Recent Advances in Understanding the Pathogenesis of Cardiovascular Diseases and Development of Treatment Modalities

Author(s): Rahul Mittal*, Vasanti M. Jhaveri, Sae-In Samantha Kay, Aubrey Greer, Kyle J. Sutherland, Hannah S. McMurry , Nicole Lin, Jeenu Mittal, Arul K. Malhotra, Amit P. Patel.

Journal Name: Cardiovascular & Hematological Disorders-Drug Targets

Volume 19 , Issue 1 , 2019

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Graphical Abstract:


Abstract:

Cardiovascular Diseases (CVDs) are a leading cause of morbidity and mortality worldwide. The underlying pathology for cardiovascular disease is largely atherosclerotic in nature and the steps include fatty streak formation, plaque progression and plaque rupture. While there is optimal drug therapy available for patients with CVD, there are also underlying drug delivery obstacles that must be addressed. Challenges in drug delivery warrant further studies for the development of novel and more efficacious medical therapies. An extensive understanding of the molecular mechanisms of disease in combination with current challenges in drug delivery serves as a platform for the development of novel drug therapeutic targets for CVD. The objective of this article is to review the pathogenesis of atherosclerosis, first-line medical treatment for CVD, and key obstacles in an efficient drug delivery.

Keywords: Cardiovascular diseases, drug delivery, atherosclerosis, treatment modalities, plaque progression, fatty streak formation.

[1]
Yusuf, S.; Hawken, S.; Ôunpuu, S. Dans, T.; Avezum, A.; Lanas, F.; McQueen, M.; Budaj, A.; Pais, P.; Varigos, J.; Lisheng, L.; INTERHEART Study Investigators. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): Case-control study. Lancet, 2004, 364(9438), 937-952.
[2]
Moran, A.E.; Forouzanfar, M.H.; Roth, G.A.; Mensah, G.A.; Ezzati, M.; Flaxman, A.; Murray, C.J.; Naghavi, M. The global burden of ischemic heart disease in 1990 and 2010: The Global Burden of Disease 2010 study. Circulation, 2014, 129(14), 1493-1501.
[3]
Bentzon, J.F.; Otsuka, F.; Virmani, R.; Falk, E. Mechanisms of plaque formation and rupture. Circ. Res., 2014, 114(12), 1852-1866.
[4]
Lim, S.S.; Vos, T.; Flaxman, A.D.; Danaei, G.; Shibuya, K.; Adair-Rohani, H.; Amann, M.; Anderson, H.R.; Andrews, K.G.; Aryee, M.; Atkinson, C.; Bacchus, L.J.; Bahalim, A.N.; Balakrishnan, K.; Balmes, J.; Barker-Collo, S.; Baxter, A.; Bell, M.L.; Blore, J.D.; Blyth, F.; Bonner, C.; Borges, G.; Bourne, R.; Boussinesq, M.; Brauer, M.; Brooks, P.; Bruce, N.G.; Brunekreef, B.; Bryan-Hancock, C.; Bucello, C.; Buchbinder, R.; Bull, F.; Burnett, R.T.; Byers, T.E.; Calabria, B.; Carapetis, J.; Carnahan, E.; Chafe, Z.; Charlson, F.; Chen, H.; Chen, J.S.; Cheng, A.T.; Child, J.C.; Cohen, A.; Colson, K.E.; Cowie, B.C.; Darby, S.; Darling, S.; Davis, A.; Degenhardt, L.; Dentener, F.; Des Jarlais, D.C.; Devries, K.; Dherani, M.; Ding, E.L.; Dorsey, E.R.; Driscoll, T.; Edmond, K.; Ali, S.E.; Engell, R.E.; Erwin, P.J.; Fahimi, S.; Falder, G.; Farzadfar, F.; Ferrari, A.; Finucane, M.M.; Flaxman, S.; Fowkes, F.G.; Freedman, G.; Freeman, M.K.; Gakidou, E.; Ghosh, S.; Giovannucci, E.; Gmel, G.; Graham, K.; Grainger, R.; Grant, B.; Gunnell, D.; Gutierrez, H.R.; Hall, W.; Hoek, H.W.; Hogan, A.; Hosgood, H.D. 3rd, Hoy, D.; Hu, H.; Hubbell, B.J.; Hutchings, S.J.; Ibeanusi, S.E.; Jacklyn, G.L.; Jasrasaria, R.; Jonas, J.B.; Kan, H.; Kanis, J.A.; Kassebaum, N.; Kawakami, N.; Khang, Y.H.; Khatibzadeh, S.; Khoo, J.P.; Kok, C.; Laden, F.; Lalloo, R.; Lan, Q.; Lathlean, T.; Leasher, J.L.; Leigh, J.; Li, Y.; Lin, J.K.; Lipshultz, S.E.; London, S.; Lozano, R.; Lu, Y.; Mak, J.; Malekzadeh, R.; Mallinger, L.; Marcenes, W.; March, L.; Marks, R.; Martin, R.; McGale, P.; McGrath, J.; Mehta, S.; Mensah, G.A.; Merriman, T.R.; Micha, R.; Michaud, C.; Mishra, V.; Mohd Hanafiah, K.; Mokdad, A.A.; Morawska, L.; Mozaffarian, D.; Murphy, T.; Naghavi, M.; Neal, B.; Nelson, P.K.; Nolla, J.M.; Norman, R.; Olives, C.; Omer, S.B.; Orchard, J.; Osborne, R.; Ostro, B.; Page, A.; Pandey, K.D.; Parry, C.D.; Passmore, E.; Patra, J.; Pearce, N.; Pelizzari, P.M.; Petzold, M.; Phillips, M.R.; Pope, D.; Pope, C.A.; 3rd, Powles, J.; Rao, M.; Razavi, H.; Rehfuess, E.A.; Rehm, J.T.; Ritz, B.; Rivara, F.P.; Roberts, T.; Robinson, C.; Rodriguez-Portales, J.A.; Romieu, I.; Room, R.; Rosenfeld, L.C.; Roy, A.; Rushton, L.; Salomon, J.A.; Sampson, U.; Sanchez-Riera, L.; Sanman, E.; Sapkota, A.; Seedat, S.; Shi, P.; Shield, K.; Shivakoti, R.; Singh, G.M.; Sleet, D.A.; Smith, E.; Smith, K.R.; Stapelberg, N.J.; Steenland, K.; Stöckl, H.; Stovner, L.J.; Straif, K.; Straney, L.; Thurston, G.D.; Tran, J.H.; Van Dingenen, R.; van Donkelaar, A.; Veerman, J.L.; Vijayakumar, L.; Weintraub, R.; Weissman, M.M.; White, R.A.; Whiteford, H.; Wiersma, S.T.; Wilkinson, J.D.; Williams, H.C.; Williams, W.; Wilson, N.; Woolf, A.D.; Yip, P.; Zielinski, J.M.; Lopez, A.D.; Murray, C.J.; Ezzati, M.; AlMazroa, M.A.; Memish, Z.A. A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990-2010: A systematic analysis for the Global Burden of Disease Study 2010. Lancet, 2012, 380(9859), 2224-2260.
