Abstract 14736: Association of Periarterial Low-Echoic Appearance with Progression of Coronary Allograft Vasculopathy and Long-Term Clinical Outcomes in Heart Transplant Patients
Introduction: Pathologic reports have indicated that cell-mediated rejection after heart transplant can affect the cardiac structures beyond the myocardium and coronary arteries. In clinical IVUS examination, a distinctive appearance of periarterial low-echoic area (PLEA) surrounding the coronary artery is observed in a substantial fraction of heart transplant recipients. This study aimed to evaluate the potential impact of this finding on early progression of cardiac allograft vasculopathy and long-term clinical outcomes.
Methods: Serial IVUS was performed in 90 patients at early (1 month) and late (12 months) follow-up after heart transplantation. PLEA was defined as a low-echoic structure in the periarterial tissue with >1 mm in axial length, evaluated in the first 50 mm of the left anterior descending artery. The signal voids due to branches, veins, or myocardial bridging were excluded. The patients were stratified by the presence of acute-PLEA observed at 1 month and late-developed PLEA (late-PLEA) detected at 12 months.
Results: Overall, 32% of patients had acute-PLEA, 27% developed late-PLEA, and 6% had both acute- and late-PLEA. Acute-PLEA was related to greater intima at 1 month (p<0.01 for volume; p=0.01 for thickness), whereas late-PLEA was accompanied by greater intimal growth from 1 to 12 months (p<0.01 for volume and thickness). Consequently, patients with both acute- and late-PLEA showed the largest amount of intima at 12 months among the 4 patient groups. Despite no significant difference in the incidence of acute cellular rejection among the groups, the incidence of subsequent cardiac death tended to be higher in acute-PLEA groups, especially the group with both acute- and late-PLEA (Figure).
Conclusions: The periarterial low-echoic appearance observed by IVUS, potentially reflecting perivascular edema or inflammation, is related to progression of cardiac allograft vasculopathy and possibly to adverse events after heart transplantation.
Author Disclosures: H. Kitahara: None. K. Okada: None. H. Yang: None. H. Lim: None. K. Otagiri: None. S. Tanaka: None. Y. Kobayashi: None. P.G. Yock: None. A.C. Yeung: None. P.J. Fitzgerald: None. K.K. Khush: None. W.F. Fearon: None. Y. Honda: None.
- © 2014 by American Heart Association, Inc.