Research Topics
Species | Mark I FurmanSummaryAffiliation: University of Massachusetts Medical School Country: USA Publications
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Detail Information
Publications
GPIIb/IIIa inhibitor-induced dethrombosisMark I Furman
Center for Platelet Function Studies, Division of Cardiovascular Medicine, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA
J Thromb Thrombolysis 18:11-7. 2004....- Quantification of abciximab-induced platelet inhibition is assay dependent: a comparative study in patients undergoing percutaneous coronary interventionMark I Furman
Center for Platelet Function Studies and Division of Cardiovascular Medicine, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01655, USA
Am Heart J 145:e6. 2003.... - Circulating monocyte-platelet aggregates are an early marker of acute myocardial infarctionM I Furman
Center for Platelet Function Studies, Division of Cardiovascular Medicine, Worcester, Massachusetts 01655, USA
J Am Coll Cardiol 38:1002-6. 2001..We investigated whether elevated levels of circulating monocyte-platelet aggregates (MPA) can be used to identify patients with acute myocardial infarction (AMI)... - Twenty-two year (1975 to 1997) trends in the incidence, in-hospital and long-term case fatality rates from initial Q-wave and non-Q-wave myocardial infarction: a multi-hospital, community-wide perspectiveM I Furman
Department of Medicine, University of Massachusetts Medical School, Worcester 01655, USA
J Am Coll Cardiol 37:1571-80. 2001.... - GPIIb-IIIa antagonists reduce thromboinflammatory processes in patients with acute coronary syndromes undergoing percutaneous coronary interventionM I Furman
Cardiac Catheterization Laboratories, UMass Memorial Medical Center, University of Massachusetts Medical School, Worcester, MA 01605, USA
J Thromb Haemost 3:312-20. 2005.... - Elevated leukocyte count and adverse hospital events in patients with acute coronary syndromes: findings from the Global Registry of Acute Coronary Events (GRACE)Mark I Furman
Division of Cardiovascular Medicine, University of Massachusetts Medical School, Worcester, Mass 01655, USA
Am Heart J 147:42-8. 2004..To examine the association between elevated leukocyte count and hospital mortality and heart failure in patients enrolled in the multinational, observational Global Registry of Acute Coronary Events (GRACE)... - Antiplatelet strategies: evaluating their current role in the setting of acute coronary syndromesEugene Braunwald
TIMI Study Group, Cardiovascular Division, Brigham and Women s Hospital, Department of Medicine, Harvard Medical School, 350 Longwood Avenue, Boston, Massachusetts 02115, USA
Clin Cardiol 31:I2-9. 2008..Currently, it appears that the use of GP IIb/IIIa antagonists might be most beneficial in high-risk ACS patients scheduled to undergo PCI, who demonstrate non-ST-segment elevation myocardial infarction and elevated troponin levels... - Investigating the mechanisms of hyporesponse to antiplatelet approachesEugene Braunwald
TIMI Study Group, Cardiovascular Division, Brigham and Women s Hospital, Department of Medicine, Harvard Medical School, 350 Longwood Avenue, Boston, Massachusetts 02115, USA
Clin Cardiol 31:I21-7. 2008..Results from these studies could cause a paradigm shift toward individualized antiplatelet therapy, improving predictability of platelet inhibition, and diminishing the likelihood for hyporesponsiveness... - Clinical considerations with the use of antiplatelet therapy in patients undergoing percutaneous coronary interventionEugene Braunwald
TIMI Study Group, Cardiovascular Division, Brigham and Women s Hospital, Department of Medicine, Harvard Medical School, 350 Longwood Avenue, Boston, Massachusetts 02115, USA
Clin Cardiol 31:I28-35. 2008..Patient nonadherence to treatment and premature discontinuation and underutilization of antiplatelet therapies by physicians remain important clinical problems with potentially dire consequences... - The problem of persistent platelet activation in acute coronary syndromes and following percutaneous coronary interventionEugene Braunwald
TIMI Study Group, Cardiovascular Division, Brigham and Women s Hospital, Department of Medicine, Harvard Medical School, 350 Longwood Avenue, Boston, Massachusetts 02115, USA
Clin Cardiol 31:I17-20. 2008..Aspirin, thienopyridines, and glycoprotein IIb/IIIa inhibitors, the 3 major pharmacologic approaches to persistent platelet activation, target various levels of the hemostatic pathways and thrombus formation... - Residual arachidonic acid-induced platelet activation via an adenosine diphosphate-dependent but cyclooxygenase-1- and cyclooxygenase-2-independent pathway: a 700-patient study of aspirin resistanceAndrew L Frelinger