[5]
Yusuf, S.; Hawken, S.; Ounpuu, S. Dans, T.; Avezum, A.; Lanas, F.; McQueen, M.; Budaj, A.; Pais, P.; Varigos, J.; Lisheng, L.; INTERHEART Study Investigators. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): Case-control study. Lancet, 2004, 364(9438), 937-952.
[6]
Wu, M.Y.; Li, C.J.; Hou, M.F.; Chu, P.Y. New insights into the role of inflammation in the pathogenesis of atherosclerosis. Int. J. Mol. Sci., 2017, 18(10), E2034.
[7]
Libby, P.; Ridker, P.M.; Hansson, G.K. Inflammation in atherosclerosis: From pathophysiology to practice. J. Am. Coll. Cardiol., 2009, 54(23), 2129-2138.
[8]
Hansson, G.K.; Libby, P.; Tabas, I. Inflammation and plaque vulnerability. J. Intern. Med., 2015, 278(5), 483-493.
[9]
Tabas, I.; Williams, K.J.; Boren, J. Subendothelial lipoprotein retention as the initiating process in atherosclerosis: Update and therapeutic implications. Circulation, 2007, 116(16), 1832-1844.
[10]
Ference, B.A.; Yoo, W.; Alesh, I.; Mahajan, N.; Mirowska, K.K.; Mewada, A.; Kahn, J.; Afonso, L.; Williams, K.A. Sr, Flack, J.M. Effect of long-term exposure to lower low-density lipoprotein cholesterol beginning early in life on the risk of coronary heart disease: A Mendelian randomization analysis. J. Am. Coll. Cardiol., 2012, 60(25), 2631-2639.
[11]
Ross, R.; Glomset, J.A. The pathogenesis of atherosclerosis (first of two parts). N. Engl. J. Med., 1976, 295(7), 369-377.
[12]
Ross, R.; Glomset, J.A. Atherosclerosis and the arterial smooth muscle cell: Proliferation of smooth muscle is a key event in the genesis of the lesions of atherosclerosis. Science, 1973, 180(4093), 1332-1339.
[13]
Cornhill, J.F.; Roach, M.R. A quantitative study of the localization of atherosclerotic lesions in the rabbit aorta. Atherosclerosis, 1976, 23(3), 489-501.
[14]
Glagov, S.; Zarins, C.; Giddens, D.P.; Ku, D.N. Hemodynamics and atherosclerosis. Insights and perspectives gained from studies of human arteries. Arch. Pathol. Lab. Med., 1988, 112(10), 1018-1031.
[15]
Giddens, D.P.; Zarins, C.K.; Glagov, S. The role of fluid mechanics in the localization and detection of atherosclerosis. J. Biomech. Eng., 1993, 115(4b), 588-594.
[16]
Wentzel, J.J.; Chatzizisis, Y.S.; Gijsen, F.J.; Giannoglou, G.D.; Feldman, C.L.; Stone, P.H. Endothelial shear stress in the evolution of coronary atherosclerotic plaque and vascular remodelling: Current understanding and remaining questions. Cardiovasc. Res., 2012, 96(2), 234-243.
[17]
Warboys, C.M.; de Luca, A.; Amini, N.; Luong, L.; Duckles, H.; Hsiao, S.; White, A.; Biswas, S.; Khamis, R.; Chong, C.K.; Cheung, W.M.; Sherwin, S.J.; Bennett, M.R.; Gil, J.; Mason, J.C.; Haskard, D.O.; Evans, P.C. Disturbed flow promotes endothelial senescence via a p53-dependent pathway. Arterioscler. Thromb. Vasc. Biol., 2014, 34(5), 985-995.
[18]
Harrison, D.; Griendling, K.K.; Landmesser, U.; Hornig, B.; Drexler, H. Role of oxidative stress in atherosclerosis. Am. J. Cardiol., 2003, 91(3a), 7a-11a.
[19]
Gimbrone, M.A.; García-Cardeña, G. Endothelial cell dysfunction and the pathobiology of atherosclerosis. Circ. Res., 2016, 118(4), 620-636.
[20]
Doddaballapur, A.; Michalik, K.M.; Manavski, Y.; Lucas, T.; Houtkooper, R.H.; You, X.; Chen, W.; Zeiher, A.M.; Potente, M.; Dimmeler, S.; Boon, R.A. Laminar shear stress inhibits endothelial cell metabolism via KLF2-mediated repression of PFKFB3. Arterioscler. Thromb. Vasc. Biol., 2015, 35(1), 137-145.
[21]
Davis, M.E.; Grumbach, I.M.; Fukai, T.; Cutchins, A.; Harrison, D.G. Shear stress regulates endothelial nitric-oxide synthase promoter activity through nuclear factor kappaB binding. J. Biol. Chem., 2004, 279(1), 163-168.
[22]
Korenaga, R.; Ando, J.; Kosaki, K.; Isshiki, M.; Takada, Y.; Kamiya, A. Negative transcriptional regulation of the VCAM-1 gene by fluid shear stress in murine endothelial cells. Am. J. Physiol., 1997, 273(5 Pt 1), C1506-C1515.
[23]
Resnick, N.; Collins, T.; Atkinson, W.; Bonthron, D.T.; Dewey, C.F. Jr., Gimbron, M.A.; Jr. Platelet-derived growth factor B chain promoter contains a cis-acting fluid shear-stress-responsive element. Proc. Natl. Acad. Sci. USA, 1993, 90(16), 7908.
[24]
Stary, H.C.; Blankenhorn, D.H.; Chandler, A.B.; Glagov, S.; Insull, W. ; Jr., Richardson, M.; et al. A definition of the intima of human arteries and of its atherosclerosis-prone regions. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. Circulation, 1992, 85(1), 391-405.
[25]
Shigematsu, K.; Yasuhara, H.; Shigematsu, H.; Muto, T. Direct and indirect effects of pulsatile shear stress on the smooth muscle cell. Int. Angiol., 2000, 19(1), 39-46.
[26]
Skalen, K.; Gustafsson, M.; Rydberg, E.K.; Hulten, L.M.; Wiklund, O.; Innerarity, T.L.; Borén, J. Subendothelial retention of atherogenic lipoproteins in early atherosclerosis. Nature, 2002, 417(6890), 750-754.
[27]
Steinberg, D.; Witztum, J.L. Oxidized low-density lipoprotein and atherosclerosis. Arterioscler. Thromb. Vasc. Biol., 2010, 30(12), 2311-2316.
[28]
Moore, K.J.; Sheedy, F.J.; Fisher, E.A. Macrophages in atherosclerosis: A dynamic balance. Nat. Rev. Immunol., 2013, 13(10), 709-721.
[29]
Kume, N.; Cybulsky, M.I.; Gimbrone, M.A. Jr. Lysophosphatidylcholine, a component of atherogenic lipoproteins, induces mononuclear leukocyte adhesion molecules in cultured human and rabbit arterial endothelial cells. J. Clin. Invest., 1992, 90(3), 1138-1144.
[30]
Raines, E.W.; Ferri, N. Thematic review series: The immune system and atherogenesis. Cytokines affecting endothelial and smooth muscle cells in vascular disease. J. Lipid Res., 2005, 46(6), 1081-1092.
