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Biomedical subjects

Andreas M Zeiher

Publications and source records attributed to Andreas M Zeiher.

At least 73 records · Page 4Linked to original sources
PubMed2004

[Acute coronary syndrome and inflammation. Biomarkers for diagnostics and risk stratification].

Inflammation plays a pivotal role in atherosclerosis and coronary heart disease. Inflammatory processes of the coronary arterial wall are involved in plaque formation, progression and, finally, plaque instability consecutively leading to the clinical manifestations of stable coronary artery disease or acute coronary syndromes (unstable angina, non-ST elevation and ST elevation myocardial infarction). Acute coronary syndromes result from plaque rupture or erosion leading to local thrombus formation with consecutive necrosis of myocytes due to ischemia, which is associated with widespread and diffuse pancoronary and panmyocardial inflammation. Accordingly, markers of myocardial necrosis (e. g., cardiac troponins) do have crucial diagnostic and prognostic value. In case of troponin-negative acute coronary syndromes, however, markers of inflammation emerged as potentially useful tools for risk stratification. C-reactive protein has been shown to serve as a powerful predictor of future cardiovascular events following acute coronary syndromes, even if troponins are not (yet) positive. Moreover, a variety of pro- (soluble CD40 ligand, placental growth factor, interleukin-6, pregnancy-associated plasma protein A, myeloperoxidase, monocyte chemoattractant protein-1) and anti-inflammatory markers (interleukin-10, activin A) have been suggested to provide relevant prognostic information in patients with acute coronary syndrome. However, the clinical utility of these novel markers has not been established so far.

Acute Disease↗
PubMed2004

Vascular repair by circulating endothelial progenitor cells: the missing link in atherosclerosis?

The integrity and functional activity of the endothelial monolayer play a crucial role in the prevention of atherosclerosis. Increasing evidence suggests that risk factors for coronary artery disease increase endothelial cell apoptosis and lead to a disturbance in the endothelial monolayer. Recent insights suggest that the injured endothelial monolayer is regenerated by circulating bone marrow derived endothelial progenitor cells, which accelerates reendothelialization and limits atherosclerotic lesion formation. However, risk factors for coronary artery disease such as age and diabetes reduce the number and functional activity of these circulating endothelial progenitor cells, thus limiting the regenerative capacity. The impairment of stem/progenitor cells by risk factors may contribute to atherogenesis and atherosclerotic disease progression. We discuss this novel concept of endothelial regeneration and highlight possible novel strategies to interfere with the balance of injury and repair mechanisms.

Animals↗
PubMed2004

Inflammatory markers and coronary artery disease.

In the past decade, the important role of inflammatory processes in the development and progression of atherosclerosis has been clearly established. Over the past two years, different circulating (inflammatory) biomarkers indicating the instability of atherosclerotic plaques have been identified. These new markers do not only serve as diagnostic tools for the identification of patients with unstable angina or acute myocardial infarction but also help us to identify high-risk patients. As a result, different markers are used clinically for risk stratification in stable coronary artery disease as well as in acute coronary syndromes.

Biomarkers↗
PubMed2004

Percutaneous coronary interventions in Europe 1992-2001.

AIMS: The purpose of this registry is to collect data on trends in interventional cardiology within Europe. Special interest focuses on relative increases and ratios in newer re-vascularisation approaches and its distribution in different regions in Europe. We report the data of the year 2001 and give an overview of the development of coronary interventions since 1992, when the first data collection was performed. METHODS AND RESULTS: Questionnaires were distributed to delegates of the individual national societies of cardiology represented in the European Society of Cardiology. These were completed by the local institutions and operators and showed that 1,806,238 angiograms and 617,176 percutaneous transluminal coronary angioplasties (PTCAs) were performed in 2001. This is an increase of 10% and 17%, respectively, compared with the year 2000. The population-adjusted PTCA rate rose from nearly 800 procedures per 10(6) inhabitants in the year 2000 to approximately 990 procedures per 10(6) inhabitants in 2001. Coronary stenting increased by 25% to about 488,900 stents implanted in 2001. Complication rates remained unchanged, and the need for emergency coronary artery bypass grafting is still at 0.2% per percutaneous intervention. CONCLUSION: Interventional cardiology in Europe is still expanding, mainly due to rapid growth in countries with lower socio-economical levels. Most central European countries reported only minor increases in procedures performed. Coronary stenting remains the only noteworthy adjunctive strategy to balloon angioplasty.

