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Incidence of non-cellular acute rejection in heart transplant recipients
88
Abstracts
The Journal of Heart and Lung Transplantation January 2002
regression(MLR) to identify which factors predicted long-term survival well. Results: A total of 623 adult HTxs were performed in the CsA era (1980 to May 2001). Five hundred forty one adults survived more than 6 months and 192 died between 6 months and 10 years. One hundred forty three survived more than 10 years and 40 of them died until May 2001. The survival rate at 10 years was 47.5%(Kaplan-Meier survival analysis). Two hundred thirty two adults who survived more than 6 months and died until May 2001 were the subject of MLR and the following factors were significantly correlated with survival time: recipient’s age and donor’s age (p⫽0.004 and 0.02). The following table shows comparisons between 2 groups. Initial immunosuppressive regimen after HTx was not significantly different between the 2 groups.
Reason for HTx Recipient’s age at HTx Donor’s age at HTx Race mismatch Ischemic time (min) Blood type mismatch Gender mismatch
Coronary disease Cardiomyopathy
AAR CI (1/min/m2) HR (beats/min) MAP (mmHg) LVEF (%)
Baseline
During HR
First FU
Last FU
0.21 ⫾ 0.42 3.49 ⫾ 0.91 87.0 ⫾ 12.48 128.35 ⫾ 23.27 0.58 ⫾ 0.09
0.56 ⫾ 0.79* 2.13 ⫾ 0.73* 99.5 ⫾ 15.7* 125.93 ⫾ 21.36 0.37 ⫾ 0.14*
0.26 ⫾ 0.55 2.59 ⫾ 0.72* 100.54 ⫾ 17.3* 124.33 ⫾ 17.97 0.45 ⫾ 0.12*
0.39 ⫾ 0.78 2.49 ⫾ 0.57* 98.7 ⫾ 16.7* 117.4 ⫾ 22.36 0.42 ⫾ 0.16*
One year survival post-HT was 26/33 (78.8%) and three year survival was 18/29 (62.0%).
Conclusions: Our data demonstrate that the incidence of SHR was as high as high as 15.9% in HT recipients. Although, once SHR was diagnosed, the aggressive augmentation of immunosuppression rapidly improved and sustained LV function in the majority of surviving HT recipients. *p⬍0.05 in comparison to baseline.
Group 0.5–10y (n ⴝ 192)
Group >10y (n ⴝ 143)
p
94
50.0% 45.3% 47.1 ⫾ 10.8 26.5 ⫾ 9.2 47.3% 148.1 ⫾ 50.5 29.3% 24.1%
34.3% 60.8% 41.4 ⫾ 11.6 24.7 ⫾ 8.2 22.6% 139.8 ⫾ 50.3 29.3% 18.9%
0.005 0.006 ⬍0.0001 0.07 0.002 NS NS NS
REGRESSION OF DONOR-TRANSMITTED ATHEROSCLEROSIS. EVIDENCE FROM SERIAL INTRAVASCULAR ULTRASOUND IMAGING S.A. Haji, M.H. Yamani, R.C. Starling, P. Schoenhagen, S.R. Kapadia, T.D. Crowe, J.B. Young, E.M. Tuzcu, Cardiology, Cleveland Clinic Foundation, Cleveland, OH
Conclusion: Long-term survival is common after HTx in the CsA era. The following are seen to be associated with long-term survival: underlying idiopathic cardiomyopathy, younger recipient or donor age, race match.
93 INCIDENCE OF NON-CELLULAR ACUTE REJECTION IN HEART TRANSPLANT RECIPIENTS J.P. Naour, K. Malinowska, B.A. Pisani, J.C. Mendez, R.C. Lichtenberg, J.A. Robinson, M.J. Stout, B.K. Foy, M. Bakhos, G.M. Mullen, Advanced Heart Failure/Heart Transplant Program, Loyola University Health System, Maywood, IL Background: Heart transplant (HT) recipients can experience hemodynamic compromise due to suspected acute allograft rejection without evidence of cellular rejection. This is commonly referred to as suspected “humoral” rejection (SHR) although the diagnostic criteria for this entity remain controversial. In such cases the positive response to augmented immunosuppression indeed suggests such a “humoral” mechanism. We wish to review our experience in treatment outcome of SHR. Methods: We retrospectively reviewed medical records of 264 HT recipients who underwent HT in our institution between 9/91 to 9/00. Thirty-three HT recipients were diagnosed and treated for SHR associated with hemodynamic compromise defined as a decline in CI by 25% from baseline, new wall motion abnormalities, restrictive abnormalities or cardiac arrest with proven tissue diagnosis. We evaluated parameters of hemodynamic compromise such as cardiac index (CI), heart rate (HR), mean arterial pressure (MAP) and left ventricular ejection fraction (LVEF) at baseline, during SHR, first follow-up and the most recent followup. Results: There were 73% men and 27% women with mean age of 48.8⫾13.6 (14-68) years. These 33 (12.5%) HT recipients experienced 42 (15.95) episodes of SHR with onset from 6 to 1855 days post-HT, and follow up from 4 to 2862 days post-SHR treatment.
