Atherosclerosis: from etiology to its possible influencing
Authors:
Michal Vrablík
Authors place of work:
Centrum preventivní kardiologie III. interní kliniky 1. LF UK a VFN Praha, přednosta prof. MUDr. Štěpán Svačina, DrSc., MBA
Published in the journal:
Vnitř Lék 2015; 61(11): 925-931
Category:
Reviews
Summary
Atherosclerosis as an inflammatory process affecting vessel wall has more forms usually occurring together. Classical atherosclerotic vascular lesion characterised by lipid accumulation in the subendothelial space is frequently accompanied by changes in deeper layers of arterial wall, in which increased extracellular tissue mass and smooth muscle cells activation represent the most prominent feature. Due to a specific constellation of risk factors the first or second pathology may be more expressed. While initiation and progression of classical atherosclerosis are mostly driven by lipoproteins (especially of LDL class) the most important factor of arterial media changes seem to be different risk factors e.g. hyperactivity of renin-angiotensin-aldosterone system (RAS). Influencing these two basic pathogenic mechanisms undoubtedly slows down the course of vascular changes and impacts positively on the prognosis of the patients. It is noteworthy, that simultaneous targeting of both of these mechanisms yields synergistic effects as evidenced both by experimental and clinical works. Using the opportunities offered by intensive lowering of atherogenic plasma lipids and over activation of the RAS system reduce not only the incidence of typical atherotromobotic complications (e.g. acute coronary syndrome) but also the events caused by changes of medial part of arterial wall or left myocardial ventricle (malignant arrhythmia, heart failure). These two strategies represent necessary conditions for successful cardiovascular prevention.
Key words:
atherosclerosis – cardiovascular prevention – dyslipidemia – RAS system – systemic inflammation
Zdroje
1. Getz GS, Vesselinovitch D, Wissler RW. A dynamic pathology of atherosclerosis. Am J Med 1969; 46(5): 657–673.
2. Ross R, Harker L. Hyperlipidemia and atherosclerosis. Science 1976; 193(4258): 1094–1100.
3. Steinberg D, Witzum JL. Lipoproteins and atherogenesis. Current Concepts JAMA 1990; 264(23): 3047–3052.
4. Camici GG, Savarese G, Akhmedov A et al. Molecular mechanism of endothelial and vascular aging: implications for cardiovascular disease. Eur Heart J 2015; pii: ehv587 (e-publikace v tisku).
5. Hansson GK. Immune and inflammatory mechanisms in the pathogenesis of atherosclerosis. J Atheroscler Thromb 1994; 1(Suppl 1): S6-S9.
6. Libby P. Inflammation in atherosclerosis. Nature 2002; 420(6917): 868–874.
7. Stemme S. Plaque T-cell activity: not so specific? Arterioscler Thromb Vasc Biol 2001; 21(7): 1099–1101.
8. Galkina E, Ley K. Vascular adhesion molecules in atherosclerosis. Arterioscler Thromb Vasc Biol 2007; 27(11): 2292–2301.
9. Luo BH, Carman CV, Springer TA. Structural basis of integrin regulation and signaling. Annu Rev Immunol 2007; 25: 619–647.
10. Skålén K, Gustafsson M, Rydberg EK et al. Subendothelial retention of atherogenic lipoproteins in early atherosclerosis. Nature 2002; 417(6890): 750–754.
11. Gerrity RG. The role of the monocyte in atherogenesis: I. Transition of blood-borne monocytes in to foam cells in fatty lesions. Am J Pathol 1981; 103(2): 181–190.
12. Libby P, Simon DI. Inflammation and thrombosis: the clot thickens. Circulation 2001; 103(13): 1718–1720.
13. Geng YJ, Libby P. Progression of atheroma: a strug glebet ween death and procreation. Arterioscler Thromb Vasc Biol 2002; 22(9): 1370–1380.
14. Libby P. Collagenases and cracks in the plaque. J Clin Invest 2013; 123(8): 3201–3203.
15. Navab M. Ananthramaiah GM, Reddy ST et al. The oxidation hypothesis of atherogenesis: the role ofoxidizedphospholipids and HDL. J Lipid Res 2004; 45(6): 993–1007.
16. Dichtl W, Nilsson L, Goncalves I al. Very low-density lipoprotein activates nuclear factor-κB in endothelial cells. Circ Res 1999; 84(9): 1085–1094.
17. Hansson GK, Hermansson A. The immune system in atherosclerosis. Nat Immunol 2011; 12(3): 204–212.
18. Varbo A, Benn M, Nordestgaard BG. Remnant cholesterol as a cause of ischemic heart disease: evidence, definition, measurement, atherogenicity, high risk patients, and present and future treatment. Pharmacol Ther 2014; 141(3): 358–367.
