Pr. Rickenbacher et al., CORONARY-ARTERY INTIMAL THICKENING IN THE TRANSPLANTED HEART - AN IN-VIVO INTRACORONARY ULTRASOUND STUDY OF IMMUNOLOGICAL AND METABOLIC RISK-FACTORS, Transplantation, 61(1), 1996, pp. 46-53
This study examined the hypothesis that immunologic factors are the ma
jor correlates of coronary artery intimal thickening and luminal steno
sis. The study population included 116 adult heart transplant recipien
ts with a mean age of 44.7 +/- 12.0 years (89 men and 27 women) underg
oing annual coronary angiography and intracoronary ultrasound 3.4 +/-
2.7 (range, 1.0-14.6) years after transplantation. Mean intimal thickn
ess was obtained from several distinct sites along the left anterior d
escending and/or left circumflex coronary artery by intracoronary ultr
asound. Coronary artery stenosis defined by angiography was classified
as mild (< 30% luminal stenosis), moderate (greater than or equal to
30-70% luminal stenosis), or severe (> 70% luminal stenosis or diffuse
pruning of distal vessels). Prevalence of any transplant coronary art
ery disease (TxCAD) was 85% by intracoronary ultrasound and 15% by ang
iography. By multiple regression analysis, only average fasting plasma
triglyceride level (P < 0.006) and average weight (P < 0.007) were si
gnificantly correlated with severity of intimal thickening (R = 0.54,
P < 0.0001). Donor age (P < 0.006) and average fasting plasma triglyce
ride level (P < 0.009) were significantly correlated with stenosis by
angiography. Correlation of multiple immunologic and metabolic factors
with intimal thickness by univariate analysis suggests a multifactori
al etiology for TxCAD. Among the multiple univariate correlates of TxC
AD, higher fasting plasma triglyceride levels and body weight are the
only independent correlates of TxCAD. The absence of acute rejection a
s an independent predictor of intimal thickening suggests that mechani
sms beyond those mediating typical cellular rejection should be target
ed for advancing our understanding of TxCAD.