Center for Platelet Function Studies, Department of Pediatrics, UMass Memorial Medical Center, 55 Lake Ave N, Worcester, Massachusetts 01655, USA
Circulation 113:2888-96. 2006.... - The active metabolite of prasugrel inhibits ADP-stimulated thrombo-inflammatory markers of platelet activation: Influence of other blood cells, calcium, and aspirinAndrew L Frelinger
Center for Platelet Function Studies, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA
Thromb Haemost 98:192-200. 2007..This inhibition is enhanced in the presence other blood cells and calcium, but not aspirin... - Application of flow cytometry to platelet disordersMatthew D Linden
Center for Platelet Function Studies, University of Massachusetts Medical School, Worcester, MA 01655, USA
Semin Thromb Hemost 30:501-11. 2004..Accordingly, this review summarizes the key technical and methodologic components of flow cytometric analysis of platelets, as well as specific examples of its application to diagnosis and patient care... - Release of soluble CD40L from platelets is regulated by glycoprotein IIb/IIIa and actin polymerizationMark I Furman
Center for Platelet Function Studies, University of Massachusetts Medical School, Worcester, Massachusetts 01655, USA
J Am Coll Cardiol 43:2319-25. 2004..In addition to their well-characterized inhibition of platelet aggregation, GP IIb/IIIa antagonists may obviate the proinflammatory and prothrombotic effects of sCD40L... - Whole blood analysis of leukocyte-platelet aggregatesMarc R Barnard
University of Massachusetts Medical School, Worcester, Massachusetts, USA
Curr Protoc Cytom . 2003..Light scatter and at least one leukocyte-specific antibody are used to gate the desired population, and the presence of associated platelets is detected by immunostaining for abundant platelet-specific markers... - Immunophenotypic analysis of plateletsLori A Krueger
University of Massachusetts Medical School, Worcester, Massachusetts, USA
Curr Protoc Cytom . 2002..Detailed discussion of appropriate sample handling, reagent preparation, flow cytometric set-up, and data interpretation are provided for three independent assays... - Combined effects of mild hypothermia and glycoprotein IIb/IIIa antagonists on platelet-platelet and leukocyte-platelet aggregationAndrew L Frelinger
Center for Platelet Function Studies, Department of Pediatrics, University of Massachusetts Medical School, Worcester 01655, USA
Am J Cardiol 92:1099-101. 2003.... - Increased platelet reactivity and circulating monocyte-platelet aggregates in patients with stable coronary artery diseaseM I Furman
Cardiovascular Thrombosis Research Center, Department of Medicine, University of Massachusetts Medical Center, Worcester 01655, USA
J Am Coll Cardiol 31:352-8. 1998..We sought to examine whether patients with stable coronary artery disease (CAD) have increased platelet reactivity and an enhanced propensity to form monocyte-platelet aggregates... - Assessing the current role of platelet function testingEugene Braunwald
TIMI Study Group, Cardiovascular Division, Brigham and Women s Hospital, Department of Medicine, Harvard Medical School, 350 Longwood Avenue, Boston, Massachusetts 02115, USA
Clin Cardiol 31:I10-6. 2008..The ideal platelet function test for clinical practice would be rapid, easy-to-use, inexpensive, and reliable... - Current options in platelet function testingAlan D Michelson
Center for Platelet Function Studies, Division of Cardiovascular Medicine, Department of Pediatrics and Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01655, USA
Am J Cardiol 98:4N-10N. 2006..In patients treated with antiplatelet drugs, the degree of platelet inhibition, as determined by several of these new platelet function assays, has been shown to predict major adverse cardiac events... - Leukocytosis and adverse hospital outcomes after acute myocardial infarctionVandana Menon
Department of Medicine, Division of Clinical Care Research, Tufts University School of Medicine/New England Medical Center, Boston, Massachusetts, USA
Am J Cardiol 92:368-72. 2003..These findings suggest that the WBC count should be considered an important prognostic factor associated with adverse hospital outcomes in patients with AMI... - Circulating monocyte-platelet aggregates are a more sensitive marker of in vivo platelet activation than platelet surface P-selectin: studies in baboons, human coronary intervention, and human acute myocardial infarctionA D Michelson