19. Schulz C, Massberg S. Atherosclerosis-Multiple Pathways to Lesional Macrophages. Sci Transl Med 2014; 6(239):239ps2. Dostupné z DOI: <http://dx.doi.org/10.1126/scitranslmed.3008922>.
20. Bonaa KH, Njølstad I, Ueland PM et al. Homocysteine lowering and cardiovascular events after acute myocardial infarction. N Engl J Med 2006; 354(15): 1578–1588.
21. Salomon RN, Hughes CC, Schoen FJ et al. Human coronary transplantation-associated arteriosclerosis. Evidence for a chronic immune reaction to activated graft endothelial cells. Am J Pathol 1991; 138(4): 791–798.
22. Verberckmoes SC, Persy V, Behets GJ et al. Uremia-related vascular calcification: more than apatite deposition. Kidney Int 2007; 71(4): 298–303.
23. Mafham M, Emberson J, Landray MJ et al. Estimated glomerular filtration rate and the risk of major vascular events and all-cause mortality: a meta-analysis. PLoSOne 2011; 6(10): e25920. Dostupné z DOI: <http://dx.doi.org/10.1371/journal.pone.0025920>.
24. Widimský J Jr, Štrauch B, Petrák O et al. Vascular disturbances in primary aldosteronism: clinical evidence. Kidney Blood Press Res 2012; 35(6): 529–533.
25. ONTARGET Investigators. Yusuf S, Teo KK, Pogue J et al. Telmisartan, ramipril, orbothin patients at high risk for vascular events. N Engl J Med 2008; 358(15): 1547–1559.
26. Couture R, Blaes N, Girolami JP. Kinin receptors in vascular biology and pathology. Curr Vasc Pharmacol 2014; 12(2): 223–248.
27. Savarese G, Costanzo P, Cleland JG et al. A meta-analysis reporting effects of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in patients without the art failure. J Am Coll Cardiol 2013; 61(2): 131–142.
28. Lazartigues E, Feng Y, Lavoie JL. Thetw of ACEs of the tissue renin-angiotensin systems: implication in cardiovascular diseases. Curr Pharm Des 2007; 13(12): 1231–1245.
29. Mac Fadyen RJ, Lees KR, Reid JL. Tissue and plasma angiotensin converting enzyme and the response to ACE inhibitor drugs. Br J Clin Pharmacol 1991; 31(1): 1–13.
30. Ceconi C, Francolini G, Bastianon D et al. Differences in the effect of angiotensin-converting enzyme inhibitors on the rate of endothelial cell apoptosis: in vitro and in vivo studies. Cardiovasc Drugs Ther 2007; 21(6): 423–429.
31. Tropeano AI, Boutouyrie P, Pannier B et al. Brachial pressure-independent reduction in carotid stiffness after long-term angiotensin-converting enzyme inhibition in diabetic hypertensives. Hypertension 2006; 48(1): 80–86.
32. Verdecchia P, Gentile G, Angeli F et al. Beyond blood pressure: evidence for cardiovascular, cerebrovascular, and renal protective effects of renin-angiotensin system blockers. Ther Adv Cardiovasc Dis 2012; 6(2): 81–91.
33. Rodriguez-Granillo GA, de Winter S, Bruining N et al. EUROPA/PERSPECTIVE Investigators. Effect of perindopril on coronary remodeling in sights from a multicentre, randomized study. Eur Heart J 2007; 28(19): 2326–2331.
34. Dahlöf B, Sever PS, Poulter NR et al. ASCOT investigators. Prevention of cardiovascular events with an antihypertensive regimen of amlodipine adding perindopril as required versus atenolol adding bendroflumethiazide as required, in the Anglo-Scandinavian Cardiac Outcomes Trial-Blood Pressure Lowering Arm (ASCOT-BPLA): a multicentre randomised controlled trial. Lancet 2005; 366(9489): 895–906.
35. Sever P, Poulter NR, Mastorantonakis S et al. ASCOT Investigators. Coronary heart disease benefits from blood pressure and lipid-lowering. Int J Cardiol 2009; 135(2): 218–222.
36. Vrablík M, Freiberger T, Lánská I et al. Projekt Atractiv: zlepšení kardiovaskulární prevence v podmínkách primární péče v České republice. Vnitř Lék 2008; 54(12): 1131–1139.
37. Ridker PM, Thuren T, Zalewski A et al. Interleukin-1ß inhibition and the prevention of recurrent cardiovascular events: rationale and design of the Canakinumab Anti-inflammatory Thrombosis Outcomes Study (CANTOS). Am Heart J 2011; 162(4): 597–605.
38. Ridker PM. Testing the inflammatory hypothesis of atherothrombosis: scientific rationale for the cardiovascular inflammation reduction trial (CIRT). J Thromb Haemost 2009; 7(Suppl 1): 332–339.
Štítky
Diabetology Endocrinology Internal medicineČlánok vyšiel v časopise
Internal Medicine
2015 Číslo 11
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