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F J Neumann

Publications and source records attributed to F J Neumann.

At least 73 records · Page 4Linked to original sources
PubMed1998

Coronary artery stent placement with postprocedural antiplatelet therapy in acute myocardial infarction.

BACKGROUND: We have shown that coronary artery stent implantation in acute myocardial infarction (AMI) is feasible and safe when combined with effective postprocedural antiplatelet therapy. However, the concept of coronary stenting in AMI has not been validated in large cohorts. In this observational study, we investigated the outcome in 318 consecutive patients. METHODS AND RESULTS: From January 1995 until December 1996, 420 of 455 (92.3%) patients admitted to our institutions with AMI underwent infarct artery stent placement. This report describes the 318 patients treated with combined antiplatelet therapy whose AMI was not complicated by cardiogenic shock or mechanical ventilation before the intervention. Postinterventional therapy consisted of 100 mg aspirin and 250 mg ticlopidine twice daily. There were 21 (6.6%) cardiac events during 30-day follow-up: five cardiac deaths (1.6%), four nonfatal re-infarctions (1.3%) and 13 target vessel revascularizations (4.1%). Six months of clinical follow-up yielded a 94.7% survival rate free of repeat AMI. The rate of repeat interventions was 11%. Quantitative computerized angiography at 6 months, performed in 79.4% of the eligible patients, revealed a binary restenosis rate of 25%. CONCLUSIONS: With postprocedural antiplatelet therapy, coronary stenting in AMI yields favorable short- and long-term outcomes.

Angioplasty, Balloon, Coronary↗
PubMed1998

Glycoprotein IIb/IIIa receptor blockade with coronary stent placement.

GP IIb/IIIa blockade for stenting offers almost complete inhibition of platelet aggregation and can bridge the delayed onset of action of ticlopidine. In the EPISTENT trial, GP IIb/IIIa blockade with abciximab reduced the 30-day cardiac event rate after stenting by more than 50% compared to placebo. Economic constraints may demand to restrict the use of GP IIb/IIIa blockade to subgroups that benefit most. Bail-out stenting constitutes one of these subgroups. Another group are patients with acute myocardial infarction. Moreover, the exquisitely high risk of residual dissection after stenting suggests to always employ GP IIb/IIIa blockade in this instance.

Angioplasty, Balloon, Coronary↗
PubMed1998

Myocardial perfusion scintigraphy to evaluate patients after coronary stent implantation.

UNLABELLED: Coronary stent implantation is an increasingly accepted revascularization method. The 20%-30% restenosis rate during the first 6 mo requires a close follow-up of the patients. Since there is very little data available defining the role of perfusion scintigraphy in the management of this population, the aim of this study was to assess the diagnostic performance of stress myocardial perfusion imaging for detecting restenosis in patients after coronary stent implantation. METHODS: In 82 patients, 93 rest or stress SPECT studies were performed using 201Tl and 99mTc-hexakis-2-methoxyisobutyl isonitrile to evaluate 99 vascular territories with implanted coronary stents. The average interval between the stent implantation and the scintigraphic study was 210.5 +/- 129.6 days. The scintiscans were visually evaluated. A stress-induced perfusion defect with reversibility at rest was used as the criterion for stent restenosis. RESULTS: Coronary angiography revealed a stenosis of > 50% diameter in the region of the stent in 19 arteries, while in 80 arteries there was no evidence of restenosis angiographically. With perfusion scintigraphy, 15/19 vascular territories with restenosed stents showed stress-induced perfusion abnormalities (sensitivity = 79%), while 62/80 territories without restenosis did not (specificity = 78%). In territories without a myocardial infarction (n = 48), sensitivity and specificity values were 8/8 (100%) and 36/44 (82%), and in territories with a myocardial infarction (n = 47) 7/11 (64%) and 26/36 (72%), respectively. Side branch stenosis was fairly frequent in patients without stent restenosis but with a reversible perfusion pattern on their scintiscan (8/18); however, these stenoses were induced infrequently by the stents (3 cases). CONCLUSION: Using the criterion of defect reversibility, stress perfusion SPECT can accurately detect restenoses of coronary artery stents. This method is most accurate for evaluating patients without a previous myocardial infarction in the stented vascular territory.

