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Role of Platelets and Thrombosis in Coronary Atherosclerotic Disease and Sudden Death

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Role of Platelets and Thrombosis in Coronary Atherosclerotic Disease and Sudden Death JACC Vol. 5, No.6 175B June 1985:175B-184B Role of Platelets and Thrombosis in Coronary Atherosclerotic Disease and Sudden Death VALENTIN FUSTER, MD, FACC, PETER M. STEELE, MB, JAMES H. CHESEBRO, MD, FACC New York, New York and Rochester, Minnesota During the last decade, significant advances have been sion during the acute coronary artery syndromes, post­ made in the understanding of the pathogenesis of coro­ mortem coronary arteriography, and methods for serial nary atherosclerotic disease. Two facts are important: histopathologic and histochemical studies, have brought 1) the early and some of the advanced coronary athero­ to light the clinical importance of the processes of plaque sclerotic lesionsprogress very slowly,probably by means rupture, dissecting hemorrhage and, most important, of a complex stepwise biologic process with one of the thrombosis. These complicated processes appear to be steps being an interaction between platelets and the ar­ of paramount importance in the Pllthogenesis of some terial Wall; the process can be favored by the so-called of the acute coronary syndromes including unstable an­ risk factors of atherosclerotic disease, and 2) some of the gina, myocardial infarction and sudden coronary death. advanced coronary atherosclerotic lesions progress very Antithrombotic and platelet inhibitor therapy is under rapidly, probably by means of complicating anatomic investigation and appears promising in some of these events, one of whichis related to a thrombogenic process. patient subsets. From a clinical point of view, technologic improve­ (J Am Coil CardioI1985;5:175B-184B) ments, such as serial coronary arteriography, reperfu- Natural Evolution of Atherosclerotic Lesions to clinically relevant advanced atherosclerotic lesions (such The International Atherosclerosis Project 0), which in­ as fibrous plaques) frequently occurs in those persons with volved 14 countries with 19 different racial groups, had the the so-called risk factors of atherosclerotic disease; 2) the objective of describing the incidence and natural history of early and some of the advanced atherosclerotic lesions pro­ atherosclerotic lesions found in coronary arteries or the aorta gress very slowly, probably by means of a complex stepwise at autopsy in these different populations. In the study, 23,000 biologic process in which one of the steps is related to sets of coronary arteries and aortas were evaluated. The interaction between platelets and the arterial wall; and 3) findings demonstrated that raised fatty streaks are a universal some of the advanced atherosclerotic lesions progress very phenomenon in young persons in all geographic and racial rapidly, probably by means of complicating anatomic events, groups; however, their evolution into clinically relevant fi­ one of which is related to a thrombogenic process. brous plaques and complicated lesions varies in incidence and extent among different geographic and racial groups Pathogenesis of Early Atherosclerotic Lesions and also among the various arterial systems, being predom­ inant in the coronary artery system (2). The major critical events in the development of the early atherosclerotic lesions (Table 1, Fig. 1) (3) are: 1) hemo­ In the natural history of the atherosclerotic lesion (Fig. dynamic turbulence, endothelial injury and smooth muscle 1 and 2), three facts are important: 1) the progression of early coronary atherosclerotic lesions (raised fatty streaks) cell proliferation; 2) interaction between platelets and the arterial wall; 3) proliferation of fibrous tissue; and 4) ac­ cumulation of lipoproteins. From the Division of Cardiology, Mount Sinai MedicalCenter, New Hemodynamic tpfbulence, endothelial injury and York, New York and the Divisionof Cardiovascular Diseaseand Internal smooth muscle cell ppoliferation. Arterial branch points Medicine,MayoClinicand MayoFoundation,Rochester,Minnesota. This study was supportedin part by researchGrants HL 17430, HL 21533and and other areas where atherosclerotic plaques usually de­ HL 23550 from the National Heart, Lung, and Blood Institute, National velop have been shown to be sites of endothelial injury (4), Institutesof Health, Bethesda, Marylandand Grant CRC-RR585 fromthe There is some evidence that hemodynamic factors are in­ United States Public Health Service, Bethesda, Maryland. Addressfor reprints: ValentinFuster, MD, MountSinai MedicalCen­ volved in causing such focal and chronic or continuous ter, One Gustave L. Levy Place, New York, New York 10029. minimal endothelial injury. From experiments in which hy- ©1985 by the American ColIege of Cardiology 0735-1097/85/$3.30 176B FUSTER ET AL. JACC