Acute coronary syndrome (ACS), one of the life-threatening manifestations of coronary artery disease, ranges from unstable angina, to acute myocardial infarction (non—ST elevation and ST elevation), to sudden cardiac death. The pathophysiology of ACS in the vast majority of cases involves coronary thrombosis overlying a disrupted atherosclerotic plaque [1]. Several autopsy studies have demonstrated that 70% to 80% of coronary thrombi occur at sites where the fi brous cap of coronary artery plaque has ruptured, with extension of the thrombus into the plaque and into the lumen, as well as with propagation of the thrombus upstream from the site of cap rupture [2, 3]. Although it would be preferable to prevent ACS rather than treat it after its occurrence, currently there is no optimal laboratory or imaging modality to predict its timing. Therefore, risk-factor modifi cation is the best approach until reliable, noninvasive tests become available.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Farb A, Tang AL, Burke AP, et al. Sudden coronary death. Frequency of active coronary lesions, inactive coronary lesions, and myocardial infarction. Circulation 1995; 92:1701–1709.
Falk E. Plaque rupture with severe pre-existing stenosis precipitating coronary thrombosis. Characteristics of coronary atherosclerotic plaques underlying fatal occlusive thrombi. Br Heart J 1983;50:127–134.
Constantinides P. Atherosclerosis—a general survey and synthesis. Surv Synth Pathol Res 1984;3:477–498.
Narula J, Finn AV, Demaria AN. Picking plaques that pop. J Am Coll Cardiol 2005; 45:1970–1973.
Warnes CA, Roberts WC. Sudden coronary death: comparison of patients with to those without coronary thrombus at necropsy. Am J Cardiol 1984;54:1206–1211.
Davies MJ, Bland JM, Hangartner JR, et al. Factors influencing the presence or absence of acute coronary artery thrombi in sudden ischaemic death. Eur Heart J 1989;10:203–208.
Takada A, Saito K, Ro A, et al. Acute coronary syndrome as a cause of sudden death in patients with old myocardial infarction: a pathological analysis. Leg Med (Tokyo) 2003;5(Suppl 1):S292–S294.
Thom T, Haase N, Rosamond D, et al. Heart disease and stroke statistics—2006 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2006;113:e85–151.
Hurst W. The Heart, arteries and veins. 10th ed. New York: McGraw-Hill; 2002.
Lloyd-Jones DM, Wang TJ, Leip EP, et al. Lifetime risk of developing coronary heart disease. Lancet 1999;353:89–92.
Jones D. Risk factors for coronary heart disease in African Americans. Arch Intern Med 2002;162:2565.
Libby P, Ridker PM, Maseri A. Inflammation and atherosclerosis. Circulation 2002; 105:1135–1143.
Falk E. Pathogenesis of atherosclerosis. J Am Coll Cardiol 2006;47(Suppl 1):C7–C12.
Davies MJ. Stability and instability: the two faces of coronary atherosclerosis. The Paul Dudley White Lecture, 1995. Circulation 1996;94:2013–2020.
Libby P. Current concepts of the pathogenesis of the acute coronary syndromes. Circulation 2001;104:365–372.
Yokoya K, Takatsu H, Suzuki T, et al. Process of progression of coronary artery lesions from mild or moderate stenosis to moderate or severe stenosis: a study based on four serial coronary arteriograms per year. Circulation 1999;100:903–909.
Falk E. Plaque rupture with severe pre-existing stenosis precipitating coronary thrombosis. Characteristics of coronary atherosclerotic plaques underlying fatal occlusive thrombi. Br Heart J 1983;50:127–134.
Muller JE, Tofler GH, Stone PH. Circadian variation and triggers of onset of acute cardiovascular disease. Circulation 1989;79:733–743.
Shah PK. Mechanisms of plaque vulnerability and rupture. J Am Coll Cardiol 2003; 41(Suppl S):15S–22S.
Maseri A, Fuster V. Is there a vulnerable plaque? Circulation 2003;107:2068–2071.
Topper JN, Cai J, Falb D, et al. Identification of vascular endothelial genes differentially responsive to fluid mechanical stimuli: cyclooxygenase-2, manganese super-oxide dismutase, and endothelial cell nitric oxide synthase are selectively up-regulated by steady laminar shear stress. Proc Natl Acad Sci U S A 1996;93:10417–10422.
Nagel T, Resnick N, Atkinson WJ, et al. Shear stress selectively upregulates intercellular adhesion molecule-1 expression in cultured human vascular endothelial cells. J Clin Invest 1994;94:885–891.
Gu L, Okada Y, Clinton SK, et al. Absence of monocyte chemoattractant protein-1 reduces atherosclerosis in low-density lipoprotein-deficient mice. Mol Cell 1998;2: 275–281.
Qiao JH, Tripathi J, Mishra NK, et al. Role of macrophage colony-stimulating factor in atherosclerosis: studies of osteopetrotic mice. Am J Pathol 1997;150: 1687–1699.