Angioplasty, Balloon, Coronary↗
PubMed2004

C-reactive protein levels determine systemic nitric oxide bioavailability in patients with coronary artery disease.

AIM: Elevated C-reactive protein (CRP) levels are associated with impaired endothelial vasoreactivity in patients with coronary artery disease (CAD). Because inflammatory cytokines experimentally reduce basal and stimulated endothelial nitric oxide (NO) release, we hypothesised that patients with elevated CRP-levels are characterised by a systemic impairment in NO bioavailability. METHODS AND RESULTS: Forearm blood flow (FBF) responses were measured by venous occlusion plethysmography in 75 male patients with documented CAD. Inhibition of NO synthesis by infusion of L-NMMA significantly reduced baseline FBF (2.2 +/- 0.5 vs. 1.9 +/- 0.5 mL/min/100 mL of forearm tissue, P < 0.001) and acetylcholine-stimulated FBF responses (AUC: 35.0 +/- 16.0 vs. 25.9 +/- 11.9; P < 0.001). CRP serum levels were inversely correlated with L-NMMA-induced decreases in baseline as well as acetylcholine-stimulated FBF responses. Co-infusion of the oxygen-derived free radical scavenger vitamin C significantly increased baseline FBF from 2.0 +/- 0.5 to 2.5 +/- 0.7 (mL/min/100 mL forearm tissue (P < 0.001)) and acetylcholine-stimulated FBF responses in patients with elevated CRP, but not in patients with low CRP serum levels. Vitamin C-induced increases in baseline FBF and in acetylcholine-stimulated FBF responses were significantly correlated with CRP serum levels. By multivariable analysis, CRP serum levels remained the only statistically significant independent predictor of NO bioavailability in the systemic circulation of patients with CAD. CONCLUSIONS: In patients with CAD, low grade systemic inflammation is associated with increased in vivo oxidative stress leading to impaired systemic bioavailability of NO, which might significantly contribute to the transition from stable coronary artery disease to acute coronary syndromes.

Biological Availability↗
PubMed2004

The pro-apoptotic serum activity is an independent mortality predictor of patients with heart failure.

AIM: Systemic inflammation with elevated serum levels of circulating pro-inflammatory cytokines is a major determinant of prognosis in heart failure (HF). Since serum of patients with HF induces apoptosis of endothelial cells (EC), we aimed to determine whether the pro-apoptotic activity in the serum may predict prognosis of patients with HF. METHODS AND RESULTS: We measured the pro-apoptotic activity in the serum of 48 patients with HF of different aetiology by an ex vivo cell culture assay and subsequently monitored these patients for the single endpoint all-cause mortality. During follow-up, 16 patients died and 11 patients received a heart transplant. Survivors had a lower pro-apoptotic serum activity (P=0.007). By univariate analysis, pro-apoptotic serum activity, NYHA class, pro-BNP, low blood pressure, and creatinine levels were significantly associated with mortality. In a multivariable stepwise Cox-regression model, the pro-apoptotic serum activity (adjusted hazard ratio, HR=1.85 per %, P=0.008), elevated pro-BNP levels (HR=9.35 per log[pro-BNP], P=0.001), and low blood pressure (HR=0.96 per mmHg, P=0.041) remained as independent predictors of death. CONCLUSION: In this exploratory study, the pro-apoptotic serum capacity is independently associated with a worse prognosis in patients with HF, suggesting that the assessment of serum-induced EC apoptosis could provide an integrative estimate of the deleterious effects of various pro-inflammatory cytokines and other cytotoxic factors in HF.

Apoptosis↗
PubMed2004

Elevated secretory non-pancreatic type II phospholipase A2 serum activity is associated with impaired endothelial vasodilator function in patients with coronary artery disease.

