The Experts below are selected from a list of 312 Experts worldwide ranked by ideXlab platform
J W Jukema - One of the best experts on this subject based on the ideXlab platform.
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cc chemokine ligand 5 ccl5 rantes and cc chemokine ligand 18 ccl18 parc are specific markers of refractory Unstable Angina Pectoris and are transiently raised during severe ischemic symptoms
Circulation, 2007Co-Authors: Adriaan O Kraaijeveld, S C A De Jager, W De Jager, Berent J Prakken, Shaun R Mccoll, I Haspels, Hein Putter, T J C Van Berkel, L Nagelkerken, J W JukemaAbstract:Background— Chemokines play an important role in atherogenesis and in ischemic injury and repair; however, prospective data on individual chemokines in Unstable Angina Pectoris (UAP) are scarce. Th...
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cc chemokine ligand 5 ccl5 rantes and cc chemokine ligand 18 ccl18 parc are specific markers of refractory Unstable Angina Pectoris and are transiently raised during severe ischemic symptoms
Circulation, 2007Co-Authors: Adriaan O Kraaijeveld, S C A De Jager, W De Jager, Berent J Prakken, Shaun R Mccoll, I Haspels, Hein Putter, L Nagelkerken, T J C Van Berkel, J W JukemaAbstract:BACKGROUND - Chemokines play an important role in atherogenesis and in ischemic injury and repair; however, prospective data on individual chemokines in Unstable Angina Pectoris (UAP) are scarce. Therefore, we assessed chemokine patterns in a prospective cohort of patients with UAP. METHODS AND RESULTS - Plasma samples of 54 patients with Braunwald class IIIB UAP were examined at baseline for 11 chemokines and 5 inflammatory mediators via multiplex analysis. Levels of CC chemokine ligand (CCL)-5 (also known as RANTES [regulated on activation, normally T-cell expressed, and secreted]; 32.7 versus 23.1 ng/mL, P=0.018) and CCL18 (also known as PARC [pulmonary and activation-regulated chemokine]; 104.4 versus 53.7 ng/mL, P=0.011) were significantly elevated in patients with refractory ischemic symptoms versus stabilized patients. Temporal monitoring by ELISA of CCL5, CCL18, and soluble CD40 ligand (sCD40) levels revealed a drop in CCL5 and sCD40L levels in all UAP patients from day 2 onward (CCL5 12.1 ng/mL, P<0.001; sCD40L 1.35 ng/mL, P<0.05), whereas elevated CCL18 levels were sustained for at least 2 days, then were decreased at 180 days after inclusion (34.5 ng/mL, P<0.001). Peripheral blood mononuclear cells showed increased protein expression of chemokine receptors CCR3 and CCR5 in CD3 and CD14 cells at baseline compared with 180 days after inclusion, whereas mRNA levels were downregulated, which was attributable in part to a postischemic release of human neutrophil peptide-3-positive neutrophils and in part to negative feedback. Finally, elevated CCL5 and CCL18 levels predicted future cardiovascular adverse events, whereas C-reactive protein and sCD40L levels did not. CONCLUSIONS - We are the first to report that CCL18 and CCL5 are transiently raised during episodes of UAP, and peak levels of both chemokines are indicative of refractory symptoms. Because levels of both chemokines, as well as of cognate receptor expression by circulating peripheral blood mononuclear cells, are increased during cardiac ischemia, this may point to an involvement of CCL5/CCL18 in the pathophysiology of UAP and/or post-UAP responses. © 2007 American Heart Association, Inc. Chemicals / CAS: C reactive protein, 9007-41-4; CD40 ligand, 226713-27-5; C-Reactive Protein, 9007-41-4; CCL18 protein, human; CCL5 protein, human; CD40 Ligand, 147205-72-9; Chemokine CCL5; Chemokines, CC; Receptors, CCR
Raban Jeger - One of the best experts on this subject based on the ideXlab platform.