Center for Platelet Function Studies, Departments of Pediatrics and Medicine, University of Massachusetts Medical School, Worcester, MA 01655, USA
Circulation 104:1533-7. 2001..Platelet surface P-selectin is considered the "gold standard" marker of platelet activation. Degranulated, P-selectin-positive platelets, however, aggregate with leukocytes in vitro and rapidly lose surface P-selectin in vivo... - Evaluation of platelet function by flow cytometryA D Michelson
Center for Platelet Function Studies, University of Massachusetts Medical School, Worcester, Massachusetts, 01655, USA
Methods 21:259-70. 2000.... - 'Postconditioning' the human heart: multiple balloon inflations during primary angioplasty may confer cardioprotectionChad E Darling
Dept of Emergency Medicine, University of Massachusetts Medical School, 55 Lake Avenue, North Worcester, MA, 01655, USA
Basic Res Cardiol 102:274-8. 2007..05), an outcome consistent with the concept that relief of sustained ischemia in a stuttered manner (analogous to postconditioning) may evoke cardioprotection in the clinical setting... - The cleaved peptide of PAR1 is a more potent stimulant of platelet-endothelial cell adhesion than is thrombinR Brannon Claytor
Department of Surgery, Division of Vascular Surgery, and Center for Platelet Function Studies, University of Massachusetts Medical School, Worcester, Mass 01655, USA
J Vasc Surg 37:440-5. 2003..We examined the effect of TR(1-41) on platelet activation and on platelet-endothelial cell adhesion... - Antithrombotic therapy in the cardiac catheterization laboratory: focus on antiplatelet agentsM I Furman
Division of Cardiovascular Medicine, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA
Curr Cardiol Rep 2:386-94. 2000..Despite the growing use of GP IIb/IIIa antagonists, much information remains unknown as to the proper dosing and the effects these agents have on other elements of the hemostatic and vascular systems... - The active metabolite of prasugrel inhibits adenosine diphosphate- and collagen-stimulated platelet procoagulant activitiesA L Frelinger
Center for Platelet Function Studies, and Department of Pediatrics, University of Massachusetts Medical School, Worcester, MA 01655, USA
J Thromb Haemost 6:359-65. 2008..We therefore examined whether R-138727 inhibits ADP- and collagen-triggered platelet procoagulant activities... - Evidence that pre-existent variability in platelet response to ADP accounts for 'clopidogrel resistance'A D Michelson
Center for Platelet Function Studies, University of Massachusetts Medical School, Worcester, MA 01655, USA
J Thromb Haemost 5:75-81. 2007..Clopidogrel is a widely used antithrombotic agent that inhibits the platelet P2Y(12) adenosine diphosphate (ADP) receptor. There is increasing interest in 'clopidogrel resistance'... - Indices of platelet activation and the stability of coronary artery diseaseM D Linden
Center for Platelet Function Studies, University of Massachusetts Medical School, Worcester, MA 01655, USA
J Thromb Haemost 5:761-5. 2007..To determine whether indices of platelet activation are associated with the stability of coronary artery disease (CAD)... - Effects of platelet binding on whole blood flow cytometry assays of monocyte and neutrophil procoagulant activityM R Barnard
Center for Platelet Function Studies, University of Massachusettes Medical School, Worcester, MA 01655, USA
J Thromb Haemost 3:2563-70. 2005.... - Laser scanning cytometry: a novel method for the detection of platelet--endothelial cell adhesionR B Claytor
Department of Surgery, Division of Vascular Surgery, University of Massachusetts Medical School, Worcester, Massachusetts 01655, USA
Cytometry 43:308-13. 2001..We report a novel method for in vitro detection of platelet-endothelial cell adhesion that allows endothelial cells to remain as an intact monolayer and for visualization of individual platelets... - Dissociation of glycoprotein IIb/IIIa antagonists from platelets does not result in fibrinogen binding or platelet aggregationA L Frelinger
Center for Platelet Function Studies, University of Massachusetts Medical School, Worcester, MA 01655, USA
Circulation 104:1374-9. 2001..These apparently paradoxical results have been extensively referenced in the cardiology literature... - Ten-year trends in the incidence, treatment, and outcome of Q-wave myocardial infarctionH L Dauerman
Cardiovascular Division, University of Massachusetts Memorial Medical Center, Worcester 01655, USA
