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2298 Part XII: Hemostasis and Thrombosis Chapter 134: Atherothrombosis: Disease Initiation, Progression, and Treatment 2299
ATHEROEMBOLISM 11. Mallika V, Goswami B, Rajappa M: Atherosclerosis pathophysiology and the role of
novel risk factors: A clinicobiochemical perspective. Angiology 58:513–522, 2007.
12. Hemkens LG, Bucher HC: HIV infection and cardiovascular disease. Eur Heart J
Atheromatous embolism refers to the dislodgment into the bloodstream 35:1373–1381, 2014.
of arterial plaque material, including cholesterol crystals (“cholesterol 13. Kline ER, Sutliff RL: The roles of HIV-1 proteins and antiretroviral drug therapy in
embolism”) from ulcerated vascular plaques. The cholesterol embol- HIV-1-associated endothelial dysfunction. J Investig Med 56:752–769, 2008.
ization syndrome involves systemic microembolism to the end arteries 14. Calza L, Manfredi R, Pocaterra D, Chiodo F: Risk of premature atherosclerosis and
ischemic heart disease associated with HIV infection and antiretroviral therapy. J Infect
of almost any circulatory bed. Atheroembolism most characteristically 57:16–32, 2008.
originates from lesions in the abdominal aorta and ileofemoral arter- 15. de Zeeuw D. Renal disease: A common and a silent killer. Nat Clin Pract Cardiovasc
ies. Cholesterol emboli that lodge in an arteriole incite an acute inflam- Med 5 Suppl 1:S27–S35, 2008.
matory response, followed by a foreign-body reaction, intravascular 16. Budoff MJ, Rader DJ, Reilly MP, et al: Relationship of estimated GFR and coronary
artery calcification in the CRIC (Chronic Renal Insufficiency Cohort) Study. Am J
thrombus formation, endothelial proliferation, and eventually fibrosis. Kidney Dis 58:519–526, 2011.
These processes generally result in ischemia that sometimes leads to 17. Said S, Hernandez GT: The link between chronic kidney disease and cardiovascular
disease. J Nephropathol 3:99–104, 2014.
infarction and necrosis. Mortality rate of clinically diagnosed athe- 18. Vonend O, Rump LC, Ritz E: Sympathetic overactivity—The Cinderella of cardiovascu-
277
roembolism can be as high as 80 percent, depending on the anatomic lar risk factors in dialysis patients. Semin Dial 21:326–330, 2008.
location and size of the vascular beds involved. 278 19. Bradley TD, Floras JS: Obstructive sleep apnoea and its cardiovascular consequences.
Lancet 373:82–93, 2009.
Patients with atheroembolism, including the cholesterol embol- 20. Skalen K, Gustafsson M, Rydberg EK, et al: Subendothelial retention of atherogenic
ization syndrome, generally have advanced atherosclerosis, often com- lipoproteins in early atherosclerosis. Nature 417:750–754, 2002.
plicated by a history of hypertension, diabetes mellitus, renal failure, 21. Passerini AG, Polacek DC, Shi C, et al: Coexisting proinflammatory and antioxidative
or aortic aneurysms. Atherosclerotic plaques can disrupt and embolize endothelial transcription profiles in a disturbed flow region of the adult porcine aorta.
Proc Natl Acad Sci U S A 101:2482–2487, 2004.
spontaneously; however, the clinical syndrome typically is triggered 22. Weber C, Zernecke A, Libby P: The multifaceted contributions of leukocyte subsets to
by vascular intervention, including vascular surgery, catheteriza- atherosclerosis: Lessons from mouse models. Nat Rev Immunol 8:802–815, 2008.
tion, angioplasty, endarterectomy, or angiography. Anticoagulation or 23. Stary HC, Chandler AB, Dinsmore RE, et al: A definition of advanced types of athero-
thrombolytic therapy may be risk factors with atheroembolism. Clin- sclerotic lesions and a histological classification of atherosclerosis. A report from the
278
Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart
ical presentation depends on the sites of embolization. When these sites Association. Circulation 92:1355–1374, 1995.
involve the distal extremity microcirculation, the “blue toe syndrome” 24. Johnson JL: Matrix metalloproteinases: Influence on smooth muscle cells and athero-
may develop. The syndrome presents with the acute appearance of pain- sclerotic plaque stability. Expert Rev Cardiovasc Ther 5:265–282, 2007.
ful and tender discoloration or mottled blue and patchy appearance of 25. Hunt JL, Fairman R, Mitchell ME, et al: Bone formation in carotid plaques: A clinico-
pathological study. Stroke 33:1214–1219, 2002.
one or more toes that may progress to ulceration and gangrene. Other 26. Curtis AM, Edelberg J, Jonas R, et al: Endothelial microparticles: Sophisticated vesicles
common cutaneous manifestations are livedo reticularis involving the modulating vascular function. Vasc Med 18:204–214, 2013.
legs, buttocks, or abdomen, painful nodules, and purpura. Cerebrovas- 27. Furchgott RF, Zawadzki JV: The obligatory role of endothelial cells in the relaxation of
arterial smooth muscle by acetylcholine. Nature 288:373–376, 1980.
cular embolism can cause transient neurologic abnormalities. Choles- 28. Loscalzo J: The identification of nitric oxide as endothelium-derived relaxing factor.
terol emboli lodged in retinal arterial bifurcations can be visualized by Circ Res 113:100–103, 2013.
ophthalmoscopy as bright, refractile, yellow rectangular crystals. Vis- 29. Lubos E, Handy DE, Loscalzo J: Role of oxidative stress and nitric oxide in atheroth-
rombosis. Front Biosci 13:5323–5344, 2008.
ceral organs most commonly affected by atheroembolism include the 30. Guzik TJ, Chen W, Gongora MC, et al: Calcium-dependent NOX5 nicotinamide
kidneys, sometimes causing renal failure, and the gastrointestinal tract, adenine dinucleotide phosphate oxidase contributes to vascular oxidative stress in
where abdominal pain, ischemic colitis, and bleeding may ensue. human coronary artery disease. J Am Coll Cardiol 52:1803–1809, 2008.