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impact of clinical presentation stable Angina Pectoris vs Unstable Angina Pectoris or non st elevation myocardial infarction vs st elevation myocardial infarction on long term outcomes in women undergoing percutaneous coronary intervention with drug
American Journal of Cardiology, 2015Co-Authors: Gennaro Giustino, Usman Baber, Giulio G Stefanini, Melissa Aquino, Gregg W Stone, Samantha Sartori, Philippe Gabriel Steg, William Wijns, Pieter C Smits, Raban JegerAbstract:The long-term risk associated with different coronary artery disease (CAD) presentations in women undergoing percutaneous coronary intervention (PCI) with drug-eluting stents (DES) is poorly characterized. We pooled patient-level data for women enrolled in 26 randomized clinical trials. Of 11,577 women included in the pooled database, 10,133 with known clinical presentation received a DES. Of them, 5,760 (57%) had stable Angina Pectoris (SAP), 3,594 (35%) had Unstable Angina Pectoris (UAP) or non-ST-segment-elevation myocardial infarction (NSTEMI), and 779 (8%) had ST-segment-elevation myocardial infarction (STEMI) as clinical presentation. A stepwise increase in 3-year crude cumulative mortality was observed in the transition from SAP to STEMI (4.9% vs 6.1% vs 9.4%; p <0.01). Conversely, no differences in crude mortality rates were observed between 1 and 3 years across clinical presentations. After multivariable adjustment, STEMI was independently associated with greater risk of 3-year mortality (hazard ratio [HR] 3.45; 95% confidence interval [CI] 1.99 to 5.98; p <0.01), whereas no differences were observed between UAP or NSTEMI and SAP (HR 0.99; 95% CI 0.73 to 1.34; p = 0.94). In women with ACS, use of new-generation DES was associated with reduced risk of major adverse cardiac events (HR 0.58; 95% CI 0.34 to 0.98). The magnitude and direction of the effect with new-generation DES was uniform between women with or without ACS (pinteraction = 0.66). In conclusion, in women across the clinical spectrum of CAD, STEMI was associated with a greater risk of long-term mortality. Conversely, the adjusted risk of mortality between UAP or NSTEMI and SAP was similar. New-generation DESs provide improved long-term clinical outcomes irrespective of the clinical presentation in women.
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impact of clinical presentation stable Angina Pectoris vs Unstable Angina Pectoris or non st elevation myocardial infarction vs st elevation myocardial infarction on long term outcomes in women undergoing percutaneous coronary intervention with drug
American Journal of Cardiology, 2015Co-Authors: Gennaro Giustino, Usman Baber, Giulio G Stefanini, Melissa Aquino, Gregg W Stone, Samantha Sartori, Philippe Gabriel Steg, William Wijns, Pieter C Smits, Raban JegerAbstract:The long-term risk associated with different coronary artery disease (CAD) presentations in women undergoing percutaneous coronary intervention (PCI) with drug-eluting stents (DES) is poorly characterized. We pooled patient-level data for women enrolled in 26 randomized clinical trials. Of 11,577 women included in the pooled database, 10,133 with known clinical presentation received a DES. Of them, 5,760 (57%) had stable Angina Pectoris (SAP), 3,594 (35%) had Unstable Angina Pectoris (UAP) or non–ST-segment-elevation myocardial infarction (NSTEMI), and 779 (8%) had ST-segment-elevation myocardial infarction (STEMI) as clinical presentation. A stepwise increase in 3-year crude cumulative mortality was observed in the transition from SAP to STEMI (4.9% vs 6.1% vs 9.4%; p interaction = 0.66). In conclusion, in women across the clinical spectrum of CAD, STEMI was associated with a greater risk of long-term mortality. Conversely, the adjusted risk of mortality between UAP or NSTEMI and SAP was similar. New-generation DESs provide improved long-term clinical outcomes irrespective of the clinical presentation in women.
Adriaan O Kraaijeveld - One of the best experts on this subject based on the ideXlab platform.
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cc chemokine ligand 5 ccl5 rantes and cc chemokine ligand 18 ccl18 parc are specific markers of refractory Unstable Angina Pectoris and are transiently raised during severe ischemic symptoms
Circulation, 2007Co-Authors: Adriaan O Kraaijeveld, S C A De Jager, W De Jager, Berent J Prakken, Shaun R Mccoll, I Haspels, Hein Putter, T J C Van Berkel, L Nagelkerken, J W JukemaAbstract:Background— Chemokines play an important role in atherogenesis and in ischemic injury and repair; however, prospective data on individual chemokines in Unstable Angina Pectoris (UAP) are scarce. Th...
