Abstract 18002: Coronary Collaterals Predict Improved Survival and Allograft Function in Patients with Coronary Allograft Vasculopathy
Coronary allograft vasculopathy (CAV) remains the most prevalent cause of allograft failure and cardiac mortality beyond the first year following heart transplantation. To date there are few proven therapies for this important disease. The presence of coronary collaterals has previously been demonstrated to impart a favorable prognosis in patients with ischemic heart disease. To determine whether the development of coronary collaterals is also associated with improved outcomes in patients with CAV, we performed a retrospective cohort study of all patients followed in the heart transplant clinic at Barnes Jewish Hospital between 1994 and 2008. The primary endpoint was the composite of all cause mortality, retransplantation, and inotrope dependence. LV end diastolic pressure and NYHA class served as surrogate measures of allograft function and heart failure symptoms. We screened 493 patients and identified 60 (13%) with moderate to severe CAV as defined by the International Society of Heart and Lung Transplantation. Coronary collaterals were present in 34 (57%) subjects. Patients with collaterals had a significantly lower risk of death, retransplanation, or inotrope dependence compared to patients without collaterals (OR 0.15, 95% CI 0.05-0.48, p= 0.002). In addition, patients with collaterals had lower LV end diastolic pressures and NYHA class. Multivariate analysis confirmed that the presence of collaterals independently predicted each of these outcomes. Immunohistochemical staining of biopsy specimens collected from patients with CAV revealed alterations in microvascular density that correlated with the presence of angiographically visible collaterals. Together these data demonstrate that the development of coronary collaterals predicts a favorable prognosis in patients with CAV and suggests that interventions aimed at promoting collateral growth may serve as effective therapies for this disease.
- © 2011 by American Heart Association, Inc.