[31]
Osborn, L.; Hession, C.; Tizard, R.; Vassallo, C.; Luhowskyj, S.; Chi-Rosso, G.; Lobb, R. Direct expression cloning of vascular cell adhesion molecule 1, a cytokine-induced endothelial protein that binds to lymphocytes. Cell, 1989, 59(6), 1203-1211.
[32]
Rice, G.E.; Munro, J.M.; Bevilacqua, M.P. Inducible cell adhesion molecule 110 (INCAM-110) is an endothelial receptor for lymphocytes. A CD11/CD18-independent adhesion mechanism. J. Exp. Med., 1990, 171(4), 1369-1374.
[33]
Elices, M.J.; Osborn, L.; Takada, Y.; Crouse, C.; Luhowskyj, S.; Hemler, M.E.; Lobb, R.R. VCAM-1 on activated endothelium interacts with the leukocyte integrin VLA-4 at a site distinct from the VLA-4/fibronectin binding site. Cell, 1990, 60(4), 577-584.
[34]
Hansson, G.K. Immune mechanisms in atherosclerosis. Arterioscler. Thromb. Vasc. Biol., 2001, 21(12), 1876-1890.
[35]
Hermansson, A.; Ketelhuth, D.F.; Strodthoff, D.; Wurm, M.; Hansson, E.M.; Nicoletti, A.; Paulsson-Berne, G.; Hansson, G.K. Inhibition of T cell response to native low-density lipoprotein reduces atherosclerosis. J. Exp. Med., 2010, 207(5), 1081-1093.
[36]
Doran, A.C.; Meller, N.; McNamara, C.A. Role of smooth muscle cells in the initiation and early progression of atherosclerosis. Arterioscler. Thromb. Vasc. Biol., 2008, 28(5), 812-819.
[37]
Stary, H.C.; Chandler, A.B.; Glagov, S.; Guyton, J.R.; Insull, W. Jr., Rosenfeld, M.E.; Schafer, S.A.; Schwartz, C.J.; Wagner, W.D.; Wissler, R.W. A definition of initial, fatty streak, and intermediate lesions of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. Arterioscler. Thromb., 1994, 14(5), 840-856.
[38]
Rong, J.X.; Shapiro, M.; Trogan, E.; Fisher, E.A. Trans-differentiation of mouse aortic smooth muscle cells to a macrophage-like state after cholesterol loading. Proc. Natl. Acad. Sci. USA, 2003, 100(23), 13531-13536.
[39]
Johnson, J.L. Emerging regulators of vascular smooth muscle cell function in the development and progression of atherosclerosis. Cardiovasc. Res., 2014, 103(4), 452-460.
[40]
Feil, S.; Hofmann, F.; Feil, R. SM22alpha modulates vascular smooth muscle cell phenotype during atherogenesis. Circ. Res., 2004, 94(7), 863-865.
[41]
Galis, Z.S.; Khatri, J.J. Matrix metalloproteinases in vascular remodeling and atherogenesis: the good, the bad, and the ugly. Circ. Res., 2002, 90(3), 251-262.
[42]
Belo, V.A.; Guimaraes, D.A.; Castro, M.M. Matrix metalloproteinase 2 as a potential mediator of vascular smooth muscle cell migration and chronic vascular remodeling in hypertension. J. Vasc. Res., 2015, 52(4), 221-231.
[43]
Camejo, G.; Fager, G.; Rosengren, B.; Hurt-Camejo, E.; Bondjers, G. Binding of low density lipoproteins by proteoglycans synthesized by proliferating and quiescent human arterial smooth muscle cells. J. Biol. Chem., 1993, 268(19), 14131-14137.
[44]
Chait, A.; Wight, T.N. Interaction of native and modified low-density lipoproteins with extracellular matrix. Curr. Opin. Lipidol., 2000, 11(5), 457-463.
[45]
Ross, R. Atherosclerosis-an inflammatory disease. N. Engl. J. Med., 1999, 340(2), 115-126.
[46]
Park, B.; Yim, J.H.; Lee, H.K.; Kim, B.O.; Pyo, S. Ramalin inhibits VCAM-1 expression and adhesion of monocyte to vascular smooth muscle cells through MAPK and PADI4-dependent NF-kB and AP-1 pathways. Biosci. Biotechnol. Biochem., 2015, 79(4), 539-552.
[47]
Cai, Q.; Lanting, L.; Natarajan, R. Interaction of monocytes with vascular smooth muscle cells regulates monocyte survival and differentiation through distinct pathways. Arterioscler. Thromb. Vasc. Biol., 2004, 24(12), 2263-2270.
[48]
Cai, Q.; Lanting, L.; Natarajan, R. Growth factors induce monocyte binding to vascular smooth muscle cells: Implications for monocyte retention in atherosclerosis. Am. J. Physiol. Cell Physiol., 2004, 287(3), C707-C714.
[49]
Clarke, M.C.; Bennett, M.R. Cause or consequence: What does macrophage apoptosis do in atherosclerosis? Arterioscler. Thromb. Vasc. Biol., 2009, 29(2), 153-155.
[50]
Arbab-Zadeh, A.; Nakano, M.; Virmani, R.; Fuster, V. Acute coronary events. Circulation, 2012, 125(9), 1147-1156.
[51]
Libby, P. Mechanisms of acute coronary syndromes and their implications for therapy. N. Engl. J. Med., 2013, 368(21), 2004-2013.
[52]
Glagov, S.; Weisenberg, E.; Zarins, C.K.; Stankunavicius, R.; Kolettis, G.J. Compensatory enlargement of human atherosclerotic coronary arteries. N. Engl. J. Med., 1987, 316(22), 1371-1375.
[53]
Pant, R.; Marok, R.; Klein, L.W. Pathophysiology of coronary vascular remodeling: Relationship with traditional risk factors for coronary artery disease. Cardiol. Rev., 2014, 22(1), 13-16.
[54]
Narula, J.; Nakano, M.; Virmani, R.; Kolodgie, F.D.; Petersen, R.; Newcomb, R.; Malik, S.; Fuster, V.; Finn, A.V. Histopathologic characteristics of atherosclerotic coronary disease and implications of the findings for the invasive and noninvasive detection of vulnerable plaques. J. Am. Coll. Cardiol., 2013, 61(10), 1041-1051.
[55]
Virmani, R.; Burke, A.P.; Farb, A.; Kolodgie, F.D. Pathology of the vulnerable plaque. J. Am. Coll. Cardiol., 2006, 47(8)(Suppl.), C13-C18.
[56]
Canto, J.G.; Kiefe, C.I.; Rogers, W.J.; Peterson, E.D.; Frederick, P.D.; French, W.J.; Gibson, C.M.; Pollack, C.V., Jr; Ornato, J.P.; Zalenski, R.J.; Penney, J.; Tiefenbrunn, A.J.; Greenland, P. NRMI Investigators. Number of coronary heart disease risk factors and mortality in patients with first myocardial infarction. JAMA, 2011, 306(19), 2120-2127.