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cc chemokine ligand 5 ccl5 rantes and cc chemokine ligand 18 ccl18 parc are specific markers of refractory Unstable Angina Pectoris and are transiently raised during severe ischemic symptoms
Circulation, 2007Co-Authors: Adriaan O Kraaijeveld, S C A De Jager, W De Jager, Berent J Prakken, Shaun R Mccoll, I Haspels, Hein Putter, L Nagelkerken, T J C Van Berkel, J W JukemaAbstract:BACKGROUND - Chemokines play an important role in atherogenesis and in ischemic injury and repair; however, prospective data on individual chemokines in Unstable Angina Pectoris (UAP) are scarce. Therefore, we assessed chemokine patterns in a prospective cohort of patients with UAP. METHODS AND RESULTS - Plasma samples of 54 patients with Braunwald class IIIB UAP were examined at baseline for 11 chemokines and 5 inflammatory mediators via multiplex analysis. Levels of CC chemokine ligand (CCL)-5 (also known as RANTES [regulated on activation, normally T-cell expressed, and secreted]; 32.7 versus 23.1 ng/mL, P=0.018) and CCL18 (also known as PARC [pulmonary and activation-regulated chemokine]; 104.4 versus 53.7 ng/mL, P=0.011) were significantly elevated in patients with refractory ischemic symptoms versus stabilized patients. Temporal monitoring by ELISA of CCL5, CCL18, and soluble CD40 ligand (sCD40) levels revealed a drop in CCL5 and sCD40L levels in all UAP patients from day 2 onward (CCL5 12.1 ng/mL, P<0.001; sCD40L 1.35 ng/mL, P<0.05), whereas elevated CCL18 levels were sustained for at least 2 days, then were decreased at 180 days after inclusion (34.5 ng/mL, P<0.001). Peripheral blood mononuclear cells showed increased protein expression of chemokine receptors CCR3 and CCR5 in CD3 and CD14 cells at baseline compared with 180 days after inclusion, whereas mRNA levels were downregulated, which was attributable in part to a postischemic release of human neutrophil peptide-3-positive neutrophils and in part to negative feedback. Finally, elevated CCL5 and CCL18 levels predicted future cardiovascular adverse events, whereas C-reactive protein and sCD40L levels did not. CONCLUSIONS - We are the first to report that CCL18 and CCL5 are transiently raised during episodes of UAP, and peak levels of both chemokines are indicative of refractory symptoms. Because levels of both chemokines, as well as of cognate receptor expression by circulating peripheral blood mononuclear cells, are increased during cardiac ischemia, this may point to an involvement of CCL5/CCL18 in the pathophysiology of UAP and/or post-UAP responses. © 2007 American Heart Association, Inc. Chemicals / CAS: C reactive protein, 9007-41-4; CD40 ligand, 226713-27-5; C-Reactive Protein, 9007-41-4; CCL18 protein, human; CCL5 protein, human; CD40 Ligand, 147205-72-9; Chemokine CCL5; Chemokines, CC; Receptors, CCR
Eugene Braunwald - One of the best experts on this subject based on the ideXlab platform.
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prognosis in the thrombolysis in myocardial ischemia iii registry according to the braunwald Unstable Angina Pectoris classification
American Journal of Cardiology, 2002Co-Authors: Benjamin M Scirica, Christopher P Cannon, Carolyn H. Mccabe, Peter H Stone, William J Rogers, Vernon H Anderson, Sabina A Murphy, Eugene BraunwaldAbstract:The Unstable Angina Pectoris (UAP) classification proposed by Braunwald in 1989, although often used, has never been validated in a large, prospective multicenter study in which all subgroups of patients were included. Patients with UAP or non-ST-elevation myocardial infarction (NSTEMI) were enrolled in the Thrombolysis In Myocardial Ischemia III Registry and classified according to the Braunwald classification for UAP. Clinical end points were compared at 6 weeks and 1 year. Of 3,318 patients, those with primary UAP had lower rates of recurrent myocardial infarction (MI) or death when compared with patients with secondary UAP and post-MI UAP at 6 weeks (4.1% vs 6.4% vs 13.4%, respectively; p <0.001) and 1 year (9.7% vs 16.7% vs 19.7%; p <0.001). Recurrent ischemia at 6 weeks followed the same gradient (13.2% vs 18.5% vs 20.8%; p <0.001). Patients with secondary UAP had similar extent of disease at angiography as primary UAP. Patients with nonresting UAP had lower rates of death or MI than patients with UAP at rest (3.0% vs 5.6%, p = 0.011 at 6 weeks, and 8.2% vs 12.5%, p = 0.004 at 1 year). Patients with ST-segment deviation and those who had received prior antiAnginal medical treatment also had worse outcomes. Thus, the Braunwald classification of UAP predicts prognosis with secondary UAP, post-MI UAP, and patients with pain at rest who have a higher risk for death or recurrent cardiac events. Given their high risk for adverse events, patients with secondary UAP should be treated aggressively.