Diagnosis is based on clinical presentation associated with imaging 31. De Pascali F, Hemann C, Samons K, et al: Hypoxia and reoxygenation induce endothe-
lial nitric oxide synthase uncoupling in endothelial cells through tetrahydrobiopterin
evidence of atherosclerosis of the arterial supply of affected organs. depletion and S-glutathionylation. Biochemistry 53:3679–3688, 2014.
278
Transient eosinophilia occurs in most cases. Treatment of athero- 32. Tiefenbacher CP, Bleeke T, Vahl C, et al: Endothelial dysfunction of coronary resis-
279
embolism should include surgical removal or bypass of the source of tance arteries is improved by tetrahydrobiopterin in atherosclerosis. Circulation 102:
2172–2179, 2000.
emboli. No medical treatment modalities have been established to be 33. Kim CS, Jung SB, Naqvi A, et al: P53 impairs endothelium-dependent vasomotor func-
effective. Anticoagulation or fibrinolytic therapy may increase the risk tion through transcriptional upregulation of p66shc. Circ Res 103:1441–1450, 2008.
of further atheroembolism. 34. Creager MA, Gallagher SJ, Girerd XJ, et al: l-Arginine improves endothelium-dependent
vasodilation in hypercholesterolemic humans. J Clin Invest 90:1248–1253, 1992.
35. Chen S, Li N, Deb-Chatterji M, et al: Asymmetric dimethylarginine as marker and
REFERENCES mediator in ischemic stroke. Int J Mol Sci 13:15983–16004, 2012.
36. Niu PP, Cao Y, Gong T, et al: Hypermethylation of DDAH2 promoter contributes to the
1. Virchow R: Cellular Pathology: As Based upon Physiological and Pathological Histology. dysfunction of endothelial progenitor cells in coronary artery disease patients. J Transl
New York: Dover, 1863. Med 12:170, 2014.
2. Ross R: Atherosclerosis-an inflammatory disease. N Engl J Med 340:115–126, 1999. 37. Ludmer PL, Selwyn AP, Shook TL, et al: Paradoxical vasoconstriction induced by acet-
3. Ridker PM: Inflammation, C-reactive protein, and cardiovascular disease: Moving past ylcholine in atherosclerotic coronary arteries. N Engl J Med 315:1046–1051, 1986.
the marker versus mediator debate. Circ Res 114:594–595, 2014. 38. Kuhn FE, Mohler ER, Satler LF, et al: Effects of high-density lipoprotein on
4. Duewell P, Kono H, Rayner KJ, et al: NLRP3 inflammasomes are required for athero- acetylcholine-induced coronary vasoreactivity. Am J Cardiol 68:1425–1430, 1991.
genesis and activated by cholesterol crystals. Nature 464:1357–1361, 2010. 39. Kuhn FE, Mohler ER 3rd, Rackley CE: Cholesterol and lipoproteins: Beyond atherogen-
5. Enos WF, Holmes RH, Beyer J: Coronary disease among United States soldiers killed in esis. Clin Cardiol 15:883–890, 1992.
action in Korea; preliminary report. J Am Med Assoc 152:1090–1093, 1953. 40. Luscher TF, Landmesser U, von Eckardstein A, Fogelman AM: High-density lipopro-
6. Joseph A, Ackerman D, Talley JD, et al: Manifestations of coronary atherosclerosis in tein: Vascular protective effects, dysfunction, and potential as therapeutic target. Circ
young trauma victims—an autopsy study. J Am Coll Cardiol 22:459–467, 1993. Res 114:171–182, 2014.
7. Tuzcu EM, Kapadia SR, Tutar E, et al: High prevalence of coronary atherosclerosis in 41. Oakley R, Tharakan B: Vascular hyperpermeability and aging. Aging Dis 5:114–125,
asymptomatic teenagers and young adults: Evidence from intravascular ultrasound. 2014.
Circulation 103:2705–2710, 2001. 42. van den Heuvel M, Sorop O, Koopmans SJ, et al: Coronary microvascular dysfunction
8. Ross R, Glomset JA: The pathogenesis of atherosclerosis (first of two parts). N Engl J in a porcine model of early atherosclerosis and diabetes. Am J Physiol Heart Circ Physiol
Med 295:369–377, 1976. 302:H85–H94, 2012.
9. Ross R, Glomset JA: The pathogenesis of atherosclerosis (second of two parts). N Engl J 43. Mohler ER 3rd, O’Hare K, Darze ES, et al: Cardiovascular function in normotensive
Med 295:420–425, 1976. offspring of persons with essential hypertension and black race. J Clin Hypertens
10. Yusuf S, Hawken S, Ounpuu S, et al: Effect of potentially modifiable risk factors asso- (Greenwich) 9:506–512, 2007.
ciated with myocardial infarction in 52 countries (the INTERHEART study): Case- 44. Yong PJ, Koh CH, Shim WS: Endothelial microparticles: Missing link in endothelial
control study. Lancet 364:937–952, 2004. dysfunction? Eur J Prev Cardiol 20:496–512, 2013.
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