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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.
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.
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