Mach F, Sauty A, Larossi AS, et al. Differential expression of three T lymphocyte-activating CXC chemokines by human atheroma-associated cells. J Clin Invest 1999; 104:1041–1050.
Hansson G. The role of the lymphocyte. In: Fuster V, Ross R, Topol E, eds. Atherosclerosis and coronary artery disease. New York: Lippincott-Raven; 1996:557–568.
Libby P, Simon DI. Inflammation and thrombosis: the clot thickens. Circulation 2001;103:1718–1720.
Libby P, Geng YJ, Aikawa M, et al. Macrophages and atherosclerotic plaque stability. Curr Opin Lipidol 1996;7:330–335.
Ohara Y, Peterson TE, Harrison DG. Hypercholesterolemia increases endothelial superoxide anion production. J Clin Invest 1993;91:2546–2551.
De Caterina R, Libby P, Peng HB, et al. Nitric oxide decreases cytokine-induced endothelial activation. Nitric oxide selectively reduces endothelial expression of adhesion molecules and proinflammatory cytokines. J Clin Invest 1995;96:60–68.
Thurberg BI, Collins T. The nuclear factor-kappa B/inhibitor of kappa B autoregula-tory system and atherosclerosis. Curr Opin Lipidol 1998;9:387–396.
Fuster V, Badimon L, Badimon JJ, et al. The pathogenesis of coronary artery disease and the acute coronary syndromes (2). N Engl J Med 1992;326:310–318.
Falk E, Shah PK, Fuster V. Coronary plaque disruption. Circulation 1995;92:657–671.
Davies MJ. A macro and micro view of coronary vascular insult in ischemic heart disease. Circulation 1990;82(Suppl):II38–46.
Virmani R, Kolodgie FD, Burke AP, et al. Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler Thromb Vasc Biol 2000;20:1262–1275.
Toschi V, Gallo R, Lettino M, et al. Tissue factor modulates the thrombogenicity of human atherosclerotic plaques. Circulation 1997;95:594–599.
Faggiotto A, Ross R, Harker L. Studies of hypercholesterolemia in the nonhuman primate. I. Changes that lead to fatty streak formation. Arteriosclerosis 1984;4: 323–340.
Davies MJ, Thomas A. Thrombosis and acute coronary-artery lesions in sudden cardiac ischemic death. N Engl J Med 1984;310:1137–1140.
Rioufol G, Finet G, Ginon I, et al. Multiple atherosclerotic plaque rupture in acute coronary syndrome: a three-vessel intravascular ultrasound study. Circulation 2002; 106:804–808.
Maehara A, Mintz GS, Bui AB, et al. Morphologic and angiographic features of coronary plaque rupture detected by intravascular ultrasound. J Am Coll Cardiol 2002; 40:904–910.
Shin J, Edelberg JE, Hong MK. Vulnerable atherosclerotic plaque: clinical implications. Curr Vasc Pharmacol 2003;1:183–204.
Fujii K, Kobayashi Y, Mintz GS, et al. Intravascular ultrasound assessment of ulcerated ruptured plaques: a comparison of culprit and nonculprit lesions of patients with acute coronary syndromes and lesions in patients without acute coronary syndromes. Circulation 2003;108:2473–2478.
Libby P. Coronary artery injury and the biology of atherosclerosis: inflammation, thrombosis, and stabilization. Am J Cardiol 2000;86:3J–8J.
Virmani R, Kolodgie FD, Burke AP, et al. Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler Throm Vasc Biol 2000;20:1262–1275.
Uchida Y, Nakamura F, Tomaru T, et al. Prediction of acute coronary syndromes by percutaneous coronary angioscopy in patients with stable angina. Am Heart J 1995;130:195–203.
Kolodgie FD, Gold HK, Burke AP, et al. Intraplaque hemorrhage and progression of coronary atheroma. N Engl J Med 2003;349:2316–2325.
Heistad DD. Unstable coronary-artery plaques. N Engl J Med 2003;349:2285–2287.
Loree HM, Kamm RD, Stringfellow AP, et al. Effects of fibrous cap thickness on peak circumferential stress in model atherosclerotic vessels. Circ Res 1992;71:850–858.
Huang H, Virmani R, Younis H, et al. The impact of calcification on the biomechani-cal stability of atherosclerotic plaques. Circulation 2001;103:1051–1056.
Kaartinen M, van der Wal AC, van der Loos CM, et al. Mast cell infiltration in acute coronary syndromes: implications for plaque rupture. J Am Coll Cardiol 1998; 32(3):606–612.
Felton CV, Crook D, Davies MJ, et al. Relation of plaque lipid composition and morphology to the stability of human aortic plaques. Arterioscler Thromb Vasc Biol 1997;17:1337–1345.
van der Wal AC, Becker AE, van der Loos CM, et al. Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflamma-tory process irrespective of the dominant plaque morphology. Circulation 1994; 89:36–44.
Laine P, Kaartinen M, Penttila A, et al. Association between myocardial infarction and the mast cells in the adventitia of the infarct-related coronary artery. Circulation 1999;99:361–369.