Coronary Disease↗
PubMed1998

Effect of glycoprotein IIb-IIIa receptor antagonism on platelet membrane glycoproteins after coronary stent placement.

Platelet membrane glycoproteins play a crucial role in ischemic complications after coronary stenting. Glycoprotein IIb-IIIa blockade reduces adverse clinical events after angioplasty but is associated with rare but profound thrombocytopenia that might increase hemorrhagic complications. Changes in platelet membrane glycoproteins of patients with angina who underwent coronary stenting and were treated with the GPIIb-IIIa antagonist abciximab (n=20) or with heparin (n=23) were studied. GPIb-IIIa receptor blockade and membrane glycoproteins were evaluated with immunological markers in venous blood samples taken before. 10, 24, 48, 72, and 96 h after initial treatment with either abciximab or heparin. Patients receiving abciximab therapy showed a rapid inhibition of binding of fluorochrome-conjugated mAb CD41 and c7E3 concomitant with a reduction in platelet aggregation which was restored in part in the days after termination of abciximab infusion. Induction of ligand-induced binding sites on GPIIb-IIIa was increased in patients receiving abciximab. The expression of ligand-induced binding sites correlated inversely with platelet count. No significant change in platelet membrane markers were found in the heparin group. In vitro studies showed that abciximab induces ligand-induced binding sites on isolated platelets and on nuclear cells bearing recombinant GPIIb-IIIa. Abciximab rapidly achieves GPIIb-IIIa receptor blockade after coronary stent placement that might be beneficial in high-risk settings to bridge the delayed action of ticlopidine. Significant alterations of platelet membrane glycoproteins during GPIIb-IIIa antagonism might contribute to development of acute profound thrombocytopenia.

Abciximab↗
PubMed1997

Predictive factors of restenosis after coronary stent placement.

OBJECTIVES: The objective of this study was to identify clinical, lesional and procedural factors that can predict restenosis after coronary stent placement. BACKGROUND: Coronary stent placement reduces the restenosis rate compared with that after percutaneous transluminal coronary angioplasty (PTCA). However, restenosis remains an unresolved issue, and identification of its predictive factors may allow further insight into the underlying process. METHODS: All patients with successful coronary stent placement were eligible for this study unless they had had a major adverse cardiac event during the 1st 30 days after the procedure. Of the 1,349 eligible patients (1,753 lesions), follow-up angiography at 6 months was performed in 80.4% (1,084 patients, 1,399 lesions). Demographic, clinical, lesional and procedural data were prospectively recorded and analyzed for any predictive power for the occurrence of late restenosis after stenting. Restenosis was evaluated by using three outcomes at follow-up: binary restenosis as a diameter stenosis > or =50%, late lumen loss as lumen diameter reduction and target lesion revascularization (TLR) as any repeat PTCA or coronary artery bypass surgery involving the stented lesion. RESULTS: Multivariate analysis demonstrated that diabetes mellitus, placement of multiple stents and minimal lumen diameter (MLD) immediately after stenting were the strongest predictors of restenosis. Diabetes increased the risk of binary restenosis with an odds ratio (OR) [95% confidence interval] of 1.86 [1.56 to 2.16] and the risk of TLR with an OR of 1.45 [1.11 to 1.80]. Multiple stents increased the risk of binary restenosis with an OR of 1.81 [1.55 to 2.06] and that of TLR with an OR of 1.94 [1.66 to 2.22]. An MLD <3 mm at the end of the procedure augmented the risk of binary restenosis with an OR of 1.81 [1.55 to 2.06] and that of TLR with an OR of 2.05 [1.77 to 2.34]. Classification and regression tree analysis demonstrated that the incidence of restenosis may be as low as 16% for a lesion without any of these risk factors and as high as 59% for a lesion with a combination of these risk factors. CONCLUSIONS: Diabetes, multiple stents and smaller final MLD are strong predictors of restenosis after coronary stent placement. Achieving an optimal result with a minimal number of stents during the procedure may significantly reduce this risk even in patients with adverse clinical characteristics such as diabetes.

