Platelets in Atherothrombosis David A. Vorchheimer, MD, Richard Becker, MD  Mayo Clinic Proceedings  Volume 81, Issue 1, Pages 59-68 (January 2006) DOI: 10.4065/81.1.59 Copyright © 2006 Mayo Foundation for Medical Education and Research Terms and Conditions

FIGURE 1 Platelet adhesion and activation. From Antiplatelet Therapy in Clinical Practice,7 with permission. Mayo Clinic Proceedings 2006 81, 59-68DOI: (10.4065/81.1.59) Copyright © 2006 Mayo Foundation for Medical Education and Research Terms and Conditions

FIGURE 2 Platelet shape changes and aggregation. From Arterioscler Thromb Vasc Biol,9 with permission from Lippincott Williams & Wilkins. Mayo Clinic Proceedings 2006 81, 59-68DOI: (10.4065/81.1.59) Copyright © 2006 Mayo Foundation for Medical Education and Research Terms and Conditions

FIGURE 3 Traditional cascade model of coagulation. The intrinsic system represents the clotting factors in the circulating blood. The extrinsic system represents tissue factor in complex with factor VII. HK = high-molecular-weight kininogen; PK = prekallikrein; TF = tissue factor. From Anesthesiology,10 with permission from Lippincott Williams & Wilkins. Mayo Clinic Proceedings 2006 81, 59-68DOI: (10.4065/81.1.59) Copyright © 2006 Mayo Foundation for Medical Education and Research Terms and Conditions

FIGURE 4 Cell-based model of coagulation. Activated cofactors Va and VIIIa occupy sites in the activated platelet before binding of the respective enzymes, factors Xa and IXa. Factor Xa on the activated platelets is recruited from circulating factor X. The burst of thrombin generation takes place on the platelet surface. Thrombin generation can be boosted by further activation of factor IX by factor XIa. The burst of thrombin is sufficient to convert fibrinogen to fibrin. TF = tissue factor. From Anesthesiology,10 with permission from Lippincott Williams & Wilkins. Mayo Clinic Proceedings 2006 81, 59-68DOI: (10.4065/81.1.59) Copyright © 2006 Mayo Foundation for Medical Education and Research Terms and Conditions

FIGURE 5 Rolling of polymorphonuclear leukocytes (PMN) on adherent, activated platelets is mediated via interactions between P-selectin and P-selectin glycoprotein 1 (PSGL-1). From J Thromb Haemost,22 with permission from Blackwell Publishing. Mayo Clinic Proceedings 2006 81, 59-68DOI: (10.4065/81.1.59) Copyright © 2006 Mayo Foundation for Medical Education and Research Terms and Conditions

FIGURE 6 Interactions between platelets (PLT) and endothelial cells (EC) mediated by arachidonic acid (AA) metabolites. Activators of each cell type induce phospholipase A2 (PLA2)-mediated hydrolysis of free AA from membrane phospholipid (PL) pools. The AA is converted by cyclooxygenase (COX) to the prostaglandin endoperoxides, PGG2 and PGH2. Endoperoxides are metabolized to thromboxane A2 (TXA2) by thromboxane synthase (TxS) in platelets and to PGI2 by prostacyclin synthase (PS) in endothelial cells. The TXA2 binds to platelet receptors to stimulate platelet activation; PGI2 binds to separate platelet receptors to inhibit platelet activation. From Am J Med,44 with permission from Excerpta Medica, Inc. Mayo Clinic Proceedings 2006 81, 59-68DOI: (10.4065/81.1.59) Copyright © 2006 Mayo Foundation for Medical Education and Research Terms and Conditions