Shah PK. Plaque disruption and thrombosis: potential role of inflammation and infection. Cardiol Rev 2000;8:31–39.
Richardson PD, Davies MJ, Born GV. Influence of plaque configuration and stress distribution on fissuring of coronary atherosclerotic plaques. Lancet 1989;2: 941–944.
Galis ZS, Sukhova GK, Lark MW, et al. Increased expression of matrix metallopro-teinases and matrix degrading activity in vulnerable regions of human atherosclerotic plaques. J Clin Invest 1994;94:2493–2503.
Steinberg D, Witztum JL. Lipoproteins and atherogenesis. Current concepts. JAMA 1990;264:3047–3052.
Pearson AM. Scavenger receptors in innate immunity. Curr Opin Immunol 1996;8: 20–28.
Hansson GK. Cell-mediated immunity in atherosclerosis. Curr Opin Lipidol 1997;8: 301–311.
Frostegard J, Wu R, Giscombe R, et al. Induction of T-cell activation by oxidized low density lipoprotein. Arterioscler Thromb 1992;12:461–467.
Stemme S, Faber B, Holm J, et al. T lymphocytes from human atherosclerotic plaques recognize oxidized low density lipoprotein. Proc Natl Acad Sci USA 1995;92:3893–3897.
Hansson GK, Jonasson L, Seifert PS, et al. Immune mechanisms in atherosclerosis. Arteriosclerosis 1989;9:567–578.
Biasucci LM, Liuzzo G, Fantozzi G, et al. Increasing levels of interleukin (IL)-1Ra and IL-6 during the first 2 days of hospitalization in unstable angina are associated with increased risk of in-hospital coronary events. Circulation 1999;99:2079–2084.
Farb A, Burke AP, Tang AL, et al. Coronary plaque erosion without rupture into a lipid core. A frequent cause of coronary thrombosis in sudden coronary death. Circulation 1996;93:1354–1363.
Virmani R, Burke AP, Farb A. Plaque rupture and plaque erosion. Thromb Haemost, 1999;82(Suppl 1):1–3.
Burke AP, Farb A, Malcolm GT, et al. Coronary risk factors and plaque morphology in men with coronary disease who died suddenly. N Engl J Med 1997;336:1276–1282.
Rauch U, Bonderman D, Bohrmann B, et al. Transfer of tissue factor from leukocytes to platelets is mediated by CD15 and tissue factor. Blood 2000;96:170–175.
Mallat Z, Benamer H, Hugel B, et al. Elevated levels of shed membrane microparti-cles with procoagulant potential in the peripheral circulating blood of patients with acute coronary syndromes. Circulation 2000;101:841–843.
Laszik ZG, Zhou XJ, Ferrell GL, et al. Down-regulation of endothelial expression of endothelial cell protein C receptor and thrombomodulin in coronary atherosclerosis. Am J Pathol 2001;159:797–802.
Willich SN, Jimenez AH, Tofler GH, et al. Pathophysiology and triggers of acute myocardial infarction: clinical implications. Clin Invest 1992;70(Suppl 1):S73–78.
Willich SN, MacLure M, Mittleman M, et al. Sudden cardiac death. Support for a role of triggering in causation. Circulation 1993;87:1442–1450.
Mittleman MA, Lewis RA, MacLure M, et al. Triggering myocardial infarction by marijuana. Circulation 2001;103:2805–2809.
Muller JE. Triggering of cardiac events by sexual activity: findings from a case-crossover analysis. Am J Cardiol 2000;86(2A):14F–18F.
Peters A, Dockery DW, Muller JE, et al. Increased particulate air pollution and the triggering of myocardial infarction. Circulation 2001;103:2810–2815.
Fernandez-Ortiz A, Badimon JJ, Falk E, et al. Characterization of the relative throm-bogenicity of atherosclerotic plaque components: implications for consequences of plaque rupture. J Am Coll Cardiol 1994;23:1562–1569.
Mallat Z, Hugel B, Ohan J, et al. Shed membrane microparticles with procoagulant potential in human atherosclerotic plaques: a role for apoptosis in plaque thrombo-genicity. Circulation 1999;99:348–353.
Matetzky S, Tani S, Kangavari S, et al. Smoking increases tissue factor expression in atherosclerotic plaques: implications for plaque thrombogenicity. Circulation 2000; 102:602–604.
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2008 Springer-Verlag London Limited
About this chapter
Cite this chapter
Eftekhari, H., Bukharovich, I., Aziz, E., Hong, M.K. (2008). Epidemiology and Pathophysiology of Acute Coronary Syndrome. In: Hong, M.K., Herzog, E. (eds) Acute Coronary Syndrome. Springer, London. https://doi.org/10.1007/978-1-84628-869-2_4
Download citation
DOI: https://doi.org/10.1007/978-1-84628-869-2_4
Publisher Name: Springer, London
Print ISBN: 978-1-84628-868-5
Online ISBN: 978-1-84628-869-2
eBook Packages: MedicineMedicine (R0)