Aged↗
PubMed1997

Recovery of myocardial perfusion in acute myocardial infarction after successful balloon angioplasty and stent placement in the infarct-related coronary artery.

OBJECTIVES: This study sought to investigate changes in myocardial perfusion after direct percutaneous transluminal coronary angioplasty (PTCA) in acute myocardial infarction (MI). BACKGROUND: After initially successful recanalization of the infarct-related artery, coronary perfusion may deteriorate as a result of reocclusion, distal embolization of platelet aggregates formed at the dilated plaque or microvascular reperfusion injury. This change could offset the benefit from early intervention. METHODS: The study included 19 patients in whom the infarct-related artery was successfully recanalized by PTCA with Palmaz-Schatz stent placement within 24 h after the onset of pain. Basal and papaverine-induced coronary blood flow were assessed by Doppler flow velocity measurements and quantitative coronary angiography. In addition, basal and adenosine-induced myocardial blood flow were measured by nitrogen-13 ammonia positron emission tomography (PET). RESULTS: Immediately after completion of the intervention, the average coronary flow reserve (CR) in the recanalized vessel was 1.56 +/- 0.51; it increased to 2.04 +/- 0.65 at 1 h (p = 0.013) and to 2.66 +/- 0.72 at 2 weeks after reperfusion (p = 0.008, n = 16). PET studies in 12 patients revealed that perfusion defect size and CR in the infarct region (2.19 +/- 0.89 vs. 2.33 +/- 0.86) did not change significantly between day 2 after recanalization and 2 weeks. However, we found significant (p < 0.03) increases in basal (by 26%) and adenosine-induced (by 40%) blood flow in the infarct region. CONCLUSIONS: Despite the persistence of a perfusion defect after successful recanalization of the occluded artery in acute MI, CR of the infarct region improves in most patients within 1 h and further improves within 2 weeks.

Adult↗
PubMed1997

Vitronectin receptor (alpha(v)beta3) mediates platelet adhesion to the luminal aspect of endothelial cells: implications for reperfusion in acute myocardial infarction.

BACKGROUND: Platelet interaction with endothelium plays an important role in the pathophysiology of coronary microcirculation. We assessed the role of the vitronectin receptor (integrin alpha(v)beta3) in platelet/endothelium adhesion. METHODS AND RESULTS: We investigated the effect on platelet/endothelium adhesion of plasma obtained from patients with acute myocardial infarction during reperfusion (before and 8, 24, 48, and 72 hours and 5 to 7 days after direct angioplasty) and with pretreatment with alpha-thrombin (2 U/mL) and recombinant human interleukin-1beta. Platelet/endothelium adhesion was significantly enhanced by approximately 20% after pretreatment of endothelium with patient plasma for 4 hours (P<.05) compared with endothelium treated with pooled control plasma. Plasma-induced platelet/endothelium adhesion was, in part, RGD peptide dependent. Pretreatment of endothelial cells with alpha-thrombin or recombinant human interleukin-1beta enhanced platelet/endothelium adhesion and surface expression of alpha(v)beta3 on the luminal aspect of endothelium (P<.05). The adhesion of platelets, isolated platelet microparticles, and Chinese hamster ovary cells bearing human recombinant alpha(IIb)beta3 (platelet glycoprotein IIb-IIIa) to activated endothelial cells was inhibited by antiadhesive peptides GRGDSP and c(RGDfV) and monoclonal antibodies 4F10, LM609, and 7E3. CONCLUSIONS: The expression of vitronectin receptor exposed on the luminal aspect of activated endothelium is enhanced and mediates platelet/endothelium adhesion. Vitronectin receptor-mediated platelet attachment to activated endothelium during reperfusion may contribute to reperfusion injury and could be a target for antiadhesive therapy.

Adult↗
PubMed1997

Restenosis after coronary stent placement and randomization to a 4-week combined antiplatelet or anticoagulant therapy: six-month angiographic follow-up of the Intracoronary Stenting and Antithrombotic Regimen (ISAR) Trial.

