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1.
Figure 6

Figure 6. From: MANAGEMENT OF ALLOSENSITIZED CARDIAC TRANSPLANT CANDIDATES.

Survival according to CDC crossmatch results in 636 cardiac transplant recipients between 1982 and 1992. (From Smith JD, Danskine AJ, Laylor RM, et al. Transplant Immunol 1993;1:60–65, with permission).

Mauricio Velez, et al. Transplant Rev (Orlando). ;23(4):235-247.
2.
Figure 8

Figure 8. From: MANAGEMENT OF ALLOSENSITIZED CARDIAC TRANSPLANT CANDIDATES.

Survival curve comparing patients that exhibit de novo anti-HLA Class II antibodies vs. patients without anti-HLA Class II antibodies. Patients who produce Class II antibodies have significantly worse survival (p=0.006). (From Tambur AR, Pamboukian SV, Constanzo MR, et al. Transplantation 2005;80:1019–1025, with permission).

Mauricio Velez, et al. Transplant Rev (Orlando). ;23(4):235-247.
3.
Figure 4

Figure 4. From: MANAGEMENT OF ALLOSENSITIZED CARDIAC TRANSPLANT CANDIDATES.

Effect of IgG anti-HLA Class I antibodies on waiting time to cardiac transplantation. In 37 allosensitized VAD recipients (△), presence of anti-HLA Class I IgG increased waiting time to cardiac transplantation compared with 18 non-sensitized VAD recipients (□)(p<0.001). (From John R, Lietz K, Burke E, et al. Circulation 1999;100(19 Suppl):II229-II235, with permission).

Mauricio Velez, et al. Transplant Rev (Orlando). ;23(4):235-247.
4.

Fig 5. From: MANAGEMENT OF ALLOSENSITIZED CARDIAC TRANSPLANT CANDIDATES.

Panel A shows the effect of IVIG therapy on reduction of serum anti-HLA Class I IgG alloreactivity. Maximal reduction in serum alloreactivity occurs within 1 week of IVIG therapy. Panel B shows the effect of plasmapheresis on anti-HLA Class I IgG alloreactivity. Maximal reduction in alloreactivity occurs 4 weeks after treatment. (From John R, Lietz K, Burke E, et al. Circulation 1999;100(19 Suppl):II229-II235, with permission).

Mauricio Velez, et al. Transplant Rev (Orlando). ;23(4):235-247.
5.
Figure 7

Figure 7. From: MANAGEMENT OF ALLOSENSITIZED CARDIAC TRANSPLANT CANDIDATES.

Intravascular ultrasound example of a de novo lesion of transplant vasculopathy. No lesions are shown at baseline examination (A). When the same site is identified on follow-up examination, significant intimal thickening is seen at that site (B). This lesion is defined as a de novo lesion of transplant vasculopathy. Note that this lesion is circumferential and non-eccentric. (From Kapadia SR, Nissen SE, Tuzcu EM. Curr Opin Cardiol 1999;14:140–150, with permission).

Mauricio Velez, et al. Transplant Rev (Orlando). ;23(4):235-247.
6.
Figure 2

Figure 2. From: MANAGEMENT OF ALLOSENSITIZED CARDIAC TRANSPLANT CANDIDATES.

PRA levels in VAD-supported versus non-supported cardiac transplant candidates. Patients who underwent VAD support before transplantation demonstrate an increase in 90th percentile (taller bar) and mean (the horizontal line within each bar) PRA levels when compared to non-VAD controls (p<0.0001) (From Joyce DL, Southard RE, Torre-Amione G, et al. J Heart Lung Transplant 2005;24:2054–2059, with permission).

Mauricio Velez, et al. Transplant Rev (Orlando). ;23(4):235-247.
7.
Figure 3

Figure 3. From: MANAGEMENT OF ALLOSENSITIZED CARDIAC TRANSPLANT CANDIDATES.

Increased levels of soluble CD40 ligand (CD40L) in the circulation of allosensitized left ventricular assist device (LVAD) recipients. Sensitized LVAD recipients had over eight-fold higher levels of serum CD40L when compared with either non-sensitized LVAD recipients, heart failure controls, or healthy volunteers. Results are expressed as the mean ± SEM of experiments using sera from 12 sensitized LVAD recipients, 10 non-sensitized LVAD recipients, 8 NYHA class IV heart failure controls, and 6 healthy volunteers. (From Schuster M, Kocher A, John R, et al. Human Immunology 2002;63:211–220, with permission).

Mauricio Velez, et al. Transplant Rev (Orlando). ;23(4):235-247.
8.
Figure 1

Figure 1. From: MANAGEMENT OF ALLOSENSITIZED CARDIAC TRANSPLANT CANDIDATES.

Mechanisms of action of ventricular assist devices. The volume displacement VAD (A) consists of a chamber or sac that fills and empties cyclically. A percutaneous driveline provides electrical power to a motor that moves a pusher plate up and down repeatedly, compressing the volume chamber and resulting in pulsatile blood flow. The backward regurgitation of blood flow is prevented by inflow and outflow valves. Some of these VADs feature a textured lining that promotes neo-intimal proliferation, and may be responsible for immune activation and allosensitization. The axial flow VAD (B) is smaller in size, and features a helical rotor that drives blood flow from the left ventricle into the ascending aorta. A percutaneous driveline provides electrical power to a motor that makes the impeller spin while levitating inside the pump with the use of electromagnetism. This mechanism provides continuous, non-pulsatile blood flow. (From Baughman KL, Jarcho JA. N Engl J Med 2007;357:846–849, with permission. Copyright ©2007 Massachussetts Medical Society. All rights reserved).

Mauricio Velez, et al. Transplant Rev (Orlando). ;23(4):235-247.

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