Low-grade inflammatory activity is associated with an increased risk for ischaemic coronary events. sPLA(2) (secretory non-pancreatic type II phospholipase A(2)) serum activity is increased in chronic inflammatory diseases and may also contribute to atherogenesis. Since the endothelium is a major target for inflammatory cytokines, we hypothesized that elevated serum activity of sPLA(2) is associated with an impaired vasodilator function in patients with documented CAD (coronary artery disease). Endothelium-dependent (acetylcholine, 10-50 microg/min) and endothelium-independent (sodium nitroprusside, 2-8 microg/min) FBF (forearm blood flow) responses were measured by venous occlusion plethysmography in 50 male patients with angiographically documented CAD. sPLA(2) serum activity was inversely correlated with acetylcholine-induced FBF responses ( r =-0.36; P <0.05). In addition, there was a significant correlation between sPLA(2) and CRP (C-reactive protein; r =0.33, P <0.02). In contrast, FBF responses to sodium nitroprusside did not correlate with sPLA(2) serum activity. In order to identify independent predictors of an impaired endothelium-dependent vasodilator function in patients with CAD, a multivariate analysis was performed including the inflammatory serum markers as well as classical risk factors of CAD. This analysis demonstrated that both sPLA(2) ( P <0.05) and CRP serum levels ( P <0.05) were the only significant independent predictors of an impaired acetylcholine-induced FBF response. In conclusion, elevated sPLA(2) serum activity is associated with a significant impairment in systemic endothelial vasodilator function in patients with CAD. The identification of sPLA(2) as a novel independent predictor for endothelial dysfunction provides another important clue to link a systemic marker of inflammation with coronary atherosclerotic disease.

Adult↗
PubMed2004

Effects of statins on endothelium and endothelial progenitor cell recruitment.

Statins appear to be potent drugs with a variety of pleiotropic effects with vasculoprotective and cardioprotective activity. The beneficial effects of statins on endothelial cells as well as on endothelial cell function appear to be related to improved nitric oxide bioavailability. Mechanistically, statins induce endothelial nitric oxide synthase mRNA stability in endothelial cells and promote endothelial nitric oxide synthase activity through a PI3K/Akt dependent pathway, which is a common signal transduction pathway shared by growth factors such as vascular endothelial growth factors or fibroblast growth factors (FGFs), estrogens, or statins. Furthermore, statins have potent antiinflammatory capacities by potently interfering with the generation of reactive oxygen species or activating scavenging systems for free radicals such as the thioredoxin system. These mechanisms might all contribute to improved NO bioavailability and confer the beneficial actions of statins. The proangiogenic properties of statins and their effects on reendothelialization following vessel injury include novel actions such as the mobilization, differentiation, and improved survival of endothelial progenitor cells. Statin therapy might reverse the impaired functional regeneration capacities seen in patients with risk factors for coronary artery disease or documented active coronary artery disease by specifically interacting with progenitor cell function. Accordingly, augmentation of functionally active endothelial progenitor cells with improved homing capacity will be a critical step in advancing therapeutic neovascularization as well as reendothelialization in patients with coronary artery disease.

Animals↗
PubMed2004

Effects of statins on endothelium and their contribution to neovascularization by mobilization of endothelial progenitor cells.

Statins are potent drugs with a variety of cardiovascular protective effects which appear to occur independent of cholesterol reduction. The vasculoprotective effects of statins might be due to their direct effect on endothelial cells leading to improved nitric oxide (NO) bioavailability. Mechanistically, statins induce endothelial nitric oxide synthesis (eNOS) mRNA stability in endothelial cells and promote eNOS activity through a PI3K/Akt dependent pathway. Novel targets of statins are pro-angiogenic actions including the mobilization and differentiation of bone marrow derived endothelial progenitor cells, which accelerate angiogenesis or re-endothelialization. The functional improvement and increased homing capacity of endothelial progenitor cells induced by statin treatment might reverse impaired functional regeneration capacities seen in patients with risk factors for coronary artery disease or documented active coronary artery disease.

Angiogenesis Inducing Agents↗
PubMed2004

Microvascular dysfunction in angiographically normal or mildly diseased coronary arteries predicts adverse cardiovascular long-term outcome.

OBJECTIVE: To study the role of coronary flow reserve for the prediction of long-term cardiovascular event rate. DESIGN: Observational, longitudinal. SETTING: Single-center, coronary vasomotor testing at university hospital. PARTICIPANTS: One hundred and twenty patients with angiographically normal or minimally diseased coronary vessel. METHODS: Coronary flow reserve was assessed by intracoronary Doppler and quantitative coronary angiography. Cardiovascular events during follow-up (6.5+/-3 years, range 14-125 months) were defined as sudden death, myocardial infarction, unstable angina, ischemic stroke or the need for revascularization by percutaneous transluminal coronary angioplasty or coronary as well as peripheral bypass surgery. RESULTS: Reduced coronary flow reserve was significantly associated with a poor long-term outcome: cardiovascular events occurred in seven (18%) patients in the lowest tertile of coronary flow reserve compared with four patients in the middle tertile (10%) and two patients in the upper tertile (5%) (P=0.019 by Kaplan-Meier analysis). The multivariate Cox proportional hazard model revealed coronary flow reserve as an independent predictor of prognosis (P=0.017) in addition to angiographic evidence of atherosclerosis (P=0.047) and arterial hypertension (P=0.013). CONCLUSIONS: Coronary flow reserve in normal to mildly diseased arteries is an independent predictor of long-term prognosis of atherosclerosis within the next decade.