BACKGROUND: Platelets and mural thrombus at the lesion site may play a key role in initiating the restenosis process after coronary interventions. The ISAR Trial provides a comparison of the outcomes of patients randomized to two different antithrombotic regimens administered for 4 weeks after successful coronary stent placement: combined antiplatelet therapy (aspirin plus ticlopidine) or a conventional anticoagulant regimen (phenprocoumon with initial overlapping heparin plus aspirin). Within the first 4 weeks after stent placement, combined antiplatelet therapy has been associated with a significant reduction of ischemic complications. In the present study, we examined whether combined antiplatelet therapy administered for 4 weeks after stent placement is able to reduce the process of restenosis at 6 months. METHODS AND RESULTS: Of 517 patients initially randomized, 496 were eligible for 6-month angiographic follow-up. Scheduled angiography was performed in 432 of the eligible patients (87.1%), 216 in each group. In a comparison of the two groups, there were no significant differences in clinical and procedural variables or in qualitative and quantitative lesion characteristics before and after stenting. At 6 months, minimal luminal diameter was 1.95+/-0.86 mm in the group with initial combined antiplatelet therapy and 1.90+/-0.87 mm in the group with initial anticoagulant therapy (P=.55). Late lumen loss was 1.10+/-0.81 and 1.15+/-0.75 mm (P=.54), and the restenosis rate was 26.8% and 28.9%, respectively (P=.70). Target lesion revascularization rate was 14.6% in the antiplatelet therapy group and 15.6% in the anticoagulant therapy group (P=.85). CONCLUSIONS: This study shows that combined antiplatelet therapy (aspirin plus ticlopidine) administered for 4 weeks after coronary Palmaz-Schatz stent placement does not result in a detectable benefit for the prevention of restenosis compared with conventional anticoagulant therapy (phenprocoumon with initial overlapping heparin plus aspirin).

Administration, Oral↗
PubMed1997

Induction of cytokine expression in leukocytes by binding of thrombin-stimulated platelets.

BACKGROUND: Activated platelets tether and activate myeloid leukocytes. To investigate the potential relevance of this mechanism in acute myocardial infarction (AMI), we examined cytokine induction by leukocyte-platelet adhesion and the occurrence of leukocyte-platelet conjugates in patients with AMI. METHODS AND RESULTS: We obtained peripheral venous blood samples in 20 patients with AMI before and daily for 5 days after direct percutaneous transluminal coronary angioplasty (PTCA) and in 20 patients undergoing elective PTCA. Throughout the study period, CD41 immunofluorescence of leukocytes (flow cytometry) revealed increased leukocyte-platelet adhesion in patients with AMI compared with control patients (mean +/- SE of fluorescence [channels] before PTCA: 77 +/- 16 versus 35 +/- 9; P = .003). In vitro, thrombin-stimulated fixed platelets bound to neutrophils and monocytes. Within 2 hours, this resulted in increased mRNA for interleukin (IL),1 beta, IL-8, and monocyte chemoattractant protein (MCP)-1 in unfractionated leukocytes. After 4 hours, IL-1 beta and IL-8 concentration of the cell-free supernatant had increased by 268 +/- 36% and 210 +/- 7%, respectively, and cellular MCP-1 content had increased by 170 +/- 8%. Addition of activated platelets to adherent monocytes had a similar effect and was associated with nuclear factor-kappa B activation. Inhibition of binding by anti-P selectin antibodies reduced the effect of activated platelets on cytokine production. CONCLUSIONS: In patients with AMI, leukocyte-platelet adhesion is increased. Binding of activated platelets induces IL-1 beta, IL-8, and MCP-1 in leukocytes. Our findings suggest that leukocyte-platelet adhesion contributes to the regulation of inflammatory responses in AMI.

Adult↗
PubMed1997

Comparison of angiography and intravascular ultrasound for the assessment of lumen size after coronary stent placement: impact of dilation pressures.