[57]
Greenland, P. Major risk factors as antecedents of fatal and nonfatal coronary heart disease events. JAMA, 2003, 290(7)
[58]
Knot. Prevalence of conventional risk factors in patients with coronary heart disease. JAMA, 2003, 290(7)
[59]
Jain, K.K. Personalized management of cardiovascular disorders. Med. Princ. Pract., 2017, 26(5), 399-414.
[60]
Spring, B.; Moller, A.C.; Colangelo, L.A.; Siddique, J.; Roehrig, M.; Daviglus, M.L.; Polak, J.F.; Reis, J.P.; Sidney, S.; Liu, K. Healthy lifestyle change and subclinical atherosclerosis in young adults: Coronary Artery Risk Development in Young Adults (CARDIA) study. Circulation, 2014, 130(1), 10-17.
[61]
Mongraw-Chaffin, M.L.; Allison, M.A.; Burke, G.L.; Criqui, M.H.; Matsushita, K.; Ouyang, P.; Shah, R.V.; Shay, C.M.; Anderson, C.A.M. CT derived body fat distribution and incident cardiovascular disease: The Multi-Ethnic Study of Atherosclerosis. J. Clin. Endocrinol. Metab., 2017, 102(11), 4173-4183.
[62]
Chou, R.; Dana, T.; Blazina, I.; Daeges, M.; Jeanne, T.L. Statins for prevention of cardiovascular disease in adults: Evidence report and systematic review for the US preventive services task force. JAMA, 2016, 316(19), 2008-2024.
[63]
Oesterle, A.; Laufs, U.; Liao, J.K. Pleiotropic effects of statins on the cardiovascular system. Circ. Res., 2017, 120(1), 229-243.
[64]
Zhong, P.; Wu, D.; Ye, X.; Wu, Y.; Li, T.; Tong, S.; Liu, X. Secondary prevention of major cerebrovascular events with seven different statins: A multi-treatment meta-analysis. Drug Des. Devel. Ther., 2017, 11, 2517-2526.
[65]
Arad, Y.; Ramakrishnan, R.; Ginsberg, H. Lovastatin therapy reduces low density lipoprotein apoB levels in subjects with combined hyperlipidemia by reducing the production of apoB-containing lipoproteins- implications for the pathophysiology of apoB production; J. Lip. Res, 1990, p. 30.
[66]
Ness, G.; Zhao, Z.; Lopez, D. Inhibitors of cholesterol biosynthesis increase hepatic low-density lipoprotein receptor protein degradation. Arch. Biochem. Biophys., 1996, 325(2), 242-248.
[67]
Feig, J.E.; Shang, Y.; Rotllan, N.; Vengrenyuk, Y.; Wu, C.; Shamir, R.; Torra, I.P.; Fernandez-Hernando, C.; Fisher, E.A.; Garabedian, M.J. Statins promote the regression of atherosclerosis via activation of the CCR7-dependent emigration pathway in macrophages. PLoS One, 2011, 6(12), e28534.
[68]
Feig, J.E.; Feig, J.L.; Kini, A.S. Statins, atherosclerosis regression and HDL: Insights from within the plaque. Int. J. Cardiol., 2015, 189, 168-171.
[69]
Schartl, M.; Bocksch, W.; Koschyk, D.H.; Voelker, W.; Karsch, K.R.; Kreuzer, J.; Hausmann, D.; Beckmann, S.; Gross, M. Use of intravascular ultrasound to compare effects of different strategies of lipid-lowering therapy on plaque volume and composition in patients with coronary artery disease. Circulation, 2001, 104(4), 387-392.
[70]
Crisby, M.; Nordin-Fredriksson, G.; Shah, P.K.; Yano, J.; Zhu, J.; Nilsson, J. Pravastatin treatment increases collagen content and decreases lipid content, inflammation, metalloproteinases, and cell death in human carotid plaques implications for plaque stabilization. Circulation, 2001, 103(7), 926-933.
[71]
Van Nieuw Amerongen Gea.Simvastatin improves disturbed endothelial barrier function.pdf. Circulation, 2000, 102(23)
[72]
Giugliano, D.; Maiorino, M.I.; Bellastella, G.; Esposito, K. Type 2 diabetes and cardiovascular prevention: The dogmas disputed. Endocrine, 2018, 60(2), 224-228.
[73]
Nathan, D.M.; Cleary, P.A.; Backlund, J.Y.; Genuth, S.M.; Lachin, J.M.; Orchard, T.J.; Raskin, P.; Zinman, B. ; Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC) Study Research Group. Intensive diabetes treatment and cardiovascular disease in patients with type 1 diabetes. N. Engl. J. Med., 2005, 353(25), 2643-2653.
[74]
Kannel, W.B.M.D. Diabetes and glucose tolerance as risk factors for cardiovascular disease- the framingham study. Diabetes Care, 1979, 2(2), 120-126.
[75]
Emerging Risk Factors Collaboration, Di Angelantonio, E.; Gao, P.; Khan, H.; Butterworth, A.S.; Wormser, D.; Kaptoge, S.; Kondapally, Seshasai, S.R.; Thompson, A.; Sarwar, N.; Willeit, P.; Ridker, P.M.; Barr, E.L.; Khaw, K.T.; Psaty, B.M.; Brenner, H.; Balkau, B.; Dekker, J.M.; Lawlor, D.A.; Daimon, M.; Willeit, J.; Njølstad, I.; Nissinen, A.; Brunner, E.J.; Kuller, L.H.; Price, J.F.; Sundström, J.; Knuiman, M.W.; Feskens, E.J.; Verschuren, W.M.; Wald, N.; Bakker, S.J.; Whincup, P.H.; Ford, I.; Goldbourt, U.; Gómez-de-la- Cámara, A.; Gallacher, J.; Simons, L.A.; Rosengren, A.; Sutherland, S.E.; Björkelund, C.; Blazer, D.G.; Wassertheil-Smoller, S.; Onat, A.; Marín Ibañez, A.; Casiglia, E.; Jukema, J.W.; Simpson, L.M.; Giampaoli, S.; Nordestgaard, B.G.; Selmer, R.; Wennberg, P.; Kauhanen, J.; Salonen, J.T.; Dankner, R.; Barrett-Connor, E.; Kavousi, M.; Gudnason, V.; Evans, D.; Wallace, R.B.; Cushman, M.; D'Agostino, R.B.; Sr, Umans, J.G.; Kiyohara, Y.; Nakagawa, H.; Sato, S.; Gillum, R.F.; Folsom, A.R.; van der Schouw, Y.T.; Moons, K.G.; Griffin, S.J.; Sattar, N.; Wareham, N.J.; Selvin, E.; Thompson, S.G.; Danesh, J. Glycated hemoglobin measurement and prediction of cardiovascular disease. 2014, 311(12), 1225-1233.
[76]
Miura, K.; Daviglus, M.L.; Dyer, A.R.; Liu, K.; Garside, D.B.; Stamler, J.; Greenland, P. Relationship of blood pressure to 25-year mortality due to coronary heart disease, cardiovascular diseases, and all causes in young adult men- the Chicago Heart Association Detection Project in Industry. Arch. Intern. Med., 2001, 161, 1501-1508.
[77]
Collaboration, P.S. Age-specific relevance of usual blood pressure to vascular mortality: A meta-analysis of individual data for one million adults in 61 prospective studies. Lancet, 2002, 360(9349), 1903-1913.