Background: Previous serial studies of donor-transmitted atherosclerosis in transplant patients have demonstrated progression of these lesions. However, it is unclear if regression of donor atherosclerosis occurs. Methods: 55 patients had intravascular ultrasound studies at baseline (1 month) and 1 year after transplantation, using an automated pullback system. Lesions (maximum plaque thickness ⬎ 0.5mm) present at baseline examination of the LAD were defined as donor lesions and classified as diffuse (maximum plaque thickness ⬎ 0.5mm throughout the lesion and ⬎ 5 mm in length) or focal. Volumetric analysis was performed by manual measurements of evenly spaced images 1 mm apart. Lumen (L), vessel wall (EEM) and the plaque volumes (P ⫽ EEM-L) were measured in the donor lesions at baseline and in the corresponding matched segments at follow up examination and average changes were calculated. Progression and regression of donor lesions was defined as ⬎ 10% increase or decrease in plaque volume respectively. Results: 48 donor lesions (average length 7mm, range 3-27mm) were identified in 27/55 (49 %) patients consisting of both diffuse (54%) and focal (46%) lesions. At one year, 14 (29%) lesions showed progression (average plaque change ⫽ 2.34 ⫾ 1.14 mm3/mm). However, 16 (33%) lesions showed regression of the plaque (average plaque change ⫽ 1.08 ⫾ 0.41 mm3/mm). Regression of donor plaque was less dramatic than progression (maximum 39 % vs 140%). Regression of donor lesions was associated with shrinkage of vessel wall (in all but 2 lesions) which was significantly different from vessel wall changes seen in donor lesions showing progression (average EEM change ⫽ -2.65 vs 1.24 mm3/mm p⫽ 0.0006). Conclusion: Our results demonstrate that regression of donor transmitted atherosclerosis occurs in one-third of involved coronary sites and is associated with shrinkage of the vessel wall. 95 MILD CARDIAC ALLOGRAFT CORONARY DISEASE DOES NOT CHANGE THE PROGNOSIS OF PATIENTS AFTER HEART TRANSPLANTATION
Abstracts
The Journal of Heart and Lung Transplantation January 2002
regression(MLR) to identify which factors predicted long-term survival well. Results: A total of 623 adult HTxs were performed in the CsA era (1980 to May 2001). Five hundred forty one adults survived more than 6 months and 192 died between 6 months and 10 years. One hundred forty three survived more than 10 years and 40 of them died until May 2001. The survival rate at 10 years was 47.5%(Kaplan-Meier survival analysis). Two hundred thirty two adults who survived more than 6 months and died until May 2001 were the subject of MLR and the following factors were significantly correlated with survival time: recipient’s age and donor’s age (p⫽0.004 and 0.02). The following table shows comparisons between 2 groups. Initial immunosuppressive regimen after HTx was not significantly different between the 2 groups.
Reason for HTx Recipient’s age at HTx Donor’s age at HTx Race mismatch Ischemic time (min) Blood type mismatch Gender mismatch
Coronary disease Cardiomyopathy
AAR CI (1/min/m2) HR (beats/min) MAP (mmHg) LVEF (%)
Baseline
During HR
First FU
Last FU
0.21 ⫾ 0.42 3.49 ⫾ 0.91 87.0 ⫾ 12.48 128.35 ⫾ 23.27 0.58 ⫾ 0.09
0.56 ⫾ 0.79* 2.13 ⫾ 0.73* 99.5 ⫾ 15.7* 125.93 ⫾ 21.36 0.37 ⫾ 0.14*
0.26 ⫾ 0.55 2.59 ⫾ 0.72* 100.54 ⫾ 17.3* 124.33 ⫾ 17.97 0.45 ⫾ 0.12*
0.39 ⫾ 0.78 2.49 ⫾ 0.57* 98.7 ⫾ 16.7* 117.4 ⫾ 22.36 0.42 ⫾ 0.16*
One year survival post-HT was 26/33 (78.8%) and three year survival was 18/29 (62.0%).
Conclusions: Our data demonstrate that the incidence of SHR was as high as high as 15.9% in HT recipients. Although, once SHR was diagnosed, the aggressive augmentation of immunosuppression rapidly improved and sustained LV function in the majority of surviving HT recipients. *p⬍0.05 in comparison to baseline.