This study was designed to assess the extent of potential discrepancies between intravascular ultrasound (IVUS) and quantitative coronary angiography (QCA) measurement of intrastent minimal luminal diameter and to evaluate the impact of dilation pressures and the balloon:artery ratio on the assessment of the minimal lumen diameter (MLD) by these imaging modalities. IVUS is recommended as an adjunct to angiography to assess stent expansion; however, the extent of potential discrepancies between the two imaging modalities is not well defined. Included were 225 patients in whom coronary Palmaz-Schatz stents were successfully placed after PTCA. IVUS and QCA were performed at the end of the intervention. We compared the MLD assessed by QCA and IVUS in the instent and reference site. The MLD assessed by IVUS and QCA were 2.68 +/- 0.41 mm and 3.08 +/- 0.47 mm (P < 0.001), respectively, at the tightest intrastent site and 3.19 +/- 0.50 mm and 3.17 +/- 0.52 ns at the reference site. There was a correlation between the dilation pressure and the difference between QCA- and IVUS-based intrastent MLD measurement (y = -0.05x + 1.11; r = -0.53; P < 0.0001). At low dilation pressures, a significant difference between the image modalities was found, but after high dilation pressures no discrepancies were detected. No relation was found with the balloon:artery ratio. These data provide clear evidence that in the case of low-pressure dilation, the exclusive reliance on data obtained by QCA will not yield sufficiently accurate information on intrastent MLD, whereas after high dilation pressure, the differences between the imaging modalities are minimized.

Adult↗
PubMed1997

Systemic and cardiac catecholamines during elective PTCA and during immediate PTCA for acute myocardial infarction.

This study investigated arterial and coronary venous catecholamine concentrations in patients undergoing either elective coronary angioplasty (PTCA) or direct PTCA for acute myocardial infarction. We included 17 patients with stenoses of the left anterior descending coronary artery (LAD) and 10 patients with acute anterior myocardial infarction (AMI) undergoing PTCA. During the initial balloon dilatation arterial and coronary venous plasma concentrations of norepinephrine and epinephrine were determined. In elective PTCA, coronary occlusion (2 min) resulted in a transient increase of arterial concentrations of norepinephrine (2.04 +/- 0.30 vs. 1.26 +/- 0.13 nmol/L before dilatation) and epinephrine (0.52 +/- 0.08 vs. 0.34 +/- 0.04 nmol/L) in the first minute of reperfusion, whereas coronary venous concentrations of catecholamines were not changed after dilatation. Among the 10 patients with AMI, immediate reperfusion of the LAD (TIMI grade 3) was achieved in 6 patients. In these patients, baseline arterial concentrations for norepinephrine (3.91 +/- 1.16 nmol/L) and epinephrine (4.68 +/- 2.07 nmol/L) were elevated and no transcardiac gradient for catecholamines was found. In the first minute after successful reopening of the LAD we detected a distinct rise of the transcardiac norepinephrine gradient from -0.10 +/- 0.53 to 85.02 +/- 24.64 nmol/L, which declined in the fifth minute of reperfusion of 4.36 +/- 2.30 nmol/L. Conversely, venous epinephrine and arterial concentrations for both catecholamines remained unchanged within the observation period. In the four patients with incomplete (TIMI 0-2) reopening of the LAD, we found no cardiac washout of norepinephrine. In summary, a transient rise of systemic catecholamines, but no cardiac release of norepinephrine was observed in patients after brief coronary occlusion. Conversely, a massive washout of norepinephrine from the infarcted myocardium occurred during AMI.

Acute Disease↗
PubMed1997

Platelet function in septic multiple organ dysfunction syndrome.

