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Commentary

Intravascular Quantification of Coronary Calcification — Current and Future Utility

*Daniel H. Steinberg, MD and §Neil J. Weissman, MD Author Affiliations: From the *Division of Cardiology, Medical University of South Carolina, Charleston, South Carolina, and §MedStar Research Institute, Washington Hospital Center, Washington, D.C. Disclosures: Dr. Weissman has received research grants from Boston Scientific Corp.; Dr. Steinberg has received speaker honoraria from the same. Address for Correspondence: Neil J. Weissman, MD, Washington Hospital Center, 100 Irving Street N.W., Suite EB 5123, Washington, D.C. 20010. E-mail: Neil.J.Weissman@Medstar.net
November 2008
Coronary calcification has long been known to reflect underlying atherosclerotic coronary artery disease. In fact, the presence of coronary calcification has become an important component of screening for coronary artery disease and the extent of calcification on electron beam computed tomography has been shown to correlate with prediction of future cardiovascular events.1,2 Intravascular ultrasound (IVUS), by virtue of its ability to image at high resolution, allows not only assessment of the location of coronary calcification, but also the number, depth, arc and length of calcified plaque. Assessing coronary calcium by IVUS, prior research has demonstrated that a greater calcium burden correlates directly with a greater extent of coronary disease3,4 and future cardiovascular events. Additionally, compared to stable plaque, calcification in unstable plaque (i.e., culprit lesion in acute coronary syndromes) tends to be less frequent, of lesser quantity and more deeply located.3,5,6 In the current study, Wang et al attempt to further characterize the extent of coronary calcification by combining two IVUS measures of calcium (arc and length) to form the “arc area”.7 This extends previous work by others attempting to improve the quantification of calcification with IVUS beyond standard arc or length measurements.8,9 By multiplying the two measures (degrees of calcium) and length (in millimeters), they derive a non-anatomic measure (degree-mm) which may have a stronger correlate to true coronary calcium volume (burden), but the validation of this measure has not been performed. Via this new method, they postulate that the arc area may correlate more with the amount of plaque seen in different clinical states (stable versus unstable angina versus acute myocardial infarction [AMI]). Care must be taken whenever a new method is introduced in the same paper that proclaims that the new measure is superior to older measures and then goes on to use that new method to test a hypothesis. A new measure should undergo validation versus a gold standard first. After validation, it can be used on a different sample to test the hypothesis. Introducing a new method prior to validation and purporting that the measure forwards a new finding is risky. The current study evaluated 201 patients, including 71 patients with AMI, 75 patients with unstable angina pectoris and 55 patients with stable angina pectoris. All patients underwent IVUS imaging of a presumed de novo culprit artery. Lesions of patients with AMI contained significantly more calcified plaques (2.21 ± 1.98) compared to patients with unstable angina (1.20 ± 1.15) or stable angina (1.15 ± 1.01), however the overall calcium burden was less, as both the amount of calcium per lesion and total arc area were significantly less in patients with AMI (301 ± 401) compared to those with stable angina pectoris (0.3 ± 1,018). Interestingly, patients with AMI had a significantly higher arc area than those with unstable angina pectoris.7 The question remains as to what these findings do to advance our current knowledge and help tailor future research and treatments. Regarding our current knowledge, it confirms what is already known. Coronary calcium represents advanced coronary disease and the extent of calcium may predict future events. These events, as demonstrated both previously and in the current study, tend to occur in spotty areas of lesser calcium burden. With regard to future research and treatment approaches, the current study does not address the clinically relevant issue of vulnerable plaque. Revascularization in the acute setting is no longer a debated question. For severe symptoms refractory to medical therapy or associated with a significant ischemic burden, revascularization is an established therapy. However, the ability to prevent myocardial infarction by early and aggressive local treatment of plaque prone to rupture remains elusive at best. Identifying vulnerable plaque remains the first step, and unfortunately, coronary calcification measured by “arc area” does little to bring us any closer.

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7. Wang X, Lu C, Chen X, et al. A new method to quantify coronary calcification by intravascular ultrasound — The different patterns of acute myocardial infarction, unstable angina pectoris and stable angina pectoris. J Invasive Cardiol 2008;20:587–590.
8. Scott DS, Arora UK, Farb A, et al. Pathologic validation of a new method to quantify coronary calcific deposits in vivo using intravascular ultrasound. Am J Cardiol 2000;85:37–40.
9. Ehara S, Kobayashi Y, Kataoka T, et al. Quantification of coronary calcification by intravascular ultrasound. Circ J 2007;71:530–535.

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