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Journal of Cardiovascular Translational Research

Published in:

01-06-2013

Clinical Implications of Platelet—Vessel Interaction

Authors: Fabio Mangiacapra, Emanuele Barbato

Published in: Journal of Cardiovascular Translational Research | Issue 3/2013

Abstract

The interaction of platelets with endothelial and inflammatory cells might trigger atherogenesis. Different pathways are responsible for this contribution of platelets to atherogenesis. A significant association has been described between increased platelet activation and the extent of atherosclerosis. Platelet reactivity also plays a key role in determining outcomes of patients undergoing percutaneous coronary intervention (PCI). Despite dual antiplatelet therapy, platelet reactivity increases early after the procedure proportionally to the degree of vascular damage and endothelial dysfunction induced by coronary interventions, and large increases in platelet reactivity are also associated with an increased risk of periprocedural myonecrosis. The interaction between platelets and vessel wall has important clinical implications, especially in patients treated with PCI. These include the appropriate selection of antiplatelet drugs when more aggressive procedures are needed, the prognostic significance of periprocedural variations of platelet reactivity, and the correct timing for platelet function testing.

Davi, G., & Patrono, C. (2007). Platelet activation and atherothrombosis. The New England Journal of Medicine, 357, 2482–94.PubMedCrossRef

Ombrello, C., Block, R. C., & Morrell, C. N. (2010). Our expanding view of platelet functions and its clinical implications. Journal of Cardiovascular Translational Research, 3, 538–46.PubMedCrossRef

Gawaz, M., Neumann, F. J., Dickfeld, T., Reininger, A., Adelsberger, H., Gebhardt, A., et al. (1997). Vitronectin receptor (alpha(v)beta3) mediates platelet adhesion to the luminal aspect of endothelial cells: implications for reperfusion in acute myocardial infarction. Circulation, 96, 1809–18.PubMedCrossRef

Bombeli, T., Schwartz, B. R., & Harlan, J. M. (1998). Adhesion of activated platelets to endothelial cells: evidence for a GPIIbIIIa-dependent bridging mechanism and novel roles for endothelial intercellular adhesion molecule 1 (ICAM-1), alphavbeta3 integrin, and GPIbalpha. The Journal of Experimental Medicine, 187, 329–39.PubMedCrossRef

Gawaz, M., Langer, H., & May, A. E. (2005). Platelets in inflammation and atherogenesis. The Journal of Clinical Investigation, 115, 3378–84.PubMedCrossRef

May, A. E., Seizer, P., & Gawaz, M. (2008). Platelets: inflammatory firebugs of vascular walls. Arteriosclerosis, Thrombosis, and Vascular Biology, 28, s5–10.PubMedCrossRef

Henn, V., Slupsky, J. R., Grafe, M., Anagnostopoulos, I., Forster, R., Muller-Berghaus, G., et al. (1998). CD40 ligand on activated platelets triggers an inflammatory reaction of endothelial cells. Nature, 391, 591–94.PubMedCrossRef

May, A. E., Kalsch, T., Massberg, S., Herouy, Y., Schmidt, R., & Gawaz, M. (2002). Engagement of glycoprotein IIb/IIIa (alpha(IIb)beta3) on platelets upregulates CD40L and triggers CD40L-dependent matrix degradation by endothelial cells. Circulation, 106, 2111–17.PubMedCrossRef

Mayadas, T. N., Johnson, R. C., Rayburn, H., Hynes, R. O., & Wagner, D. D. (1993). Leukocyte rolling and extravasation are severely compromised in P selectin-deficient mice. Cell, 74, 541–54.PubMedCrossRef

10.

Subramaniam, M., Saffaripour, S., Watson, S. R., Mayadas, T. N., Hynes, R. O., & Wagner, D. D. (1995). Reduced recruitment of inflammatory cells in a contact hypersensitivity response in P-selectin-deficient mice. The Journal of Experimental Medicine, 181, 2277–82.PubMedCrossRef

11.

Husain, S., Andrews, N. P., Mulcahy, D., Panza, J. A., & Quyyumi, A. A. (1998). Aspirin improves endothelial dysfunction in atherosclerosis. Circulation, 97, 716–20.PubMedCrossRef

12.

Heitzer, T., Ollmann, I., Koke, K., Meinertz, T., & Munzel, T. (2003). Platelet glycoprotein IIb/IIIa receptor blockade improves vascular nitric oxide bioavailability in patients with coronary artery disease. Circulation, 108, 536–41.PubMedCrossRef

13.

