Morphologic Differences of Vessel Wall at Sites of Focal and Diffuse Coronary Vasospasm by Intravascular Ultrasound(IVUS)

BACKGROUND AND OBJECTIVES: The coronary vasospasm has been shown to play an important role in the pathogenesis of not only variant angina but also ischemic heart disease in general, including other forms of angina pectoris, acute myocardial infarct, and sudden death. The angiographic features of coronary vasospasm are focal and diffuse patterns in clinical setting. We attempted to clarify the differences in vessel wall morphologic appearance between the sites of focal and diffuse vasospasm by intravascular ultrasound(IVUS). MATERIAL AND METHODS: We studied 23 patients(32 segments) with variant angina in whom coronary angiograms were normal and coronary spasm was documented by intracoronary injection of acetylcholine. Coronary spasm was defined as luminal diameter reduction > or = 90% compared with baseline coronary artery diameter. Focal spasm was defined if the length of spastic narrowing was less than 10mm. By IVUS, we observed atheromatous plaques in 32 spasm segments with either focal or diffuse vasospasm. We measured maximal intimal thickness, luminal cross-sectional area(CSA), and external elastic membrane-CSA in spasm sites. RESULT: When comparing maximal intimal thickness between focal (n=15) and diffuse vasospasm segments(n=17), there was significantly greater thickness at focal spasm segments(1.21+/-0.36mm vs. 0.70+/-0.23mm, P<0.001). The maximal plaque area was similar between two groups but tended to be greater in focal spasm segments(6.03+/-2.06mm2 vs. 4.92+/-2.59mm2, P=NS). When circular shaped factor(CSF : standardized index of eccentricity) was compared, focal spasm segments were greater than diffuse spasm segments(0.89+/-0.06 vs. 0.97+/-0.02, P<0.001). At the segments of focal spasm, remodeling index was greater compared to the segments of diffuse spasm(1.02+/-0.16 vs. 0.86+/-0.13, P<0.001). CONCLUSION: Focal spasm segments were more eccentric and had greater atheromatous plaque than diffuse spasm segments. Positive remodeling pattern was observed at the segments of focal spasm and negative remodeling pattern at the segments of diffuse spasm. There were morphologic differences of vessel wall appearance between focal and diffuse spasm sites.

Inhibition of Neointimal Hyperplasia by External Radiation in Rat Carotid Injury Model-The Possible Role of Intercellular Adhesion Molecule-1 and Vascular Cell Adhesion Molecule-1-

BACKGROUND AND OBJECTIVES: Despite significant improvement in the field of angioplasty, restenosis remains a major obstacle to the long-term success of the procedure. Radiation can effectively inhibit neointimal hyperplasia by causing the arrest of mitosis during cell division and limiting proliferation by reducing the number of regenerating clonal progenitors. Balloon injury could induce the cell adhesion molecule, ICAM-1 and VCAM-1, on SMCs and regenerating endothelial cells (ECs). ICAM-1 and/or VCAM-1 may play a role in the progression of neointimal hyperplasia induced by balloon injury and external radiation may effectively inhibit neointimal hyperplasia by attenuating their expression. The purpose of this study was to examine the effect of external radiation against ICAM-1 and VCAM-1 on neointimal hyperplasia after balloon injury in rat carotid arteries. MATERIAL AND METHODS: A standardized carotid balloon catheter arterial injury was produced in 51 rats and external beam radiation with doses from 5-20 Gy were delivered in 28 rats (radiation treated group) at 24 hours after injury. To investigate the effect of the external radiation on neointimal hyperplasia, the intima area and the intima/medial area of arteries were measured at day 14 after injury. The expressions of ICAM-1 and VCAM-1 at day 2, day 7, and day 10 after injury were studied in control group and radiation treated group by immunohistochemistry. RESULTS: Means of intimal area and intima/medial ratio in radiation treated group were significantly lower than those in control group and significantly reduced with increasing radiation dosage. At day 2 after injury, medial SMCs of injury group extensively expressed ICAM-1, while it was focally expressed with 10 Gy radiation treated group. At day 7 and day 10 after injury, ICAM-1 expression on medial SMCs was attenuated and neointimal ICAM-1 expression was increased. As compared with control group, ICAM-1 expression after radiation was weak and focal just around the internal elastic lamina. At 2 days after injury, medial SMCs moderately expressed VCAM-1, which was weakly and focally expressed with 10 Gy radiation treated group. At day 7 and day 10 after injury, focal expression of VCAM-1 was noted around the internal elastic lamina, but there was no VCAM-1 expression on neointima with radiation. CONCLUSION: External radiation after carotid arterial injury may potentially inhibit SMC proliferation and neointimal hyperplasia, and balloon injury-induced or upregulated expressions of ICAM-1 and VCAM-1 may be attenuated with external radiation.