Role of compensatory enlargement and shrinkage in transplant coronary artery disease - Serial intravascular ultrasound study CIRCULATION Lim, T. T., Liang, D. H., Botas, J., Schroeder, J. S., Oesterle, S. N., Yeung, A. C. 1997; 95 (4): 855-859

Abstract

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.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 (delta IA) and TA (delta TA) between baseline and follow-up IVUS were compared: delta IA, 2.9 +/- 0.2 mm2: delta TA, 2.7 +/- 0.4 mm2. A remodeling index (RI) was defined as RI = delta TA/delta IA. Three subgroups could be distinguished: over compensation (RI > I), partial compensation (RI 0 to 1), and no compensation or shrinkage (RI < or = 0). Seventy-four segments (49%) showed overcompensation, 44 (29%) showed partial compensation, and 33 (22%) showed no compensation or shrinkage.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.

View details for Web of Science ID A1997WJ28200021

View details for PubMedID 9054742