PubMed · 14094243
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LAVAL-JEANTET, H SCALA. 1963. [DIFFUSE ARTICULAR CHONDROCALCINOSIS].. https://pubmed.ncbi.nlm.nih.gov/14094243/
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BACKGROUND: Coronary artery calcification measured by electron-beam computerized tomography (EBCT) correlates with plaque burden and vessel stenosis and is predictive of future cardiac events in the general population. Uremic vascular calcification is common and widespread, tends to be medial as well as intimal, and may not relate solely to atherosclerotic lesions. Despite this difference and in the absence of any direct evidence in uremic patients, it is generally implied that coronary artery calcification equates to occlusive atherosclerosis. METHODS: We set out to compare the predictive value of coronary artery calcification assessed by EBCT with contemporaneous coronary angiography. We studied 18 patients with end-stage renal disease undergoing maintenance dialysis. Seventy-two coronary vessels were analyzed for angiographic evidence of stenotic disease and correlated with individual vessel calcification score. RESULTS: There was no significant correlation between degree of vessel stenosis and calcification score for individual vessels in patients with a positive calcium scan. Specificity was 48% and the positive predictive value was 53%. However, a calcification score <20 strongly correlated with the absence of significant luminal narrowing, and a 0 calcification score had a negative predictive value of 87.5%. CONCLUSION: Coronary artery calcification measured by EBCT is not an accurate marker of the degree of vessel stenosis in coronary artery disease in uremic patients and should not be used as a single screening test for atherosclerotic coronary disease.
Dialysis patients have increased cardiovascular morbidity, mortality, and vascular calcification, and the latter appears to impact the former. Recent evidence indicates that vascular calcification is an active, cell-mediated process. Osteoblast differentiation factor Cbfa1 and several bone-associated proteins (osteopontin, bone sialoprotein, alkaline phosphatase, type I collagen) are present in histologic sections of arteries obtained from patients with end-stage renal disease (chronic kidney disease stage V [CKD-V]). This supports the theory that vascular smooth muscle cells can dedifferentiate or transform to osteoblast-like cells, possibly by up-regulation of Cbfa1. In in vitro experiments, addition of pooled serum from dialysis patients (versus normal healthy controls) accelerated mineralization and increased expression of Cbfa1, osteopontin, and alkaline phosphatase in cultured vascular smooth muscle cells. Clinically, the pathogenesis of vascular calcification is not completely understood, although increased levels of phosphorus and/or other potential uremic toxins may play an important role by transforming vascular smooth muscle cells into osteoblast-like cells. Presumably, once this process begins, increased serum calcium X phosphorus product, or calcium load from binders, accelerates this process. In addition, it is likely that circulating inhibitors of calcification are also important. Further understanding of the pathophysiology of vascular calcification is needed to intervene appropriately.