PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY OF FOCAL CORONARY LESIONS AFTER CARDIAC TRANSPLANTATION

Citation
W. Vonscheidt et al., PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY OF FOCAL CORONARY LESIONS AFTER CARDIAC TRANSPLANTATION, The Clinical investigator, 71(7), 1993, pp. 524-530
Citations number
28
Categorie Soggetti
Medicine, General & Internal
Journal title
ISSN journal
09410198
Volume
71
Issue
7
Year of publication
1993
Pages
524 - 530
Database
ISI
SICI code
0941-0198(1993)71:7<524:PTCAOF>2.0.ZU;2-F
Abstract
Transplant coronary artery disease is the greatest impediment to long- term survival beyond the first year after cardiac transplantation. Tra nsplant coronary artery disease shows a heterogeneous angiographic app earance, but focal stenoses can occur alone or at least predominate. B ased on an angiographic indication 35 critical focal lesions causing n arrowing by 75% or more were treated by PTCA during 23 procedures in s even patients 18-84 months after cardiac transplantation. Three patien ts each underwent only one procedure and four underwent repeated proce dures [2, 3, 4 and 11, respectively). Primary success was achieved wit hout any complication in 35 of 35 lesions (100%). The mean degree of s tenosis was reduced from 86 +/- 9% to 28 +/- 17% (P<0.001). The rate o f restenosis was 18/29 (62%) at a mean of 4 months after angioplasty. Four patients are alive and free of adverse effects (symptoms, myocard ial infarction, repeated percutaneous transluminal coronary angioplast y, retransplantation) 16 +/- 10 months after their last angioplasty. O ne patient underwent a successful second heart transplantation 26 mont hs after the first angioplasty. Two patients died, 1 and 31 months aft er the last angioplasty. In conclusion, percutaneous transluminal coro nary angioplasty can be performed safely with an excellent primary suc cess rate in critical focal transplant coronary artery disease. The ra te of restenosis is higher than in native coronary artery disease. Lon g-term follow-up depends on the individually variable accelerated natu re of graft atherosclerosis.