Jakubowski, A., Chlopicki, S., Olszanecki, R., Jawien, J., Lomnicka, M., Dupin, J. P., et al. (2005). Endothelial action of thienopyridines and thienopyrimidinones in the isolated guinea pig heart. Prostaglandins, Leukotrienes, and Essential Fatty Acids, 72, 139–45.PubMedCrossRef

14.

Ziemianin, B., Olszanecki, R., Uracz, W., Marcinkiewicz, E., & Gryglewski, R. J. (1999). Thienopyridines: effects on cultured endothelial cells. Journal of Physiology and Pharmacology, 50, 597–604.PubMed

15.

Heitzer, T., Rudolph, V., Schwedhelm, E., Karstens, M., Sydow, K., Ortak, M., et al. (2006). Clopidogrel improves systemic endothelial nitric oxide bioavailability in patients with coronary artery disease: evidence for antioxidant and antiinflammatory effects. Arteriosclerosis, Thrombosis, and Vascular Biology, 26, 1648–52.PubMedCrossRef

16.

Warnholtz, A., Ostad, M. A., Velich, N., Trautmann, C., Schinzel, R., Walter, U., et al. (2008). A single loading dose of clopidogrel causes dose-dependent improvement of endothelial dysfunction in patients with stable coronary artery disease: results of a double-blind, randomized study. Atherosclerosis, 196, 689–95.PubMedCrossRef

17.

Muller, O., Hamilos, M., Bartunek, J., Ulrichts, H., Mangiacapra, F., Holz, J. B., et al. (2010). Relation of endothelial function to residual platelet reactivity after clopidogrel in patients with stable angina pectoris undergoing percutaneous coronary intervention. The American Journal of Cardiology, 105, 333–38.PubMedCrossRef

18.

Hamilos, M., Muller, O., Ntalianis, A., Trana, C., Bartunek, J., Sarno, G., et al. (2011). Relationship between peripheral arterial reactive hyperemia and residual platelet reactivity after 600 mg clopidogrel. Journal of Thrombosis and Thrombolysis, 32, 64–71.PubMedCrossRef

19.

Patti, G., Grieco, D., Dicuonzo, G., Pasceri, V., Nusca, A., & Di Sciascio, G. (2011). High versus standard clopidogrel maintenance dose after percutaneous coronary intervention and effects on platelet inhibition, endothelial function, and inflammation results of the ARMYDA-150 mg (antiplatelet therapy for reduction of myocardial damage during angioplasty) randomized study. Journal of the American College of Cardiology, 57, 771–78.PubMedCrossRef

20.

Barbato, E., Bartunek, J., Wyffels, E., Wijns, W., Heyndrickx, G. R., & De Bruyne, B. (2003). Effects of intravenous dobutamine on coronary vasomotion in humans. Journal of the American College of Cardiology, 42, 1596–601.PubMedCrossRef

21.

Barbato, E., Piscione, F., Bartunek, J., Galasso, G., Cirillo, P., De Luca, G., et al. (2005). Role of beta2 adrenergic receptors in human atherosclerotic coronary arteries. Circulation, 111, 288–94.PubMedCrossRef

22.

Methia, N., Andre, P., Denis, C. V., Economopoulos, M., & Wagner, D. D. (2001). Localized reduction of atherosclerosis in von Willebrand factor-deficient mice. Blood, 98, 1424–28.PubMedCrossRef

23.

Egan, K. M., Wang, M., Fries, S., Lucitt, M. B., Zukas, A. M., Pure, E., et al. (2005). Cyclooxygenases, thromboxane, and atherosclerosis: plaque destabilization by cyclooxygenase-2 inhibition combined with thromboxane receptor antagonism. Circulation, 111, 334–42.PubMedCrossRef

24.

Pratico, D., Cyrus, T., Li, H., & FitzGerald, G. A. (2000). Endogenous biosynthesis of thromboxane and prostacyclin in 2 distinct murine models of atherosclerosis. Blood, 96, 3823–26.PubMed

25.

Dixon, D. A., Tolley, N. D., Bemis-Standoli, K., Martinez, M. L., Weyrich, A. S., Morrow, J. D., et al. (2006). Expression of COX-2 in platelet-monocyte interactions occurs via combinatorial regulation involving adhesion and cytokine signaling. The Journal of Clinical Investigation, 116, 2727–38.PubMed

26.

