angioplasty for restenosis within the stent. BACKGROUND: There is still little angiographic information about lumen renarrowing and its correlates after emergency stenting, and data with regard to the angiographic outcome of repeat angioplasty within the stent are almost nonexistent. METHODS: This study was based on the quantitative evaluation of angiograms performed before and immediately after intervention and at 6-month follow-up. The study included 164 of the 183 eligible patients with emergency Palmaz-Schatz stent implantation and 31 of those with restenosis within the stent who had repeat angioplasty. RESULTS: Stenting produced an improvement in minimal lumen diameter from 0.82 +/- 0.41 to 2.76 +/- 0.47 mm (mean +/- SD) and in diameter stenosis from 74.9 +/- 11.5% to 18.3 +/- 8.1%. Elastic recoil was 0.51 +/- 0.34 mm, or 16%. At 6-month follow-up, 32.3% of the patients had restenosis (> or = 50% stenosis). Minimal lumen diameter decreased to 1.84 +/- 0.78 mm, and diameter stenosis increased to 41.7 +/- 21.0%. The degree of lumen loss correlated significantly with the length of the original stenosis and the initial lumen gain achieved by stenting. Thirty-one patients with in-stent restenosis underwent repeat angioplasty. The primary success rate was 100%, and no abrupt vessel closure was verified. Minimal lumen diameter increased from 0.85 +/- 0.35 to 2.18 +/- 0.39 mm, and diameter stenosis decreased from 69.7 +/- 12.9% to 28.6 +/- 9.4%. Elastic recoil was 0.82 +/- 0.38 mm, or 27%. At follow-up, 38.5% of the patients had restenosis. Minimal lumen diameter was reduced to 1.72 +/- 0.67 mm, and diameter stenosis increased to 42.4 +/- 18.1%. CONCLUSIONS: Angiographic results of emergency coronary stenting compare favorably with those of conventional angioplasty. In-stent balloon redilation in patients with restenosis is associated with excellent short-term results and a restenosis rate not different from that reported for nonstented vessels.

Aged↗