A. Michael Lincoff – författare

One of the most important developments in the field of cardiovascular medicine over the last two decades has been recognition of the key role played by arterial thrombosis in the pathogenesis of acute coronary syndromes, ischemic complications of percutane- ous coronary revascularization, and coronary and peripheral atherosclerosis. The phar- macologic armamentarium directed against vascular thrombosis has thus expanded substantially during that time, with development of new fibrinolytic agents, low-molecu- lar-weight heparins, direct thrombin inhibitors, antagonists to platelet activation, and the platelet glycoprotein lIb/IlIa inhibitors. Though clinical investigations of these com- pounds have been marked by failures as well as successes, there is little doubt that enhanced antithrombotic therapies have markedly improved the outcome of patients undergoing coronary revascularization or with acute coronary syndromes. Glycoprotein IIblIlIa receptor antagonists were introduced into clinical practice to overcome the limitations of approaches that inhibit only individual pathways of platelet activation.Multiple mechanisms of platelet activation in response to different agonists converge on the platelet membrane glycoprotein IIblIlIa complex, the "final common pathway" of platelet aggregation. The clinical hemorrhagic syndrome caused by a rare inherited defect in this receptor (Glanzmann' s thrombasthenia), characterized by muco- cutaneous and postsurgical bleeding, but infrequent spontaneous organ (particularly central nervous system) bleeding, suggested that therapeutic inhibition of this receptor might be a potent, yet well-tolerated means of treating thrombotic disorders.

Substantial morbidity and mortality remains associated with thrombotic events has stimulated the rapid expansion of the available armamentarium to combat pathologic thrombosis. Pathologic thrombosis plays an essential role in the pathogenesis of acute coronary syndromes (ACS), ischemic complications of percutaneous coronary intervention (PCI), venous thromboembolic disease, and embolic complications of arrhythmias and various cardiomyopathies.Written by experts in the field, Antithrombotic Drug Therapy in Cardiovascular Disease carefully examines individual and various combinations of the available antithrombotic regimens including fibrinolytic agents, antiplatelet therapies (aspirin, thieneopyridines, glycoprotein IIb/IIIa inhibitors), and anticoagulant therapies (unfractionated heparin, low-molecular-weight heparins, direct thrombin inhibitors, and synthetic factor X inhibitors), non-ST-segment elevation (NSTE) ACS and ST-segment elevation myocardial infarction (STEMI). A detailed overview, Antithrombotic Drug Therapy in Cardiovascular Disease presents the evidence demonstrating the efficacy of available antithrombotic therapies in specific disease states such as atrial fibrillation, cardiomyopathy, valvular heart disease, and heparin-induced thrombocytopenia (HIT).

One of the most important developments in the field of cardiovascular medicine over the last two decades has been recognition of the key role played by arterial thrombosis in the pathogenesis of acute coronary syndromes, ischemic complications of percutane- ous coronary revascularization, and coronary and peripheral atherosclerosis. The phar- macologic armamentarium directed against vascular thrombosis has thus expanded substantially during that time, with development of new fibrinolytic agents, low-molecu- lar-weight heparins, direct thrombin inhibitors, antagonists to platelet activation, and the platelet glycoprotein lIb/IlIa inhibitors. Though clinical investigations of these com- pounds have been marked by failures as well as successes, there is little doubt that enhanced antithrombotic therapies have markedly improved the outcome of patients undergoing coronary revascularization or with acute coronary syndromes. Glycoprotein IIblIlIa receptor antagonists were introduced into clinical practice to overcome the limitations of approaches that inhibit only individual pathways of platelet activation.Multiple mechanisms of platelet activation in response to different agonists converge on the platelet membrane glycoprotein IIblIlIa complex, the "final common pathway" of platelet aggregation. The clinical hemorrhagic syndrome caused by a rare inherited defect in this receptor (Glanzmann' s thrombasthenia), characterized by muco- cutaneous and postsurgical bleeding, but infrequent spontaneous organ (particularly central nervous system) bleeding, suggested that therapeutic inhibition of this receptor might be a potent, yet well-tolerated means of treating thrombotic disorders.