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Role of calcified spots detected by intravascular ultrasound in patients with ST-segment elevation acute myocardial infarction.

van der Hoeven BL, Liem SS, Oemrawsingh PV, Dijkstra J, Jukema JW, Putter H, Atsma DE, van der Wall EE, Bax JJ, Reiber JC, Schalij MJ

Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands.

Electron beam computed tomographic studies have demonstrated that the extent of intracoronary calcium is related to risk of coronary events. This study was performed to gain further insight into the distribution of focal calcifications and their relation to the site of plaque rupture within the culprit artery in consecutive patients (n = 60) with acute myocardial infarction (AMI) using intravascular ultrasound imaging. Calcifications in the culprit lesion and adjacent segments were classified and counted according to their arc (< 45 degrees, 45 degrees to 90 degrees, 90 degrees to 180 degrees, > 180 degrees), length (< 1.5, 1.5 to 3.0, 3.0 to 6.0, > 6.0 mm), and dispersion (number of spots per millimeter). Calcifications at the edge of a visible rupture or ulceration were considered related to the AMI. Compared with adjacent proximal and distal segments, the culprit lesion contained more calcified spots per millimeter (0.14, 0.10, and 0.21, respectively, p < 0.05). Small calcified spots (arc < 45 degrees, length < 1.5 mm) were more common (p < 0.05). Plaque rupture or ulceration was manifest in 31 culprit lesions (52%), 14 (45%) of which contained focal calcifications. These calcified spots extended more often to 90 degrees to 180 degrees of the vessel circumference and were more often of moderate length (3 to 6 mm) compared with culprit lesions without visible plaque rupture (p < 0.05). In conclusion, culprit lesions in patients with AMI contain more and smaller calcifications compared with adjacent segments. Calcifications related to plaque rupture appear to be larger and extend over a wider arc compared with these calcified spots. Those larger calcified spots may play a role in plaque instability in a subgroup of lesions.

Published 24 July 2006 in Am J Cardiol, 98(3): 309-13.
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