Vol. 5. No.6 CORONARY ATHEROSCLEROTIC DISEASE June 1985:1758-184B Coronary Atherosclerotic Disease Complicated lesion (Thrombosis) IPathology I Early Figure 1. Scheme of evolution of coronary artery Norma l lesion atherosclerosis . The progression of early lesions to clinically relevant advanced lesions tends to occur in those persons with the so-called risk factors of atherosclerotic disease. The early and some of the • clinically relevant advanced lesions can progress to total occlusion of an artery either through slow pro­ gression or rapidly by thrombus formation with sub­ Myocardial Infarction sequent fibrotic organization. Icr ical l Ulstable Angina Asymptomatic Sudden Death Sudden death I I i 10 50 60 Age (years) draulic models of various flow patterns were used, it was (9) was very superficial, the possibility arises that the mi­ possible to predict from the site of maximal turbulence the gration and proliferation of smooth muscle cells are related areas of predilection for occurrence of atherosclerosis within to an interaction between blood components and the injured the human aorta (5); similarly, the localization of athero­ surface of the arterial wall. sclerotic plaques in the coronary artery tree appears to cor­ Interaction between platelets and the arterial wall. relate with sites of hemodynamic turbulence (2,6,7). There Evidence that platelets and other formed elements of the is increasing evidence that some of the so-called risk factors blood can interact with the minimally injured vascular en­ of atherosclerotic disease may contribute to this chronic dothelium in regions of blood turbulence has been obtained process of endothelial injury (8). in a number of studies . Formed elements, mainly platelets, The concept that atherosclerosis is a local response to have been detected on the endothelial surface of arteries chronic or continuous minimal endothelial injury has also from rabbits, pigs and young human subjects who died received further support (9). Experimental endothelial injury suddenly; these elements occurred near those sites where reproduces the full spectrum of early atherosclerotic lesions. atherosclerosis develops (10). In such experiments, as in spontaneous atherosclerosis, one Thus far, it appears that the observed attachment of plate­ of the first structural changes is an intimal proliferation of lets to damaged endothelial surfaces, and particularly their smooth muscle cells that presumably derive from the media activation, depends mainly on a complex molecule related of the artery. Because the arterial injury in these experiments to factor VIII (II). This molecule, called the Willebrand Figure 2. Progression of coronary ar­ tery atherosclerosis. Slow progres­ sion: A, normal artery; B, fatty streak A with fibrosis; C, advanced fibrous plaque. Rapid progression: D, occlu­ sion by thrombus formation over su­ perficial plaque damage; E, thrombus in process of fibrotic organization. (Reproduced from Fuster V [3], with permission .) JACC Vol. 5. No.6 FUSTER ET AL. 1778 June 1985:1758-1848 CORONARY ATHEROSCLEROTIC DISEASE Table 1. Simplified Unified Concept of Probable Sequential erties (16). It is conceivable that, during the platelet-arterial Events in Coronary Atherosclerotic Disease: Role of Platelets wall interaction, platelet factor 4 and platelet-derived growth and Thrombosis* factor penetrate the vessel wall; then platelet factor 4 may Early lesions-asymptomatic stage attract the smooth muscle cells from the media toward the Hemodynamic factors-endothelial damage intima, and platelet-derived growth factor, together with Platelet deposition other growth factors, may playa role in the proliferation of Smooth muscle cell migration and proliferation Connective tissue synthesis intimal smooth muscle cells. Lipid transformation and deposition Insight into the contribution ofplatelets to the initiation Growing lesions-angina pectoris of atherosclerosis has also been gained by investigating Progression of above (slow process) whether inhibition of platelet function occurs in experi­ Organization of thrombi (rapid processi' mental animals resistant to the development of atheroscle­ Clinical complications Unstable angina rosis. For several years, a breeding colony of pigs with Plaque rupture. thrombosis' severely impaired platelet function in the form of homo­ Myocardial infarction zygous von Willebrand's disease has been maintained in Plaque rupture. thrombotic occlusion' Rochester, Minnesota. Fuster et al. (17,18) showed that Sudden death such pigs have a marked impairment in platelet attachment Chronic myocardial fibrosis to the vascular wall, and they are resistant to the initiation Myocardial infarction} . T MyocardiiaI'ISChemierma thrombosis and progression of both spontaneous atherosclerosis (17) ? Microemboli and atherosclerosis induced by a diet mildly high in cho­ *Italic type indicates
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