Adult↗
PubMed2004

111In-labeled CD34+ hematopoietic progenitor cells in a rat myocardial infarction model.

UNLABELLED: Transplantation of progenitor cells (PCs) has been shown to improve neovascularization and left ventricular function after myocardial ischemia. The fate of transplanted PCs has been monitored by fluorescence labeling or by genetic modifications introducing reporter genes. However, these techniques are limited by the need to kill the experimental animal. The aim of this study was to radiolabel CD34(+) hematopoietic PCs (HPCs) with (111)In-oxine and to evaluate the feasibility of this in vivo method for monitoring myocardial homing of transplanted cells in a rat myocardial infarction model. METHODS: Human HPCs were isolated from mobilized peripheral blood and labeled with (111)In-oxine. Labeled HPCs were injected into the cavity of the left ventricle in nude rats 24 h after induction of myocardial infarction (n = 4) or sham operation (n = 4). Scintigraphic images were acquired up to 96 h after HPC injection. After animals were killed, tissue samples of various organs were harvested to calculate tissue-specific activity and for immunostaining. RESULTS: Labeling efficiency of HPCs was 32% +/- 11%. According to trypan-blue staining, viability of radiolabeled HPCs was impaired by 30% after 48 and 96 h in comparison with unlabeled cells, whereas proliferation and differentiation of HPCs was nullified after 7 d, as assessed by colony-forming assays. After injection of HPCs, the specific activity ratio of heart to peripheral muscle tissue increased from 1.10 +/- 0.32 in sham-operated rats to 2.47 +/- 0.92 (P = 0.020) in infarcted rats. However, the overall radioactivity detected in the heart was only about 1%. A transient high lung uptake of 17% +/- 6% was observed within the first hour after infusion of HPCs. At 24 h after injection, the initial lung activity had shifted toward liver, kidneys, and spleen, resulting in an increase of radioactivity in these organs from 37% +/- 6% to 57% +/- 5%. CONCLUSION: Radiolabeling with (111)In-oxine is a feasible in vivo method for monitoring transplanted HPCs in a rat myocardial infarction model. The potential to detect differences in myocardial homing between infarcted and normal hearts suggests that this method may provide a noninvasive imaging approach for clinical trials using transplanted HPCs in patients. Our findings, however, also demonstrated a negative effect of (111)In-oxine on cellular function, which resulted in complete impairment of HPC proliferation and differentiation. For future trials in stem cell imaging with (111)In-oxine, therefore, it will be mandatory to carefully check for radiation-induced cell damage.

Animals↗
PubMed2003

Inhibition of cytochrome P450 2C9 improves endothelium-dependent, nitric oxide-mediated vasodilatation in patients with coronary artery disease.

BACKGROUND: Nitric oxide (NO)- and prostacyclin-independent vasodilatation in several vascular beds has been linked to the activation of cytochrome P450 (CYP) epoxygenases expressed in endothelial cells. However, these enzymes, which generate vasodilator epoxyeicosatrienoic acids, may also produce oxygen-derived free radicals, which attenuate the bioavailability of NO. Here, we studied the involvement of CYP 2C9 in modulating endothelium-dependent and -independent changes in forearm blood flow (FBF) in healthy volunteers and in patients with manifest coronary artery disease. METHODS AND RESULTS: The effects of sulfaphenazole, a selective inhibitor of CYP 2C9, on endothelium-dependent (acetylcholine) and endothelium-independent (sodium nitroprusside, SNP) FBF responses were measured by venous occlusion plethysmography in 5 healthy subjects and in 16 patients with angiographically documented stable coronary artery disease. Sulfaphenazole did not modify FBF responses to acetylcholine or SNP in healthy subjects. In contrast, sulfaphenazole markedly and dose-dependently enhanced the FBF response to acetylcholine without affecting the response to SNP. Vitamin C also increased the FBF response to acetylcholine, but this effect was further potentiated by sulfaphenazole. In the presence of N(omega)-monomethyl-l-arginine, sulfaphenazole failed to significantly improve acetylcholine-induced vasodilatation. The oxidation of serum proteins was enhanced in patients with coronary artery disease, and this effect was significantly attenuated by sulfaphenazole. CONCLUSIONS: The CYP 2C9 inhibitor sulfaphenazole enhances endothelium-dependent vasodilator responses in patients with manifest coronary artery disease. This effect seems to be related to an increase in the bioavailability of NO, probably as a consequence of an attenuated generation of reactive oxygen species by CYP 2C9 in endothelial cells.

