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Systemic Up‐Regulation of Angiotensin II Type 1 Receptor in Cardiac Donors with Spontaneous Intracerebral Hemorrhage
Author(s) -
Yamani Mohamad H.,
Cook Daniel J.,
Tuzcu E. Murat,
Abdo Ashraf,
Paul Philip,
Ratliff Norman B.,
Yu Yang,
Yousufuddin Mohammad,
Feng Jing,
Hobbs Robert,
Rincon Gustavo,
BottSilverman Corinne,
McCarthy Patrick M.,
Young James B.,
Starling Randall C.
Publication year - 2004
Publication title -
american journal of transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.89
H-Index - 188
eISSN - 1600-6143
pISSN - 1600-6135
DOI - 10.1111/j.1600-6143.2004.00463.x
Subject(s) - medicine , intracerebral hemorrhage , spontaneous intracerebral hemorrhage , angiotensin ii , receptor , angiotensin ii receptor type 1 , cardiology , subarachnoid hemorrhage
Donor spontaneous intracerebral hemorrhage (ICH) is a potential risk factor for morbidity and mortality after cardiac transplantation. We hypothesized that donor ICH is associated with systemic up‐regulation of angiotensin II receptor type 1 (AT1R). We evaluated mRNA expression of AT1R and AT2R in donor spleen lymphocytes and in heart biopsies from 20 recipients of hearts from donors with spontaneous ICH which were compared with 20 recipients from trauma donors. Heart biopsies showed 4.7‐fold increased mRNA expression of AT1R (p < 0.0001) in the ICH group compared with the Trauma group. The ICH group also showed 2.6‐fold (p < 0.01) increased mRNA expression of AT1R in the donor spleen lymphocytes, suggesting the presence of systemic activation before transplantation. At 1 year, the ICH group had increased coronary vasculopathy by vascular ultrasound. Using multivariate regression analysis, mRNA expression of AT1R in the donor spleen lymphocytes was found to be a strong independent predictor of transplant vasculopathy (odds ratio = 4.397, CI = 1.243–15.553, adjusted p = 0.02). This is the first report to describe splenic up‐regulation of AT1R in the presence of spontaneous ICH and its association with subsequent development of transplant vasculopathy.