Group 0.5–10y (n ⴝ 192)
Group >10y (n ⴝ 143)
p
94
50.0% 45.3% 47.1 ⫾ 10.8 26.5 ⫾ 9.2 47.3% 148.1 ⫾ 50.5 29.3% 24.1%
34.3% 60.8% 41.4 ⫾ 11.6 24.7 ⫾ 8.2 22.6% 139.8 ⫾ 50.3 29.3% 18.9%
0.005 0.006 ⬍0.0001 0.07 0.002 NS NS NS
REGRESSION OF DONOR-TRANSMITTED ATHEROSCLEROSIS. EVIDENCE FROM SERIAL INTRAVASCULAR ULTRASOUND IMAGING S.A. Haji, M.H. Yamani, R.C. Starling, P. Schoenhagen, S.R. Kapadia, T.D. Crowe, J.B. Young, E.M. Tuzcu, Cardiology, Cleveland Clinic Foundation, Cleveland, OH
Conclusion: Long-term survival is common after HTx in the CsA era. The following are seen to be associated with long-term survival: underlying idiopathic cardiomyopathy, younger recipient or donor age, race match.
93 INCIDENCE OF NON-CELLULAR ACUTE REJECTION IN HEART TRANSPLANT RECIPIENTS J.P. Naour, K. Malinowska, B.A. Pisani, J.C. Mendez, R.C. Lichtenberg, J.A. Robinson, M.J. Stout, B.K. Foy, M. Bakhos, G.M. Mullen, Advanced Heart Failure/Heart Transplant Program, Loyola University Health System, Maywood, IL Background: Heart transplant (HT) recipients can experience hemodynamic compromise due to suspected acute allograft rejection without evidence of cellular rejection. This is commonly referred to as suspected “humoral” rejection (SHR) although the diagnostic criteria for this entity remain controversial. In such cases the positive response to augmented immunosuppression indeed suggests such a “humoral” mechanism. We wish to review our experience in treatment outcome of SHR. Methods: We retrospectively reviewed medical records of 264 HT recipients who underwent HT in our institution between 9/91 to 9/00. Thirty-three HT recipients were diagnosed and treated for SHR associated with hemodynamic compromise defined as a decline in CI by 25% from baseline, new wall motion abnormalities, restrictive abnormalities or cardiac arrest with proven tissue diagnosis. We evaluated parameters of hemodynamic compromise such as cardiac index (CI), heart rate (HR), mean arterial pressure (MAP) and left ventricular ejection fraction (LVEF) at baseline, during SHR, first follow-up and the most recent followup. Results: There were 73% men and 27% women with mean age of 48.8⫾13.6 (14-68) years. These 33 (12.5%) HT recipients experienced 42 (15.95) episodes of SHR with onset from 6 to 1855 days post-HT, and follow up from 4 to 2862 days post-SHR treatment.
Background: Previous serial studies of donor-transmitted atherosclerosis in transplant patients have demonstrated progression of these lesions. However, it is unclear if regression of donor atherosclerosis occurs. Methods: 55 patients had intravascular ultrasound studies at baseline (1 month) and 1 year after transplantation, using an automated pullback system. Lesions (maximum plaque thickness ⬎ 0.5mm) present at baseline examination of the LAD were defined as donor lesions and classified as diffuse (maximum plaque thickness ⬎ 0.5mm throughout the lesion and ⬎ 5 mm in length) or focal. Volumetric analysis was performed by manual measurements of evenly spaced images 1 mm apart. Lumen (L), vessel wall (EEM) and the plaque volumes (P ⫽ EEM-L) were measured in the donor lesions at baseline and in the corresponding matched segments at follow up examination and average changes were calculated. Progression and regression of donor lesions was defined as ⬎ 10% increase or decrease in plaque volume respectively. Results: 48 donor lesions (average length 7mm, range 3-27mm) were identified in 27/55 (49 %) patients consisting of both diffuse (54%) and focal (46%) lesions. At one year, 14 (29%) lesions showed progression (average plaque change ⫽ 2.34 ⫾ 1.14 mm3/mm). However, 16 (33%) lesions showed regression of the plaque (average plaque change ⫽ 1.08 ⫾ 0.41 mm3/mm). Regression of donor plaque was less dramatic than progression (maximum 39 % vs 140%). Regression of donor lesions was associated with shrinkage of vessel wall (in all but 2 lesions) which was significantly different from vessel wall changes seen in donor lesions showing progression (average EEM change ⫽ -2.65 vs 1.24 mm3/mm p⫽ 0.0006). Conclusion: Our results demonstrate that regression of donor transmitted atherosclerosis occurs in one-third of involved coronary sites and is associated with shrinkage of the vessel wall. 95 MILD CARDIAC ALLOGRAFT CORONARY DISEASE DOES NOT CHANGE THE PROGNOSIS OF PATIENTS AFTER HEART TRANSPLANTATION