[78]
Group, S.R.; Wright, J.T. Jr., Williamson, J.D.; Whelton, P.K.; Snyder, J.K.; Sink, K.M.; Rocco, M.V.; Reboussin, D.M.; Rahman, M.; Oparil, S.; Lewis, C.E.; Kimmel, P.L.; Johnson, K.C.; Goff, D.C.; Fine, L.J.; Jaiden, C.; Cushman, W.C.; Cheung, A.K.; Ambrosius, W.T.; Bansal, S. A randomized trial of intensive versus standard blood-pressure control. N. Engl. J. Med., 2015, 373(22), 2103-2116.
[79]
Group, A.S. Effects of intensive blood-pressure control in type 2 diabetes mellitus. N. Engl. J. Med., 2010, 362(17), 1575.
[80]
Baker, W.L.; Coleman, C.I.; Kluger, J.; Reinhart, K.M.; Talati, R.; Quercia, R.; Phung, O.J.; White, C.M. Systematic review- comparative effectiveness of angiotensinconverting enzyme inhibitors or angiotensin ii–receptor blockers for ischemic heart disease. Ann. Intern. Med., 2009, 151(12), 861-871.
[81]
Elgendy, I.Y.; Winchester, D.E.; Pepine, C.J. Experimental and early investigational drugs for angina pectoris. Expert Opin. Investig. Drugs, 2016, 25(12), 1413-1421.
[82]
Piccolo, R.; Giustino, G.; Mehran, R.; Windecker, S. Stable coronary artery disease: revascularisation and invasive strategies. Lancet, 2015, 386(9994), 702-713.
[83]
Nossaman, V.E.; Nossaman, B.D.; Kadowitz, P.J. Nitrates and nitrites in the treatment of ischemic cardiac disease. Cardiol. Rev., 2010, 18(4), 190-197.
[84]
Kristina, E.; Torfgard, J.A. Mechanisms of action of nitrates. Cardiovas. Drugs Therap., 1994, 8(5).
[85]
Brown, B.G.; Bolson, E.; Petersen, R.B.; Pierce, C.D.; Dodge, H.T. The mechanisms of nitroglycerin action- stenosis vasodilatation as a major component of the drug response. Circulation, 1981, 64(4), 1089-1097.
[86]
Pearlman, A.S.; Goldstein, R.A.; Kent, K.M.; Epstein, S.E. Relative effects of nitroglycerin and nitroprusside during experimental acute myocardial ischemia. Eur. J. Prev. Cardiol., 1980, 11(4), 295-313.
[87]
Boudonas, G.E. β-Blockers in coronary artery disease management. Hippokratia, 2010, 14(4), 231-235.
[88]
Physicians NCGCURCo. Stable Angina: Methods, Evidence Guidance [Internet]. 7, Beta blockers vs. calcium channel blockers. Available from: . NICE Clinical Guidelines, 2011; 12
[89]
Ladage, D.; Schwinger, R.H.; Brixius, K. Cardio-selective beta-blocker: Pharmacological evidence and their influence on exercise capacity. Cardiovasc. Ther., 2013, 31(2), 76-83.
[90]
Bangalore, S.S.G.; Deedwania, P.; Crowley, K.; Eagle, K.A.; Goto, S.; Ohman, E.M.; Cannon, C.P.; Smith, S.C.; Zeymer, U.; Hoffman, E.B.; Messerli, F.H.; Bhatt, D.L. REACH Registry Investigators β-Blocker use and clinical outcomes in stable outpatients with and without coronary artery disease. JAMA, 2012, 308(13), 1340.
[91]
Motivala, A.A.; Parikh, V.; Roe, M.; Dai, D.; Abbott, J.D.; Prasad, A.; Mukherjee, D. Predictors, trends, and outcomes (among older patients >/=65 years of age) associated with beta-blocker use in patients with stable angina undergoing elective percutaneous coronary intervention: insights from the ncdr registry. JACC Cardiovasc. Interv., 2016, 9(16), 1639-1648.
[92]
Andersson, C.; Shilane, D.; Go, A.S.; Chang, T.I.; Kazi, D.; Solomon, M.D.; Boothroyd, D.B.; Hlatky, M.A. Beta-blocker therapy and cardiac events among patients with newly diagnosed coronary heart disease. J. Am. Coll. Cardiol., 2014, 64(3), 247-252.
[93]
Bhatia, V.; Bajaj, N.S.; Sanam, K.; Hashim, T.; Morgan, C.J.; Prabhu, S.D.; Fonarow, G.C.; Deedwania, P.; Butler, J.; Carson, P.; Love, T.E.; Kheirbek, R.; Aronow, W.S.; Anker, S.D.; Waagstein, F.; Fletcher, R.; Allman, R.M.; Ahmed, A. Beta-blocker use and 30-day all-cause readmission in medicare beneficiaries with systolic heart failure. Am. J. Med., 2015, 128(7), 715-721.
[94]
Wikstrand, J.; Wedel, H.; Castagno, D.; McMurray, J.J. The large-scale placebo-controlled beta-blocker studies in systolic heart failure revisited: results from CIBIS-II, COPERNICUS and SENIORS-SHF compared with stratified subsets from MERIT-HF. J. Intern. Med., 2014, 275(2), 134-143.
[95]
Chatterjee, S.; Biondi-Zoccai, G.; Abbate, A.; D’Ascenzo, F.; Castagno, D.; Van Tassell, B.; Mukherjee, D.; Lichstein, E. Benefits of beta blockers in patients with heart failure and reduced ejection fraction: Network meta-analysis. BMJ, 2013, 346, f55.
[96]
Belsey, J.; Savelieva, I.; Mugelli, A.; Camm, A.J. Relative efficacy of antianginal drugs used as add-on therapy in patients with stable angina: A systematic review and meta-analysis. Eur. J. Prev. Cardiol., 2015, 22(7), 837-848.
[97]
Braunwald, E. Mechanism of calcium-channel-blocking agents. N. Engl. J. Med., 1882, 307, 1618-1627.
[98]
Pascual, I.; Moris, C.; Avanzas, P. Beta-blockers and calcium channel blockers: First line agents. Cardiovasc. Drugs Ther., 2016, 30(4), 357-365.
[99]
Conti, C.R. Re-thinking angina. Clin. Cardiol., 2007, 30(2)(Suppl. 1), I1-I13.
[100]
Bavry, A.A.; Park, K.E.; Choi, C.Y.; Mahmoud, A.N.; Wen, X.; Elgendy, I.Y. Improvement of Subjective Well-Being by Ranolazine in Patients with Chronic Angina and Known Myocardial Ischemia (IMWELL Study). Cardiol. Ther., 2017, 6(1), 81-88.
