Coronary Artery Calcification and Its Progression: What Does It Really Mean?
abstract
This abstract is available on the publisher's site.
Access this abstract now Full Text Available for ClinicalKey SubscribersCoronary artery calcification is concomitant with the development of advanced atherosclerosis. Coronary artery calcification pathologically begins as microcalcifications (0.5 to 15.0 μm) and grows into larger calcium fragments, which eventually result in sheet-like deposits (>3 mm). This evolution is observed to occur concurrently with the progression of plaque. These fragments and sheets of calcification can be easily identified by radiography as well as by computed tomography and intravascular imaging. Many imaging modalities have proposed spotty calcification to be a predictor of unstable plaque and have suggested more extensive calcification to be associated with stable plaques and perhaps the use of statin therapy. We will review the pathology of coronary calcification in humans with a focus on risk factors, relationship with plaque progression, correlation with plaque (in)stability, and effect of pharmacologic interventions.
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Coronary Artery Calcification and Its Progression: What Does It Really Mean?
JACC Cardiovasc Imaging 2018 Jan 01;11(1)127-142, H Mori, S Torii, M Kutyna, A Sakamoto, AV Finn, R VirmaniFrom MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.
One of the great, unaddressed issues in the practice of cardiovascular disease is how and whether to routinely incorporate the use of coronary artery calcium scoring (CACS) into patient management. With contemporary imaging technology, CACS can be easily measured—usually by computed tomography—rapidly with very low cost and very low radiation exposure. Hundreds of papers involving thousands of patients have shown that those individuals with a CACS of zero are at very low subsequent risk of events (likely because most do not have atherosclerotic coronary disease) and also that there is a graded relationship between the CACS (usually assessed by the Agatston score) and risk of subsequent events. There is incremental risk prediction value of knowing the CACS above clinical risk scores. Yet we do not really know how to react to such information, and questions such as whether asymptomatic people with non-zero CACS be put on high-intensity statin therapy regardless of their underlying pooled risk equation score have not been rigorously assessed in prospective randomized trials.
This week, a highly comprehensive review of coronary artery calcification was published. The authors are premier cardiovascular pathologists; thus, the perspective is from the pathological viewpoint. Patterns and possible mechanisms of coronary vascular calcification are reviewed, relative to the various types of atherosclerotic plaques. The authors address some of the conundrums in the literature, such as the apparent progression of coronary calcium as a consequence of statin therapy in concert with the risk reduction afforded by such therapy. They also address the interesting issue of whether calcium deposition may be associated with plaque stability, and describe how some patterns of deposition such as spotty calcification appear to be associated with plaque vulnerability, whereas others such as dense calcification may be associated with plaque stability. Issues of population risk vs an individual’s risk are discussed relative to how a clinician might incorporate the CACS information. This highly comprehensive review summarizes the state of knowledge and points to areas requiring further study. A good read!