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validation of the thrombolysis in myocardial infarction timi risk score for Unstable Angina Pectoris and non st elevation myocardial infarction in the timi iii registry
American Journal of Cardiology, 2002Co-Authors: Benjamin M Scirica, Christopher P Cannon, Carolyn H. Mccabe, Sabina A Murphy, Marc S Sabatine, Elliott M Antman, David A Morrow, Michael C Gibson, Eugene BraunwaldAbstract:The 1.4 million patients admitted with Unstable Angina Pectoris and non‐ST-elevation myocardial infarction (UAP/NSTEMI) each year are a heterogenous population with varying risks of death and recurrent cardiac events. The Thrombolysis In Myocardial Infarction (TIMI) risk score for UAP/NSTEMI was created to better stratify patients according to easily obtainable information gathered from the initial history, electrocardiogram, and cardiac markers. 1 The TIMI risk score was derived and validated in the TIMI 11B and Efficacy and Safety of Subcutaneous Enoxaparin in Non‐Q-wave Coronary Events (ESSENCE) trials and accurately predicted adverse outcomes through 14 days. It has also been applied in the Platelet Receptor Inhibition for Ischemic Syndrome Management in Patients Limited by Unstable Signs and Symptoms (PRISM-PLUS) and Treat Angina with Aggrastat and determine Cost of Therapy with an Invasive or Conservative Strategy (TACTICS)-TIMI 18 Trials. 2,3 However, because clinical trials of UAP/ NSTEMI usually select higher risk patients (with electrocardiographic changes and/or positive cardiac markers), there has been questions whether the TIMI risk score would be valid in an unselected population of patients representative of general clinical practice. The goal of this study was to validate the TIMI risk score in a large unselected population of patients with UAP/NSTEMI and assess its long-term predictive value. ••• The details of the TIMI III Registry have been previously reported. 4 Briefly, patients admitted be
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association of white blood cell count with increased mortality in acute myocardial infarction and Unstable Angina Pectoris
American Journal of Cardiology, 2001Co-Authors: Christopher P Cannon, Carolyn H. Mccabe, Robert G Wilcox, Jane H. Bentley, Eugene BraunwaldAbstract:Markers of inflammation assessed by a number of techniques, including high-sensitivity C-reactive protein, have been found to be powerful risk factors for the development of myocardial infarction and other acute coronary events, 1,2 and to be valuable predictors of adverse prognosis in patients with Unstable Angina. 3‐ 6 Another, even simpler and universally available marker of inflammation is the white blood cell (WBC) count. Previous studies of patients with acute myocardial infarction (AMI), performed in an era before aggressive fibrinolytic-antithrombotic and interventional therapies, have observed that patients with elevated WBC counts were at higher risk of mortality and recurrent AMI. 7‐11 We hypothesized that the WBC count would be useful for risk stratification in these conditions as well. ••• The trial design and results of the Orbofiban in Patients with Unstable Coronary Syndromes trial have recently been reported. 12 Briefly, between October 16, 1997, and November 5, 1998, 10,288 patients with AMI or high-risk Unstable Angina Pectoris were enrolled into the trial at 888 hospitals in 29 countries. Patients had to have either AMI or Unstable Angina Pectoris with an associated high-risk feature, and be enrolled within 72 hours from the onset of their acute coronary syndrome. Eligible patients were treated with 150 to 162 mg of aspirin daily and were randomized in a 1:1:1 fashion to receive 1 of 2 dosing regimens of the oral IIb/IIIa inhibitor orbofiban, or placebo. Patients were seen in follow-up at 14 and 30 days and every 3 months, with a complete blood count performed at baseline (the time of enrollment) in 7,651 patients that was analyzed in the central laboratory. The primary end point was a composite of death, AMI, recurrent ischemia at rest leading to rehospitalization or urgent revascularization, or stroke. Patients were stratified by WBC count at baseline, and 30-day and 10-month outcomes were compared between the groups. Outcomes are presented as Kaplan-Meier event rates with p values from log-rank tests (with follow-up censored at 30 days or 10 months). Multivariate analysis using Cox regression analysis was used to control for differences in baseline characteristics.