OBJECTIVE: Altered platelet function plays a role in the pathophysiology of multiple organ failure in sepsis. The purpose of the present study was to evaluate various aspects of platelet adhesive function in septic patients and its putative relevance for prognosis. DESIGN: Prospective clinical study. SETTING: Intensive Care Unit of the University Hospital. PATIENTS AND METHODS: A total of 41 patients admitted to the medical Intensive Care Unit were studied. On the day of admission, patients were evaluated by intensive care scoring systems (Elebute, APACHE II) to assess the severity of sepsis and multiple organ dysfunction syndrome (MODS), and platelet function tests were performed. All patients were observed for 28 days to assess their clinical outcomes. Eleven patients revealed septicemia without MODS (Elebute > or = 12, APACHE II < 20) and 20 septic patients suffered from MODS (Elebute > or = 12, APACHE II > or = 20). Ten non-septic patients without MODS served as a control group (Elebute < 12, APACHE II < 20). Flow cytometric determination of the activated fibrinogen (fg) receptor GPIIb-IIIa and as well as thrombospondin (TSP) on platelets and platelet-neutrophil adhesion (CD 41 immunofluorescence) ex vivo was performed using monoclonal antibodies. The effect of plasma obtained from patients on normal platelet aggregation in vitro, and adhesion to cultured endothelial cells was evaluated. RESULTS: The surface expression of TSP on platelets was increased in septic patients with MODS compared to controls (p < 0.03). Platelet-neutrophil adhesion was not significantly altered in septicemia (p < 0.09) but decreased significantly in the presence of MODS (p < 0.05) when compared to controls. Logistic regression analysis showed that platelet-neutrophil adhesion was an independent predictor for poor clinical outcome (p < 0.01). Plasma from septic patients sensitized normal platelets to hyperaggregate and to adhere to cultured endothelium (p < 0.01). CONCLUSION: In septic patients platelets become activated and are hyperadhesive to other vascular cells including neutrophils and endothelium. This may induce sequestration of platelets and microcirculatory arrest, thus the development of MODS.

APACHE↗
PubMed1997

Coronary stent placement in patients with acute myocardial infarction: comparison of clinical and angiographic outcome after randomization to antiplatelet or anticoagulant therapy.

OBJECTIVES: The Intracoronary Stenting and Antithrombotic Regimen (ISAR) trial is a randomized comparison of combined antiplatelet with anticoagulant therapy after coronary Palmaz-Schatz stent placement. The objective of this study was to compare early and late clinical and angiographic outcome in a subgroup of patients with stent placement for acute myocardial infarction. BACKGROUND: Stenting has become a treatment option for acute myocardial infarction, but it is not known which antithrombotic regimen is more adequate after stent implantation. METHODS: One hundred twenty-three patients with successful stenting after acute myocardial infarction were randomized to receive aspirin plus ticlopidine (n = 61) or intense anticoagulant therapy (n = 62). Six-month repeat angiography was performed in 101 (86.3%) eligible patients. RESULTS: During the first 30 days after stenting, patients with antiplatelet therapy had a significantly lower clinical event rate (3.3% vs. 21.0%, p = 0.005) and stent vessel occlusion rate (0% vs. 9.7%, p = 0.03) and a trend to fewer cardiac events (1.6% vs. 9.7%, p = 0.12). After 6 months, the survival rate free of recurrent myocardial infarction was higher in patients with antiplatelet therapy (100% vs. 90.3%, p = 0.03), and the rate of stent vessel occlusion was lower (1.6% vs. 14.5%, p = 0.02). Both groups had comparable restenosis rates (26.5% vs. 26.9%, p = 0.87). CONCLUSIONS: This study demonstrates that combined antiplatelet therapy after stent placement in patients with acute myocardial infarction is associated with an overall better clinical and angiographic outcome than anticoagulant therapy.

Anticoagulants↗
PubMed1997

Antiplatelet effect of ticlopidine after coronary stenting.

OBJECTIVES: This study sought to investigate the contribution of ticlopidine to the inhibition of platelet activation after coronary stent placement. BACKGROUND: After coronary stenting, antiplatelet therapy with aspirin and ticlopidine improves stent patency compared with anticoagulation. However, the specific role of ticlopidine has not been elucidated. METHODS: After successful coronary stent placement, we randomized 22 patients to receive ticlopidine and aspirin (ticlopidine group) and 25 to receive aspirin alone (aspirin group). Surface expression on platelets of the activated fibrinogen receptor and of P-selectin was assessed by flow cytometry. RESULTS: In the aspirin group the percent of platelets with activated fibrinogen receptors increased between days 1 and 5 (p = 0.001), whereas there were no substantial changes in the ticlopidine group. The percent of P-selectin-positive platelets did not change significantly in the aspirin group but decreased in the ticlopidine group (p = 0.019). At day 5 after the intervention, the percent of platelets with activated fibrinogen receptors in the ticlopidine group was significantly lower (median [interquartile range]: 8.5 [3.1 to 17.8] vs. 18.1 [8.5 to 35.5], p = 0.025), and there was a trend to fewer P-selectin-positive platelets than in the aspirin group (5.8 [3.4 to 9.5] vs. 8.8 [4.0 to 15.8], p = 0.073). CONCLUSIONS: Combined antiplatelet therapy with ticlopidine plus aspirin is superior to treatment with aspirin alone in suppressing platelet activation after coronary stenting.