[101]
Windecker, S.; Stortecky, S.; Stefanini, G.G.; da Costa, B.R.; Rutjes, A.W.; Di Nisio, M.; Silletta, M.G.; Maione, A.; Alfonso, F.; Clemmensen, P.M.; Collet, J.P.; Cremer, J.; Falk, V.; Filippatos, G.; Hamm, C.; Head, S.; Kappetein, A.P.; Kastrati, A.; Knuuti, J.; Landmesser, U.; Laufer, G.; Neumann, F.J.; Richter, D.; Schauerte, P.; Sousa Uva, M.; Taggart, D.P.; Torracca, L.; Valgimigli, M.; Wijns, W.; Witkowski, A.; Kolh, P.; Jüni, P. Revascularisation versus medical treatment in patients with stable coronary artery disease: network meta-analysis. BMJ, 2014, 348, g3859.
[102]
Deb, S.; Wijeysundera, H.C.; Ko, D.T.; Tsubota, H.; Hill, S.; Fremes, S.E. Coronary artery bypass graft surgery vs percutaneous interventions in coronary revascularization: A systematic review. JAMA, 2013, 310(19), 2086-2095.
[103]
Katz, B.; Rosenberg, A.; Frishman, W.H. Controlled-release drug delivery systems in cardiovascular medicine. Am. Heart J., 1995, 129(2), 359-368.
[104]
Zhang, H.; Zhang, J.; Streisand, J.B. Oral mucosal drug delivery. Clin. Pharmacokinet., 2002, 41(9), 661-680.
[105]
Henrikson, C.A.; Howell, E.E.; Bush, D.E.; Miles, J.S.; Meininger, G.R.; Friedlander, T.; Bushnell, A.C.; Chandra-Strobos, N. Chest pain relief by nitroglycerin does not predict active coronary artery disease. Ann. Intern. Med., 2003, 139(12), 979-986.
[106]
Noonan, P.K.; Benet, L.Z. The bioavailability of oral nitroglycerin. J. Pharm. Sci., 1986, 75(3), 241-243.
[107]
Noonan, P.K.; Benet, L.Z. Incomplete and delayed bioavailability of sublingual nitroglycerin. Am. J. Cardiol., 1985, 55(1), 184-187.
[108]
Kamiya, A.; Ogata, H.; Fung, H-L. Rectal absorption of nitro-glycerin in the rat: Avoidance of first-pass metabolism as a function of rectal length exposure. J. Pharm. Sci., 1982, 71(6), 621-624.
[109]
Wei, J.; Wu, T.; Yang, Q.; Chen, M.; Ni, J.; Huang, D. Nitrates for stable angina: a systematic review and meta-analysis of randomized clinical trials. Int. J. Cardiol., 2011, 146(1), 4-12.
[110]
Yang, J.; Jamei, M.; Yeo, K.R.; Tucker, G.T.; Rostami-Hodjegan, A. Prediction of intestinal first-pass drug metabolism. Curr. Drug Metab., 2007, 8(7), 676-684.
[111]
Narang, N.; Sharma, J. Sublingual mucosa as a route for systemic drug delivery. Int. J. Pharma Sci., 2011, 3(Suppl. 2), 18-22.
[112]
Sudhakar, Y.; Kuotsu, K.; Bandyopadhyay, A. Buccal bioadhesive drug delivery—a promising option for orally less efficient drugs. J. Control. Release, 2006, 114(1), 15-40.
[113]
Kammona, O.; Kiparissides, C. Recent advances in nanocarrier-based mucosal delivery of biomolecules. J. Control. Release, 2012, 161(3), 781-794.
[114]
Shojaei, A.H. Buccal mucosa as a route for systemic drug delivery: A review. J. Pharm. Sci., 1998, 1(1), 15-30.
[115]
Giannola, L.I.; De Caro, V.; Giandalia, G.; Siragusa, M.G.; Tripodo, C.; Florena, A.M.; Campisi, G. Release of naltrexone on buccal mucosa: permeation studies, histological aspects and matrix system design. Eur. J. Pharm. Biopharm., 2007, 67(2), 425-433.
[116]
Di Colo, G.; Zambito, Y.; Zaino, C. Polymeric enhancers of mucosal epithelia permeability: Synthesis, transepithelial penetration-enhancing properties, mechanism of action, safety issues. J. Pharm. Sci., 2008, 97(5), 1652-1680.
[117]
Werle, M.; Bernkop-Schnürch, A. Thiolated chitosans: Useful excipients for oral drug delivery. J. Pharm. Pharmacol., 2008, 60(3), 273-281.
[118]
Laffleur, F.; Bernkop-Schnürch, A. Strategies for improving mucosal drug delivery. Nanomedicine (Lond.), 2013, 8(12), 2061-2075.
[119]
Bernkop-Schnürch, A. The use of inhibitory agents to overcome the enzymatic barrier to perorally administered therapeutic peptides and proteins. J. Control. Release, 1998, 52(1), 1-16.
[120]
Müller, C.; Leithner, K.; Hauptstein, S.; Hintzen, F.; Salvenmoser, W.; Bernkop-Schnürch, A. Preparation and characterization of mucus-penetrating papain/poly (acrylic acid) nanoparticles for oral drug delivery applications. J. Nanopart. Res., 2013, 15(1), 1353.
[121]
Rao, S.; Tan, A.; Thomas, N.; Prestidge, C.A. Perspective and potential of oral lipid-based delivery to optimize pharmacological therapies against cardiovascular diseases. J. Control. Release, 2014, 193, 174-187.
[122]
Hilmer, S.N.; Shenfield, G.M.; Le Couteur, D.G. Clinical implications of changes in hepatic drug metabolism in older people. Ther. Clin. Risk Manag., 2005, 1(2), 151-156.
[123]
Lennernäs, H. Clinical pharmacokinetics of atorvastatin. Clin. Pharmacokinet., 2003, 42(13), 1141-1160.
[124]
Lai, S.K.; Wang, Y-Y.; Hanes, J. Mucus-penetrating nanoparticles for drug and gene delivery to mucosal tissues. Adv. Drug Deliv. Rev., 2009, 61(2), 158-171.
[125]
Ensign, L.M.; Cone, R.; Hanes, J. Oral drug delivery with polymeric nanoparticles: The gastrointestinal mucus barriers. Adv. Drug Deliv. Rev., 2012, 64(6), 557-570.
[126]
Yu, T.; Wang, Y-Y.; Yang, M.; Schneider, C.; Zhong, W.; Pulicare, S.; Choi, W.J.; Mert, O.; Fu, J.; Lai, S.K.; Hanes, J. Biodegradable mucus-penetrating nanoparticles composed of diblock copolymers of polyethylene glycol and poly (lactic-co-glycolic acid). Drug Deliv. Transl. Res., 2012, 2(2), 124-128.
[127]
Tang, B.C.; Dawson, M.; Lai, S.K.; Wang, Y-Y.; Suk, J.S.; Yang, M.; Zeitlin, P.; Boyle, M.P.; Fu, J.; Hanes, J. Biodegradable polymer nanoparticles that rapidly penetrate the human mucus barrier. Proc. Natl. Acad. Sci. USA, 2009, 106(46), 19268-19273.
[128]
Kararli, T.T. Comparison of the gastrointestinal anatomy, physiology, and biochemistry of humans and commonly used laboratory animals. Biopharm. Drug Dispos., 1995, 16(5), 351-380.
[129]
Corfield, A.P.; Carroll, D.; Myerscough, N.; Probert, C. Mucins in the gastrointestinal tract in health and disease. Front. Biosci., 2001, 6(10), D1321-D1357.
