Risk Factor Analysis for the Major Hazards Following Heart Transplantation—rejection, Infection, and Coronary Occlusive Disease

Sharples, Linda D.; Caine, N; Mullins, P. A.; Scott, John; Solis, E.; English, T. A. H.; Large, Stephen; Schofield, Peter M.; Wallwork, J.

doi:10.1097/00007890-199108000-00012

Cited by 153 publications

(62 citation statements)

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“…CMV has been linked to the development of left ventricular dysfunction (293) and an increased incidence of graft atherosclerosis that is believed to be a manifestation of chronic rejection (144,171,229,292,415). However, a study of serial blood and endomyocardial tissue specimens from heart transplant recipients showed no association between acute rejection and the detection of CMV by using culture and a semi-quantitative PCR assay (46).…”

Section: Allograft Dysfunction and Rejectionmentioning

confidence: 99%

New Strategies for Prevention and Therapy of Cytomegalovirus Infection and Disease in Solid-Organ Transplant Recipients

Sia¹,

Patel²

2000

Clinical Microbiology Reviews

220

181

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Section: Allograft Dysfunction and Rejectionmentioning

confidence: 99%

New Strategies for Prevention and Therapy of Cytomegalovirus Infection and Disease in Solid-Organ Transplant Recipients

Sia¹,

Patel²

2000

Clinical Microbiology Reviews

220

181

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“…Transplant-associated arteriosclerosis, characterized by diffuse and concentric intimal thickening in blood vessels of the transplanted organ, is the major cause of graft failure after the first year of transplantation (1)(2)(3). Although the pathogenesis of this disease remains unclear, clinical and laboratory studies both indicate that transplant arteriosclerosis is a local, immune-mediated process involving an interaction between the recipient's mononuclear cells and cells of the donor vessel wall (4)(5)(6).…”

Section: Introductionmentioning

confidence: 99%

Donor MHC and adhesion molecules in transplant arteriosclerosis

Shi¹,

Feinberg²,

Zhang³

et al. 1999

J. Clin. Invest.

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Transplant-associated arteriosclerosis remains an obstacle to long-term graft survival. To determine the contribution to transplant arteriosclerosis of MHC and adhesion molecules from cells of the donor vasculature, we allografted carotid artery loops from six mutant mouse strains into immunocompetent CBA/CaJ recipients. The donor mice were deficient in either MHC I molecules or MHC II molecules, both MHC I and MHC II molecules, the adhesion molecule P-selectin, intercellular adhesion molecule (ICAM)-1, or both P-selectin and ICAM-1. Donor arteries in which ICAM-1, MHC II, or both MHC I and MHC II were absent showed reductions in neointima formation of 52%, 33%, and 38%, respectively, due primarily to a reduction in smooth muscle cell (SMC) accumulation. In P-selectin-deficient donor arteries, neointima formation did not differ from that in controls. In donor arteries lacking both P-selectin and ICAM-1, the size of the neointima was similar to that in those lacking ICAM-1 alone. In contrast, neointima formation increased by 52% in MHC I-deficient donor arteries. The number of CD4-positive T cells increased by 2.8-fold in MHC I-deficient arteries, and that of α-actin-positive SMCs by twofold. These observations indicate that ICAM-1 and MHC II molecules expressed in the donor vessel wall may promote transplant-associated arteriosclerosis. MHC I molecules expressed in the donor may have a protective effect.

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“…In coronary angiography, the incidence of cardiac allograft arteriosclerosis is between 6% and 18% at 1 yr, 23% at 2 yr, and 50% at 5 yr (4,5), with angiographic underestimation of this disorder in some patients (6). This phenomenon is probably due to several risk factors, such as humoral and cellular immune injury, hyperlipidemia, and infections (7)(8)(9)(10).…”

Section: Introductionmentioning

confidence: 99%

Cytomegalovirus infection enhances smooth muscle cell proliferation and intimal thickening of rat aortic allografts.

Lemström¹,

Bruning²,

Bruggeman³

et al. 1993

J. Clin. Invest.

131

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Inbred DA (AG-B4, RT1 a) and WF (AG-B2, RT1') rats were used as donors and recipients of aortic allografts. The recipient rats were inoculated i.p. either on day 1 (early infection) or on day 60 (late infection) with iOs plaque-forming units of rat cytomegalovirus (RCMV). The control rats were left noninfected. The presence of viral infection was demonstrated by plaque assays from biopsies of the salivary glands, liver, and spleen at sacrifice. The rats received 300 gCi 13H Ithymidine by i.v. injection 3 h before sacrifice, and the grafts were removed at various time points for histology, immunohistochemistry, and autoradiography. RCMV infection significantly enhanced the generation of allograft arteriosclerosis. Infection at the time of transplantation had two important effects. First, the infection was associated with an early, prominent inflammatory episode and proliferation of inflammatory cells in the allograft adventitia. Second, the viral infection doubled the proliferation rate of smooth muscle cells and the arteriosclerotic alterations in the intima. In late infection the impact of RCMV infection on the allograft histology was nearly nonexistent. RCMV infection showed no effect in syngeneic grafts. These results suggest that early infection is more important to the generation of accelerated allograft arteriosclerosis than late infection, and that an acute alloimmune response must be associated with virus infection, to induce accelerated allograft arteriosclerosis. RCMVinfected aortic allografts, as described here, provide the first experimental model to investigate the interaction between the virus and the vascular wall of the transplant. (J. Clin. Invest. 1993. 92:549-558.)

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Risk Factor Analysis for the Major Hazards Following Heart Transplantation—rejection, Infection, and Coronary Occlusive Disease

Cited by 153 publications

References 0 publications

New Strategies for Prevention and Therapy of Cytomegalovirus Infection and Disease in Solid-Organ Transplant Recipients

New Strategies for Prevention and Therapy of Cytomegalovirus Infection and Disease in Solid-Organ Transplant Recipients

Donor MHC and adhesion molecules in transplant arteriosclerosis

Cytomegalovirus infection enhances smooth muscle cell proliferation and intimal thickening of rat aortic allografts.

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