Role of Compensatory Enlargement and Shrinkage in Transplant Coronary Artery Disease
- 18 February 1997
- journal article
- research article
- Published by Wolters Kluwer Health in Circulation
- Vol. 95 (4) , 855-859
- https://doi.org/10.1161/01.cir.95.4.855
Abstract
Background Compensatory enlargement of the vessel wall has been described in the early stages of native atherosclerosis. Whether compensatory enlargement plays a role in transplant coronary artery disease is not known. The objective of this study was to determine, by use of serial intravascular ultrasound (IVUS), whether compensatory dilation occurs in transplant coronary artery disease over time. Methods and Results Seventy-five heart transplant recipients with 151 matched coronary segments were selected for the presence of intimal disease progression as detected by serial IVUS examinations 1 to 3 years apart. Intimal disease progression was defined as a >10% increase in intimal area (IA). IVUS catheter location in follow-up studies was verified angiographically in relation to branch vessels. Luminal area (LA) and total vessel area (TA) were measured at each site. Intimal area (IA=TA−LA) was calculated. Changes in IA (ΔIA) and TA (ΔTA) between baseline and follow-up IVUS were compared: ΔIA, 2.9±0.2 mm2; ΔTA, 2.7±0.4 mm2. A remodeling index (RI) was defined as RI=ΔTA/ΔIA. Three subgroups could be distinguished: overcompensation (RI >1), partial compensation (RI 0 to 1), and no compensation or shrinkage (RI ≤0). Seventy-four segments (49%) showed overcompensation, 44 (29%) showed partial compensation, and 33 (22%) showed no compensation or shrinkage. Conclusions In this study, serial IVUS shows that early after cardiac transplantation, a large proportion of the coronary segments with progression of intimal thickening have compensatory dilation of the vessel wall. However, a substantial number of coronary segments (22%) show no compensatory dilation or shrinkage. The progressive luminal narrowing in transplant patients may be due in part to vessel shrinkage or the lack of compensatory dilation over time.Keywords
This publication has 18 references indexed in Scilit:
- 935-32 Differing Mechanisms of Late Arterial Responses to Transcatheter Therapy: A Serial Quantitative Angiographic and Intravascular Ultrasound StudyJournal of the American College of Cardiology, 1995
- Focal compensatory enlargement of human arteries in response to progressive atherosclerosis. In vivo documentation using intravascular ultrasound.Circulation, 1994
- Differences in compensatory vessel enlargement, not intimal formation, account for restenosis after angioplasty in the hypercholesterolemic rabbit model.Circulation, 1994
- In vivo validation of compensatory enlargement of atherosclerotic coronary arteriesThe American Journal of Cardiology, 1993
- Intravascular ultrasound imaging of angiographically normal coronary arteries: An in vivo comparison with quantitative angiographyJournal of the American College of Cardiology, 1991
- Control of shear stress in the epicardial coronary arteries of humans: Impairment by atherosclerosisJournal of the American College of Cardiology, 1989
- Accelerated coronary vascular disease in the heart transplant patient: Coronary arteriographic findingsJournal of the American College of Cardiology, 1988
- Differential enlargement of artery segments in response to enlarging atherosclerotic plaquesJournal of Vascular Surgery, 1988
- Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factorNature, 1987
- Compensatory Enlargement of Human Atherosclerotic Coronary ArteriesNew England Journal of Medicine, 1987