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management of Unstable Angina Pectoris and non q wave acute myocardial infarction in the united states and canada the timi iii registry
American Journal of Cardiology, 1997Co-Authors: Vernon H Anderson, Christopher P Cannon, Peter H Stone, Frank V Aguirre, Robert S Gibson, Bruce Thompson, Genell L Knatterud, Eugene BraunwaldAbstract:Management of Q-wave acute myocardial infarction (AMI) has been shown to differ between the United States and Canada, with more catheterization and revascularization procedures performed in the United States, but with little or no apparent difference in clinical outcomes. No previous studies have evaluated management differences for the acute coronary syndromes of Unstable Angina Pectoris and non-Q-wave AMI. We therefore compared treatments and outcomes between 14 United States and 4 Canadian tertiary care centers participating in an observational registry of all consecutive admissions for Unstable Angina or non-Q-wave AMI between 1990 and 1993. A random, stratified sample was selected for detailed assessment and follow-up. There were 1,733 patients enrolled in United States centers and 642 in Canadian ones. In United States centers patients were less likely to receive intravenous nitroglycerin, heparin, beta blockers, calcium antagonists, or > or = 2 anti-ischemic agents. Coronary arteriography during index hospitalization was equally frequent in both countries (63.4% vs 66.9%, p = 0.781), but at 6 weeks and 1 year coronary arteriography was slightly less frequent in the United States patients. Revascularization by coronary angioplasty or bypass surgery was equivalent at 6 weeks and 1 year; however, there were trends toward less angioplasty and more bypass surgery in the United States than in Canada. Patients at United States centers stayed in the hospital fewer days than patients at Canadian centers (mean 8.2 vs 12.1 days, p <0.001). Death or AMI by 6 weeks was not different (4.8% vs 4.4%, p = 0.633), nor was it different at 1 year (10.0% vs 10.2%, p = 0.836). The combined outcome of death, AMI, or recurrent ischemia was more common in United States than in Canadian patients at 6 weeks (18.4% vs 13.9%, p = 0.004). Our findings indicate that United States physicians and hospitals did not consistently utilize more resources and were not more aggressive than their Canadian counterparts when treating acute coronary syndromes during this period.
Gilles Montalescot - One of the best experts on this subject based on the ideXlab platform.
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relation of timing of cardiac catheterization to outcomes in patients with non st segment elevation myocardial infarction or Unstable Angina Pectoris enrolled in the multinational global registry of acute coronary events
American Journal of Cardiology, 2005Co-Authors: Gilles Montalescot, Omar H Dabbous, Michael J Lim, Marcus Flather, Rajendra H MehtaAbstract:We assessed whether timing of catheterization is associated with the type of non-ST-segment elevation acute coronary syndrome and/or outcome in patients who were enrolled in the Global Registry of Acute Coronary Events. Overall, 8,853 patients who had Unstable Angina Pectoris or non-ST-elevation myocardial infarction were categorized according to timing of catheterization: expeditive ( 48 hours). Patients in the delayed group were older, more frequently had previous myocardial infarction or stroke, and had a higher risk score compared with those in the expeditive and early groups (all p ≤0.001). Killip class IV at admission, non-ST-elevation myocardial infarction, and Q waves after the index electrocardiogram were more common in the expeditive group (all p
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comparison of effects on markers of blood cell activation of enoxaparin dalteparin and unfractionated heparin in patients with Unstable Angina Pectoris or non st segment elevation acute myocardial infarction the armada study
American Journal of Cardiology, 2003Co-Authors: Gilles Montalescot, Claire Balditsollier, Daniela Chibedi, Jeanphilippe Collet, Thierry Soulat, Miles Dalby, Emi R Choussat, Ariel Cohen, Michel Slama, Phillipe Gabriel StegAbstract:Abstract The low-molecular-weight heparins (LMWHs) enoxaparin and dalteparin have shown superior and equivalent efficacy, respectively, over unfractionated heparin (UFH) in patients with Unstable Angina Pectoris (UAP) or non–ST-segment elevation myocardial infarction (NSTEMI). This study aimed to identify markers of blood cell activation that are independent predictors of outcomes at 1 month and to compare the effects of enoxaparin, dalteparin, and UFH on any such markers. In this multicenter, prospective, open-label study, 141 patients with UAP or NSTEMI were randomized to treatment for 48 to 120 hours with enoxaparin (n = 46), dalteparin (n = 48), or UFH (n = 47). Blood samples were taken at the time of randomization and after ≥48 hours of treatment but before catheterization. Multivariate analysis identified increased plasma levels of von Willebrand factor (vWF) and decreased platelet levels of glycoprotein Ib/IX complexes as independent predictors of 1-month adverse outcome (a composite of death, myocardial infarction, and recurrent ischemia). vWF release was strongly related to and may have been released by inflammation as measured by C-reactive protein. Both LMWHs reduced the release of vWF in plasma (as well as C-reactive protein) compared with UFH. Enoxaparin had a more favorable effect on glycoprotein Ib/IX complexes than either dalteparin or UFH. The incidence of the composite clinical efficacy end point was: 13% (enoxaparin), 19% (dalteparin), and 28% (UFH). vWF and its receptor glycoprotein Ib/IX play a key role in acute coronary syndromes. vWF is linked to inflammation and, like glycoprotein Ib/IX, is affected more favorably by the LWMHs than by UFH.