Aged↗
PubMed1997

Induction of cytokine expression in leukocytes in acute myocardial infarction.

OBJECTIVES: This study sought to investigate whether cytokine expression in leukocytes may be induced by plasma from the reperfused heart of patients with an acute myocardial infarction (MI). BACKGROUND: Reperfusion in acute MI is associated with deleterious local and systemic inflammatory responses that are regulated by cytokines. Induction of cytokine expression in resident leukocytes could contribute to inflammatory responses of the ischemic and reperfused heart. METHODS: Blood samples of 10 patients with an acute MI were obtained simultaneously from the coronary sinus and the aorta before and 5 min after recanalization of the coronary occlusion. Ten patients with elective percutaneous transluminal coronary angioplasty served as a control group. We incubated leukocytes from healthy donors with plasma samples and analyzed mRNA expression of interleukin (IL)-1 beta, IL-6, IL-8 and tumor necrosis factor-alpha (TNF-alpha) by Northern blot analysis. RESULTS: In patients with an acute MI, plasma obtained from the coronary sinus after recanalization increased the mRNA expression of IL-1 beta and IL-8 compared with that of plasma before recanalization (median [quartiles] difference before vs. after recanalization: 34.5 [4, 137], p = 0.017, for IL-1 beta; 18.5 [4, 35], p = 0.032, for IL-8) and simultaneously obtained aortic plasma (median [quartiles] coronary sinus-aortic differences after recanalization: 45.5 [-3, 115], p = 0.021, for IL-1 beta; 16 [4, 52], p = 0.005, for IL-8). No induction of IL-6 and TNF-alpha expression could be observed. No changes found in the study patients were detectable in the control group. CONCLUSIONS: Plasma from the ischemic and reperfused heart stimulates the expression of IL-1 beta and IL-8 in leukocytes. Therefore, leukocyte-derived cytokines may contribute to the regulation of cardiac inflammatory responses in patients with an acute MI.

Adult↗
PubMed1997

Reduction of monocyte-platelet interaction and monocyte activation in patients receiving antiplatelet therapy after coronary stent implantation.

BACKGROUND: Monocyte activation induces different procoagulant and proadhesive inflammatory responses and thus may play a role in thrombotic complications after coronary interventions. Monocyte-platelet interaction may trigger these effects inducing monocyte activation. AIMS: To characterize the effect of antiplatelet vs anticoagulation therapy on monocyte-platelet interaction and monocyte function after intracoronary stenting. METHODS AND RESULTS: Immediately before, and during the first 12 days after successful coronary stenting, monocyte-platelet conjugates and monocyte function were assessed by flow cytometric detection of GPIIb/IIIa (CD41) on monocytes and by monocyte surface exposure of Mac-1 (CD11b/CD18) and L-selectin (CD62L). Twenty patients receiving combined antiplatelet therapy (ticlopidine, aspirin) were compared to 20 patients with standard anticoagulation (phenprocoumon, overlapping heparin, aspirin). Before stenting, monocyte-platelet conjugates and Mac-1 surface expression in both groups were significantly increased, while L-selectin was significantly diminished. Anticoagulation did not change these variables significantly during the subsequent 12 days. In contrast, antiplatelet therapy reduced platelet-monocyte conjugates by 46 +/- 9.3% (mean +/- SEM, P = 0.0019) within 4 days, which was associated with a decrease in Mac-1 expression (28 +/- 6.7%, P = 0.0013) and an increase in L-selectin (56 +/- 15.0%, P = 0.0061). CONCLUSION: After intracoronary stenting, combined antiplatelet therapy, but not anticoagulation, causes reduction of monocyte-platelet interaction, which is associated with monocyte deactivation. This may contribute to a decreased risk for thrombotic events.

Adult↗