Atherosclerosis

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ΕΤΥΜΟΛΟΓΙΑ

(German early 20th century) ← Latin. atheroma ← Greek. athare/athere - groats, sklerosis - hardening
Cross-section of a coronary artery showing stenosis by atheroma.

This is a complex pathophysiological process which appears to involve four distinct but interacting elements:

In essence, in due course the three main hypothesis resulted in effective treatments and were proved, as well as fine tuned by such treatment success. It is thought that chronic intramural inflammation, caused by say diabetes mellitus or smoking promotes the deposition of lipids, particularly cholesterol. These lipids become organised in a plaque by macrophage infiltration. The resulting plaque is weak and prone to rupture. Rupture exposes the vessel wall collagen, which appropriately activates pro-coagulant pathways.

Smoking promotes inflammation of vasa vasorum by producing chronic tissue hypoxia. The mechanism involved in diabetes is less readily understood.

Chronic inflammation resolves with the production of fibrotic areas and calcification.

Plaques are most commonly produced at the intersections of vessels, an effect attributable to alteration of flow at those points, which probably allows for attachment of apolipoproteins to the vessel wall.

While there is evidence that a diet characterised by high intake of antioxidants tends to reduce atherosclerosis selective supplimentation with vitamins such as Vitamin E can be ineffectual[1] [2] or harmful[3][4]. Positive results may be confined to subpopulations with nutritional deficiency for cultural or other reasons.[5].[6] This may be because antioxidants have other properties than just a role in scavenging the free radicals produced by chronic inflammation.

Modification of these processes offers the possibility of disease modification (see below).

Thrombi produced by exposure of mural collagen may cause infarction of distal territories. This is an important mechanism for stroke and myocardial infarction.

Prevention therefore focuses on modifiable risk factors. These include:

References

  1. Heart Protection Study Collaborative Group.MRC/BHF Heart Protection Study of antioxidant vitamin supplementation in 20,536 high-risk individuals: a randomised placebo-controlled trial. Lancet. 2002 ;360(9326):23-33.
  2. Lonn E, Yusuf S, Arnold MJ, Sheridan P, Pogue J, Micks M, et al. Homocysteine lowering with folic acid and B vitamins in vascular disease. The New England journal of medicine 2006;354:1567-77. (Direct link – subscription may be required.)
  3. Rapola JM, Virtamo J, Ripatti S, Huttunen JK, Albanes D, Taylor PR, et al. Randomised trial of alpha-tocopherol and beta-carotene supplements on incidence of major coronary events in men with previous myocardial infarction. Lancet 1997;349:1715-20.
  4. Tarnwall ME, Virtamo J, Korhonen PA, Virtanen MJ, Taylor PR, Albanes D, et al. Effect of alpha-tocopherol and beta-carotene supplementation on coronary heart disease during the 6-year post-trial follow-up in the ATBC study. European heart journal 2004;25:1171-8. (Direct link – subscription may be required.)
  5. Hercberg S, Galan P, Preziosi P, Bertrais S, Mennen L, Malvy D, et al. The SU.VI.MAX Study: a randomized, placebo-controlled trial of the health effects of antioxidant vitamins and minerals. Archives of internal medicine 2004;164:2335-42. (Direct link – subscription may be required.)
  6. Jaxa-Chamiec T, Bednarz B, Drozdowska D, Gessek J, Gniot J, Janik K, et al. Antioxidant effects of combined vitamins C and E in acute myocardial infarction. The randomized, double-blind, placebo controlled, multicenter pilot Myocardial Infarction and VITamins (MIVIT) trial. Kardiologia polska 2005;62:344-50.
  7. Brunekreef B, Hoffmann B. Air pollution and heart disease. Lancet (London, England). 2016 Aug 13; 388(10045):640-2.(Link to article – subscription may be required.)
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