1. Genetic Determinants of Arterial Calcification Associated With Atherosclerosis 
Terence M. Doherty, BA, Lorraine A. Fitzpatrick, MD, Aisha Shaheen, BA, Tripathi B. Rajavashisth, PhD, Robert C. Detrano, MD, PhD 
Mayo Clinic Proceedings 
Volume 79, Issue 2, Pages (February 2004)
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2. Figure 1
Computed tomographic (A and B) and intravascular ultrasonic (IVUS) (C-E) images of coronary arterial calcification. Computed tomography is a widely used noninvasive method to quantify coronary calcium. A, Horizontal tomographic image of a healthy heart without coronary calcification. The spine is the bright semicircular region at the bottom; the sternum is at the top; and the aorta is the gray circular structure adjacent to the spine, with a small focus of calcification (bright dot). B, Similar tomographic image from a patient with a moderate amount of calcification in the left coronary artery distribution (bright radiographically dense regions near the right border of the heart). C-E, IVUS is invasive, uses ultrasonography rather than radiography, and is performed in conjunction with coronary arteriography. C, Normal artery with no atherosclerosis or calcification. D, A large plaque without calcification, visible in the lower half of the artery. E, Extensive, echodense, nearly circumferential calcification is evident in the artery. Computed tomographic images courtesy of R.C.D.; IVUS images courtesy of Steven L. Goldberg, MD, Division of Cardiology, University of Washington, Seattle.
Mayo Clinic Proceedings  , DOI: ( / )
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3. Figure 2
In the early stages of atherogenesis, circulating cells of the immune and mononuclear phagocytic lineages converge on sites of subendothelial inflammation. Lipoproteins become trapped in the subendothelial matrix and are modified into moieties such as oxidized low-density lipoprotein (Ox-LDL). This results in overlying endothelial cells expressing adhesion molecules, which guide circulating leukocytes to the nascent plaque. The leukocytes engage the endothelial cells transiently, and if the endothelial cells have expressed appropriate additional adhesion molecules on their surface, this acts as a braking mechanism, stabilizing the leukocyte-endothelial cell interaction. The leukocyte “rolls” along the surface of the endothelium and may begin to transmigrate into the subendothelial matrix by squeezing between adjacent endothelial cells in a process called diapedesis. On subendothelial entry, the leukocytes migrate toward the inflammatory nidus.
Mayo Clinic Proceedings  , DOI: ( / )
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