Association of Arterial Expansion (Expansive Remodeling) of Bifurcation Lesions Determined by Intravascular Ultrasonography With Unstable Clinical Presentation

B of unique hemodynamic properties, vessel bifurcations are predisposed to early and eccentric plaque development. Early lesion development is associated with compensatory changes of the external elastic membrane (EEM) area, called arterial remodeling. However, angiographic and intravascular ultrasound (IVUS) studies have questioned whether remodeling occurs at vessel bifurcations. Recent studies in nonbifurcation lesions report that positive (expansive) arterial remodeling, defined as an expansion of the EEM area at atherosclerotic lesions, is associated with an unstable clinical presentation. We hypothesized that the absence of expansive remodeling at bifurcations found in previous clinical studies might have been related to inclusion of relatively stable patients. We therefore specifically compared remodeling of stable and unstable lesions at vessel bifurcations. • • • Preinterventional angiographic and IVUS images of 216 consecutive patients with isolated de novo coronary lesions in native vessels were screened. The examinations were performed between January 1993 and May 1998. Bifurcation lesions were identified by angiography as lesions involving the common vessel stem and both branches. IVUS pullback performed from 1 branch into the vessel stem typically shows a short segment of the other branch distal to the bifurcation. We compared the size of the 2 branches and included only lesions with branches of similar size. (Figure 1) We excluded lesions involving a vessel stem and a minor side branch. Twenty-four lesions at vessel bifurcations fulfilling the inclusion criteria were identified. Clinical data including age, gender, risk factors for coronary artery disease, and information about the clinical presentation were collected from the interventional database at our institution and from patient charts. The unstable group included patients with unstable angina (Canadian Cardiovascular Society class IV angina; new onset or changed pattern), or recent myocardial infarction ( 14 days). The stable group included patients with stable angina (Canadian Cardiovascular Society class I or II angina unchanged for 2 months). The IVUS imaging method used has been previously described. Briefly, a 30-MHz 3.5Fr monorail ultrasound catheter (Boston Scientific, Scimed Inc., Maple Grove, Minnesota) interfaced with a scanner (Hewlett-Packard, Andover, Massachusetts) was employed. After anticoagulation with heparin, intracoronary nitroglycerin was administered and the ultrasound catheter was placed over a guidewire beyond the target lesion site in the vessel branch with more severe disease. The ultrasound catheter was then withdrawn manually into the vessel stem during continuous imaging. The ultrasound images were recorded on 1/2-in SuperVHS videotape. A single operator blinded to the clinical presentation selected the target (culprit) lesion site and a proximal reference site. The culprit lesion was defined as the site with the minimal lumen diameter, which was always located in the branch. The proximal reference segment was chosen in the common stem as the site with the least amount of plaque. For each site, a short segment (10 to 20 seconds) of videotape was digitized at 30 frames/s into a 640 480 pixel image matrix with an 8-bit gray scale. At each selected site, the lumen and EEM areas were traced manually using the intimal leading edge boundary and the leading edge of the adventitia, respectively. The plaque area was calculated as the difference between lumen and EEM area. Percent cross-sectional narrowing (%CSN) was calculated as: