Abstract
Coronary artery calcifications appear to be an indicator of total atherosclerotic disease burden, but their relation to the stability of individual atherosclerotic plaques is not well understood. Plaque rupture and acute coronary syndromes can occur without plaque calcification and may be more often associated with noncalcified, soft plaque. Pharmacologic control of calcium and phosphate metabolism should be guided by the nephrologic and endocrinologic needs of the renal failure patient and not withheld out of concern about coronary calcifications. Efforts to slow coronary artery disease progression in patients with end-stage renal disease should emphasize aggressive control of recognized cardiovascular risk factors.
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