Am J Cardiol 86:730-5. 2000..The decrease in mortality occurs in the setting of broader use of reperfusion and adjunctive therapy (including primary angioplasty)... - Leukocyte-platelet aggregation, platelet surface P-selectin, and platelet surface glycoprotein IIIa after percutaneous coronary intervention: Effects of dalteparin or unfractionated heparin in combination with abciximabM I Furman
Center for Platelet Function Studies and the Division of Cardiovascular Medicine, Departments of Medicine, Pediatrics, and Cell Biology, University of Massachusetts Medical School, Worcester, MA 01655, USA
Am Heart J 142:790-8. 2001..Low-molecular-weight heparins have been reported to cause less platelet activation than unfractionated heparin... - Laboratory markers of platelet activation and their clinical significanceA D Michelson
Center for Platelet Function Studies, Department of Pediatrics, University of Massachusetts Medical School, Worcester 01655, USA
Curr Opin Hematol 6:342-8. 1999.... - GPIIb-IIIa antagonist-induced reduction in platelet surface factor V/Va binding and phosphatidylserine expression in whole bloodM I Furman
Center for Platelet Function Studies, University of Massachusetts Medical School, Worcester, PA 01655, USA
Thromb Haemost 84:492-8. 2000..Fibrinogen binding to GPIIb-IIIa is important in the generation of platelet procoagulant activity... - The role of platelet inhibition in the drug-eluting stent eraMichael R Tamberella
Department of Medicine and the Center for Platelet Function Studies, UMass Memorial Medical Center and University of Massachusetts Medical School, Worcester, MA 01655, USA
Coron Artery Dis 15:327-9. 2004..Drug-eluting stents now account for greater than 50% of stenting procedures. This review focuses on the limited available data describing the use of antiplatelet agents in patients undergoing drug-eluting stent implantation... - The cleaved peptide of the thrombin receptor is a strong platelet agonistM I Furman
Center for Platelet Function Studies, University of Massachusetts Medical Center, Worcester, MA 01655, USA
Proc Natl Acad Sci U S A 95:3082-7. 1998..TR1-41-induced platelet activation was synergistic with TR42-55. In summary, the cleaved peptide of the seven-transmembrane domain TR (TR1-41) is a strong platelet agonist... - Activated clotting times in the setting of eptifibatide use during percutaneous coronary interventionHarold L Dauerman
Cardiac Unit, University of Vermont College of Medicine, Burlington, Vermont 05401, USA
J Thromb Thrombolysis 13:127-32. 2002..The impact of the short acting glycoprotein (GP) IIb-IIIa inhibitor, eptifibatide, on ACT measurements has not been studied... - The Ultegra rapid platelet-function assay: comparison to standard platelet function assays in patients undergoing percutaneous coronary intervention with abciximab therapyGuy L Wheeler
Wake Forest University School of Medicine, Winston-Salem, NC 27157-1045, USA
Am Heart J 143:602-11. 2002..Ultegra RPFA measurements are not operator-dependent and are not influenced by concomitant medications, hematologic parameters, or demographics... - An additional mechanism of action of abciximab: dispersal of newly formed platelet aggregatesStanley J Marciniak
Centocor, Malvern, PA 19355, USA
Thromb Haemost 87:1020-5. 2002..In vivo, abciximab may destabilize coronary thrombi by preventing aggregate formation and dispersing mural thrombi... - Measuring antiplatelet drug effects in the laboratoryPaul Harrison
Oxford Haemophilia Centre and Thrombosis Unit, Churchill Hospital, Oxford, United Kingdom
Thromb Res 120:323-36. 2007..A clinically meaningful definition of "resistance" to antiplatelet drugs needs to be developed, based on data linking drug-dependent laboratory tests to clinical outcomes in patients... - A novel point-of-care enoxaparin monitor for use during percutaneous coronary intervention. Results of the Evaluating Enoxaparin Clotting Times (ELECT) StudyDavid J Moliterno
Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA
J Am Coll Cardiol 42:1132-9. 2003..Morrisville, North Carolina), a new point-of-care test... - Platelet-monocyte aggregates in patients with chronic venous insufficiency remain elevated following correction of refluxMichael J Rohrer
Division of Vascular Surgery and the Center for Platelet Function Studies, The University of Massachusetts Medical School, 55 Lake Avenue, North Worcester 01655, USA
Cardiovasc Surg 10:464-9. 2002..The purpose of this study was to determine whether patients with CVI maintain elevated levels of PMAs following complete surgical correction of chronic venous insufficiency...