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A calcified nodule is a type of potentially vulnerable plaque accounting for approximately 2% to 7% of coronary events. Because its intravascular ultrasound (IVUS) features have never been validated, the aim of this study was to assess the IVUS characteristics of calcified nodules in comparison to histopathology. IVUS was performed in 856 pathologic slices in 29 coronary arteries (11 left anterior descending, 5 left circumflex, and 13 right coronary arteries) in 18 autopsy hearts. Pathologic sections were analyzed every 2 mm; qualitative and quantitative findings of matched IVUS were analyzed. IVUS detected calcification in 285 frames; 17 (6.0%) were calcified nodules, and 268 (94.0%) were non-nodular calcium by histopathology. Two calcified nodules (11.8%) were solitary, and 15 (88.2%) were adjacent to non-nodular calcium. IVUS characteristics of calcified nodules were (1) a convex shape of the luminal surface (94.1% in calcified nodules vs 9.7% in non-nodular calcium, p <0.001), (2) a convex shape of the luminal side of calcium (100% vs 16.0%, p <0.001), (3) an irregular luminal surface (64.7% vs 11.6%, p <0.001), and (4) an irregular leading edge of calcium (88.2% vs 19.0%, p <0.001). Luminal area at the calcified nodule site was larger (6.2 ± 2.4 vs 4.3 ± 1.6 mm(2), p <0.001) and plaque burden less (57 ± 6% vs 68 ± 5%, p <0.001) than at the minimum luminal area site. In conclusion, calcified nodules have distinct IVUS features (irregular and convex luminal surface) permitting their prospective identification in vivo., (Copyright © 2011 Elsevier Inc. All rights reserved.)

BACKGROUND AND MORPHOLOGIC STUDIES: Because coronary artery calcification correlates highly with plaque burden, it is an excellent disease marker for atherosclerosis. However, it is not a sensitive indicator of disease activity, and does not predict luminal compromise because of compensatory remodeling. In addition, most data do not support the concept that plaque calcification is related to plaque instability. Plaques demonstrating acute rupture usually show mild or moderate calcification, and biophysical models do not predict that calcium should result in an increased propensity to rupture. This review outlines morphologic studies relating calcification to risk factors and coronary plaque morphology.

Background: Increased biomechanical stresses in the fibrous cap of atherosclerotic plaques contribute to plaque rupture and, consequently, to thrombosis and myocardial infarction. Thin fibrous caps and large lipid pools are important determinants of increased plaque stresses. Although coronary calcification is associated with worse cardiovascular prognosis, the relationship between atheroma calcification and stresses is incompletely described., Methods and Results: To test the hypothesis that calcification impacts biomechanical stresses in human atherosclerotic lesions, we studied 20 human coronary lesions with techniques that have previously been shown to predict plaque rupture locations accurately. Ten ruptured and 10 stable lesions derived from post mortem coronary arteries were studied using large-strain finite element analysis. Maximum stress was not correlated with percentage of calcification, but it was positively correlated with the percentage of lipid (P:=0.024). When calcification was eliminated and replaced with fibrous plaque, stress changed insignificantly; the median increase in stress for all specimens was 0.1% (range, 0% to 8%; P:=0.85). In contrast, stress decreased by a median of 26% (range, 1% to 78%; P:=0.02) when lipid was replaced with fibrous plaque., Conclusions: Calcification does not increase fibrous cap stress in typical ruptured or stable human coronary atherosclerotic lesions. In contrast to lipid pools, which dramatically increase stresses, calcification does not seem to decrease the mechanical stability of the coronary atheroma.

Background: Neither clinical prediction models nor noninvasive imaging tests that detect coronary artery calcification identify all patients who experience acute coronary events. Variations in culprit plaque morphology may account for these inaccuracies., Methods and Results: We compared the 10-year Framingham risk index, histologic coronary calcification, and culprit plaque morphology in 79 consecutive adults with sudden cardiac death. There was a modest relationship between the Framingham risk index and the extent of histologic coronary calcification (r=0.35, P=0.002). Agreement in risk classification between the histologic calcification score and the Framingham risk index occurred in 50 of 79 cases (63.3%, P=0. 039). Either a focus of coronary artery calcification >/=40 micromol/L (62% of cases) or a Framingham risk index score >/= average risk for age (62% of cases) were present in 66 of 79 (83.5%) cases. Cases with plaque erosion (n=22) had significantly less coronary calcification (P=0.003) and lower Framingham risk index (P=0.001) scores than stable (n=27) or ruptured (n=30) plaques. Fourteen of 22 (63.6%) cases of plaque erosion were classified as low risk by both the Framingham risk index and the histologic calcification score., Conclusions: The prediction of sudden cardiac death using the Framingham risk index and the measurement of coronary calcification are distinct methods of assessing risk for sudden cardiac death. Excessive reliance on either method alone will produce errors in risk classification, particularly for patients at risk of plaque erosion, but their combination may be complementary.

We studied 108 cases of sudden coronary death at autopsy. Any calcification was present in 55% of men and women under 40 years; all hearts showed some calcification by age 50 in men, and by age 60 in women. The only risk factor independently associated with increased calcification was diabetes mellitus, in women only. The degree of calcification was greatest for acute and healed plaque ruptures, and the least for plaque erosion. Calcification in coronary atherosclerosis appears to be delayed in women, is greatest in women diabetics, and is associated with one type of plaque instability, namely plaque rupture.