Acetylcholine↗
PubMed2003

Relevance of monocytic features for neovascularization capacity of circulating endothelial progenitor cells.

BACKGROUND: Transplantation of ex vivo expanded circulating endothelial progenitor cells (EPCs) from peripheral blood mononuclear cells improves the neovascularization after critical ischemia. However, the origin of the endothelial progenitor lineage and its characteristics have not yet been clearly defined. Therefore, we investigated whether the phenotype and functional capacity of EPCs to improve neovascularization depend on their monocytic origin. METHODS AND RESULTS: Monocytic CD14+ cells were isolated from mononuclear cells and incubated on fibronectin-coated dishes in endothelial medium in the presence of vascular endothelial growth factor. After 4 days of cultivation, adherent cells deriving from CD14+ or CD14- mononuclear cells showed equal expression of endothelial marker proteins and capacity for clonal expansion as determined by measuring endothelial colony-forming units. In addition, transplanted EPCs (5x10(5) cells) deriving from CD14+ or CD14- cells were incorporated into vascular structures of nude mice after hind-limb ischemia and significantly improved neovascularization from 0.27+/-0.12 (no cells) to 0.66+/-0.12 and 0.65+/-0.17, respectively (P<0.001; laser Doppler-derived relative blood flow). In contrast, no functional improvement of neovascularization was detected when freshly isolated CD14+ mononuclear cells without ex vivo expansion were used (0.33+/-0.17). Moreover, macrophages or dendritic cells differentiated from isolated CD14+ cells were significantly less effective in improving neovascularization than EPCs cultivated from the same starting population (P<0.01). CONCLUSIONS: These data demonstrate that EPCs can be generated from nonmonocytic CD14- peripheral blood mononuclear cells and exhibit a unique functional activity to improve neovascularization after hind-limb ischemia.

Animals↗
PubMed2003

A randomized trial of polytetrafluoroethylene-membrane-covered stents compared with conventional stents in aortocoronary saphenous vein grafts.

We compared a conventional stent (Jostent Flex, Jomed GmbH, Rangendingen, Germany) with a polytetrafluoroethylene (PTFE)-membrane-covered stent (Jostent Stentgraft) in patients undergoing intervention of a stenosis in an obstructed vein graft. The use of stents improved results of percutaneous revascularization of obstructed vein grafts, but did not demonstrate the reduced elevated restenosis rate. In addition, long-term clinical event rate is still high compared with intervention in native vessels. Observational studies suggested that stents covered with a PTFE membrane might be associated with a low complication and restenosis rate in venous bypass grafts. This prospective multicenter study included a total of 211 patients who were randomly assigned to receive either a Flex stent or Stentgraft. The primary end point was binary restenosis rate at six months by core lab quantitative coronary angiography. Acute success and procedural events were comparable between the two groups. Restenosis rate was not significantly different between the Flex (20%) and the Stentgraft (29%) groups (p = 0.15), although there was a nonsignificant trend toward a higher late occlusion rate in the Stentgraft group (7% vs. 16%, p = 0.069) at follow-up. Likewise, after a mean observation period of 14 months, cumulative event rates (death, myocardial infarction, or target lesion revascularization) were comparable in the two groups (31% vs. 31%, p = 0.93). This controlled trial does not indicate a superiority of the PTFE-membrane-covered Stentgraft compared with a conventional stent with respect to acute results, restenosis, or clinical event rates.

Aged↗
PubMed2003

Statin therapy in patients with coronary artery disease improves the impaired endothelial progenitor cell differentiation into cardiomyogenic cells.

