Rm. Mills et al., HEART-TRANSPLANT REJECTION WITH HEMODYNAMIC COMPROMISE - A MULTIINSTITUTIONAL STUDY OF THE ROLE OF ENDOMYOCARDIAL CELLULAR INFILTRATE, The Journal of heart and lung transplantation, 16(8), 1997, pp. 813-821
Citations number
15
Categorie Soggetti
Cardiac & Cardiovascular System",Transplantation,"Respiratory System
Background: The natural history of patients experiencing hemodynamic c
ompromise with rejection has been incompletely characterized, This mul
tiinstitutional study examined the outcome of such episodes, particula
rly with regard to the extent of cellular infiltrate on the index endo
myocardial biopsy, Methods: From January 1, 1990, through June 30, 199
4, 3367 patients in the Cardiac Transplant Research Database experienc
ed 4137 episodes of rejection. Severe hemodynamic compromise occurred
in approximately 5% of the rejection episodes, and this proportion rem
ained relatively constant over time. Results: Recipient risk factors f
or rejection with severe hemodynamic compromise included black race, f
emale recipient sex, and diabetes, The 3-month actuarial survival rate
was 60% after rejection with severe hemodynamic compromise versus 95%
after rejection with no or mild compromise. Low initial biopsy score
conferred a higher early survival, but a lower survival at 2 years aft
er rejection with severe hemodynamic compromise, Among patients who su
rvive an initial rejection episode with severe hemodynamic compromise,
survival at 2 years after an episode was 46% among those who had a lo
w initial biopsy score versus 84% with a high biopsy score, Conclusion
s: Rejection with hemodynamic compromise, although rare, represents a
major complication of heart transplantation with a poor long-term outc
ome, Survivors of hemodynamically compromising rejection episodes asso
ciated with low biopsy scores in the International Society for Heart a
nd Lung Transplantation grading system have a significantly worse long
-term outcome than survivors of episodes associated with high scores,
These findings suggest that immunologic mechanisms other than lymphocy
tic infiltration of the cardiac allograft are important and distinct c
auses of allograft dysfunction.