Bk. Julius et al., Incidence, progression and functional significance of cardiac allograft vasculopathy after heart transplantation, TRANSPLANT, 69(5), 2000, pp. 847-853
Background, Cardiac allofraft vasculopathy after heart transplantation le:l
ds to an accelerated form of atherosclerosis with mar ked and often diffuse
vessel wall changes that limit Long-term survival. Previous studies showed
contradictory results relating vessel wall changes to endothelial vasodila
tor response.
Methods. A total of 30 cardiac transplant recipients were studied 3, 12, an
d 24 months after heart transplantation. Coronary angiography was performed
at rest, during supine bicycle ergometry, and after 1.6 mg sublingual nitr
oglycerin. Coronary cross-sectional area (biplane coronary angiography) and
coronary artery wall changes (intravascular ultrasound) were assessed and
extent of intimal changes correlated to vasodilator responses to nitroglyce
rine and bicycle ergometry,
Results, Intravascular ultrrasound showed significant intimal thickening in
43, 64, and 58% of patients at 3, 12, and 24 months. Intimal thickening 3
months after transplantation was related to donor age (r=0.70, P<0.01) but
did not predict progression of disease that manifested itself angiographica
lly as a decrease in coronary cross-sect;iona]: area at 12 and 24 months (P
<0.005) and significant coronary stenosis in 12% of patients after 24 month
s. Endothelium-independent vasodilatation after nitroglycerin (33+/-15, 44/-20, and 43+/-24%) was normal. Endothelium-dependent, flow-induced vasodil
atation during exercise was decreased (14+/-11, 18+/-14, and 16+/-17%) but
did not correlate to intimal changes assessed by ultrasound.
Conclusions. The study confirms the high incidence of intimal thickening af
ter heart transplantation as assessed by intravascular ultrasound. Impaired
exercise-induced vasodilatation suggests diminished bioavailability of end
othelium-derived nitric oxide to physiological stimulation but the lack of
relationship between coronary wall changes and this functional impairment s
uggests intermittent and presumably reversible endothelial injury in graft
atherosclerosis.