TY - JOUR
T1 - Angiotensin II receptors from peritransplantation through first-year post-transplantation and the risk of transplant coronary artery disease
AU - Yousufuddin, Mohammed
AU - Cook, Daniel J.
AU - Starling, Randall C.
AU - Abdo, Ashraf
AU - Paul, Philip
AU - Tuzcu, E. Murat
AU - Ratliff, Norman B.
AU - McCarthy, Patrick M.
AU - Young, James B.
AU - Yamani, Mohamad H.
N1 - Funding Information:
A portion of the data in this study was presented for the 2003 Young Investigator Award in Physiology, Pharmacology, and Pathology of the American College of Cardiology, March 2003, Chicago, Illinois. This study was supported by a grant from AstraZeneca.
PY - 2004/5/5
Y1 - 2004/5/5
N2 - Objectives We evaluated whether the angiotensin II (Ang II) receptors from perioperation through one-year post-transplantation predict the transplant coronary artery disease (TCAD) progression. Background The role of Ang II receptors (type 1: AT1R; type 2: AT2R) in TCAD is uncertain. Methods We investigated 28 heart donors and the corresponding recipients. The levels of AT1R and AT2R messenger ribonucleic acid (mRNA) were examined in lymphocytes from the donor spleen and in the donor heart at one-week and one-year posttransplantation to determine their association with the progression of TCAD, measured as changes in maximal intimal thickness (CMIT) and plaque volume (CPV) by intravascular ultrasound (IVUS) examinations. Results The AT1R mRNA in lymphocytes from the donor spleen (CMIT: r = 0.73, p < 0.0001; CPV: r = 0.69, p < 0.0001) and in the donor hearts at one-week (CMIT: r = 0.52, p = 0.005; CPV: r = 0.56, p = 0.002) and at one-year (CMIT: r = 0.63, p < 0.0001; CPV: r = 0.43, p = 0.004) post-transplantation along with AT2R mRNA in the donor hearts at one-year post-transplantation (CMIT: r = 0.3, p < 0.0001; CPV: r = 0.53, p = 0.009) were univariate predictors, whereas AT1R mRNA in lymphocytes and in the donor hearts at one-year post-transplantation proved to be multivariate predictors of the progression of TCAD. Conclusions These data suggest a role for Ang II receptors in the pathogenesis of TCAD and support a novel concept that TCAD may have its origin in the donor per se and may be modulated by the recipient's inherent biological factors.
AB - Objectives We evaluated whether the angiotensin II (Ang II) receptors from perioperation through one-year post-transplantation predict the transplant coronary artery disease (TCAD) progression. Background The role of Ang II receptors (type 1: AT1R; type 2: AT2R) in TCAD is uncertain. Methods We investigated 28 heart donors and the corresponding recipients. The levels of AT1R and AT2R messenger ribonucleic acid (mRNA) were examined in lymphocytes from the donor spleen and in the donor heart at one-week and one-year posttransplantation to determine their association with the progression of TCAD, measured as changes in maximal intimal thickness (CMIT) and plaque volume (CPV) by intravascular ultrasound (IVUS) examinations. Results The AT1R mRNA in lymphocytes from the donor spleen (CMIT: r = 0.73, p < 0.0001; CPV: r = 0.69, p < 0.0001) and in the donor hearts at one-week (CMIT: r = 0.52, p = 0.005; CPV: r = 0.56, p = 0.002) and at one-year (CMIT: r = 0.63, p < 0.0001; CPV: r = 0.43, p = 0.004) post-transplantation along with AT2R mRNA in the donor hearts at one-year post-transplantation (CMIT: r = 0.3, p < 0.0001; CPV: r = 0.53, p = 0.009) were univariate predictors, whereas AT1R mRNA in lymphocytes and in the donor hearts at one-year post-transplantation proved to be multivariate predictors of the progression of TCAD. Conclusions These data suggest a role for Ang II receptors in the pathogenesis of TCAD and support a novel concept that TCAD may have its origin in the donor per se and may be modulated by the recipient's inherent biological factors.
KW - ACE
KW - ATR
KW - ATR
KW - Ang II
KW - CMIT
KW - CPV
KW - HBSS
KW - angiotensin II
KW - angiotensin II type 1 receptor
KW - angiotensin II type 2 receptor
KW - angiotensin-converting enzyme
KW - changes in maximal intimal thickness
KW - changes in plaque volume
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U2 - 10.1016/j.jacc.2003.11.060
DO - 10.1016/j.jacc.2003.11.060
M3 - Article
C2 - 15120813
AN - SCOPUS:2342436624
SN - 0735-1097
VL - 43
SP - 1565
EP - 1573
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 9
ER -