Abstract 16130: Early Invasive Assessment of the Coronary Microcirculation Predicts Subsequent Acute Rejection After Heart Transplantation
Background: Acute rejection plays an important role in the development of cardiac allograft vasculopathy (CAV) and long-term mortality after heart transplantation; therefore, more emphasis should be placed on characterizing clinical factors associated with subsequent acute rejection, especially focusing on early anatomic and physiologic measures.
Methods: This study enrolled 85 patients who underwent invasive physiology measurements (fractional flow reserve (FFR), coronary flow reserve (CFR) and the index of microcirculatory resistance (IMR)) and intravascular ultrasound (IVUS) in the left anterior descending artery at baseline (4-6 weeks post-transplant). Baseline right heart catheterization and echocardiography (left ventricular ejection fraction: LVEF) were also evaluated. Acute rejection was defined as acute cellular rejection of grade ≥2R and/or antibody-mediated rejection of grade ≥2.
Results: During the first year post-transplant, 28.3% of patients experienced acute rejection. Baseline values of IVUS indices, FFR and LVEF were not significantly different between patients with and without subsequent acute rejection, whereas baseline values of pulmonary capillary wedge pressure (16.6±5.4 vs. 13.3±5.8), CFR (2.8±1.0 vs. 3.8±1.8) and IMR (30.7±18.0 vs. 20.8±14.8) were significantly more abnormal in patients with subsequent acute rejection (p<0.05 respectively). There were also higher rates of recipient obesity (body mass index ≥25 kg/m2) and sirolimus use and a lower rate of anti-thymocyte globulin use in patients with acute rejection during the first year. In multivariate analysis, high baseline IMR value (≥15) was independently associated with subsequent acute rejection during the first year.
Conclusions: Elevated microvascular resistance (high IMR) early after cardiac transplantation is an independent determinant of subsequent acute rejection, suggesting that early measurement of IMR may improve risk stratification.
Author Disclosures: K. Okada: None. Y. Honda: None. H. Luikart: None. P. Yock: None. P. Fitzgerald: None. A. Yeung: None. H. Valantine: None. K. Khush: None. W. Fearon: None.
- © 2016 by American Heart Association, Inc.