Barbato, E., Rubattu, S., Bartunek, J., Berni, A., Sarno, G., Vanderheyden, M., et al. (2009). Human coronary atherosclerosis modulates cardiac natriuretic peptide release. Atherosclerosis, 206, 258–64.PubMedCrossRef

27.

Jayachandran, M., Litwiller, R. D., Lahr, B. D., Bailey, K. R., Owen, W. G., Mulvagh, S. L., et al. (2011). Alterations in platelet function and cell-derived microvesicles in recently menopausal women: relationship to metabolic syndrome and atherogenic risk. Journal of Cardiovascular Translational Research, 4, 811–22.PubMedCrossRef

28.

Koyama, H., Maeno, T., Fukumoto, S., Shoji, T., Yamane, T., Yokoyama, H., et al. (2003). Platelet P-selectin expression is associated with atherosclerotic wall thickness in carotid artery in humans. Circulation, 108, 524–29.PubMedCrossRef

29.

Fateh-Moghadam, S., Li, Z., Ersel, S., Reuter, T., Htun, P., Plockinger, U., et al. (2005). Platelet degranulation is associated with progression of intima-media thickness of the common carotid artery in patients with diabetes mellitus type 2. Arteriosclerosis, Thrombosis, and Vascular Biology, 25, 1299–303.PubMedCrossRef

30.

Furman, M. I., Benoit, S. E., Barnard, M. R., Valeri, C. R., Borbone, M. L., Becker, R. C., et al. (1998). Increased platelet reactivity and circulating monocyte-platelet aggregates in patients with stable coronary artery disease. Journal of the American College of Cardiology, 31, 352–58.PubMedCrossRef

31.

Furman, M. I., Barnard, M. R., Krueger, L. A., Fox, M. L., Shilale, E. A., Lessard, D. M., et al. (2001). Circulating monocyte-platelet aggregates are an early marker of acute myocardial infarction. Journal of the American College of Cardiology, 38, 1002–06.PubMedCrossRef

32.

Keating, F. K., Whitaker, D. A., Kabbani, S. S., Ricci, M. A., Sobel, B. E., & Schneider, D. J. (2004). Relation of augmented platelet reactivity to the magnitude of distribution of atherosclerosis. The American Journal of Cardiology, 94, 725–28.PubMedCrossRef

33.

Mangiacapra, F., De Bruyne, B., Muller, O., Trana, C., Ntalianis, A., Bartunek, J., et al. (2010). High residual platelet reactivity after clopidogrel: extent of coronary atherosclerosis and periprocedural myocardial infarction in patients with stable angina undergoing percutaneous coronary intervention. JACC. Cardiovascular Interventions, 3, 35–40.PubMedCrossRef

34.

Tcheng, J. E., Lim, I. H., Srinivasan, S., Jozic, J., Gibson, C. M., O’Shea, J. C., et al. (2009). Stent parameters predict major adverse clinical events and the response to platelet glycoprotein IIb/IIIa blockade: findings of the ESPRIT trial. Circulation. Cardiovascular Interventions, 2, 43–51.PubMedCrossRef

35.

Wang, T. H., Bhatt, D. L., Fox, K. A., Steinhubl, S. R., Brennan, D. M., Hacke, W., et al. (2007). An analysis of mortality rates with dual-antiplatelet therapy in the primary prevention population of the CHARISMA trial. European Heart Journal, 28, 2200–07.PubMedCrossRef

36.

Mangiacapra, F., Barbato, E., Patti, G., Gatto, L., Vizzi, V., Ricottini, E., et al. (2010). Point-of-care assessment of platelet reactivity after clopidogrel to predict myonecrosis in patients undergoing percutaneous coronary intervention. JACC. Cardiovascular Interventions, 3, 318–23.PubMedCrossRef

37.

Mangiacapra, F., Patti, G., Peace, A., Gatto, L., Vizzi, V., Ricottini, E., et al. (2010). Comparison of platelet reactivity and periprocedural outcomes in patients with versus without diabetes mellitus and treated with clopidogrel and percutaneous coronary intervention. The American Journal of Cardiology, 106, 619–23.PubMedCrossRef

38.

Breet, N. J., van Werkum, J. W., Bouman, H. J., Kelder, J. C., Ruven, H. J., Bal, E. T., et al. (2010). Comparison of platelet function tests in predicting clinical outcome in patients undergoing coronary stent implantation. JAMA: The Journal of the American Medical Association, 303, 754–62.CrossRef

39.

