Background It is unclear to what extent the ＂Glagov phenomenon＂ occurs in transplant coronary artery disease （TCAD）. The objective of this study was to evaluate the relationship between intimal hyperplasia and com...Background It is unclear to what extent the ＂Glagov phenomenon＂ occurs in transplant coronary artery disease （TCAD）. The objective of this study was to evaluate the relationship between intimal hyperplasia and compensatory enlargement in TCAD. Methods Intravascular ultrasound imaging was performed on 190 cardiac transplant recipients at （1.4±0.6） months and again （12.1±0.7） months after cardiac transplantation. Studies 1 year apart were matched at 625 sites. There were 545 coronary artery sites that had an increase in intimal area 〉10% from baseline to one year, and this comprised the data set of the present study. Results At the first year, 91% of coronary artery sites with intimal growth had a total cross-sectional area stenosis ≤40%, but 38% of the sites showed a decrease of 〉10% in lumen area. Receiver operating characteristic curve demonstrated that the change in cross-sectional area stenosis cut-off level at year 1 was 8% with a sensitivity of 75% and a specificity of 82% in predicting lumen loss. At a total cross-sectional area stenosis of 20%, sensitivity was 65% with a specificity of 81% in predicting lumen loss. Conclusions In TCAD, vessel enlargement as a compensatory mechanism for plaque growth is generally inadequate. Instead of continued vessel expansion, luminal narrowing develops when there is more than 8% cross-sectional area filled with intimal hyperplasia. In distinction to native coronary artery atherosclerotic disease, the transition point in transplant vasculopathy where the lumen is diminished by increasing intimal growth, occurs at a lower threshold, 20% vs 40% of vessel crossectional area.展开更多
文摘Background It is unclear to what extent the ＂Glagov phenomenon＂ occurs in transplant coronary artery disease （TCAD）. The objective of this study was to evaluate the relationship between intimal hyperplasia and compensatory enlargement in TCAD. Methods Intravascular ultrasound imaging was performed on 190 cardiac transplant recipients at （1.4±0.6） months and again （12.1±0.7） months after cardiac transplantation. Studies 1 year apart were matched at 625 sites. There were 545 coronary artery sites that had an increase in intimal area 〉10% from baseline to one year, and this comprised the data set of the present study. Results At the first year, 91% of coronary artery sites with intimal growth had a total cross-sectional area stenosis ≤40%, but 38% of the sites showed a decrease of 〉10% in lumen area. Receiver operating characteristic curve demonstrated that the change in cross-sectional area stenosis cut-off level at year 1 was 8% with a sensitivity of 75% and a specificity of 82% in predicting lumen loss. At a total cross-sectional area stenosis of 20%, sensitivity was 65% with a specificity of 81% in predicting lumen loss. Conclusions In TCAD, vessel enlargement as a compensatory mechanism for plaque growth is generally inadequate. Instead of continued vessel expansion, luminal narrowing develops when there is more than 8% cross-sectional area filled with intimal hyperplasia. In distinction to native coronary artery atherosclerotic disease, the transition point in transplant vasculopathy where the lumen is diminished by increasing intimal growth, occurs at a lower threshold, 20% vs 40% of vessel crossectional area.
