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Circulation. 1992;86:64-70

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Circulation, Vol 86, 64-70, Copyright © 1992 by American Heart Association


ARTICLES

Contribution of localized calcium deposits to dissection after angioplasty. An observational study using intravascular ultrasound

PJ Fitzgerald, TA Ports and PG Yock
Cardiovascular Research Institute, University of California, San Francisco 94143.

BACKGROUND. Atherosclerotic plaque fracture and dissection of the arterial wall are frequent concomitants of the balloon angioplasty process. The composition and morphology of plaque within the vessel may be critical in determining the extent of plaque fracture and dissection during balloon angioplasty. To examine this potential association in the clinical setting, we studied patients with intravascular ultrasound imaging after balloon angioplasty. METHODS AND RESULTS. Forty-one patients were studied with intravascular ultrasound after angioplasty in both peripheral and coronary arteries. Ultrasound images representing the target lesion cross section were digitized, stored on computer, and analyzed off-line. The presence of intralesional calcium and the relative size of dissection for each lesion was computed. Thirty-one patients (76%) had ultrasound evidence of significant dissection or plaque fracture immediately after balloon dilation. In 23 of 31 (74%) of the lesions, the ultrasound scans showed significant localized calcium deposits within the plaque substance. In 87% of these cases, the dissections were adjacent to the calcific portion of the vessel wall. In addition, the relative size of dissections referenced to the neolumen area were significantly larger (p less than or equal to 0.002) in the calcified vessels (27.5 +/- 12.3%) compared with the size of the dissections in lesions without calcium (11.2 +/- 5.8%). CONCLUSIONS. The presence of calcium within the vessel wall appeared to be significantly associated with both the location and size of the dissected tissue arm from the vessel wall. These data suggest that localized calcium deposits have a direct role in promoting dissection, presumably by increasing shear stresses within the plaque.


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