Author + information
- Received February 4, 2000
- Revision received May 8, 2000
- Accepted July 10, 2000
- Published online November 15, 2000.
- Paul Wexberg, MDa,* (, )
- Mariann Gyöngyösi, MD, PhDa,
- Wolfgang Sperker, BSa,
- Katharina Kiss, MDa,
- Paul Yang, BSa,
- Ali Hassan, MDa,
- Gerard Pasterkamp, MD, PhD∗ and
- Dietmar Glogar, MD, FESCa
- ↵*Reprint requests and correspondence: Dr. Paul Wexberg, Division of Cardiology, Department for Internal Medicine II, University of Vienna, Währinger Gürtel 18-20, A-1090 Vienna, Austria.
The goal of this study was to investigate the association between the atherosclerotic arterial remodeling and the incidence of cardiac events after coronary interventions in patients with stable angina.
The local mode of de novo atherosclerotic remodeling is associated with plaque vulnerability and clinical symptoms. It may, therefore, reflect plaque morphology influencing the long-term outcome after coronary interventions.
Quantitative angiography and intravascular ultrasound were obtained in 244 patients with stable angina before and after single-vessel revascularization. On the basis of the lesion and the reference segment vessel size, patients were categorized into three groups (adaptive [AR], constrictive [CR] and intermediate [IR] remodeling). The lesion was analyzed for lumen, total vessel and plaque areas. Clinical follow-up was obtained at a mean period of 7.7 ± 3.7 months.
Patients with CR had a higher rate of in-hospital complications (10.9% vs. 2.9% and 2.7% in group CR vs. AR and IR, p = 0.035). In contrast, patients with AR had the highest rate of major adverse cardiac events (MACE) (44.3% vs. 25.5% in IR and 28.1% in CR, p = 0.024) with a predominance of revascularization at follow-up. Both target lesion restenosis (p = 0.036) and nontarget lesion de novo stenosis (p = 0.007) occurred more frequently in this group. Adaptive remodeling was a significant predictor of MACE in multivariate analysis.
Adaptive remodeling is associated with a higher rate of MACE, target lesion restenosis and nontarget de novo stenosis. This finding may be due to differential responses of the adaptively remodeled vessel to revascularization and a generally accelerated course of systemic atherosclerosis.
- Received February 4, 2000.
- Revision received May 8, 2000.
- Accepted July 10, 2000.
- American College of Cardiology