Human endothelial progenitor cells (EPCs) can differentiate into cardiomyogenic cells in vitro. We tested the effects of statin therapy on the differentiation rate of EPCs from patients with coronary artery disease (CAD), who may benefit from autologous cell therapy.EPCs from 3 age-matched groups were tested: No CAD (n = 13), CAD patients with (n = 10) or without (n = 16) statin therapy. From 4 CAD patients, EPCs were tested before and after 4 weeks of therapy with 20 mg atorvastatin. After 6 days of co-culture with rat neonatal cardiomyocytes, EPC differentiation was quantified by immunostaining for alpha-sarcomeric actinin flow cytometry analysis. After 6 days of co-culture, the percentage of -sarcomeric actinin-positive EPCs was significantly (p = 0.014) higher in EPCs from adults without CAD (8.07% +/- 1.48% of EPCs) compared to EPCs from CAD patients without statin (3.56% +/- 0.72%). Importantly, patients with statin therapy revealed significantly higher numbers of alpha-sarcomeric actinin-positive EPCs (6.36% +/- 0.69%, p = 0.01) compared to CAD patients without statin. In addition, statin therapy resulted in a significant (p = 0.017) increase of EPC differentiation in all 4 CAD patients investigated before and 4 weeks after statin therapy. The survival of EPCs did not differ between the different groups suggesting that the regulation of EPC differentiation is not secondary to altered EPC survival. In vitro, EPC treatment with 0.1 micro M atorvastatin did not affect EPC differentiation (116.15% +/- 49.11% of control).EPCs from patients with CAD display impaired differentiation into cardiomyogenic cells. This defect can be improved by in vivo, statin therapy.

Adult↗
PubMed2003

Essential role of endothelial nitric oxide synthase for mobilization of stem and progenitor cells.

Endothelial nitric oxide synthase (eNOS) is essential for neovascularization. Here we show that the impaired neovascularization in mice lacking eNOS is related to a defect in progenitor cell mobilization. Mice deficient in eNOS (Nos3(-/-)) show reduced vascular endothelial growth factor (VEGF)-induced mobilization of endothelial progenitor cells (EPCs) and increased mortality after myelosuppression. Intravenous infusion of wild-type progenitor cells, but not bone marrow transplantation, rescued the defective neovascularization of Nos3(-/-) mice in a model of hind-limb ischemia, suggesting that progenitor mobilization from the bone marrow is impaired in Nos3(-/-) mice. Mechanistically, matrix metalloproteinase-9 (MMP-9), which is required for stem cell mobilization, was reduced in the bone marrow of Nos3(-/-) mice. These findings indicate that eNOS expressed by bone marrow stromal cells influences recruitment of stem and progenitor cells. This may contribute to impaired regeneration processes in ischemic heart disease patients, who are characterized by a reduced systemic NO bioactivity.

Animals↗
PubMed2003

Myeloperoxidase serum levels predict risk in patients with acute coronary syndromes.

BACKGROUND: Polymorphonuclear neutrophils (PMNs) have gained attention as critical mediators of acute coronary syndromes (ACS). Myeloperoxidase (MPO), a hemoprotein abundantly expressed by PMNs and secreted during activation, possesses potent proinflammatory properties and may contribute directly to tissue injury. However, whether MPO also provides prognostic information in patients with ACS remains unknown. METHODS AND RESULTS: MPO serum levels were assessed in 1090 patients with ACS. We recorded death and myocardial infarctions during 6 months of follow-up. MPO levels did not correlate with troponin T, soluble CD40 ligand, or C-reactive protein levels or with ST-segment changes. However, patients with elevated MPO levels (>350 microg/L; 31.3%) experienced a markedly increased cardiac risk (adjusted hazard ratio [HR] 2.25 [1.32 to 3.82]; P=0.003). In particular, MPO serum levels identified patients at risk who had troponin T levels below 0.01 microg/L (adjusted HR 7.48 [95% CI 1.98 to 28.29]; P=0.001). In a multivariate model that included other biochemical markers, troponin T (HR 1.99; P=0.023), C-reactive protein (1.25; P=0.044), vascular endothelial growth factor (HR 1.87; P=0.041), soluble CD40 ligand (HR 2.78; P<0.001), and MPO (HR 2.11; P=0.008) were all independent predictors of the patient's 6-month outcome. CONCLUSIONS: In patients with ACS, MPO serum levels powerfully predict an increased risk for subsequent cardiovascular events and extend the prognostic information gained from traditional biochemical markers. Given its proinflammatory properties, MPO may serve as both a marker and mediator of vascular inflammation and further points toward the significance of PMN activation in the pathophysiology of ACS.

Abciximab↗