Abstract

N studies have demonstrated asymmetric longitudinal and circumferential atherosclerotic plaque distribution along coronary arteries.1,2 In vivo data are limited and have primarily examined the left main artery bifurcation.3,4 In the proximal left anterior descending (LAD) artery, the wall opposite to the circumflex origin is a preferred site of plaque accumulation and is likely secondary to fluid dynamics near the bifurcation.5,6 It has been described that abnormally low or oscillatory shear forces at these sites contribute to atherogenesis.7 Assessment of plaque distribution in the proximal and mid-LAD artery has not been systematically described. Intravascular ultrasound (IVUS) is ideally suited to study distribution patterns of atherosclerotic plaque burden.8 Using a motorized pullback device that withdraws the IVUS catheter at a precisely controlled rate allows accurate mapping of the longitudinal and circumferential plaque patterns. In the present report, in vivo IVUS imaging was employed to examine plaque distribution in the LAD artery in relation to the first septal perforator in patients with mild coronary artery disease (CAD). • • • We analyzed IVUS studies in 50 patients with minimally obstructive CAD ( 50% angiographic diameter stenosis) of the native LAD artery. IVUS imaging was performed in standard fashion using either a 30-MHz, 3.2 or 2.9Fr catheter, or a 40MHz, 2.6Fr device (Cardiovascular Imaging Systems, Sunnyvale, California).9 The IVUS catheter was advanced over a guidewire to a position in the midto distal portion of the LAD artery after the administration of intracoronary nitroglycerin and anticoagulation with intravenous heparin. Motorized pullback at a rate of 0.5 mm/s was performed to the left main ostium with ultrasound images recorded on Super-VHS videotape. A long segment of the LAD artery pullback (20 to 60 seconds) was digitized from videotape into a 640 480-pixel image matrix with an 8-bit gray scale for each patient. The midpoint of the first septal perforator was identified on IVUS and angiographic images, and 7 serial cross-sectional slices were selected (midpoint of septal, 1, 2, and 3 mm proximally and distally) for a total of 350 cross sections (Figure 1). In each cross section, the vessel was divided into two 180° semicircles ipsilateral (septal) and contralateral (antiseptal) to the septal branch. In each semicircle, the external elastic membrane and lumen area were planimetered. Atheroma area (external elastic membrane lumen area) and maximum and minimum intimal thickness were calculated. All results are expressed as mean SD. Comparison of atheroma area and intimal thickness between the septal and antiseptal sides was performed using the paired, 2-tailed Student’s t test. A p value 0.05 was considered statistically significant. Fifty patients with mild coronary atherosclerotic disease of the LAD artery were included in the analysis. In the LAD artery segment adjacent to the first septal branch, mean atheroma area was substantially greater on the septal side than on the antiseptal side (3.44 1.6 vs 2.5 1.5 mm, p 0.0001). Mean intimal thickness on the septal side was also greater than the antiseptal side (1.03 0.48 vs 0.81 0.42 mm, p 0.0001; Table 1). This relation was evident for each of the 7 individual cross sections, and it was remarkably consistent throughout the cohort with 255 of 350 cross sections (73%; Figure 2). A distinctive pattern of longitudinal atheroma distribution was evident. At 3 mm proximal to the septal side, the plaque area on the septal side was much larger than that on the antiseptal side (3.69 1.8 vs 2.36 1.7 mm, p 0.0001). From a more distal position, the differences between septal plaque and the antiseptal side decreased progressively. At 3 mm distal to the septal side, the differences between the septal and antiseptal sides were the smallest (3.00 1.9 vs 2.45 1.5 mm, p 0.0086). Similar findings were noted for maximum atheroma thickness. At 3 mm proximal to the septal artery, the difference in plaque thickness between the septal and antiseptal sides was large (1.10 0.5 vs 0.76 0.4 mm, p 0.0001). The difference was smaller at a site 3 mm distal to the septal artery (0.93 0.5 vs 0.78 0.5 mm, p 0.0051). Figure 3 shows the plaque distribution (mean SD) adjacent to the first septal branch for the overall group. From The Cleveland Clinic Foundation, Cleveland, Ohio; and Yale University School of Medicine, New Haven, Connecticut. Dr. Nissen’s address is: The Cleveland Clinic Foundation, F 15, 9500 Euclid Avenue, Cleveland, Ohio 44195. E-mail: nissens@ccf.org. Manuscript received June 25, 2002; revised manuscript received and accepted October 11, 2002.

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