[130]
Ehsanullah, M.; Filipe, M.I.; Gazzard, B. Mucin secretion in inflammatory bowel disease: correlation with disease activity and dysplasia. Gut, 1982, 23(6), 485-489.
[131]
Podolsky, D.; Isselbacher, K. Composition of human colonic mucin. Selective alteration in inflammatory bowel disease. J. Clin. Invest., 1983, 72(1), 142.
[132]
Gill, S.R.; Pop, M.; DeBoy, R.T.; Eckburg, P.B.; Turnbaugh, P.J.; Samuel, B.S.; Gordon, J.I.; Relman, D.A.; Fraser-Liggett, C.M.; Nelson, K.E. Metagenomic analysis of the human distal gut microbiome. Science, 2006, 312(5778), 1355-1359.
[133]
Clayton, T.A.; Baker, D.; Lindon, J.C.; Everett, J.R.; Nicholson, J.K. Pharmacometabonomic identification of a significant host-microbiome metabolic interaction affecting human drug metabolism. Proc. Natl. Acad. Sci. USA, 2009, 106(34), 14728-14733.
[134]
Kinross, J.M.; Darzi, A.W.; Nicholson, J.K. Gut microbiome-host interactions in health and disease. Genome Med., 2011, 3(3), 14.
[135]
Wilson, I.D. Drugs, bugs, and personalized medicine: pharm-acometabonomics enters the ring. Proc. Natl. Acad. Sci. USA, 2009, 106(34), 14187-14188.
[136]
Bergin, I.L.; Witzmann, F.A. Nanoparticle toxicity by the gastrointestinal route: Evidence and knowledge gaps. Int. J. Biomed. Nanosci. Nanotechnol., 2013, 3(1-2), 163-210.
[137]
Khan, S.T.; Ahamed, M.; Al-Khedhairy, A.; Musarrat, J. Biocidal effect of copper and zinc oxide nanoparticles on human oral microbiome and biofilm formation. Mater. Lett., 2013, 97, 67-70.
[138]
Pietroiusti, A.; Magrini, A.; Campagnolo, L. New frontiers in nanotoxicology: gut microbiota/microbiome-mediated effects of engineered nanomaterials. Toxicol. Appl. Pharmacol., 2016, 299, 90-95.
[139]
Lestini, B.J.; Sagnella, S.M.; Xu, Z.; Shive, M.S.; Richter, N.J.; Jayaseharan, J.; Case, A.J.; Kottke-Marchant, K.; Anderson, J.M.; Marchant, R.E. Surface modification of liposomes for selective cell targeting in cardiovascular drug delivery. J. Control. Release, 2002, 78(1), 235-247.
[140]
Rejman, J.; Oberle, V.; Zuhorn, I.S.; Hoekstra, D. Size-dependent internalization of particles via the pathways of clathrin-and caveolae-mediated endocytosis. Biochem. J., 2004, 377(1), 159-169.
[141]
Gratton, S.E.; Ropp, P.A.; Pohlhaus, P.D.; Luft, J.C.; Madden, V.J.; Napier, M.E.; DeSimone, J.M. The effect of particle design on cellular internalization pathways. Proc. Natl. Acad. Sci. USA, 2008, 105(33), 11613-11618.
[142]
Alconcel, S.N.; Baas, A.S.; Maynard, H.D. FDA-approved poly (ethylene glycol)–protein conjugate drugs. Polym. Chem., 2011, 2(7), 1442-1448.
[143]
Fordyce, C.B.; Roe, M.T.; Ahmad, T.; Libby, P.; Borer, J.S.; Hiatt, W.R.; Bristow, M.R.; Packer, M.; Wasserman, S.M.; Braunstein, N.; Pitt, B.; DeMets, D.L.; Cooper-Arnold, K.; Armstrong, P.W.; Berkowitz, S.D.; Scott, R.; Prats, J.; Galis, Z.S.; Stockbridge, N.; Peterson, E.D.; Califf, R.M. Cardiovascular drug development: Is it dead or just hibernating? J. Am. Coll. Cardiol., 2015, 65(15), 1567-1582.
[144]
Wright, R.S.; Anderson, J.L.; Adams, C.D.; Bridges, C.R.; Casey, D.E. Jr, Ettinger, S.M.; Fesmire, F.M.; Ganiats, T.G.; Jneid, H.; Lincoff, A.M.; Peterson, E.D.; Philippides, G.J.; Theroux, P.; Wenger, N.K.; Zidar, J.P.; Anderson, J.L.; Adams, C.D.; Antman, E.M.; Bridges, C.R.; Califf, R.M.; Casey, D.E.; Jr, Chavey, W.E.; 2nd, Fesmire, F.M.; Hochman, J.S.; Levin, T.N.; Lincoff, A.M.; Peterson, E.D.; Theroux, P.; Wenger, N.K.; Wright, R.S. 2011 ACCF/AHA focused update of the Guidelines for the Management of Patients with Unstable Angina/Non-ST-Elevation Myocardial Infarction (updating the 2007 guideline): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines developed in collaboration with the American College of Emergency Physicians, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J. Am. Coll. Cardiol., 2011, 57(19), 1920-1959.
[145]
Antithrombotic Trialists’ Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ, 2002, 324(7329), 71-86.
[146]
CURRENT-OASIS 7 Investigators, Mehta, S.R.; Bassand, J.P.; Chrolavicius, S.; Diaz, R.; Eikelboom, J.W.; Fox, K.A.; Granger, C.B.; Jolly, S.; Joyner, C.D.; Rupprecht, H.J.; Widimsky, P.; Afzal, R.; Pogue, J.; Yusuf, S. Dose comparisons of clopidogrel and aspirin in acute coronary syndromes. N. Engl. J. Med., 2010, 363(10), 930-942.
[147]
Xian, Y.; Wang, T.Y.; McCoy, L.A.; Effron, M.B.; Henry, T.D.; Bach, R.G.; Zettler, M.E.; Baker, B.A.; Fonarow, G.C.; Peterson, E.D. Association of discharge aspirin dose with outcomes after acute myocardial infarction: Insights from the treatment with adp receptor inhibitors: longitudinal assessment of treatment patterns and events after acute coronary syndrome (translate-acs) study. Circulation, 2015, 132(3), 174-181.
[148]
Yusuf, S.; Zhao, F.; Mehta, S.R.; Chrolavicius, S.; Tognoni, G.; Fox, K.K. ; Clopidogrel in Unstable Angina to Prevent Recurrent Events Trial Investigators. Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. N. Engl. J. Med., 2001, 345(7), 494-502.
[149]
Foster, C.J.; Prosser, D.M.; Agans, J.M.; Zhai, Y.; Smith, M.D.; Lachowicz, J.E.; Zhang, F.L.; Gustafson, E.; Monsma, F.J., Jr; Wiekowski, M.T.; Abbondanzo, S.J.; Cook, D.N.; Bayne, M.L.; Lira, S.A.; Chintala, M.S. Molecular identification and characterization of the platelet ADP receptor targeted by thienopyridine antithrombotic drugs. J. Clin. Invest., 2001, 107(12), 1591-1598.