Mangiacapra, F., Patti, G., Barbato, E., Peace, A. J., Ricottini, E., Vizzi, V., et al. (2012). A therapeutic window for platelet reactivity for patients undergoing elective percutaneous coronary intervention: results of the ARMYDA-PROVE (antiplatelet therapy for reduction of MYocardial damage during angioplasty-platelet reactivity for outcome validation effort) study. JACC. Cardiovascular Interventions, 5, 281–89.PubMedCrossRef

40.

Mehta, S. R., Yusuf, S., Peters, R. J., Bertrand, M. E., Lewis, B. S., Natarajan, M. K., et al. (2001). Effects of pretreatment with clopidogrel and aspirin followed by long-term therapy in patients undergoing percutaneous coronary intervention: the PCI-CURE study. The Lancet, 358, 527–33.CrossRef

41.

Steinhubl, S. R., Berger, P. B., Mann, J. T., Fry, E. T., DeLago, A., Wilmer, C., et al. (2002). Early and sustained dual oral antiplatelet therapy following percutaneous coronary intervention: a randomized controlled trial. JAMA: The Journal of the American Medical Association, 288, 2411–20.CrossRef

42.

Saito, Y., Wada, H., Yamamuro, M., Inoue, A., Shimura, M., Hiyoyama, K., et al. (1999). Changes of plasma hemostatic markers during percutaneous transluminal coronary angioplasty in patients with chronic coronary artery disease. American Journal of Hematology, 61, 238–42.PubMedCrossRef

43.

Serrano, C. V. J., Ramires, J. A., Venturinelli, M., Arie, S., D'Amico, E., Zweier, J. L., et al. (1997). Coronary angioplasty results in leukocyte and platelet activation with adhesion molecule expression. Evidence of inflammatory responses in coronary angioplasty. Journal of the American College of Cardiology, 29, 1276–83.PubMedCrossRef

44.

Scharf, R. E., Tomer, A., Marzec, U. M., Teirstein, P. S., Ruggeri, Z. M., & Harker, L. A. (1992). Activation of platelets in blood perfusing angioplasty-damaged coronary arteries. Flow cytometric detection. Arterioscler Thromb, 12, 1475–87.CrossRef

45.

Gurbel, P. A., Samara, W. M., & Bliden, K. P. (2004). Failure of clopidogrel to reduce platelet reactivity and activation following standard dosing in elective stenting: implications for thrombotic events and restenosis. Platelets, 15, 95–99.PubMedCrossRef

46.

Matetzky, S., Shenkman, B., Guetta, V., Shechter, M., Beinart, R., Goldenberg, I., et al. (2004). Clopidogrel resistance is associated with increased risk of recurrent atherothrombotic events in patients with acute myocardial infarction. Circulation, 109, 3171–75.PubMedCrossRef

47.

Siller-Matula, J. M., Haberl, K., Prillinger, K., Panzer, S., Lang, I., & Jilma, B. (2009). The effect of antiplatelet drugs clopidogrel and aspirin is less immediately after stent implantation. Thrombosis Research, 123, 874–80.PubMedCrossRef

48.

Mangiacapra, F., Bartunek, J., Bijnens, N., Peace, A. J., Dierickx, K., Bailleul, E., et al. (2012). Peri-procedural variations of platelet reactivity during elective percutaneous coronary intervention. Journal of Thrombosis and Haemostasis, 10(12), 2452–61.PubMedCrossRef

49.

Price, M. J., Berger, P. B., Teirstein, P. S., Tanguay, J. F., Angiolillo, D. J., Spriggs, D., et al. (2011). Standard- vs high-dose clopidogrel based on platelet function testing after percutaneous coronary intervention: the GRAVITAS randomized trial. JAMA: The Journal of the American Medical Association, 305, 1097–105.CrossRef

50.

Collet, J. P., Cuisset, T., Range, G., et al. (2012). Bedside monitoring to adjust antiplatelet therapy for coronary stenting. The New England Journal of Medicine, 367(22), 2100–9.PubMedCrossRef

Title: Clinical Implications of Platelet—Vessel Interaction
Authors: Fabio Mangiacapra
Emanuele Barbato
Publication date: 01-06-2013
Publisher: Springer US
Published in: Journal of Cardiovascular Translational Research / Issue 3/2013
Print ISSN: 1937-5387
Electronic ISSN: 1937-5395
DOI: https://doi.org/10.1007/s12265-012-9441-0

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Clinical Implications of Platelet—Vessel Interaction

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