Universiteit Maastricht

Calcification

 

Calcium builds up in the vessels and stiffen them, laying the foundation for heart disease. Getting one's calcium score is simple, either by electron beam computed tomography (EBCT) or by multidetector CT. Studies show that in every age group people with higher vascular calcium levels have a greater risk of heart attack than do people of the same age with lower scores.

Atherosclerosis is the major cause of mortality in the Western world. It is characterized by the presence of atherosclerotic lesions in the arterial intima. Atherosclerosis is thought to progress from fatty streak to fibrous plaques, and finally to calcified atheromata.
Vascular calcification does not remain restricted to the intima, but also occurs in the media were it is known as Mönckeberg sclerosis. In contrast to intimal calcification, medial calcification occurs in the absence of inflammatory cell infiltration and lipid deposition. Although both processes are different in many ways, it is generally accepted that vascular calcification is an active process rather than a passive process resulting from the accumulation of calcium released from dying cells.

Arterial calcification is now generally accepted as an important independent risk factor for the development of atherosclerosis, myocardial infarction, stroke, and renal disease. Patients with manifest arterial calcification have an unfavorable prognosis compared to patients with no or mild calcification. Therefore, the prevention or reversal of arterial calcification may lead to improved patient outcomes.

For a long time it has been thought that calcification was a passive process and the end stage of cardiovascular disease. During the last decades, however, it has become clear that several osteoregulatory proteins, both stimulatory and inhibitory, are involved in the calcification of vascular tissue with a major role for the vitamin K-dependent matrix Gla-protein.

Recommended literature:

  • "Ross R. The pathogenesis of atherosclerosis: a perspective for the 1990s. Nature. 1993;362:801-809.
  • Wexler L, Brundage B, Crouse J, Detrano R, Fuster V, Maddahi J, Rumberger J, Stanford W, White R, Taubert K. Coronary artery calcification: pathophysiology, epidemiology, imaging methods, and clinical implications. A statement for health professionals from the American Heart Association. Writing Group. Circulation. 1996;94:1175-1192.
  • Mönckeberg JG. Uber die reine mediaverkalkung der extremitätenarterien und ihr verhalten zur arteriosklerose. Virchows Arch Pathol Anat. 1902;171:141-167.
  • Shanahan CM, Cary NR, Salisbury JR, Proudfoot D, Weissberg PL, Edmonds ME. Medial Localization of Mineralization-Regulating Proteins in Association With Mönckeberg's Sclerosis: Evidence for Smooth Muscle Cell-Mediated Vascular Calcification. Circulation. 1999;100:2168-2176.
  • Doherty, T. M. Fitzpatrick, L. A. Inoue, D. Qiao, J. H. Fishbein, M. C. Detrano, R. C. Shah, P. K. Rajavashisth, T. B. Molecular, endocrine, and genetic mechanisms of arterial calcification. 2004; 25: 629-72
  • Lehto S, Niskanen L, Suhonen M, et al. Medial artery calcification: a neglected harbinger of cardiovascular complications in non-insulin-dependent diabetes mellitus. Arterioscler Thromb Vasc Biol 1996; 16:978-983.
  • Zieman SJ, Melenovsky V, Kass DA. Mechanisms, pathophysiology, and therapy of arterial stiffness. Arterioscler Thromb Vasc Biol. 2005 May;25(5):932-43