[150]
Boersma, E.; Harrington, R.A.; Moliterno, D.J.; White, H.; Théroux, P.; Van de Werf, F.; de Torbal, A.; Armstrong, P.W.; Wallentin, L.C.; Wilcox, R.G.; Simes, J.; Califf, R.M.; Topol, E.J.; Simoons, M.L. Platelet glycoprotein IIb/IIIa inhibitors in acute coronary syndromes: a meta-analysis of all major randomised clinical trials. Lancet, 2002, 359(9302), 189-198.
[151]
Kastrati, A.; Mehilli, J.; Neumann, F.J.; Dotzer, F.; ten Berg, J.; Bollwein, H.; Graf, I.; Ibrahim, M.; Pache, J.; Seyfarth, M.; Schühlen, H.; Dirschinger, J.; Berger, P.B.; Schömig, A. Intracoronary Stenting and Antithrombotic: Regimen Rapid Early Action for Coronary Treatment 2 (ISAR-REACT 2) Trial Investigators. Abciximab in patients with acute coronary syndromes undergoing percutaneous coronary intervention after clopidogrel pretreatment: the ISAR-REACT 2 randomized trial. JAMA, 2006, 295(13), 1531-1538.
[152]
Stone, G.W.; Bertrand, M.E.; Moses, J.W.; Ohman, E.M.; Lincoff, A.M.; Ware, J.H.; Pocock, S.J.; McLaurin, B.T.; Cox, D.A.; Jafar, M.Z.; Chandna, H.; Hartmann, F.; Leisch, F.; Strasser, R.H.; Desaga, M.; Stuckey, T.D.; Zelman, R.B.; Lieber, I.H.; Cohen, D.J.; Mehran, R.; White, H.D. ACUITY Investigators. Routine upstream initiation vs deferred selective use of glycoprotein IIb/IIIa inhibitors in acute coronary syndromes: The ACUITY Timing trial. JAMA, 2007, 297(6), 591-602.
[153]
Merli, G.J.; Groce, J.B. Pharmacological and clinical differences between low-molecular-weight heparins: Implications for prescribing practice and therapeutic interchange. P&T, 2010, 35(2), 95-105.
[154]
Alfonso Ross Terres, J.; Lozano-Ortega, G.; Kendall, R.; Sculpher, M.J. Cost-effectiveness of fondaparinux versus enoxaparin in non-ST-elevation acute coronary syndrome in Canada (OASIS-5). BMC Cardiovasc. Disord., 2015, 15, 180.
[155]
Zed, P.J. Low-molecular-weight heparin should replace unfractionated heparin in the management of acute coronary syndromes. J. Thromb. Thrombolysis, 1999, 8(2), 79-87.
[156]
Wong, G.C.; Giugliano, R.P.; Antman, E.M. Use of low-molecular-weight heparins in the management of acute coronary artery syndromes and percutaneous coronary intervention. JAMA, 2003, 289(3), 331-342.
[157]
Bittl, J.A.; Strony, J.; Brinker, J.A.; Ahmed, W.H.; Meckel, C.R.; Chaitman, B.R.; Maraganore, J.; Deutsch, E.; Adelman, B. Treatment with bivalirudin (Hirulog) as compared with heparin during coronary angioplasty for unstable or postinfarction angina. Hirulog Angioplasty Study Investigators. N. Engl. J. Med., 1995, 333(12), 764-769.
[158]
Antman, E.M. Should bivalirudin replace heparin during percutaneous coronary interventions? JAMA, 2003, 289(7), 903-905.
[159]
Levine, G.N.; Bates, E.R.; Blankenship, J.C.; Bailey, S.R.; Bittl, J.A.; Cercek, B.; Chambers, C.E.; Ellis, S.G.; Guyton, R.A.; Hollenberg, S.M.; Khot, U.N.; Lange, R.A.; Mauri, L.; Mehran, R.; Moussa, I.D.; Mukherjee, D.; Nallamothu, B.K.; Ting, H.H. 2011 ACCF/AHA/ SCAI Guideline for Percutaneous Coronary Intervention: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Society for Cardiovascular Angiography and Interventions. Circulation, 2011, 124(23), e574-e651.
[160]
Lands, A.M.; Arnold, A.; McAuliff, J.P.; Luduena, F.P.; Brown, T.G., Jr Differentiation of receptor systems activated by sympathomimetic amines. Nature, 1967, 214(5088), 597-598.
[161]
Gauthier, C.; Tavernier, G.; Charpentier, F.; Langin, D.; Le Marec, H. Functional beta3-adrenoceptor in the human heart. J. Clin. Invest., 1996, 98(2), 556-562.
[162]
Krief, S.; Lönnqvist, F.; Raimbault, S.; Baude, B.; Van Spronsen, A.; Arner, P.; Strosberg, A.D.; Ricquier, D.; Emorine, L.J. Tissue distribution of beta 3-adrenergic receptor mRNA in man. J. Clin. Invest., 1993, 91(1), 344-349.
[163]
Abrams, J. Hemodynamic effects of nitroglycerin and long-acting nitrates. Am. Heart J., 1985, 110(1 Pt 2), 216-224.
[164]
Parker, J.D.; Parker, A.B.; Farrell, B.; Parker, J.O. Effects of diuretic therapy on the development of tolerance to nitroglycerin and exercise capacity in patients with chronic stable angina. Circulation, 1996, 93(4), 691-696.
[165]
Braunwald, E. Mechanism of action of calcium-channel-blocking agents. N. Engl. J. Med., 1982, 307(26), 1618-1627.
[166]
Istvan, E.S.; Deisenhofer, J. Structural mechanism for statin inhibition of HMG-CoA reductase. Science, 2001, 292(5519), 1160-1164.
[167]
Tonelli, M.; Moyé, L.; Sacks, F.M.; Kiberd, B.; Curhan, G. Cholesterol and Recurrent Events (CARE) Trial Investigators. Pravastatin for secondary prevention of cardiovascular events in persons with mild chronic renal insufficiency. Ann. Intern. Med., 2003, 138(2), 98-104.
[168]
Asano, K.; Dutcher, D.L.; Port, J.D.; Minobe, W.A.; Tremmel, K.D.; Roden, R.L.; Bohlmeyer, T.J.; Bush, E.W.; Jenkin, M.J.; Abraham, W.T.; Raynolds, M.V.; Zisman, L.S.; Perryman, M.B.; Bristow, M.R. Selective downregulation of the angiotensin II AT1-receptor subtype in failing human ventricular myocardium. Circulation, 1997, 95(5), 1193-1200.
[169]
Haywood, G.A. AT1 and AT2 angiotensin receptor gene expression in human heart failure. Circulation, 1997, 95(5), 1201-1206.
[170]
Tsutamoto, T.; Wada, A.; Maeda, K.; Mabuchi, N.; Hayashi, M.; Tsutsui, T.; Ohnishi, M.; Sawaki, M.; Fujii, M.; Matsumoto, T.; Kinoshita, M. Angiotensin II type 1 receptor antagonist decreases plasma levels of tumor necrosis factor alpha, interleukin-6 and soluble adhesion molecules in patients with chronic heart failure. J. Am. Coll. Cardiol., 2000, 35(3), 714-721.


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