INFLUENCE OF PREEXISTENT DONOR CORONARY-ARTERY DISEASE ON THE PROGRESSION OF TRANSPLANT VASCULOPATHY - AN INTRAVASCULAR ULTRASOUND STUDY

Citation
J. Botas et al., INFLUENCE OF PREEXISTENT DONOR CORONARY-ARTERY DISEASE ON THE PROGRESSION OF TRANSPLANT VASCULOPATHY - AN INTRAVASCULAR ULTRASOUND STUDY, Circulation, 92(5), 1995, pp. 1126-1132
Citations number
35
Categorie Soggetti
Cardiac & Cardiovascular System",Hematology
Journal title
ISSN journal
00097322
Volume
92
Issue
5
Year of publication
1995
Pages
1126 - 1132
Database
ISI
SICI code
0009-7322(1995)92:5<1126:IOPDCD>2.0.ZU;2-V
Abstract
Background Transplant vasculopathy (TxCAD) limits long-term survival o f allograft recipients. The possibility that preexistent donor coronar y disease (PEDD) might accelerate this process is of concern. The seri al progression of sites with and without PEDD as assessed by intravasc ular ultrasonic imaging is explored in this study. Methods and Results Thirty patients with baseline intravascular imaging within 3 weeks of cardiac transplantation who had at least one annual follow-up study w ere included in this study. Vessel luminal area (LA), total area (TA), intimal index (II=TA-LA/TA), mean intimal thickness (MIT), and Stanfo rd classification were expressed for each image site and for each pati ent at each study. Progression of sites and of patients with and witho ut PEDD on the baseline study was compared. Patients with PEDD (n=9) s till had significantly more intimal disease than those without PEDD (n =21) at the first follow-up study (MIT=0.35+/-0.13 versus 0.13+/-0.11 mm; II=0.29+/-0.11 versus 0.11+/-0.1; class=3.7+/-0.5 versus 2.2+/-0.9 4; P<.001 for all comparisons). However, the increase in intimal thick ness during the 1- year interval was not significantly different betwe en the two groups. In 4 patients in whom both types of sites were pres ent, no difference in progression was found. Data were similar for pat ients and sites studied over >1 year. Conclusions PEDD doss not accele rate the progression of TxCAD within the first few years after cardiac transplantation. The pathophysiology of TxCAD is most likely immune m ediated and does not seem to be accelerated by native coronary artery disease.